FCH, Communicable Diseases Syllabus (2020)

COLLEGE OF MEDICINE AND HEALTH SCIENCES
REPUBLIC OF RWANDA
MINISTRY OF EDUCATION
SCHOOL OF NURSING AND MIDWIFERY
MODULE NAME: FUNDAMENTALS OF COMMUNITY HEALTH
UNIT NAME: COMMUNICABLE DISEASES
YEAR OF STUDY: 1ST YEAR NURSING AND MIDWIFERY
ACADEMIC YEAR: 2015-2016
Content:1
4.1. General Information

4.1.1 Key terms
4. 1.2 Factors necessary for the existence of a communicable disease
4. 1.3 The host and infection
4. 1.4 Phases of an infectious illness evolution
4.1.5 Carrier of infection
4.1.6 Epidemiology of the infectious and parasitic illnesses
4.1.7 Principles of communicable disease control
4.1.8 Resistance to infectious diseases (immunity)

4.1.9 Symptomatology of infection or infectious syndrome
4.1.10 Classification of infectious diseases
4.1.11. General Principles of infection control
4. 2. Bacterial Diseases
4.2.1 Typhoid fever
4.2.2 Tetanus
4.2.3 Meningitis
4.2.4 Tuberculosis
FCH-- Communicable Diseases (2015-2016≈>2020)/j.p poly-. 1

4.2.5 Leprosy
4.2.6 Bacillary dysentery
4.2.7 Cholera
4.2.8 Syphilis
4.2.9 Chancroid (Soft sore)
4.2.10 Gonorrhoea
4.3. Parasitic diseases
4.3.1 Malaria
4.3.2 Amoebiasis
4.3.3 Giardiasis
4.3.4 Ascariasis
4.3.5 Hookworm
4.3.6 Trichomoniasis
4.3.7 Bilharziosis (Schistosomiasis)
4.3.8 Trypanosomiasis
4.3.9. Tapeworm (Taeniasis)
4.3.10 Filariosis
4.3.11 Trichiuriasis
4.3.12 Pinworm
4.4. Viral diseases

4.4.1 Introduction to viruses
4.4.2 Viral diseases
4.4.2.1 HV.IV/AIDS
4.4.2.2 Acute coryza (common cold or cold)
4.4.2.3 Influenza or flu
4.4.2.4 Chichenpox
4.4.2.5 Shingles /zona/zoster/herpes zoster
4.4.2.6 Viral hemorrhagic fevers
4.4.2.6.1 Ebola
4.4.2.6.2 Marburg virus
4.4.2.6.3 Lassa fever
4.4.2.7 Yellow fever

4.4.2.8 Herpes simplex virus infections
4.4.2.9 Rabies
4.4.2.10 Poliomyelitis
4.4.2.11 Infectious mononucleosis/Epstein-Barr virus infection/ “the kissing disease”
4.4.2.12 Cytomegalovirus infection
4.5. Fungal diseases

4.5.1 Candidiasis
4.5.2 Pityriasis V.Versicolor or tinea V.Versicolor
4.5.3 Dermatophyties
4.5.4 Cryptococcosis
4.5.5 Aspergillosis
CHAPTER I. INTRODUCTION TO COMMUNICABLE DISEASES
I.1 DEFINITIONS OF KEY TERMS
Infection: Invasion by and multiplication of pathogenic microorganisms (bacteria, fungi,

viruses, parasites,…) in a bodily part or tissue, which may produce subsequent tissue injury
and progress to overt disease through a variety of cellular or toxic mechanisms.
Communicable disease is a disease that can spread from one person to another or from animals
to people.
Disease: A change away from a normal state of health to an abnormal state in which health is
diminished. This means that an infection (growth and multiplication of pathogens) causes a
disease.
Sign: A sign is an objective change in body function that may be observed and measured by
an individual in addition to the patient’s feelings.
Symptom: A symptom is a change in body function felt by the patient.

Sequelae: Residual effects of the disease process.
Syndrome: A collection of signs and symptoms characterizing a disease or an abnormality.
Etiology: the cause of a disease or abnormal condition; or a branch of medical science

concerned with the causes and origins of diseases.
Koch's postulates (as addressed in 1800s):
They are used particularly for demonstration that a specific pathogen is the cause of a
specific disease.
a. The microorganism or other pathogen must be present in all cases of the disease
b. The pathogen can be isolated from the diseased host and grown in pure culture
c. The pathogen from the pure culture must cause the disease when inoculated into a healthy,
susceptible laboratory animal
d. The pathogen must be reisolated from the new host and shown to be the same as the
originally inoculated pathogen
Pathophysiology:
✔ The functional changes associated with or resulting from disease or injury.

✔ The study of such changes. It is also known as physiopathology.
Pathogenesis: The development of morbid conditions; more specifically the cellular events
and reactions and other pathologic mechanisms occurring in the development of a disease.
Pathogenecity: The ability of a microbe to cause disease.
Virulence: The degree of pathogenicity in a microorganism.
Acute infection: An infection characterized by sudden onset, rapid progression, and often with
severe symptoms.
Chronic infection: An infection characterized by delayed onset and slow progression.

Primary infection: An infection that develops in an otherwise healthy individual.
Secondary infection: An infection that develops in an individual who is already infected with
a different pathogen.
Localized infection: An infection that is restricted to a specific location or region within the
body of the host.
Systemic infection: An infection that has spread to several regions or areas in the body of the
host
Opportunistic infection: An infection caused by microorganisms that are commonly found in

the host’s environment. This term is often used to refer to infections caused by organisms in
the normal flora.
Contagious disease: A communicable disease that is easily spread from one individual to
another.
Noncommunicable disease: A disease that is not transmitted from one individual to another
Reservoir of infection: An organism in which a parasite lives and develops without damaging
it, but from which the parasite passes to another species that is damaged by it. Carrier: An
individual who carries an infectious agent without manifesting symptoms, yet who can transmit
the agent to another individual.
Fomites: Any inanimate object capable of being an intermediate in the indirect transmission
of an infectious agent.
Direct mechanisms of disease transmission: Directly from person to person
Examples:
Direct skin contact, Airborne (Aerosols)
Indirect mechanisms of disease transmission: By the intermediate agents or objects.

Examples:
Food and Waterborne transmission; Fomites; Animal vectors
Parasite: it is an organism that lives in or on a second organism, called a host, usually causing
it some harm. A parasite is generally smaller than the host and of a different species.
Many parasites do not cause diseases. Parasitic diseases can affect practically all living
organisms, including plants and mammals.
Parasitology: The study of parasitic diseases
Infestation: parasitic attack or subsistence on the skin and/or its appendages, as by insects,
mites, or ticks; sometimes used to denote parasitic invasion of the organs and tissues, as by
helminths.
I.2 FACTORS NECESSARY FOR THE EXISTENCE OF A COMMUNICABLE

DISEASE
The presence of a particular communicable disease in an area at a certain time depends on

three main factors:
a) Agent of a disease: a living organism that causes the disease e.g. bacteria, a virus,
parasite…
b) The host: a human or animal in which or on which an infectious agent lives and
develops.
c) The environment: consisting of the various elements surrounding a person.
The three factors interact in a triangular manner as follows:
Environment
Agent Host

The agents must be present in a suitable environment helping them to grow and multiply, spread
and infect other hosts. If the agents do not succeed to grow, multiply and spread, they die out.
Hosts can change the environment and thus eliminate the source of the infection, for example
by sanitation, personal hygiene, or treating the sick people. The environment can be changed
so that it doesn’t support the multiplication of the disease agent.
The environment brings the host and the agent together. The environment influences the agent,
the host, and the route of transmission of the agent from a source to the host.
The above triangle is called epidemiologic triangle or triad which is a traditional model of
infectious disease causation.
I.3 THE HOST AND INFECTION
1. DEFINITIVE HOST
This is a host in which the adult or sexually mature forms of a parasite are found e.g. Humans
in schistosomiasis, Anopheles mosquito in malaria.
2. INTERMEDIATE HOST
This is the host in which only immature forms of the parasite are found e.g. snails in
schistosomiasis, humans in plasmodium (causal agent of malaria).
NB. Definitive and intermediate hosts are terms used when there is an indirect life cycle of the
infectious agent.
E.g. Parasite like plasmodium requires two hosts: a human and Anopheles mosquito
3. SUBCLINICAL INFECTION
This is an infection that has not yet shown the clinical symptoms of the disease. The infection
can be detected by the laboratory diagnosis and not by the clinical symptoms. In some diseases,
the decline in the immunity status of the host causes the subclinical infection to become active
and symptoms appear e.g. Tuberculosis.
4. CLINICAL INFECTION

This is an infection that shows the clinical symptoms of the disease.
I.4 PHASES OF AN INFECTIOUS ILLNESS EVOLUTION
Any infectious disease develops into five distinct phases. The duration of each phase varies
from one disease to another. These phases are the following:
A. THE INCUBATION PHASE
This is the time between penetration of the pathogen in the body of the receptive host and the
onset of clinical signs of disease.
It is that period in which the germ will grow, reproduce, produce toxins and acquire skills that
will enable it to cause disease and show clinical signs.
The duration of the incubation period depends on:
✔ The amount of absorbed or inoculated germs

✔ The speed of propagation
✔ The distance between the gateway and the preferred site for the proliferation of germs
B. INVASION PHASE
This is the stage of embryo transport after multiplication and reproduction at the site of
entrance via blood or lymph to the target organ of infection or spread throughout the body.
The period of invasion is characterized by the appearance of non specific clinical signs,
prodromes of fever, malaise, fatigue.
C.THE STATE PERIOD OR PHASE
This is the period of onset of specific clinical manifestations and disease-specific response to
physiological and biological target organs caused by the pathogen. It is during this period that
the clinical diagnosis of the disease is made.
D. DEFERVESCENCE PHASE OR PERIOD

This phase is characterized by the gradual reduction of the intensity of the disease and the
gradual disappearance of clinical symptoms.
E. THE CONVALESCENT PHASE OR PERIOD
This is the phase of restoration of function and morphology of organs. No signs and symptoms
of the disease.
I.5 CARRIER OF INFECTION
This is a person who harbors the agent and disseminates subclinical infections.
⮚ TYPES OF CARRIERS OF DISEASES
1. Incubating carrier: this is a person in the incubation period of a disease before clinical
symptoms appear. E.g: HIV, Measles
2. Convalescent carrier: this is a person who continues to harbour the infection after recovery
from the disease (after disappearance of the clinical symptoms). E.g. 3% of people who recover
from typhoid and are not showing the clinical signs of the disease remain carriers for 5 months
(after recovery).
3. Temporary carrier: this is a person remaining a carrier for less than 3 months.
4. Chronic carrier: this is a person remaining a carrier for three months or more.
I.6 EPIDEMIOLOGY OF THE INFECTIOUS AND PARASITIC DISEASES
A. TRANSMISSION CYCLE OF AN INFECTIOUS AGENT
The transmission cycle is the way an infectious agent grows, multiplies and spreads.
Usually humans are an integral part of the transmission cycle as well as being the main
reservoirs. E.g.: malaria or schistosomiasis.
Cows are reservoirs for brucellosis, dogs are reservoirs for rabies, and the soil is a reservoir for
a few infectious agents (e.g. tetanus).

Three parts of the transmission cycle of an infectious agent include: Source of infection,
transmission route and susceptible host.
Transmission route Susceptible host
Source of infection
1. SOURCES OF INFECTIOUS DISEASES
● The sick person or healthy carriers

● Animals e.g.: rabies virus in dogs
● Soil: tetanus.
● Object from where the infectious agent comes from to the host e.g. water, food,
materials….
● Reservoirs of infection
2. TRANSMISSION ROUTE
This is the way the infectious agent is transferred from source (i.e. person, animals, and soil)
to the susceptible host.
The main routes of transmission of communicable diseases are:
1. Direct contact (skin, mucous membrane or sexual) e.g. syphilis, gonorrhea….
2. Vector e.g. malaria
3. Faecal contamination of soil, food and water which is ingested. It is also called faecal-
oral route e.g. cholera, typhoid…
4. Contact with animals and their products
5. Air (inhalation) e.g. tuberculosis, measles,…
6. Transplacental (during pregnancy). E.g. toxoplasmosis, syphilis
7. Blood contact (injection, surgery, blood transfusion). E.g. HIV,…
On the basis of routes of transmission, common communicable diseases can be conveniently

classified as follows:
a. Water washed diseases E.g. scabies
b. Sexually transmitted diseases or infections (STI). E.g. gonorrhea, syphilis
c. Waterborne disease. E.g. cholera

d. Airborne diseases. E.g. meningitis
e. Vectorborne diseases. E.g. malaria
f. Water based diseases. E.g. bilharziasis
g. Zoonotic diseases or Zoonoses: these are diseases that are transmitted to humans by
animals. E.g rabies, trypanosomiasis, anthrax…
h. Faecal-oral diseases. E.g. Ascariasis, staphylococcal food poisoning,etc
N.B. Some diseases can be transmitted through more than one route. E.g. Syphilis by sex or
contact with infective clothes (even if the latter route is rare).
3. SUSCEPTIBLE HOST
A susceptible host is an individual who has low resistance to the particular infection.
Low resistance may be due to the fact that:
*The person has not been infected before by the infectious agent, and therefore doesn’t have
any immunity for it. E.g. measles
*If the person has not been actively immunized
*The person has another serious illness. E.g. AIDS at the same time, whereby such people have
a high risk of developing other disease such as Tuberculosis
*The body is malnourished thereby making the infection worse.
B. MODES OF TRANSMISSION OF AN INFECTIOUS DISEASE
There are two modes of transmission:
✔ Direct transmission: there is immediate transfer of the agent from a reservoir to a susceptible
host by direct contact or droplet spread.
✔ Indirect transmission: in indirect transmission an agent is carried from a reservoir to a

susceptible host by suspended air particles or by animate (vector) or inanimate (vehicle)
intermediaries.

A vector: an insect in which the germ develops and undergoes transformations. E.g. arthropods
such as mosquitoes, flies, ticks….
N.B. The vector may carry the agent through purely mechanical means. E.g.: Flies carry
shigella and deposit the agent on the skin of a new host. In mechanical transmission, the agent
doesn’t multiply or undergo physiologic changes in the vector.
A vehicle: a support which carries mechanically an agent. E.g.: water, food, hands,
contaminated objects, biologic products (blood), handkerchiefs, etc
Thus, indirect transmission may be: Airborne, Vehicleborne, Vectorborne, Mechanical indirect
transmission
Airborne transmission is by particles that are suspended in air. Two types of those particles are
dust and droplet nuclei (the residue of dried droplets). The nuclei are less than 5 microns in
size and may remain suspended in the air for long periods, may be brown over great distances,
and are easily inhaled into the lungs and exhaled.
Tuberculosis, for example is believed to be transmitted more often indirectly, through droplet
nuclei, than directly, through droplet spread.
C.CHAIN OF SPREAD OF COMMUNICABLE DISEASES
The epidemiologic triad illustrates that infectious diseases result from the interaction of the
agent, host and environment.
More specifically, transmission occurs when the agent leaves its reservoir or host through a
portal of exit, and is conveyed by some mode of transmission, and enters through an appropriate
portal of entry to infect a susceptible host. This is sometimes called the CHAIN OF
INFECTION.
⮚ PORTAL OF EXIT
It is the pathway by which an agent leaves the source host. The portal of exit usually
corresponds to the site at which the agent is localized.
Thus, the tubercle bacilli and influenza viruses exit through the respiratory tract,
schistosomes through urine, vibrio cholerae in feces, sarcoptes scabiei in skin lesions.

Some blood borne agents can exit by crossing the placenta (syphilis...), blood-sucking
arthropods (malaria).
⮚ PORTAL OF ENTRY
An agent enters a susceptible host through a portal of entry. Often, organisms use the same
portal to enter a new host that they use to exit the source host. Portal of entry may be:
o The skin and mucous membranes, cuts, natural orifices (skin hair, sebaceous glands,…)
.E.g.: Staphylococcus
o Respiratory tract. E.g.: Meningococcus, tuberculosis bacilli,…
o Digestive tract. E.g. : S.typhi, shigella, vibrio cholerae, poliomyelitis virus.
o Genital tract. E.g.: STIs, post abortion septicemia, hepatitis B,..
o Accidental ways: during therapeutic maneuvers (injection with non sterile needles,
transfusion, venous puncture, lack of asepsis,..).
⮚ RESERVOIR
The reservoir of an agent is the habitat in which an infectious agent normally lives, grows and
multiplies and from which it can be transmitted to susceptible hosts.
Reservoirs include humans, animals and environment.
The reservoir may or may not be the source from which an agent is transferred to a host.
Human reservoirs
Two types of human reservoir are:

✔ Persons with symptomatic illness
✔ Carriers
Animal reservoirs

✔ In case of zoonoses, diseases that are transmitted from animals to humans, reservoirs
are: Cows and pigs for brucellosis; sheep for anthrax; rodents for plague; dogs for
rabies.
✔ Another group of diseases with animal reservoirs are those caused by parasites that have
complex life cycles, with different reservoirs at different stages of development such as
malaria (requiring mosquitoes) and schistosomiasis (requiring fresh water snails).
Environmental reservoirs
✔ Plants, soil, and water in the environment are also reservoirs for some infectious agents.
E.g. Soil for hookworm, Legionnaires’ bacillus lives in pools of water
D. DEFINITIONS OF SOME TERMINOLOGICAL TERMS OF EPIDEMIOLOGY
1. ENDEMIC DISEASE
This is a disease that causes almost a constant number of people to become sick all the time
when there is balance between agent, host and environment.
2. EPIDEMIC DISEASE
This is a disease that causes a larger number of cases of the disease to occur than expected for
a given time and place as a result of shifting the balance in favor of the disease agent.
3. PANDEMIC DISEASE
This is an epidemic which has become worldwide in distribution.
E.g.: AIDS
4. SPORADIC DISEASE
This is a disease that has isolated cases of the disease in various and scattered places.

I.7 PRINCIPLES OF COMMUNICABLE DISEASE CONTROL
Control of communicable diseases is the management of communicable diseases involving

both trying to protect the people from getting the disease (i.e. prevention) and looking after
people who have the disease (i.e. case management including treatment).
Therefore control of communicable disease can be achieved by:
i. Attacking the source

ii. Interrupting the route of transmission
iii. Protecting the host
This table shows main methods of communicable disease control
Attacking the source Interrupting transmission Protecting the host

● Treatment ● Environmental ● Immunization
● Isolation sanitation ● Chemoprophylaxis
/Quarantine ● Personal hygiene and ● Personal protection
● Reservoir control behavior change ● Better nutrition
● Notification ● Vector control
● Screening and ● Disinfection and
Surveillance Sterilization
Difference between isolation and quarantine
Quarantine; this is the limiting of movement of apparently healthy persons (but who have
been exposed to a communicable disease) for the length of time equal to the incubation
period to prevent contact with those not yet exposed.
Isolation of persons with a disease is to keep them away such they do not come into close
contact with other people except those who are providing care, in order to prevent the spread
of the infectious agent.

I.8 PROCEDURES FOR INVESTIGATION, MANAGEMENT AND CONTROL OF
EPIDEMICS
Investigation, management and control activities are carried out immediately and concurrently
as soon as an outbreak is reported.
The investigation team must be formed to work together and should consult higher authorities/
experts on major findings and strategies to be taken. The team must include a clinician, a
laboratory technologist, a public health expert and nurses.
The team should carry out the following 10 main activities which are also the purpose of the
investigation, management and control of the epidemics:
1. Verify and confirm that the outbreak is present through communication with local
people and medical staff; and checking medical records and laboratory results in health
facilities
2. Confirm the nature of the disease through data detailed examination of affected
individuals
3. Manage all cases according to standard treatment guidelines and as close to the site of
outbreak as possible. DO NOT REFER PATIENTS!!!!
4. Determine the extent of the outbreak. Find out the numbers of patients affected and then
specific population groups affected (e.g. age groups, sex, occupation, etc)
5. Determine the source and mode of transmission of disease through examination of
contacts (people close to the sick)
6. Determine areas and persons at risk
7. Control the epidemics by using appropriate strategies (e.g.: cleaning and protecting
sources of water, improving sanitation, treating contacts, immunization, public health
education)
8. Communicate with the community and authorities about the results of the investigation
and control measures
9. Educate the community and train health workers to prevent future outbreaks and to
ensure a rapid appropriate response in the future
10. Continue with surveillance after the epidemics has been controlled, in order to monitor
the level of the disease in the population, and detect a rise in the number of cases as
early as possible

I.9 RESISTANCE TO INFECTIOUS DISEASES (IMMUNITY)
Resistance to infectious disease is called immunity. Humans have or can develop immunity to
some diseases.
IMMUNITY: is a biological term that describes a state of having sufficient biological defenses
to avoid infection, disease, or other unwanted biological invasion.
Immunity involves both specific and non-specific immunity
1. NON-SPECIFIC IMMUNITY
It acts either as barriers or as eliminators of wide range of pathogens irrespective of antigenic

specificity (no antigen-antibody reaction).
E.g. skin barriers and mucosal immunity
The skin cannot be penetrated by most organisms unless it already has an opening such as a
scratch or a cut.
Mechanically, pathogens are expelled from the lungs by ciliary action; coughing and sneezing
eject both living and non-living things from the respiratory system; tears, saliva and urine also
force out pathogens. Sticky mucus in respiratory tract traps many microorganisms. Acid Ph
<7.0 of skin secretions inhibits bacterial growth. Hair follicles secrete sebum that contains
lactic acid and fatty acids both of which inhibit the growth of some pathogenic bacteria and
fungi. This is the reason why areas of the skin not covered with hair, such as the palms and
soles of the feet, are most susceptible to fungal infections (E.g.: athlete’s foot).
Saliva, tears, nasal secretions and perspiration contain lysozyme, an enzyme that destroys gram
positive bacterial cell walls causing cell lysis.
Spermine and zinc in semen destroy some pathogens.
Lactoperoxidase is a powerful enzyme found in mother’s milk.
2. SPECIFIC IMMUNITY
There is antigen-antibody reaction.
⮚ CLASSIFICATION OF SPECIFIC IMMUNITY
A. PASSIVE IMMUNITY

Passive immunity is the transfer of active immunity in the form of ready-made antibodies, from
one individual to another. It can occur:
✔ Naturally, when maternal antibodies are transferred to the fetus through the placenta.
✔ Artificially, when high levels of human antibodies specific for a pathogen or toxin are
transferred to non-immune individuals.
Passive immunization is used when there is a high risk of infection and insufficient time for
the body to develop its own immune response, or to reduce the symptoms of ongoing or
immunosuppressive diseases.
Passive immunity provides immediate protection, but the body doesn’t develop memory,
therefore the patient is at risk of being infected by the same pathogen later.
● Naturally acquired passive immunity
Maternal antibodies are passed through the placenta to the fetus by a receptor on placental cells.
This occurs around the third month of gestation. IgG is the only antibody that can pass through
the placenta.
This immunity can also be provided through the transfer of IgA antibodies found in breast milk
that are transferred to the gut of the infant, protecting against bacterial infections until the new
born can synthesize his own antibodies.
● Artificially acquired passive immunity
It is a short term immunization induced by the transfer of antibodies, which can be administered
in several forms, as human or animal blood plasma for intravenous or intramuscular use.
Passive transfer is used prophylactically in immunodeficiency diseases, in the treatment of
acute infections.
The artificial induction of passive immunity has been used for over a century to treat infectious
disease, and prior to the advent of antibiotics, was often the only specific treatment for certain
infections (e.g. immunoglobulin therapy in the treatment of severe respiratory diseases).
B. ACTIVE IMMUNITY
Active immunity is induced in the host itself by an antigen.

Due to the formation of immunological memory, re-infection at later time leads to a rapid
increase in antibody production.
When B cells and T cells are activated by a pathogen, memory B-cells and T-cells develop.
These memory cells will remember each specific pathogen encountered, and be able to mount
a strong response if the pathogen is detected again.
● Naturally acquired active immunity
It occurs when a person is exposed to a live pathogen, and develops a primary immune
response, which leads to immunological memory. This type of immunity is natural because it
is not induced by man.
● Artificially acquired active immunity
It can be induced by a vaccine or a substance that contains antigen.

A vaccine stimulates a primary response against an antigen without causing symptoms of the
disease.
The vaccine is defined as a suspension of attenuated or killed microorganisms (viruses,
bacteria, or rickettsiae), or antigenic proteins derived from them, administered for prevention,
amelioration, or treatment of infectious diseases.
In brief, immunity can be categorized as follows: PASSIVE e.g. breast

milk, placenta-fetus
NATURAL
ADAPTIVE OR ACTIVE e.g Infection like

ACQUIRED measles
IMMUNITY ARTIFICIAL
PASSIVE e.g. Man made:
Antibodies transfer
INNATE, the one is born

with e.g. Skin barriers,
mucosal immunity
ACTIVE e.g. Vaccination
⮚ TYPES OF VACCINES
1. Inactivated vaccines (killed vaccines): they are composed of microorganisms that have been
killed with chemicals and/ or heat and are no longer infectious.
E.g.: Flu, cholera, hepatitis A Vaccines. Most vaccines of this type are likely to require booster
shots.
2. Live attenuated vaccines: Are composed of microorganisms that have been cultivated
under conditions which disable their ability to induce disease.
These responses are more durable and do not generally require booster shots.
E.g. vaccines against yellow fever, measles, polio, rubella and mumps
3. Toxoids: Are inactivated toxic compounds from microorganisms in cases where these
(rather than the microorganism itself) cause illness.
E.g.: Vaccines against tetanus, diphtheria
4. Subunit: Vaccines are composed of small fragments of disease causing organisms
E.g. Subunit vaccine against hepatitis B virus
I.10 SYMPTOMATOLOGY OF INFECTION OR INFECTIOUS SYNDROME
In case of infection, different symptoms may occur and include the following:
✔ Fever, the more frequent symptom
✔ Chills
✔ Sweating
✔ Malaise, Asthenia, Headache, Anorexia, Thirst
✔ Delirium for adult and convulsion for children
✔ Rapid pulse and rapid respiratory rate (polypnea)
✔ Decreased diuresis (oliguria) and concentrated urine
✔ Digestive signs: vomiting, diarrhea, etc

N.B. *There are some infectious diseases without fever. E.g.: Syphilis, Cholera (the client
may even develop hypothermia).
* Furthermore, there may be fever in some non-infectious diseases (e.g.: Cancer).
I.11 CLASSIFICATION OF INFECTIOUS AND PARASITIC DISEASES
The classification of infectious disease is related to the causative organism. Thus, there are:
1. BACTERIAL DISEASES
❖ Gram-positive
E.g.: Staphylococcus, streptococcus, etc.
❖ Gram-negative bacteria
E.g.: Neisseria, vibrio, haemophilus, brucella, salmonella, shigella, Pseudomonas,etc.
2. VIRAL DISEASES
❖ DNA viruses: E.g.: Herpes zoster virus, cytomegalovirus, hepatitis B Virus.

❖ RNA viruses: E.g.: Influenza virus, poliovirus, retrovirus (HIV), Hepatitis virus A, C,
D, Rhabdovirus, Ebola virus…
❖ Enveloped vs. Non-Enveloped
3. FUNGAL DISEASES
❖ Disseminated fungal infections

❖ Localized fungal infections
4. PARASITIC DISEASES
❖ Metazoa
❖ Protozoa
⮚ PROTOZOA

1. RHIZOFLAGELLA
✔ Flagella: Trichomonas, Trypanosome, Giardia

✔ Rhizopodes : Entamoeba
2. CILIA
✔ Balantidium coli
3. SPOROZOA
✔ Plasmodium
⮚ METAZOA
1. NEMATHELMINTHES
✔ Nematodes: Ascaris, Trichocephalus, Anguillule, Ancylostoma
2. PLATYHELMINTHES
✔ Cestodes: Tapeworm (taenia)

✔ Trematodes: Schistosomas
CHAPTER II. BACTERIAL DISEASES
II.1 TYPHOID FEVER (SALMONELLOSIS)
A. DEFINITION: Typhoid fever or Salmonellosis is a contagious disease caused by

Salmonella typhi or Eberth bacilli and Salmonella paratyphi A, B or C. It is a sepsis originated
in intestines.
The Salmonella are Gram-negative bacilli and they are allocated in Enterobacter family. They
produce three kinds of antigens:

● Antigen O: Flagellar
● Antigen H: Somatic
● Antigen Vi: Capsular
Both antigen O and antigen H serve in serological diagnosis called Serodiagnosis of Widal and
Felix.
The serodiagnosis of Widal and Felix is positive since 8th day for antigen O and 12th day for
antigen H. The body produces anti O antibodies and anti H antibodies as a body defense
mechanism. These antibodies are detected during Widal and Felix serodiagnostic test.
Anti O antibodies disappear in blood after 2 to 3 months, while anti H antibodies persist for
years.
Antigen Vi, virulent, is used in vaccination (immunization).
B.MODE OF TRANSMISSION
The reservoir of bacteria is the sick or convalescent human and the carrier. The latter can harbor
germs for months or years in his bile ducts. The individual eliminates the germs through feces
and urine and the contamination occurs via the gastrointestinal tract by ingesting food and
water contaminated by infected feces or urine from cases and carriers. The role of dirty hands
and flies is very important.
C.PATHOGENESIS AND PATHOPHYSIOLOGY
In brief: The germs multiply in the lymphoid tissue of the small intestine and in mesenteric
lymph nodes. This leads to mesenteric adenolymphatitis .By there they pass the lymphatic
system and reach the blood stream where bacteremia and septicemia occur. Then they move
into kidney and the liver from where they pass out in urine and faeces.
In details: the bacteria in contaminated food or water are swallowed. If they resist to the action
of hydrochloric acid of gastric secretion, they arrive in the small intestine where they multiply
and invade the intestinal mucosal barrier. If the typhoid bacilli cannot resist to the bacterial
competition, typhoid infection cannot occur. If the multiplication of bacilli is sufficient to
overcome the activity of phagocytic cells of the intestinal mucosa, pathogens can penetrate the

mucosa. During this period, the patient is asymptomatic but the typhoid bacilli are excreted in
feces.
● After germs penetration of the intestinal mucosa, these germs that have passed the
intestinal barrier stop and multiply in the mesenteric lymph nodes, which consequently
increase in volume and present signs of acute inflammation (namely redness, swelling,
pain and heat).
● The most important lesions are found at the level of intestinal lymphoids formations
(in PEYER patches i.e. Lymph nodules in the lower part of small intestines where the
typhoid bacilli multiply) which become necrotic. These lesions may be responsible for
severe life-threatening complications (intestinal perforation, gastrointestinal
hemorrhage).
● From these nodes, the infection spreads through the lymphatic route and then through
the blood circulation, where septicemia occurs. Then, the blood culture becomes
positive.
● Most of the pathological phenomena of typhoid fever are caused by the action of
endotoxins released from killed bacteria (lysis in lymph nodes) where the signs of
the disease occur.
● The most important physiological problem and most serious is the endotoxinic septic
shock which can appear during the disease. Sometimes, the signs of endotoxinic
shock occur soon after starting treatment; in this case, it is precipitated by the use of
high doses of chloramphenicol at the beginning of treatment. These doses cause the
rapid death of large number of germs with the release of significant amounts of
endotoxins.
D.CLINICAL MANIFESTATIONS
Incubation: 10 to 15 days, biologically detectable, but contagious since 2nd day.
1st week, Invasion period, characterized by:
✔ Severe headache
✔ Asthenia
✔ Vertigo
✔ Insomnia

✔ Constipation
✔ Epistaxis
✔ The fever increases progressively up to 40oC at the end of the week while the pulse
accelerates slowly (dissociation Pulse-Temperature)
2nd week, State period:
✔ The temperature remains on top with pulse-temperature dissociation

✔ Tuphos state: the patient is completely adynamic, uninterested to everything that
surrounds him, prostration, delirium, sometimes the patient can be agitated and
aggressive.
✔ Abnormal movement e.g. shaking of extremities
✔ Diarrhea
✔ Mild abdominal swelling
✔ Rose spots occur on the trunk in 40% of patients
✔ Splenomegaly occurs in 30 to 50% of the cases
✔ The right iliac fossa is gurgling
✔ Abdominal pain
3rd week: Defervescence phase or resolution
✔ The fever decreases progressively and other signs disappear progressively , general
state of the patient improves
✔ However, it is during this phase that complications may occur
4th week: Convalescence phase
✔ It is often long and marked by asthenia
E.COMPLICATIONS
They are many and related to 2 mechanisms:
1. Septic complications: they are due to bacteria dissemination. There may be:
● Hepatic abscess

● Hepatitis
● Cholecystitis
● Purulent meningitis
● Osteomylelitis and arthritis
2. Complications due to endotoxins: they are more frequent.
● Intestinal hemorrhage: 2 to 6% of cases, due to ulcerations of Peyer patches. It is

marked by a drop in temperature, a rapid pulse and a drop in blood pressure. The
patient may fall in cardiovascular collapse.
● Intestinal perforation: 2 to 3% of the cases. It is often accompanied by abdominal
pain, vomiting and later, signs of peritonitis. This perforation occurs often silently
and its prognosis is very serious.
● Myocarditis: which may complicate into cardiac failure. It is characterized by
dyspnea, palpitations, precordial pain, and rapid heart rate.
● Neurologic complications: encephalopathy with coma
F.CLINICAL FORMS OF TYPHOID FEVER
✔ Mild or attenuated form: the signs are restricted, there is no tuphos.

✔ Severe forms: there is a choleralike diarrhea, nervous disorders (coma,). Tuphos state
is present and hemorrhage. It is often fatal.
✔ Relapsing forms: they are manifested as attenuated forms of the disease. It is like as
there are forms with incomplete treatment.
G.DIAGNOSIS
● Clinical diagnosis
● Biologic diagnosis: E.g.: Full Blood Count (FBC); Leucopenia with neutropenia.
● Certitude diagnosis, for isolating the germ.The following exams can be done:
❖ Hemoculture (blood culture): positive during the 1st and 2nd week, before
antibiotherapy.
❖ Coproculture
❖ Serodiagnosis of Widal and Felix: it detects the anti O and anti H antibodies.

H.TREATMENT
✔ Etiologic treatment. The following are the frequently used antibiotics:

1. CHLORAMPHENICOL (IV) 3x1gr/ day for adult
2. CIPROFLOXACIN (Per os) 20 to 30 mg/ kg/ day two times a day during 10-15 days
3. CEFOTAXIME ( IV) 100mg/ kg/ day or 3x 1gr/ day for adult
4. CEFTRIAXONE ( IV) 100mg/ kg/ day or 2x2gr/ day for adult
✔ Other treatment
1. Corticotherapy
2. Infusions ( rehydration) in case of shock or in case of fever persistence above 5 days
3. Sedation ( PHENOBARBITAL in case of prolonged insomnia)
4. Symptomatic treatment (for example analgesic, antipyretic)
5. Surgical treatment in case of intestinal perforation
✔ Hygieno-dietetic treatment
1. Bedrest
2. Rigorous oral and body hygiene measures for any contagious patient.
3. Diet: it must include easily digestible food, less liquid or semi-liquid.
Surveillance: the following elements must be surveilled
● BP, pulse, temperature

● Abdominal exam
● The state of the stools
● Anemia due to CHLORAMPHENICOL treatment
I.PREVENTION
● Carriers must not be allowed to work as food handlers

● Provision of good water supply
● Improvement in hygiene
● Vaccination
● Patient isolation and disinfection

N.B.:
✔ Avoid the laxative drugs and enema because they may precipitate intestinal perforation
✔ Avoid oral drugs in case of intestinal hemorrhage and give only liquid food in small
quantities
II.2 TETANUS
A. DEFINITION AND CAUSAL AGENT
Tetanus is a severe toxi-infection due to Clostridium tetani or Nicolaier bacilli (anaerobic

Gram-positive bacilli), characterized by muscle spasms and rigidity (Cardinal features of
tetanus). This anaerobic germ lives in the soil as resistance form (spore) for many years. It is
found in the intestines of animals where it lives as a saprophyte and is eliminated with the
faeces of these animals. Tetanus, commonly called lockjaw, is a serious bacterial disease that
affects muscles and nerves. It is also known as lockjaw because it often causes a person’s neck
and jaw muscles to lock, making it hard to open the mouth or swallow. It is characterized by
muscle stiffness that usually involves the jaw and neck that then progresses to involve other
parts of the body. Death can result from severe breathing difficulties or heart abnormalities.
Tetanus is a serious but preventable disease.
The tetanus vaccine can prevent tetanus but its protection does not last forever. Normally,
adults should get a tetanus shot, or booster, every 10 years.
B. PATHOGENESIS AND PATHOPHYSIOLOGY
Spores of Clostridium tetani live in faeces, soil, dust and on instruments. A tiny break in skin
or mucosa, for e.g. cuts, burns, ear piercing may admit the spores. Spores may then germinate
and only germinate in relatively hypoxic tissue such as necrotic or ischaemic tissue, or tissue
surrounding a foreign body. As clostridium tetani grows, it produces at least two exotoxins
(Tetanospasmin and Tetanolysin). The role of tetanolysin in human is unclear but it may
promote growth of clostridium tetani or contribute to the autonomic dysfunction.

Tetanospasmin causes the clinical manifestations of tetanus by travelling up peripheral nerves
and by inhibiting neurotransmitter release from a presynaptic terminal of nerves and interferes
with inhibitory synapses.
C.EPIDEMIOLOGY AND PATHOLOGY
The transmission is direct and requires portal of entry:
o Skin wounds, even very small bites such as needles, thorns, which even have already
healed. The following are also to mention: injections, surgical interventions, trauma,
etc.
o The umbilical wound in the newborn
o The uterine cavity (post-partum, post-abortion)
o Accidental injuries even small neglected wounds : 40 to 60% of the cases
o Chronic wounds: 10% of the cases
Germs once entered the body, they remain localized in the wound and secrete neurotropic
toxins which spread throughout all the body and cause the disease manifestations.
D.CLINICAL MANIFESTATIONS
✔ The incubation period: it is very variable: 4 to 30 days. More the incubation is short, more
the disease is severe.
✔ The invasion period:
● Trismus: intense, painful permanent contractures of the masseters joining two jaws.
This opposes to any opening of the mouth, feeding and speech are difficult because of the
contractions of muscles responsible for mastication (masseters). The presence of this sign must
always make to think about tetanus even in the absence of any local lesion and try to find the
portal of entry.
● Dysphagia: difficult swallowing.
✔ At the state phase :
Generalized contractures: They are intense, permanent and painful and interest:
▪ The face: where the risus sardonicus or rictus grin occurs

▪ The neck: stiff neck occurs
▪ The abdomen: abdominal muscles contractions (stick abdomen)
▪ The limbs remain in extension
▪ The back muscles: opisthotonus attitude (arched body with hyperextended neck)
These spasms are exaggerated by paroxysm induced by movement, injections, noise,
light,...and they are very painful while the client is lucid.These spasms may interest the viscera
and can cause constipation, apnea, dysphagia, dysuria and even spasm of the larynx which can
asphyxiate the patient and can be fatal if the tracheotomy is not performed immediately.
E. EVOLUTION
It is often fatal, especially if the treatment was delayed and in severe cases.
Favorable evolution is rare.
If untreated, deaths arise up to 80-90% of the cases.
If treated, mortality is 50% in average.
F.COMPLICATIONS
● Respiratory complications
o Laryngeal spasm (apnea or respiratory distress)
o Bronchial congestion
o Aspiration bronchopneumonia
o Bone fracture, especially vertebral fractures, muscle rupture.
● Other complications
o Convulsions
o Urinary Tract Infections by stasis or urinary catheterization
o Dehydration
o Renal failure
o Poor nutrition
o Cardio-vascular accident such as cardiac arrest, emboli or cardiovascular
collapse

G. PARA CLINICAL EXAMINATION
There is no required examination for diagnosis
H. NEONATAL TETANUS
⮚ Portal of entry: Umbilical cord (especially for home delivery)

Clinical signs occur from the 6th to 7th day with:
✔ Impossibility to breastfeed due to the contraction of the masseters
✔ Characteristic Risus sardonicus
✔ Opisthotonus attitude
These 3 signs are enough for Tetanus diagnosis
⮚ Evolution
✔ Untreated: 100% of mortality

✔ Treated: 60% of mortality
I.TREATMENT
❖ Preventive treatment or measures
✔ Vaccination
✔ The serum therapy: the antitetanic serum is required for any suspected wound. It is
effective if done early, it must be associated with vaccination or booster shots if the
subject has already been vaccinated.
This serotherapy may be accompanied by serious accidents and even fatal: Anaphylactic
shock. To avoid this accident, the use of BESREDKA method is necessary: it involves
injecting gradually small doses in subcutaneous injection. First a quarter of the dose is given,
15 minutes after a half of the dose, other 15 minutes after 1 cc and finally 15 minutes after, the
rest of the dose. During this period they must monitor the alarm signs.

✔ Emergency treatment for any suspected traumatic wound: surgical cleaning of
the wound.Oxygenated water is better to kill anaerobic germs.
N.B: The following must be done in case of any injury:
⮚ If the client has been properly vaccinated and that the booster shot is less than one year,
nothing to do.
⮚ If the booster shot is dated more than 1 year and less than 5 years, the booster shot is
given again.
⮚ If the client has not been vaccinated or if the vaccination is dated longer than 5 years,
serovaccsination is practiced.
❖ Curative treatment
● Obligatory hospitalization in the dark room without any light or noise.

● General antibiotherapy: IV PENICILLIN G or METRONIDAZOLE IV and apply
also local care of the wound.
● Give human tetanus immune globulin to neutralize free toxins or give horse
antitetanus serum (ATS) if available.
● Stop the contractures by giving the myorelaxants.The mostly used are DIAZEPAM
and PHENOBARBITAL.
● Respiratory reanimation: intubation and/ or tracheotomy.
N.B.:
1. Don’t give food by oral route in case of dysphagia
2. Insert a nasogastric tube (NGT) for liquid or semi-liquid feeding, especially for a newborn
3. Infusions must be used according to medical order
4. Hygiene is also an other important nursing care
For Neonatal Tetanus
● Calm the baby with a half ampoule of Diazepam( 5mg) in IM or IR

● Insert a NGT for feeding and administration of sedative drugs (Diazepam and
Phenobarbital).

● Care of the umbilical cord
● Artificial milk feeding: 60 to 100 cc , 6 times per day, and increase the quantity
according to the patient’s age and weight.
II.3 MENINGITIS
A.DEFINITION
Meningitis is an infection and inflammation of the meninges and cerebrospinal fluid

surrounding the brain and spinal cord.
The organisms responsible for meningitis enter the central nervous system (CNS) via the blood
stream at the blood-brain barrier (BBB).
BBB is the barrier that selects which substances reach the brain. The BBB is both a physical
barrier and a system of cellular transport mechanisms.
B.TRANSMISSION OF MENINGITIS
The organisms are commensals in the nose and pharynx of people. They are spread and caught
by droplet method (i.e. airborne). In a susceptible host they become invasive i.e. they enter the
blood stream and reach the meninges of the brain; they infect, and cause pus that forms on
surface of brain. The route of transmission is represented by the Upper Respiratory Tract.
C.PREDISPOSING FACTORS
• Head trauma
• Immunosuppression
• CSF fistula/leak
• Neurosurgical patients
• Alcoholism
• Congenital defects
• Splenectomized patients
• Local infections:
a. Sinusitis
b. Otitis media
c. Pharyngitis
d. Bacterial pneumonia
D.TYPES OF MENINGITIS
Classically, there are two major types of meningitis:

1. Septic meningitis or Bacterial Meningitis or Purulent Meningitis (purulent CSF)
2. Aseptic Meningitis or Clear Liquid Meningitis (clear CSF)
1. SEPTIC OR PURULENT MENINGITIS
Bacterial meningitis is an acute purulent infection within the subarachnoid space.

It is associated with a CNS inflammatory reaction that may result in decreased consciousness,
seizures, raised intracranial pressure (ICP), and stroke.
It is considered as more serious and it can be life threatening.
Acute bacterial meningitis is the most common form of meningitis. Approximately 80 percent
of all cases are acute bacterial meningitis. The bacteria most often responsible for bacterial
meningitis are common in the environment and can also be found in nose and respiratory
system without causing any harm.
a. Routes for entry
Haematogenous:
• Anatomic defect
o Congenital
o Traumatic
o Surgical
• Intraneural pathways
b. Pathogenesis

Meningitis-causing germs reach the meninges or central nervous system by any of the
following ways:
• Colonization of the oropharynx 🡪 bacteremia 🡪 CNS invasion
• Local infection (pneumonia, endocarditis, UTI) 🡪 bacteremia 🡪 CNS invasion
• Direct CNS invasion from trauma, sinusitis, mastoiditis, or surgery
• The lysis of bacteria with the subsequent release of cell-wall components into the
subarachnoid space is the initial step in the induction of the inflammatory response and
the formation of a purulent exudate in the subarachnoid space x 🡪purulent CSF
c. Responsible germs
The most frequent organisms involved in bacterial meningitis are:
✔ MENINGOCOCCI (Neisseria meningitidis), Gram-negative diplococci

✔ PNEUMOCOCCI (Streptococcus pneumoniae), Gram-positive diplococci
✔ HAEMOPHILUS INFLUENZA (Haemophilus influenza), Gram-negative bacilli
These 3 germs represent 80% of purulent meningitis.
The Meningococcal meningitis (due to Neisseria meningitidis) is less virulent but it is an
epidemic type (N.meningitidis causes outbreaks or epidemics). Its contagiosity is very high.
d .Clinical signs of meningitis
Four syndromes define and characterise meningitis:

• Infectious syndrome
• Meningeal syndrome
• Encephalitic syndrome
• IICP syndrome (Increased Intracranial Pressure Syndrome)
⮚ INFECTIOUS SYNDROME: it is characterized by:
✔ Hyperthermia of 39 -40oC
✔ Chills
✔ Increased heart rate or Rapid pulse
✔ Labial herpes
✔ Malaise
✔ Myalgia and/or polyarthralgia
✔ Asthenia
⮚ THE MENINGEAL SYNDROME
It is characterized by:
✔ Stiffness of the neck or nuchal rigidity

✔ Positive Kernig’s sign: the patient cannot fully extend his knee while the hip is flexed
at 90 degrees. Inability to stretch the leg at knee joint when the thigh is at right angle
(90 degrees). When the knee is flexed at 90 degrees, the client feels pain when the
nurse/examiner attempts to extend the knee.
✔ Positive Brudzinski’s sign:
1. Passive flexion of one thigh causes spontaneous flexion of the opposite thigh
2. Passive flexion of the neck causes bilateral flexion of hip and knees
✔ Opisthotonos
✔ Severe headache
✔ Nausea and vomiting
✔ Photophobia
N.B. For infants:
✔ Absence of stiffness of the neck, but generalized hypotonia

✔ Digestive signs at the first plan: e.g. vomiting
✔ Convulsion
✔ Refusal of breastfeeding
✔ The anterior fontanelle bulge (it swells)
⮚ ENCEPHALITIC SYNDROME
• Alteration in mental status

• Delirium
• Seizures
• Drowsiness

• Stupor and Coma
⮚ IICP SYNDROME
• Headache
• Projectile vomiting
• Diplopia (nerve VI)
• Mydriasis (nerve III)
• Decorticate posturing
• Cushing’s triad : a response involving three classic signs:
✔ Widening pulse pressure: increased systolic BP with diastolic remaining the same or
slightly elevated.
✔ Bradycardia
✔ Slowing respirations
Cushing’s triad indicates severe increased ICP!
o POSITIVE DIAGNOSIS
The classic triad of acute bacterial meningitis consists of
• Fever
• Nuchal rigidity, and a change in mental status
• Seizures
e. Diagnosis
The diagnosis of bacterial meningitis is made by:
• History and physical examination

• Lumbar puncture +CSF analysis
• Laboratory findings
⮚ CSF analysis (microscopic): the microscopic analysis of CSF concerns the following:
o Cytology (blood cells: WBC)

o Biochemistry (glucose, protein, lactic acid)
o Bacteriology (CSF stains, culture)
o PH
ANALYSIS OF CSF
● Aspect of the liquid:

✔ It flows under pressure
✔ Purulent or turbid
✔ Sometimes yellowish
● Cytology of CSF:
✔ Increased WBC: neutrophils in abundance
● Biochemistry of CSF:
✔ Increased protein in CSF
✔ Decreased glucose in CSF
✔ Increased Lactic acid in CSF
● Culture:
✔ Meningococci
✔ Pneumococci, etc depending on the causal agent
● PH: decreased
⮚ Lumbar puncture (LP) is done to obtain cerebrospinal fluid (CSF) to be analyzed.

It should be done before any antibiotherapy. The LP is done with the patient in a flexed position
to maximize the space between vertebrae. The LP needle is usually inserted between L3-L4 or
L4 and L5 to gain entry to the subarachnoid space where the CSF is located.
N.B.: LP must be done when there are no signs of increased intracranial. Examination of the
CSF is the certitude diagnosis of meningitis.
Remark: CSF CULTURE
● CSF culture is much less sensitive after antibiotics are given.

● N.meningitidis will disappear from CSF within 1 h of appropriate antibiotic therapy.
● Streptococcus pneumoniae will disappear in 4-10 hours after appropriate antibiotics.
That is why the examination of cerebrospinal fluid permits to diagnose meningitis with
precision.

f. Treatment
● Therapeutic guidelines: curative treatment
Age Probable etiology First line antibiotics

Adults and children > 6 Meningococci Chloramphenical : 1g×3/day for
years adults or 100mg/kg/ day in infants or
Pneumococci
Cefotaxime: 200 to
300mg/kg/24hours in 4 times
Association or not with gentamycin to

fight associated sepsis
Penicillin:100.000IU/kg
Infants and children of H. influenza Chloramphenical: children

3 months to 5 years :100mg/kg day or Ampicillin:
200mg/kg /day or amoxicillin: 200
mg/kg/ day or Cefotaxime: 200mg/kg
/day or ceftriaxone: 100mg/kg/day
Newborn E.Coli; Streptococcus Cefotaxime: 200mg/kg/day

Group B; Listeria
Ceftriaxone: 100mg/kg/day
Monocytogenes
● Additional procedures commonly employed include:
1. Correction of fluid and electrolyte deficits (rehydration) by infusions

2. Provision of adequate ventilation (oxygenation)
3. Monitoring of cardiovascular function:
o Pulse
o Arterial blood pressure
o Central venous pressure

4. Monitoring intracranial pressure: administer mannitol to reduce cerebral edema.
5. Diazepam in case of convulsions
6. Antipyretic drugs for e.g. aspegic
7. Corticotherapy (e.g. DEXAMETHASONE: 0.6mg/ kg) 20 min before antibiotic therapy to
reduce meningeal irritation and cerebral edema if necessary
8. Elevation of the patient’s head to 30 to 45 degrees (HOB elevated), intubation and
hyperventilation
N.B.: The duration of the treatment should be as long as follows:

⮚ 2-3 weeks for Meningococci
⮚ 3-6 weeks for Pneumococci and H.influenza
2. ASEPTIC OR CLEAR LIQUID MENINGITIS
a. Definition
A syndrome characterized by acute onset of meningeal symptoms, fever, and cerebrospinal

fluid with bacteriologically sterile cultures.
Aseptic meningitis is a syndrome of multiple etiologies, but most cases are caused by a viral
agent.
b. Clinical manifestations
The symptoms of clear liquid meningitis are almost similar to those of purulent meningitis. The
diagnosis is obtained from the result of Lumbar puncture by analyzing the CSF.
Viral meningitis is commonly characterised by:
o Fever
o Headache often associated with photophobia and pain on moving eyes
o Malaise
o Myalgia
o Anorexia, Nausea and vomiting
o Abdominal pain, and/or diarrhea.
o Nuchal rigidity

o Evidence of severe meningeal irritation such as Kernig’s and Brudzinski’s signs, is
generally absent
c. Main etiologies of clear liquid meningitis
● Viral
● Fungal (cryptococcus, histoplasma, candida,….)
● Parasitic
● Tubercular
● Syphilis, Listeria, brucella, leptospira
1. Meningitis due to Listeria monocytogenes: Symptoms similar to those of tubercular/

tuberculous meningitis.
2. Tubercular meningitis: clear liquid meningitis with abundant lymphocytes in the
CSF, decreased glucose and increased protein in the CSF.
3. Other agents: Brucellosis, syphilis, Leptospirosis, Rickettsiosis,…
4. Viral Meningitis: it is not considered as serious or potentially life threatening. It often
occurs as a sequella to a variety of viral illnesses, including measles, mumps, herpes
simplex and herpes zoster. The formation of exudate that is common in bacterial
meningitis doesn’t occur, and no organisms are obtained for culture from the CSF.
Inflammation occurs over the cerebral cortex and the meninges.
5. Fungal meningitis: it is the meningitis due to Cryptococcus neoformans. The disease
is called Cryptococcus meningitis. It is the most commonly seen fungal infection that
affects the CNS of clients with acquired immunodeficiency syndrome (AIDS). Other
possible fungi are histoplasma, candida albicans,…
Clinical manifestations include headache, nausea, vomiting and a decline in mental status, fever
or not.
6. Protozoal meningitis
Meningitis following parasitic affection: Amoeba, trypanosomiasis, toxoplasmosis,…
d. Treatment of clear CSF meningitis
The treatment of clear CSF is etiological.

E.g.: Herpetic meningoencephalitis: the treatment is Acyclovir for 10 to 15 days.

In case of Cryptococcus meningitis, AMPHOTERICINE B also called FUNGIZONE is
given. The alternative treatment is FLUCONAZOLE.
N.B. AMPHOTERICINE B is given in infusion and it must be protected against the sun light.
Give a premedication (Antihistamine and or corticoid) to the patient before giving
amphotericine for preventing the patient hypersensitivity to the drug.
e. Comparison of CSF for purulent and clear liquid meningitis
CHARACTERISTICS OF PURULENT CLEAR LIQUID

CSF MENINGITIS MENINGITIS
Aspect Purulent CSF. Clear CSF
Xanthochromic ( yellow)
Flow pressure Elevated Normal or less elevated
Leucocytes Increased >1000 WBC/mm3 , Increased (10-2000
Neutrophils in abundance WBC/mm3), Lymphocytes
in abundance
Glucose Decreased <40mg/ dl Normal >45 mg/ dl
Protein Increased > 100mg/dl Normal or slightly increased
Lactic acid Increased Normal
Gram stain Positive or negative -
Culture Often positive Negative
⚫ COMPLICATIONS OF MENINGITIS (BOTH PURULENT AND CLEAR

LIQUID MENINGITIS)
Mainly due to increased ICP, the following complications may occur:
✔ Hydrocephalus
✔ Cerebral edema
✔ Herniation of the brain due to increased ICP
✔ Hemiplegia
✔ Deafness

✔ Blindness
⚫ PREVENTION OF MENINGITIS
Bacteria, viruses and fungi cause most meningitis. There are several actions that can be taken
to help prevent infection caused by these organisms such as:
✔ Vaccination (all recommended immunizations)
✔ Health education on avoiding crowded places and improving ventilation of houses
✔ Maintaining healthy habits, like getting plenty of rest and not coming into close contact
with people who are sick as much as possible
✔ For a pregnant woman, it is advisable to prevent the risk of meningitis caused by
Listeria bacteria (listeriosis) by cooking meats thoroughly
✔ Hygiene: thorough handwashing; avoid sharing a drinking glass, eating utensil, lipstick,
or other such items with sick people.
II.4 TUBERCULOSIS
A.DEFINITION
Tuberculosis or TB (short for tubercle bacillus) is a common infectious disease caused by

various strains of mycobacteria, usually Mycobacterium tuberculosis.
Typical causative agents of tuberculosis are:
1. Mycobacterium tuberculosis or Koch bacillus
● It is the common cause of morbidity and mortality due to TB

● It is spread through droplets coughed up by sputum of positive person i.e. patient- to-
patient transmission
● M.tuberculosis is sensitive to ultraviolet light, so daytime outdoor transmission is rare.
2. Mycobacterium bovis
● Spread by ingesting non-pasteurized milk

● Domesticated and wild animals are the usual hosts

● It causes intestinal tuberculosis in humans
B. MYCOBACTERIUM TUBERCULOSIS OR KOCH BACILLI
B.1. GENERAL CHARACTERISTICS
Slender curved rods. Acid-fast and Alcohol-fast bacilli in Zielhl-Neelsen stain (Acido-Alcohol
Resistant Bacilli: AARB). Characterized by slow multiplication, these bacilli require 4-6 weeks
for a culture. They are very sensitive to heat and ultraviolet light. Resisting to the cold and
dryness, they are strict aerobic. AARB are very virulent and multiply inside macrophages
(intracellular bacilli).
The Mycobacterium tuberculosis (Koch bacillus) causes tuberculosis which can be:
1. Chronic disease that can affect mainly:
✔ The lungs resulting in pulmonary tuberculosis

✔ Other organs such as the brain, intestines, kidneys, bones and spine where it is called
extrapulmonary tuberculosis.
2. Acute disease and is called Miliary Tuberculosis
Also known as disseminated tuberculosis, miliary tuberculosis occurs when Mycobacteria

enter the blood and are disseminated widely in the lungs and other organs of the body especially
in infants and immunocompromized persons than in immunocompetent adults.
Miliary tuberculosis is so called because it causes the appearance of numerous small tubercles
(which look like millet i.e. Miliary) in organs, and it normally kills the patient if untreated. X-
rays show the numerous small tubercles.
B.2. TRANSMISSION OF TUBERCULOSIS
Primarily by air (other forms of tuberculosis are not common):

● Direct transmission through droplet spread. When the patient (person suffering from
active pulmonary TB) coughs, spits, sneezes, laughs, sings or speaks, he emits aerosol
droplets charged with bacilli (0.5 to 5 micrometers). A single sneeze can release up
to 40.000 droplets and each of these droplets may transmit the disease, since the
infectious dose of tuberculosis is very low and inhaling fewer than ten bacteria may
cause an infection. Direct inhalation of those droplets causes an infection to a new
host.
● Indirect transmission through droplet nuclei (residue of dried droplet spread, that
passes a long time suspended in the air).
B.3. RESERVOIR
Humans:
• Healthy infected
• Patient with pulmonary tuberculosis with positive microscopy
Animals:
• Bovine
• Monkeys, cats, dogs, etc.
B.4. PATHOGENESIS
After inhalation of bacilli, the development of tuberculosis in a previously uninfected child or

adult person can be of three types:
1. PRIMARY TUBERCULOSIS
2. POST-PRIMARY( OR REACTIVATION) TUBERCULOSIS
3. MILIARY TUBERCULOSIS (or DISSEMINATED
TUBERCULOSIS)
1. PRIMARY TUBERCULOSIS
A susceptible person becomes infected by inhaling Mycobacterium through droplets of sputum

(liberated by coughing or speaking) from an infectious tuberculosis patient after repeated
exposure. Risk factors include bad ventilation, overcrowding (living in a refugee camp or
shelter), weakened immune system (for example in case of HIV/AIDS, diabetes, end-stage

kidney disease, cancer treatment such as chemotherapy, drugs to prevent rejection of
transplanted organs, malnutrition, advanced age ), poverty and substance abuse, lack of medical
care, health care work.
The Mycobacteria breathed in the distant (i.e. peripheral) part of the lung tissue. There they
multiply and cause some tissue destruction especially in the mid zone of the lung ( and they
cause the peripheral lesion). While this happens, the immune system sends many lymphocytes
to the site in an attempt to conquer the invading organism.
Then the cells of the immune system including Macrophages and Lymphocytes try to eliminate
the mycobacteria by surrounding and killing them, whereby some mycobacteria are transported
to regional lymph nodes e.g. hilar lymph nodes, which tend to enlarge due to some
inflammation.
The isolated lesion (i.e. solitary peripheral lesion) in the lung together with enlarged regional
lymph node is called PRIMARY COMPLEX or GHON’S COMPLEX.
Most primary complexes heal spontaneously by action of cell-mediated immunity resulting in
fibrosis and sometimes calcification to form tubercles (i.e. swelling) 2-6 weeks after infection.
The bacilli in the tubercles die slowly but some remain alive even for 20 years or more.
The primary infection ends there in most people who have a well functioning cell-mediated
immunity.
For people who have or later may have weak cellular immunity, the infection progresses into
postprimary (i.e. reactivation) tuberculosis.
It is usually asymptomatic, but there may be fever, malaise, cough with or without sputum,
painful red rashes (erythema nodosum), sweating, and anorexia.
2. POSTPRIMARY (OR REACTIVATION) TUBERCULOSIS
1. Definition
This occurs as a result of reactivation of formally dormant Mycobacteria in the turbercles

formed during primary tuberculosis period. It can occur 20 years or more after a healed primary
tuberculosis. This is in fact the true tuberculosis disease.

2. Risk factors
● Age ( infants, small children and old people of 50 years and above due to weak cellular
immunity) and malnutrition
● Concurrent infection ( for e.g. malaria, worms, measles,etc)
● Toxic factors : e.g. alcohol and smoking
● Immunosuppression (e.g.: HIV, Steroids,etc)
● Host genetic factors
● Poverty and stress
3. Mechanism
If the immune response is weak or immunity declines, the mycobacteria may gain the upper
hand and spread to other party of the lungs. There they cause characteristic lesions. These solid
lesions, containing mycobacteria and immune response cells, then gradually involve more and
more lung tissues.
4. Location of infection
The apex of the lung is the common site of infection. Other parts such as kidneys, bones and
bone marrow, lymph nodes, brain, meninges and intestines may be involved
5. Signs and symptoms
✔ Cough soon producing purulent sputum, then haemoptysis

✔ The infection can be spread to other parts of the body leading to specific signs of the
affected part
✔ The patient loses weight, coughs blood, has night sweats and chronic fever, malaise,
anorexia (lack of appetite).
N.B.: DIFFERENCE BETWEEN TB INFECTION AND TB DISEASE

✔ TB INFECTION(PRIMARY TB): ✔ TB DISEASE(SECONDARY TB):
● TB germs stay in lungs, but they do ● TB germs stay in the lungs or move to
not multiply or make the carrier sick other parts of the body, multiply, and
● The carrier cannot pass TB germs to make the carrier sick
others ● The carrier ( TB patient) can pass the
TB germs to other people
3. MILIARY OR DISSEMINATED TUBERCULOSIS
1. Mechanism: It occurs when a large blood vessel is eroded by TB whereby the bacilli get
disseminated in the blood to almost every organ system of the body resulting in fulminating
(i.e. of sudden onset, and rapid in progress and acute) infection.
It occurs in very young children, very old people and those who are immunocompromised
2. Symptoms: They are similar to those of reactivation (postprimary) tuberculosis, but
meningitis and brain involvement are common.This form of TB is commonly fatal.
B.5. CLINICAL MANIFESTATIONS
● Cough for 2 weeks or more (Any person coughing for two weeks or more is a “TB
suspect” and must absolutely have sputum examination and HIV test done).
● Other pulmonary symptoms may be present like expectoration, sometimes stained with
blood or haemoptysis, chest pain, and dyspnea (difficult breathing).
● Constitutional symptoms: loss of appetite (anorexia), weight loss, fever, asthenia, night
sweats are also suggestive of TB. Presence of one of these signs in an HIV infected
person requires conducting an investigation for TB
● Unusual breath sounds (crackles) on auscultation
● In HIV positive people, diagnostic investigations need to be done as quickly as possible
in order to reduce the mortality linked to TB. If the TB suspect does not know his HIV
status, it is important to give him counseling for HIV testing
● Other signs according to the affected organ (in extrapulmonary tuberculosis).
● Enlarged or tender lymph nodes in the neck or other areas

B.6. DIAGNOSIS
1. Bacilloscopy (sputum examination or Sputum smear microscopy)
● It is mainly based on finding acid-fast mycobacterium in the sputum smear with Ziehl-
Neelsen stain.
● In order to have maximum chances to find bacilli, it is necessary to collect good sputum,
that is, some purulent or muco-purulent expectancy coming from the deep part of the
respiratory system.
● To reduce the risk of infection, sputum will be taken in the open air, out of view and away
from other persons.
● Collection of sputum sample: For any TB suspect, 2 sputum samples must be collected
within two days, in the following way:
o 1st day: Sample no. 1: Immediately, on the spot and under supervision.
Then give to the patient a sputum container to take home to collect the second sample.
o 2nd day: Sample no. 2: next day when s/he gets up in the morning.
Note: For treatment follow-up, the collection of sputum is as follows:

✔ One sample is enough, taken in the morning.
✔ Every positive smear at the end of the 3rd month of treatment or later shall be cultivated
and sensitivity to TB drugs shall be tested.
✔ Every positive control at the end of the 4th month or later shall be confirmed by a 2nd
sample.
2. Tuberculin (Mantoux) skin test or Intra-Dermo-Reaction (IDR)
The test is actually done as follows:

● 5 tuberculin units of purified protein derivative antigen of M.tuberculosis are injected
on the front of the forearm.
● There appears a swelling like a pimple (spot). This is monitored for hardening (i.e.
induration) 3 days later. The diameter of induration is recorded as follows:
a) Diameter over 10 mm indicates positive reaction (i.e. Previous exposure to tuberculosis

in BCG or naturally, or active tuberculosis disease).

b) Diameter 5-10 mm is questionable i.e. uncertain and so test must be repeated using 10
tuberculin units
c) Diameter of induration less than 5 mm indicates a negative test
3. Radiography or chest x-ray (especially for patient with negative microscopy)
4. Biopsy of the affected tissue (less common)
5. Other diagnostic investigations: GeneXpert, Culture and sensitivity, Ultrasound
B.7. PREVENTION AND CONTROL OF TUBERCULOSIS
1. PREVENTIVE MEASURES
✔ Treatment of the sick in order to cure illness and prevent spread of disease to others by
killing Mycobacteria as efficiently as possible and within the shortest possible time by
taking attention on the following elements:
a. WHO strategy for the treatment of TB is known as DOTS (Directly Observed

Treatment Short Course). Practically it means the following activities:
i. Directly: Identifying the sick, infection cases.
ii. Observed: Health workers or trained volunteers observe the patients
as they swallow the drugs
iii. Treatment: The TB patient must be provided with complete
treatment and monitored to assess progress until cured. There must
be good reporting and record keeping
iv. Short course: The correct combination and dosages or anti-TB drugs
must be used for the correct length of time.
b. Combination of treatment: two or more anti-TB drugs must be used at the same time to
prevent resistance to one anti-TB drug.
c. Treatment of TB is done in two phases for a total of 6 months
i. Intensive therapy phase lasting 2 months
ii. Continuation therapy phase that lasts 4 months

2. RESPECT OF INTENSIVE THERAPY PHASE
i. Combination of most powerful drugs is used to kill as many bacteria as possible

and as quickly as possible.
ii. A patient may be admitted or treated as out patient but seen daily and treatment
supervised
iii. Intensive therapy phase lasts 2 months with daily intake of (RHZE)
iv. After intensive phase, the patient is discharged from hospital to continue treatment
at home under supervised of community health workers in the continuation phase
of 4 months
v. Patient reports at health facility every month for being checked, and to get fresh
supply of drugs
vi. Follow up period involves taking sputum smear of positive patients at month 2, and
5
3. CHEMOPROPHYLAXIS
1. Isoniazid (H) can be used for 6-9 months to prevent development of subclinical infection to
active TB in exposed children and people who have recently become tuberculin positive ,for
HIV positive patients. Isoniazid reduces the risk of active tuberculosis in infected people by up
to 90%.
2. Immunoprophylaxis with BCG (Bacillus Calmette-Guerin). It is a vaccine made of
attenuated living Mycobacterium bovis. It is given to children during the first year of life, and
adults at risk of infection
3. Cases finding (screening of high-risk groups such as prisoners, homeless people, etc) and
treatment.
4. Health education to enable people to avoid spitting anywhere carelessly, overcrowding,
general hygiene and poor ventilation and isolation of patients
B.8. TREATMENT OF TUBERCULOSIS IN RWANDA
❖ CASE DEFINITIONS RELATING TO TUBERCULOSIS

1. Pulmonary tuberculosis with positive microscopy (PTM+):
It is a case of pulmonary tuberculosis where the patient presents at least 1 positive sputum
smear.
2. Pulmonary tuberculosis with negative microscopy (PTM -):
The patient presenting 2 series of negative bacilloscopy, with absence of improvement to the
antibiotics but the patient has evocative radiological abnormalities of pulmonary tuberculosis.
The decision of starting a complete antituberculosis treatment is taken by a doctor.
Or patients whose sputum smears are negative but culture is positive
3. Pulmonary tuberculosis with non-done microscopy (PTM0):

It is in fact a pulmonary tuberculosis for which the patient is diagnosed as pulmonary case of
tuberculosis without microscopic examination of sputum. The diagnosis is only clinical and/or
radiological, which is against the standards of the program (except for the children whose the
sputum cannot be got because they cannot expectorate).
4. Extra pulmonary tuberculosis (EPTB):

Any case of tuberculosis located outside the pulmonary parenchyma (or the lungs).
It is sometimes confused with non-respiratory disease. TB of the larynx for example, which is
part of the respiratory system, is respiratory disease but extrapulmonary.
Note: The patient can have both pulmonary tuberculosis and extrapulmonary tuberculosis. In
this case of two combined forms, the patient is known as pulmonary tuberculosis case because
this patient can still spread the disease to others.
5. New case:
TB patient who has never received antituberculosis treatment or has received the treatment for
a period whose duration was less than 4 weeks.
6. Retreatment:
TB patient who received antituberculosis for a period of more than 4 weeks and who has
positive sputum smear. It includes the relapse, the failure and the resumptions of treatment after
abandonment.
7. Relapse:

This case consists of the patient who was treated in the past and declared cured or having
finished the treatment successfully, and whose examinations of expectoration are again B.K.
positive (2 samples at least must be positive).
8. Failure:
TB patient whose sputum remains or becomes again B.K. positive at the 5th month or later
during the treatment (2 positive samples at least at 15 days of interval)
9. Chronic:
Patient who remains positive at the end of a retreatment (2 positive sputum samples at least)
10. Treatment after default

Patient who returns to treatment with positive sputum smears, following interruption of
treatment for 2 consecutive months or more.
11. Transfer in:

Patient who has been transferred from another CDT to continue treatment in a different CDT
(Center for Diagnosis and Treatment)
12. Others:
Any case which does not fulfil all requirements of the above mentioned definitions.
For example: relapse with negative smears, retreatment of an EP case.
❖ TREATMENT
The two aims of tuberculosis treatment are to interrupt tuberculosis transmission by rendering
patients noninfectious and to prevent morbidity and death by curing patients with tuberculosis.
✔ Principles of the treatment
1. Association of at least 4 anti-TB drugs to avoid the selection of resistant mutants

2. Sufficient duration to act on all classes of bacilli.
3. Regulation with adequate doses.
4. Administration under direct supervision in order to make sure that the patient takes his drugs
correctly and without interruption.
5. Daily dose, to reach a high serum peak and to facilitate the supervision of the treatment.
✔ Regimens
Standard short-course regimens are divided into an initial, or bactericidal phase and a
continuation or sterilizing phase. During the initial phase, the majority of the tubercle bacilli
are killed, symptoms resolve, and usually the patient becomes noninfectious. The continuation
phase is required to eliminate persisting mycobacteria and prevent relapse.
The treatment regimen of choice for virtually all forms of tuberculosis in both adults and
children consists of a 2-month initial phase of isoniazid, rifampin, pyrazinamide, and
ethambutol followed by a 4-month continuation phase of isoniazid and rifampin. Patients with
cavitary pulmonary tuberculosis and delayed sputum-culture conversion (i.e. those who remain
culture-positive at 2 months) should have the continuation phase extended by 3 months, for a
total course of 9 months. To prevent isoniazid-related neuropathy, pyridoxine (10–25 mg/d)
should be added to the regimen given to persons at high risk of vitamin B6 deficiency (e.g.,
alcoholics; malnourished persons; pregnant and lactating women; and patients with conditions
such as chronic renal failure, diabetes, and HIV infection, which are also associated with
neuropathy).
❖ STANDARD TREATMENT IN RWANDA
THERAPEUTIC DIAGRAMS:
✔ New case: Adult: 2 (RHZE)7 / 4(RH) 7
Infant: 2 (RHZ)7 / 4(RH) 7
✔ Retreatment : 2S7(RHZE)7/1(RHZE)7 /5(RHE)7
✔ Multiresitant TB: 6 Am6-Z7-Ofx7-Pto7-Cs7 / 14 Ofx7-Pto7-Cs7 (category 4)
N.B.: For multiresistant tuberculosis, please note the following:
■ Injection phase : 6 months of: Am(injectable)-Z-Ofx-Pto-Cs

■ Followed by 14 months of: Ofx-Pto-Cs per os (oral route).

E: Ethambutol, R: Rifampicin, H: Isoniazide, Am: Amikacin (INJECTABLE), Ofx:
Ofloxacine, Pto: Prothionamide, Z: Pyrazinamide, Cs: Cycloserine, S: Streptomycin
SYNTHETIC TREATMENT CATEGORIES
CATEGORIES DIAGRAM DURATION RISK OF INDICATIONS
FAILURE
PRIMOTREAT 2 (RHZE)7 / 4(RH) 7 6 months 1-3% New case

MENT (Cat. I)
PRIMOTREAT 2 (RHZ)7 / 4(RH) 7 6 months - Infants < 5 years

MENT FOR
Add E100 if indicated
CHILDREN
(Cat.III)
III.RETREAT 2S7(RHZE)7/1(RHZE 8 months 1-5% Relapse, Failure,

MENT )7/5(RHE) 7 Resumption of
(Category II) treatment (after
abandonment)
MULTIRESIST Am-Z-Ofx-Pto-CS 20-24 months - Multiresistant

ANT (Cat.IV) patient
N.B: INH 6 months - Health contacts,

PREVENTIVE children <5 years
TREATMENT
Note : For pediatric treatment (less than 5 years or 25 kg), add Ethambutol 100mg if :
• Positive sputum smear
• Negative sputum smear with extensive lesions on chest X-ray
• Severe extrapulmonary TB (miliary, osteo-articular, abdominal TB)
• TB with severe HIV infection, defined by presence of 1 of the following criteria:
✔ Child aged less than 18 months

✔ AIDS stage 3 or 4
✔ CD4 < 25%

The duration of the multiresistant TB treatment is 20 to 24 months.
NB.:
1. The multiresistant TB treatment is uniquely administered at a specialized unit with a
specialized team such as KABUTARE HOSPITAL
2. The quinolones (Ciprofloxacin, Ofloxacin) should not be used in the treatment of
respiratory tract infections based on the fact that there may be a risk of creating resistance of
Koch bacilli to quinolones that are used in multidrug resistant tuberculosis.
❖ TREATMENT OF TUBERCULOSIS IN PARTICULAR SITUATIONS
1. Pregnancy and breast-feeding

o First line antituberculosis drugs may be administered during pregnancy, except
streptomycin which is strictly contraindicated since it may cause definitive deafness to
the baby. Therefore, only primo-treatment will be prescribed during pregnancy.
o Every pregnant woman diagnosed for tuberculosis must know she may take the
prescribed regimen without any problem for her baby and that it is important to
successfully finish treatment in order to carry her pregnancy through.
o In case of bacilliform tuberculosis during breast-feeding, the mother will immediately
receive the adequate regimen in order to avoid transmission to the infant. All drugs
against tuberculosis may be administered to her, streptomycin included. She will
continue breast-feeding her baby who will receive INH prophylaxis.
o Second line drugs have potential teratogenic effects, particularly Kanamycin which
may also provoke deafness to the baby. The risks and benefits of treatment should be
carefully considered with the goal to protect the health of the mother and the child.
Birth control is strongly recommended for all non-pregnant women during the whole
duration of 2nd line treatment
2. Contraceptive pill
o Rifampicin may reduce the effect of the contraceptive pill. A more strongly dosed pill
(containing 50μg oestrogens) must be prescribed or use another method of
contraception.

3. Renal insufficiency
o Avoid drugs which are eliminated by kidneys: Streptomycin and Ethambutol, and
among 2d line drugs. Kanamycin, Capreomycin and Cycloserine.
o Replacement regimen (1st line): 2RHZ / 4 (RH)
4. Liver disorders
o Pyrazinamide, Isoniazid and Rifampicin are toxic for the liver.
o Standardized regimens may be used in case of previous history of viral hepatitis or in
case of alcoholism, except when there are signs of hepatic failure.
o In the case of jaundice of drug induced hepatitis (transaminases above 3 times the
normal value), stop antituberculosis drugs until jaundice disappears and transaminases
decrease to less than 3 times the normal value and re-introduce drugs with individual
tablets at progressive dose
o In case of severe chronic liver disease, consider a regimen using drugs which are
eliminated through the kidney (S and E) and excluding drugs that are metabolized
through the liver: Pyrazinamide, Prothionamide and PAS. It is preferable to refer the
patient to CHUK, where an alternative regimen will be established and agreed with the
TB Unit. For example:
● In case of predominant cholestatic alteration (high bilirubin, phospha-tases
alcalines andγGT) : alternative regimen : 2HES/10HE
● In case of predominant transaminases increase or not defined biological
alteration: alternative regimen :: 2RES/10RE
Hepatic function need to be controlled regularly
Note: Corticoids should be used only in a limited number of cases:

✔ In case of tuberculosis meningitis, in order to reduce the risk of hydrocephalus
✔ Pericarditis tuberculosis, in order to reduce the risk of constrictive pericarditis
✔ Miliary tuberculosis, in order to relieve the patient
✔ Airway compression by TB adenopathy in a child, in order to reduce the risk of
atelectasia
B.7. GUIDELINES FOR FOLLOW UP OF CLIENTS ON TREATMENT

✔ Bacteriological follow up of smear-positive patients.
Diagnosis New PTB+ Retreatment
● Send sputum to NRL for

culture and DST (even if a
sample was sent during
primo-treatment).
When positive • Check if treatment is ● Check if treatment is
at the end of the correctly supervised and correctly supervised and
intensive phase regularly taken. regularly taken.
• Send sputum to NRL for ● Send sputum to NRL for
culture and drug sensitivity culture and DST
test (DST) ● Prolong intensive phase by
• Prolong intensive phase by one month (RHZE) and
one month (RHZE) and motivate patient
motivate patient ● Do another control at the end
• Do another control at the of 4th month.
end of 3rd month. ● Go on to continuation phase
• Go on to the continuation
phase
When positive • Send sputum to NRL for ● Send sputum to NRL for
at the end of the culture and DST culture and DST
4th month • Do another control after 15 ● Do another control after 15
days and when positive, days and when positive,
declare failure inform the supervisor or the
• Begin retreatment until you MDR-TB focal point.
obtain DST results
When positive • Send a sputum sample to • Declare failure. It is a chronic
at the end of NRL for culture and DST patient, likely to be multidrug
treatment (2 • Declare failure and begin re- resistant.
sputum samples treatment • Inform the supervisor or the
with 15 days MDR-TB focal point.
interval)

✔ Follow up of smear-negative patients (PTB-)
● For precaution, one sputum exam is recommended at the end of the 2nd month
● When positive, either the patient is irregular (treatment incorrectly supervised), or there
was a diagnostic error (it is a false negative), or s/he is resistant.
When • Check whether treatment is correctly supervised and

positive at regularly taken.
the end of • Send sputum to NRL for culture and drug sensitivity testing.
the 2nd • Prolong intensive phase by one month (RHZE) and motivate
month patient.
• Do another sputum exam at the end of the 3d month, 4th
month and at the end of treatment.
• Total duration of treatment will be 7 months.
Note: The following are the indications of culture and drug sensitivity test:
● For any patient who fails to retreatment.

● For all patients starting a retreatment regimen (in particular for any failure to Category
1, even if a specimen was sent during first treatment).
● For any patient who remains positive at the end of the 2rd month of treatment or later.
● For any patient who is diagnosed with TB and who has been in close contact with a
known MDR-TB patient.
● For prisoners who are diagnosed with smear-positive TB
B.8. EXTRA PULMONARY TUBERCULOSIS
A. Definition
By definition, an extrapulmonary tuberculosis refers to any case of TB located outside the lungs
(or outside the pulmonary parenchyma).

B. Localisations
✔ Pleura, pericardium, peritoneum, ganglia, bone, articulation or joint, skin, meninges,

internal organs such as spleen, etc.
✔ The most frequent forms according to Koch bacilli localisation: Ganglionic TB (neck
and axillary), pleural TB, disseminated TB
✔ Less frequent: Pericardial and meningeal TB.
C. Types of extrapulmonary tuberculosis according to the localisation
1. GANGLIONIC TUBERCULOSIS
• Most frequent cause of adenopathies in the countries with high prevalence of TB

• Cervical ganglia are mostly affected (65%)
• The adenopathies are unilateral or bilateral, asymmetrical, painless, adherent, initially
elastic and then hard, cold, and chronic.
• Loss of weight, night sweats, fever
Essential examinations are:

• Bacilloscopy if cough is present
• Bacteriological examination of the secretions or the liquid of aspiration of the ganglion
(direct microscopic examination)
• Histological biopsy for examination or culture
Treatment: Chemotherapy without waiting for the results of the culture.
2. PLEURAL EFFUSION OR PLEURAL TUBERCULOSIS
• By pleural attack with Mycobacterium tuberculosis via lymphatic way.

• Often unilateral and massive.
• Young adults more affected or touched.
• Associated to PTB in 1/3 of the cases.

Diagnosis:
❖ Clinical signs: Dry cough, thoracic pain++ with often brutal beginning, reduction of
vesicular murmurs, matity on percussion, loss of weight, night sweats, fever
❖ Radiologic signs and ultrasonography for confirmation.
❖ Bacilloscopy: pleural puncture shows clear liquid or citrine yellow which coagulates in
the tube (exudate); rate of high Albumin (> 30gr/dl), low glucose, increased leucocytes
with lymphocytes in abundance; the direct examination under the microscopy is not
very sensitive (up to 25%), culture (up to 75% but it delays).
❖ Pleural biopsy = > granulomata confirming the diagnosis
Treatment:
✔ Chemotherapy
✔ Corticotherapy at a dosage of 40 mg/day by decreasing the doses gradually per a month.
✔ Pleural drainage
3. THE MILIARY TUBERCULOSIS
• Massive dissemination by circulatory way

• The lesions develop simultaneously in the whole organism.
• Especially attacks the children and immunocompromized persons.
● Acute form of TB
• No specific clinical manifestations: cough, dyspnea, slimming (weigth loss), and
sometimes, adenopathies, gastro intestinal disturbances.
• Diagnosis is done on basis of Chest X-ray = > small shadowy nodules disseminated
uniformly in the two pulmonary fields;
• Treatment: chemotherapy
• Bad prognosis without treatment
4. MENINGEAL TUBERCULOSIS
● Severe form of EPTB, more often attacks the non-vaccinated young children and
immuno-depressed

Clinical signs: general signs like fever, lethargy, vomiting, photophobia, irritability,
convulsions, neck stiffness, coma, death without treatment.
Diagnosis:
Lumbar puncture shows clear liquid under pressure, with increased proteins, decreased
glucose, increased leucocytes (lymphocytes).
The direct examination for KB is not very sensitive, the culture is sensitive but it gives late
results (2-6 weeks).
Essential examinations:
LP: liquid under pressure, clear, increased proteins, lowered glucose, increased leucocytes
(lymphocytes).
Search for KB in the CSF
HIV test can be an additional exam
Treatment:
The treatment must be started as soon as possible without waiting the results of the culture.
5. BONE TUBERCULOSIS
● It attacks the bones and the articulations.

● Articular TB often touches the large articulations (hips and knees).
● The Pott’s disease: the TB that touches usually the medio-thoracic vertebrae (by blood
or lymphatic way)
● Clinical manifestations: Back pain, anterior erosion of the vertebral body = >
compressing and kyphosis, possible paraplegia by medullar compression, para vertebral
cold abscesses.
● Diagnosis: clinical manifestations, radiological image and tissue biopsy.
● Treatment: Chemotherapy and mobilization of the column, surgery if the rachis is
unstable.
6. UROGENITAL TB
● Can touch any part of the urogenital system of both man and the woman.

● Renal TB is mainly manifested by pyuria, microscopic hematuria
● The standard culture of purulent discharge is sterile (sterile pyuria), it is necessary to
seek KB in the urines (at least 3 early morning urine samples are taken to identify acid-
fast bacilli).
● Ultrasonography.
● The tuberculous salpingitis causes female sterility, ectopic pregnancy.
● In the man TB touches the prostate, the seminal vesicles, and the epididymis
● Diagnosis is done by culture of the urine.
● Treatment: chemotherapy according to the therapeutic diagram
7. OTHER LOCALIZATIONS
● Pericardium: TB is responsible of 90% of the pericardial effusion among HIV positive

patients and for 50 to 70% among HIV negative people.
● Peritoneum and intestines
● Larynx and bronchi
● Eyes
● Skin
B.9. MULTIRESISTANT TUBERCULOSIS
1. Definitions:
● Resistant case: case of tuberculosis which is resistant to one or more antituberculosis

drugs.
● Multidrugresistance (MDR-TB): Resistance to at least Rifampicin and Isoniazid,
(confirmed by DST) which are the two most powerful TB drugs.
● Monoresistance: Resistance to one first-line antituberculosis drug
● Polyresistance: Resistance to more than one first-line antituberculosis drug, other than
both isoniazid and rifampicin.
2. Causes:

The problem can come from either patient and health care provider or one of two. The
following conditions can induce resistance to anti tuberculosis treatment:
● The prescribed treatment is inadequate: insufficient dose, insufficient duration

,incorrect diagram according to the category of the case.
● DOTS badly observed or done: bad follow-up of the patients. Consequently the
patient does not regularly take his treatment for the necessary required time.
● Bad management of programme (a poor national programme): irregular supplying
of drugs and out-of-stock condition
● The patient was infected starting from patient carrying resistant bacilli: this means
that the patient had an infection from a resistant TB patient and developed directly a
resistant TB form
3. When to suspect a case of multiresistance?
● In the event of retreatment failure well taken (chronic case)

● When a patient does not improve clinically and remains positive in spite of a correct,
regular and supervised treatment.
● When a case of tuberculosis is diagnosed among the contacts of a known multiresistant
patient.
4. Treatment: According to the therapeutic diagram as it has been

mentioned above
B.10. COMPLICATIONS OF TUBERCULOSIS

● Massive hemoptysis
● Pneumothorax; due to the rupture of cavern into pleural cavity
● Chronic respiratory failure
● Anemia : as a result of massive haemoptysis which may be massive and life threatening
● Pleurisy: inflammation of the pleural
● Tuberculorous pneumonia
● Broncho-pleural fistula and empyema and this may lead to pneumothorax
● Extrapulmonary tuberculosis such as gastro-intestinal tuberculosis, Pott’s Disease, etc.

II.5. LEPROSY (HANSEN'S DISEASE)
A. DEFINITION AND ETIOLOGY
It is an infectious disease caused by Mycobacterium leprae (HANSEN BACILLI). It attacks

the skin, mucus membranes and the nerves. Untreated, it causes the disabilities.
Mycobacterium leprae are weakly acid-fast and alcohol-fast bacilli in Ziehl-Neelsen stain.
When stained they appear as thin pink rods.
These bacilli have slow growth with generation time of 20 days in experimental animals.
In humans incubation period is 5-8 years, and the disease is chronic. It affects the skin and the
peripheral nerves.
B. RISK FACTORS FOR LEPROSY INFECTION
● Staying with an infectious patient in a poorly ventilated room

● Staying in contact with a patient who is not being treated or has not completed treatment
● Overcrowding
● Poor general nutrition and health status (i.e. influence of poverty)
● Not having been vaccinated with BCG
● HIV infection
● Recent measles
● Metabolic disorders e.g. diabetes mellitus
C.MODE OF TRANSMISSION OF REPROSY AND MECHANISM
● The mode of transmission of leprosy is not clearly understood, but it is thought to be

due to prolonged direct contact with infectious people through:
a. Droplet infection by sneezing, coughing, spitting, unhygienic nose cleaning

habits.
b. Broken skin
● Once in the body, leprosy bacilli divide inside macrophages of the skin and in nerve
fiber Schwann cells.

● Leprosy is a disease that is not easily caught by other people, mainly because of natural
resistance to Mycobacterium leprae (i.e. cellular immunity)
● That is when people are exposed to leprosy bacteria, most (about 75%) of people do
not develop leprosy and only some develop leprosy; a few of whom develop non-
infectious leprosy, and still fewer develop infection type of leprosy.
D. CLINICAL FEATURES OF LEPROSY
Leprosy is categorized into 4 clinical forms determined by the level of cellular immunity of the
individual as follows:
1. INDETERMINATE LEPROSY
Features are:
● Lesions(1-3) appear as small discolored(i.e. hypopigmanted) areas (i.e. maculae)

● Lesions are called indeterminate because they do not indicate how they will continue
to develop
● Most lesions heal spontaneously and many lesions are never noticed
● No loss of sensation or if any, it is slight
● No bacilli are found in smears
● Organs and nerves are not involved
● Lesions which do not heal may develop into tuberculoid, borderline or lepromatous
leprosy.
2. TUBERCULOID LEPROSY
This form is characterized by:
● Skin lesion patches are few, raised or flat large or small, with dry surface
● There is some loss of feeling due to damage of peripheral nerves
● Loss of hair and of sweating
● Patches show central healing
● Patches have marked hypopigmentation
● Cutaneous nerves may be enlarged under patches of lesions
● Paralysis is common

● Skin smear is negative
● It is seen in patients with high degree resistance(i.e. cell mediated immunity)
● Most common in dark skinned people than white (light) skinned people.
3. LEPROMATOUS LEPROSY
● Skin lesions are numerous , small, slightly raised or flat patches, maculae, or nodules
● Skin may appear thicker than normal especially on face and ears
● No loss of hair
● No loss of sweating
● No loss of sensation
● Nerves are affected later and get thickened
● There is positive skin smear
● Other organs are involved including eyes, hands, feet, testicles, nose, fingers, teeth loss
● Paralysis due to damage of motor neurons
4. BORDERLINE LEPROSY
● Has both features of tuberculoid and lepromatous leprosy

● Skin lesions are very many, raised or flat
● There is some loss of feeling
● Nerves are affected very early
● Smears range from negative to positive
E.CLINICAL DIAGNOSIS
A. HOW TO DIAGNOSE LEPROSY
• Examine skin
• Check for patches
• Test for sensation
• Count the number of patches
• Look for damage to nerves
B. CHECK FOR LOSS OF SKIN SENSATION

• Take a pointed soft object (feather, cotton wick)
• Lightly touch alternately the patch & normal skin
• Ask the person to point where they were touched
• Ask them to close their eyes and repeat the procedure
• In case of loss of sensation the person will be able to point to where they were touched
on the normal skin but not on the patch
The findings of clinical diagnosis may be as follows:
1. Presence of hypopigmented patches with loss of sensation:
❖ 1-5 patches mean paucibacillary leprosy characterized by:
o Having scanty (inadequate) bacilli in smears

o Being non-infectious e.g. Indeterminate and Tuberculoid forms
❖ 6 or more patches mean multibacillary leprosy characterized by:
o Having many bacilli in smears

o Being infectious e.g. Borderline and Lepromatous leprosy
2. Abnormally large peripheral nerves at points of predilection, for e.g. facial nerves, trigeminal
nerves, greater auricular nerves, ulnar nerve, median nerve, radial nerve, peroneal nerve and
posterior tibial nerve
F. LABORATORY DIAGNOSIS
It is based on finding acid-fast bacilli in the skin smears.

a. All positive smear cases and Borderline leprosy cases that have negative smears are
considered multibacillary e.g. Lepromatous and Borderline leprosy
b. All other negative smears cases are considered paucibacillary. E.g. Indeterminate and
Tuberculoid leprosy
G. PREVENTION AND CONTROL OF LEPROSY
❖ Treatment and management

Early diagnosis and treatment as well as management of reactions prevent all disabilities.
Major goals of treatment are:
1. Early detection of patients

2. Appropriate treatment
3. Adequate care for the prevention of disabilities and rehabilitation
There are several effective chemotherapeutic agents: Dapsone (diaphenylsulfone, DDS),

Rifampicin (RFP), Clofazimine (CLF), Ofloxacin (OFLX), and Minocycline (MINO)
constitute the backbone of the multidrug therapy (MDT) regimen. Pregnancy makes worse
the disease, pregnant women continues their treatment unchangeably as the drugs are not toxic
to the fetus.
Treatment recommended by WHO combines several drugs which are taken at the same time.
This form of treatment is called Multidrug therapy (MDT). Since 1995, WHO has supplied
MDT free of cost to all leprosy patients in the World.
The tables below show how MDT is taken (source: WHO).
Table to show MDT for pauci-bacillary Leprosy according to the WHO: Duration 6
months
MDT 0-5 YEARS 6-14 YEARS 15 YEARS AND
OVER
1.DAPSONE: 25mg 50mg 100mg
*It is taken daily.
*Self administered (or
by mother for kids) at
home and (+)
2.RIFAMPICIN: 300 mg 300mg 600mg
*It is taken once in 4
weeks
*It is supervised (i.e.
once monthly)

Treatment schedule for Multi-bacillary Leprosy: Duration 12 months
MDT 0-5 YEARS 6-14 YEARS 15 YEARS AND

OVER
1.DAPSONE: 25 mg 50 mg 100 mg
*It taken daily
*It is self-
administered
and (+)
2.RIFAMPICIN: 300 mg 300 mg 600mg
weeks,
*It must be supervised
and (+)
3.CLOFAZIMINE 100 mg 200 mg 300 mg
weeks
*It must be supervised
and (+)
4.CLOFAZIMINE 50 mg 50 mg 50 mg
*It is self administered
Alternating days Daily Daily
NOTE: Treatment should be done as close as possible to where patients live.
Side effects of used drugs:
• Dapsone (DDS): occasional cutaneous eruptions

• Rifampicin (RFP) : A slight reddish coloration of urine, sweat, and tears
• Clofazimine (CLF): Brownish :Black discoloration and dryness of skin
The health care provider has to reassure the patients
❖ Prevention

i. Prevention of injury, infection and deformity by:
a) Proper care of the skin of the patient

b) Proper care of minor wounds and skin infections
c) Provision of shoes
d) Physiotherapy
e) Health education
ii. Cases finding among the contacts of Leprosy patients through school and
community surveys.
iii. Improvement in housing and social economic status
iv. BCG immunization is slightly protective but no effective vaccine as yet
H.COMPLICATIONS
• In severe cases, disfigurement and deformities occur in the hands, feet and face.
• Blindness
• Testicular atrophy and sterility
• Liver involvement may manifest as gynaecomastia
• Paralysis
• Injuries: due to loss of sensibility
II.6 BACILLARY DYSENTERY (SHIGELLOSIS)
A. DEFINITION AND ETIOLOGY
It is acute human infection limited to the digestive tract, caused by the germs of the genus
Shigella. These are the bacteria, non motile bacilli (because of the lack of cilia), Gram-
negative, of the genus Shigella including the following species:
● Shigella dysenteriae ( the more common and severe one)

● Shigella flexneri
● Shigella boydii

● Shigella sonnei
They produce endotoxin and exotoxin, but Shigella dysenteriae is the only one that secretes
the exotoxin.
• Humans are the only reservoir of shigella bacilli.
• The bacilli cause acute diarrhea with blood (i.e. dysenteria) also called shigellosis.
B. TRANSMISSION OF BACILLARY DYSENTERY
❖ Sources of infection include:

o Sick persons of bacillary dysentery
o Convalescent carriers of bacillary dysentery: they can spread the bacilli for up
to 3 months
o Other carriers
❖ Transmission route
Transmission is by faeco-oral route
E.g.: The rule of F for faeco-oral route
Flies
Faeces Food and Water
Fingers
● Faeces transmitted to food by flies or fingers result into infection when the food is
ingested.
● Faeces can also be contracted from:
i. Visiting the toilet during anal cleaning
ii. Lavatory seats
iii. Door handle
iv. Crockery( plates, cups,saucers,bowls)
v. Cutlery( knives, forks, spoons)

vi. Bedding (e.g. bed sheets, blankets)
C. RISK FACTORS FOR BACILLARY DYSENTERY
1. Unsanitary disposal of human faeces

2. Shortage or lack of water which is safe
3. Presence of house flies
4. Seasonal changes
o In dry season, there is shortage of water
o In the wet season, there is faecal contamination of water sources from run off
water.
5. Malnutrition: it reduces resistance of the body
6. Old age or early age
7. Overcrowding e.g. in prisons, refugee camps
D. PATHOGENESIS
Shigellae are the pathogens specific to the digestive tract. They are never of normal flora. They
are eliminated through the faeces and can contaminate water and food. The human is
contaminated by ingesting food or drinking water contaminated by the faeces. The incubation
period is short (1-4 days). After ingesting the germs, the bacilli multiply in the large intestine,
invade the intestinal mucosa, penetrate in the enterocytes and destroy them using their toxin.
The endotoxin of the bacilli causes the irritation of the intestinal wall where the inflammatory
reaction of the intestinal mucosa occurs. This inflammation of the mucosa explains the
symptomatology of the disease. The mucous membrane can develop necrotic patches (areas)
which turn into ulcers and intestinal perforation. Exotoxin when absorbed results in toxemia
(toxic material in blood) leading to high fever and rapid pulse.
E.CLINICAL MANIFESTATIONS
After ingestion of many germs, they multiply in the large intestine where colitis occurs with
bloody diarrhea containing the mucus, abdominal pain, frequent diarrhea that can exceed
20 stools/ day, followed by tenesmus (i.e. painful contraction of anal sphincter) without
production of faecal matter except for blood and mucus. Frequent diarrhea can cause

dehydration. The death is due to severe hydro-electrolytic imbalance. This disease is often
accompanied by fever.
F. DIFFERENTIAL DIAGNOSIS
We must differentiate this disease from other diseases which are accompanied by dysentery
such as:
o The acute intestinal amoebiasis (amoebic dysentery)
o Salmonellosis (acute gastroenteritis)
o Hemorrhagic rectocolitis ulcer, Schistosomiasis…
The table below shows the difference between amoebic dysentery and bacillary dysentery
DISEASE FEVER NUMBER OF PARACLINIC DEHYDRATIO

STOOLS/ DAY EXAM N
AMOEBIC - < 20 Fresh -
DYSENTERY stool(direct
stool)
BACILLARY + (present) >20 Stool culture + (high risk of
DYSENTERY dehydration)
G. DIAGNOSIS
Stool examination by microscopy may show macrophages (leucocytes) containing

erythrocytes, but these can be confused with Entamoeba histolytica.
Thus, the Diagnosis of bacillary dysentery is aimed to isolate the bacteria by STOOL
CULTURE.
H. TREATMENT
✔ Rehydration therapy (by infusions or oral rehydration salts)

✔ Antibiotherapy such as quinolones (E.g.: Ciprofloxacin tablet 500mg twice daily for 3-
5 days).

I. PREVENTION
i. Observing strict personal hygiene among family contacts and the nursing staff
ii. Community preventive measures:
1. Health education on hygiene about the following topics:
a. Use of latrines
b. Use of safe (boiled/ filtered) water, safe food
c. Washing of hands with soap
d. Proper waste disposal
e. Proper excreta disposal
2. Examine if water supply is contaminated, and treat it accordingly
3. Early testing and treatment of carriers
iii. The carriers who work in alimentary sectors should be stopped to work until they are no
longer carriers.
N.B. There is no vaccine against shigellosis.
J. COMPLICATIONS
They are uncommon, but there can be:

✔ Perforation of the colon
✔ Digestive hemorrhage
II.7 CHOLERA
1. DEFINITION AND ETIOLOGY
It is a human toxi-infection caused by the presence in the intenstine of vibrio cholerae. It is an

acute infectious disease of the small intestine, caused by the bacterium vibrio cholerae and
characterized by profuse watery diarrhea, vomiting, muscle cramps, severe dehydration, and
depletion of electrolytes.
Vibrio cholerae is a Gram-negative, comma shaped rod, which is motile with a single terminal
flagellum.

2. TRANSMISSION AND PATHOGENESIS
It is an acute infectious disease, transmitted through water or food contaminated with infected
faeces from a case or a carrier.
Incubation period is 1-4 days
Infection remains in the intestine and doesn’t involve the blood.
The germs multiply in the small intestine where they release enterotoxin which acts on the
intestinal mucosa and disrupts the electrolyte balance (elimination of chloride and inhibition of
sodium absorption).
3. CLINICAL MANIFESTATIONS
The illness begins rapidly and is characterized by watery diarrhea without abdominal pain,
stool is very liquid, looking like “rice water” very frequent (more than 20-50 times / day),
abundant vomiting without effort and nausea, vomit of "rice water" appearance. Diarrhea
and vomiting lead to significant dehydration with painful muscle cramps, the hydro -
electrolytic disorders are severe and the patient is often in acidosis and hypokalemia. There is
also oliguria or anuria (hypovolemic shock + acute renal failure). Ultimately the patient
falls into a state of algidity: Cold extremities, severe hypotension, hypothermia, rapid
pulse, persistent skin folds.
4. DIAGNOSIS
It is essentially clinical and can be supported by stool culture.

5. CURATIVE TREATMENT
i. The most important part of treatment is to correct the fluid and electrolytes imbalance by
giving intravenous fluids (replacing fluids and salts losses). IV fluids containing 5g of NaCl,
4g of NaHCO3 and 1 g of KCl per liter are enough to reduce diarrhea. Or oral rehydration
solution (ORS) for patients who are still having strength.
N.B.: a) Ringer’s lactate is the preferred solution often with added potassium
b) Ten percent of a person's body weight in fluid may need to be given in the first 2 to
4 hours

c) If oral rehydration solutions are not available, solutions can be made as follows: 1
litre of boiled water, 1/2 teaspoon of salt, 6 teaspoons of sugar, and added mashed banana for
potassium and to improve taste
ii. Antibiotics should be given to only the most severe cases:
o Doxycycline as first line;Tetracycline 10mg/ kg/ 6h PO for 48 h reduces fluids loss
o Other drugs are indicated by antibiogram (Negram,bactrim,erythromycin, etc)
6. PREVENTION AND CONTROL
1. Measures to improve food and personal hygiene and sanitation are the most important factors
2. Killed whole cell vaccine gives only 50-60% of protection
3. Health education about:
a. Food and water hygiene and sanitation
b. Sanitary disposal of human excreta by burying or mixing with disinfectant, incineration
of solid wastes.
c. Disinfecting patients clothing by boiling for 5 minutes
d. Drying bedding in the sun
e. Burial should be done quickly and near the place of death
f. Discourage ritual washing of the dead
g. Discourage funeral feasts ( it is culturally possible)
Cholera is a notifiable disease. Therefore:

❖ Patients should be treated without being referred
❖ Notify District Medical Officer
❖ Take stool specimens for culture
7. COMPLICATIONS
✔ Severe dehydration and shock

✔ Renal failure
✔ Hypoglycemia
✔ Hypokalemia
II.8 SYPHILIS

A. DEFINITION
Syphilis is a sexually transmitted disease caused by bacteria, Treponema pallidum, a

microscopic organism called a spirochete. The highly infectious disease may also be passed,
but much less often, through blood transfusions or from mother to fetus in the womb.
Without treatment, syphilis can cause irreversible damage to the brain, nerves, and body
tissues.
B. CLINICAL MANIFESTATIONS
Syphilis is an infection that can stay in the body for years if not recognized and treated
quickly.
There are two forms: acquired and congenital syphilis
1. ACQUIRED SYPHILIS
Observed in adults, it evolves in four stages of syphilis, and each stage has distinct signs and
symptoms.
✔ Primary stage: it usually occurs 3 weeks after the infectious contact. It is characterized by
a chancre, indurated and painless ulceration, single, localized at the point of inoculation of
the external genitalia (penis, vulva).
The chancre generally appears on the genital area but can also form on the lips, tongue or
rectum if these areas have been exposed to a syphilis chancre on another person during oral
or anal sexual contact. A chancre in the vagina, mouth or rectum is generally not easily
seen.
The chancre is accompanied by a regional satellite lymphadenopathy, inguinal and often
painless. Untreated, the chancre heals spontaneously in 4 to 6 weeks.
✔ Secondary stage: corresponds to bacterial dissemination phase. If left untreated, primary

syphilis progresses to a second stage called secondary syphilis. In this stage, the bacteria
that cause syphilis spread throughout the body and cause additional symptoms. It usually

occurs around 2 months after the contamination. Symptoms begin to appear after the
chancre has resolved and include:
● Skin lesions that are very contagious: Syphilitic roseola, Papules
● Mucosal lesions that are very contagious: Painless erosions especially at the oral
mucosa and genital mucosa (mucous patches, condylomata ...). These signs
disappear spontaneously in 1 to 2 years.
● General symptoms: fever, general malaise, headache, flu-like symptoms, weight
loss, fatigue...
✔ Latent stage: This stage occurs after signs and symptoms of secondary syphilis resolve or
reduce. The latent stage is between secondary and tertiary stages. The latent stage is
characterized by little to no symptoms of syphilis.
✔ Tertiary stage: The third and final stage of syphilis is called tertiary or late-stage syphilis,
which develops from untreated secondary syphilis. When untreated secondary syphilis
symptoms disappear, the infection still continues in the body. Symptoms of tertiary syphilis
may appear within 10 to 20 years after initial infection with syphilis. During this time,
syphilis can damage organs, such as the brain (general paralysis), cardiovascular system
(aortitis, aortic aneurysm), liver (the disease is similar to cirrhosis), bones, and nerves,
leading to serious complications.
The germs can be located anywhere (in the liver, kidneys, bones, stomach)
This stage is characterized by gummas.
2. CONGENITAL SYPHILIS
Transmission of T. pallidum from a syphilitic woman to her fetus across the placenta may occur
at any stage of pregnancy, but fetal damage generally does not occur until after the fourth
month of gestation, when fetal immunologic competence begins to develop. There are two
types:
1. Early congenital syphilis: the one of the Newborn.
The earliest signs occur between 2-10 weeks after birth and are infectious.

The earliest signs of congenital syphilis include rhinitis with purulent or bloody secretions
which is soon followed by other mucocutaneous lesions: bullae (syphilitic pemphigus or
pemphigus syphiliticus) in the palm of the hands and soles of the foot, vesicles, superficial
desquamation, petechiae, and (later) papulosquamous lesions, mucous patches, and
condylomata. In this stage of congenital syphilis, it was seen that the most common early
manifestations are bone changes (61%), including osteochondritis, osteitis, and periostitis
detectable by x-ray examination of long bones; hepatosplenomegaly (50%); lymphadenopathy.
2. Late congenital syphilis: it develops among old children.
Signs and symptoms appear after 2 years and are non infectious. This type is characterized by:
o Teeth deformation
o Osteo-arthritis
o Eye affection (keratitis): more common and occurs between ages 5-25.
o Perforation of uvula
N.B. SPECIAL CLINICAL FORM is syphilis in pregnant women where it may cause:
o Spontaneous abortion
o Stillbirth
o Premature birth or at term but presenting signs of congenital syphilis.
C. PARACLINICAL DIAGNOSIS
❖ Primary stage: collect the fluid at the chancre and the direct examination by
microscopy to search for spirochetes (Treponema pallidum)
❖ Secondary and tertiary stage: serological tests are made. Serological tests are the
most effective methods. They are aimed to search for antisyphilitic antibodies. There
are two types of serological tests for syphilis:
✔ Non-treponemal antigen (cardiolipia): Non specific

✔ Treponemal antigen: Specific
1. Non-treponemal antigen tests:

o To detect anticardiolipide antibodies.

o Cardiolipide is a constituent of the cytoplasmic membrane of treponema pallidum.
Non treponemal antigen tests include:
a.VDRL (Venereal Disease Research Laboratory):

Cardiolipin antigen plus serum produces clump (agglutination) in positive result
b.RPR Test (Rapid Plasma Reagin): not in use today
2. Treponemal antigen tests:

o Use antigens of treponema pallidum and they are more specific.
They include:
i. T.P.H.A (Treponema Pallidum Hemagglutination Assay)

ii. F.T.A-Abs test (Fluorescent Treponema Antibody Absorbed): permits putting in evidence
of IgM antibodies. Highly specific and sensitive, and so widely used.
iii. ELISA (Enzyme Linked Immunosorbent Assay): It is rarely used because it is very
expensive.
N.B. In case of neurosyphilis, the CSF (cerebrospinal fluid) is used for examination.
D. TREATMENT
1. Primary and Secondary stage of Syphilis

o Benzathine Penicillin 2.4 Mega Units (MU) IM as a single dose
2. Tertiary stage of Syphilis (i.e. cardiovascular and neurosyphilis)
o Benzathine Penicillin 2.4 MU in IM weekly for 3 to 4 weeks
E. PREVENTION AND CONTROL
i.Condoms use
ii.Avoid having sex with multiple partners
iii.Screen pregnant women for syphilis infection where possible
iv.Screening and treatment of infected individuals (secondary prevention)
F.COMPLICATIONS

Complications of syphilis include:
• An increased risk for contracting HIV, which causes AIDS

• Aortic aneurysm: Dilation of aorta
• Birth defects
• Blindness
• Dementia
• Paralysis
• Stillbirth
II.9 CHANCROID (OR SOFT SORE)
1. GENERALITIES
Chancroid (also known as soft chancre or ulcus molle) is a sexually transmitted infection
caused by Haemophilus ducreyi and characterized by painful sores on the genitalia.
H.ducreyi is Gram-negative coccobacillus.
It causes a soft sore on sex organs.
Women do not show symptoms in vagina when infected. So infected males cannot have sexual
intercourse because of pain, and therefore they do not transmit infection. Buboes (lymph nodes
with pus) can also develop as one of the symptoms.
Infection is acquired as the result of a break in the epithelium during sexual contact with an
infected individual. After an incubation period of 4-7 days, the initial lesion (a papule with
surrounding erythema) appears. In 2 to 3 days, the papule evolves into a pustule, which
spontaneously ruptures and forms a sharply circumscribed ulcer that is generally not indurated.
The ulcers are painful and bleed easily, little or no inflammation of the surrounding skin is
evident. Approximately half of patients develop enlarged, tender inguinal lymph nodes, which
frequently become fluctuant and spontaneously rupture.
⮚ The CDC’s standard clinical definition for a probable case of chancroid includes
all of the following:

● Patient has one or more painful ulcers. The combination of a painful ulcer with tender
adenopathy is suggestive of chancroid; the presence of suppurative adenopathy is
almost pathognomonic.
● No evidence of Treponema pallidum is indicated by dark-field examinationof ulcer or
by a serologic test for syphilis performed at least 7 days after the onset of ulcer.
● The clinical manifestation is not typical of disease caused by human herpesvirus 2
(Herpes Simplex Virus), or result of culture for HSV is negative.
N.B.: The chancroid ulcer has typical features. The ulcer characteristically:
o Ranges in size dramatically from 3 to 50 mm

o Is painful
o Has sharply defined, undermined borders
o Has irregular or ragged borders
o Has a base that bleeds easily if traumatized or scraped
o Painful lymphadenopathy occurs in 30 to 60% of patients
About half of infected men have only a single ulcer. Women frequently have four or more
ulcers, with fewer symptoms. Most common symptoms in women are dysuria and
dyspareunia.
The initial ulcer may be mistaken as a “hard” chancre, the typical sore of primary syphilis as
opposed to the “soft chancre” of chancroid.
⮚ Comparison with syphilis
a. Similarities:
● Both originate as pustules at the site of inoculation, and progress to ulcerated lesions.
● Both lesions are typically 1-2 cm in diameter
● Both lesions are caused by sexually transmissible organisms
● Both lesions typically appear on the genitals of infected individuals
● Both lesions can present at multiple sites and with multiple lesions
b. Differences:

● Chancre is a lesion typical of infection with the bacterium that causes syphilis,
Treponema pallidum whereas Chancroid is a lesion typical of infection with the
bacterium Haemophilus ducreyi
● Chancres are typically painless, whereas chancroids are typically painful
● Chancres are typically non-exudative, whereas chancroids typically have a grey or
yellow purulent exudates
● Chancres have a hard (indurated) edge, whereas chancroid have a soft edge
● Chancres heal spontaneously within three to six weeks, even in the absence of treatment
● Chancres can occur in the pharynx as well as genitals
3. DIAGNOSIS
✔ Gram-negative coccobacilli are identified in fluid from chanchroid (but Gram stain can
be misleading because of other organisms found in most genital ulcers)
✔ Isolation of bacteria H.ducreyi in a culture from a genital ulcer
4. TREATMENT OF CHANCROID
Antibiotherapy is given and there are many alternatives:
o Norfloxacin 800 mg orally in a single dose

o Single IM dose of Ceftriaxone
o Oral ciprofloxacin for seven days: 2 times 500 mg/day
o Oral Erythromycin for seven days: 3 times 500mg/day for an adult
Partners should be examined and treated regardless of whether symptoms are present.
5. PREVENTION
i. Condoms use
ii. Not having sex until the end of treatment
iii. Avoid having sex with many partners
iv. Abstinence (not having sex)
II. 10 GONORRHEA

1. DEFINITION
Gonorrhea is an acute or chronic common sexually transmitted infection caused by the

bacterium Neisseria gonorrhoeae.
2. ETIOLOGY
Etiologic agent: Neisseria gonorrhoeae, Gram-negative intracellular diplococcus.It is found

only in humans with different epidemiological presentations for females and males.
3. TRANSMISSION
It is transmitted through sexual intercourse, but also perinatal transmission (mother-to-child) is

possible.
4. RISK FACTORS
⚫ Multiple sex partners or inconsistent condom use

⚫ Urban residence in areas with high disease prevalence
⚫ Lower socio-economic status
⚫ Have a partner with a past history of any sexually transmitted infection
⚫ No use of a condom during sex
⚫ Alcohol or illegal substances abuse
⮚ In men: (90% of infected men develop symptoms)
Symptoms in men include:
⚫ Burning and pain while urinating

⚫ Increased urinary frequency or urgency
⚫ Discharge from the penis (purulent discharge)
⚫ Red or swollen opening of penis (urethra)
⚫ Tender or swollen testicles
⚫ Sore throat (gonococcal pharyngitis)

If untreated, it can be complicated in:
✔ Epididymitis: Inflammation of the epididymis. Its symptoms include unilateral testicular

pain and swelling
✔ Prostatitis: Inflammation of prostate gland
✔ Male sterility: Due to inflammation of vas deferens
✔ Vesicle seminal inflammation
✔ Urinary retention: due to narrowing of urethra
✔ Hydronephrosis: associated with urinary retention and increased pressure in kidney
⮚ In women( 40% of infected women develop symptoms)

Symptoms in women can be very mild or nonspecific, and may be mistaken for another
type of infection. In women (40% of infected women develop symptoms). The vagina is
normally not infected because of reproductive age. However in prepubertal girls and women
after menopause the acid production in vagina is very limited, and therefore the vagina and
vulva inflammation (vulvo-vaginitis) can occur in epidemic proportions of these age groups.
They include:
● Vaginal discharge
● Burning and pain while urinating
● Increased urination
● Sore throat
● Painful sexual intercourse
● Severe pain in lower abdomen (if the infection spreads to the fallopian tubes and
stomach area)
● Fever (if the infection spreads to the fallopian tubes and stomach area)
If the infection spreads to the bloodstream, fever, rash, and arthritis-like symptoms may occur.
If untreated, for women, it can complicate in:
✔ Accessory gland infection

⚫ Bartholin’s glands: Bartholin’s abscess
⚫ Skene’s glands
✔ Pelvic Inflammatory Disease (PID)
✔ Peritonitis
✔ Endometritis: inflammation of the endometrium

✔ Sterility: due to narrowing of fallopian tubes in case of chronic salpingitis
N.B. Gonorrhea infection in children
⚫ Perinatal: The child is infected during delivery when he is passing through infected
maternal genital tract. It can cause infections of the conjunctiva (Gonococcal
Ophthalmia) , pharynx, respiratory tract
⚫ Untreated, blindness can occur
6. DIAGNOSIS
1. Gonorrhea can be quickly identified by staining a sample of tissue or discharge and then
looking at it under a microscope. This is called a Gram stain. Although this method is fast, it is
not the most certain.
Gram stain tests used to diagnose gonorrhea include:
● Cervical gram stain in women
● Gram stain of urethral discharge in men
● Joint fluid Gram stain
2. Cultures (cells that grow in a lab dish) provide absolute proof of infection. Generally,
samples for a culture are taken from the cervix, vagina, urethra, anus, or throat. Cultures can
provide a preliminary diagnosis often within 24 hours and a confirmed diagnosis within 72
hours.
Cultures used to diagnose gonorrhea include:
● Endocervical culture in women
● Urethral discharge culture in men
● Throat swab culture in both men and women
● Rectal culture in both men and women
● Culture of joint fluid
● Blood cultures
DNA tests are especially useful as a screening test. They included the ligase chain reaction
(LCR) test. DNA tests are quicker than cultures. Such tests can be performed on urine samples,
which are a lot easier to collect than samples from the genital area.

If someone has gonorrhea, s/he should ask to be tested for other sexually transmitted infections,
including chlamydia, syphilis, and HIV. If she is 21 or older, she should be sure she has had a
recent pap smear.
7. TREATMENT
⮚ First line treatment (not in pregnant woman):

Norfloxacin 800 mg orally in a single dose
Or Ciprofloxacin 500 mg orally in a single dose
Or Ofloxacin 400 mg orally in a single dose
⮚ Second line treatment:

⚫ Spectinomycin 2 g in a single IM dose
Or Cefotaxime 2 gr IM in a single dose
Or Azithromycin 1 gr orally in a single dose
⚫ Single-dose cephalosporin regimens
⚫ Ceftizoxime 500 mg IM
⚫ Cefoxitin 2 g IM with Probenecid 1 g orally
8. PREVENTION
✔ Health education: use of condoms, sexual abstinence …

✔ Early diagnosis and treatment
✔ Regular eye washing with 1% Tetracycline eye ointment in the newborn to prevent
infection
Note: Partner management

⚫ Evaluate and treat all sex partners for N.gonorrhoeae
⚫ Avoid sexual intercourse until therapy is completed and provided that both partners no
longer have symptoms.
II. 11 BORRELIOSIS OR LYME DISEASE

1. DEFINITIONS
o Borreliosis: it is an infection with spirochetes of the genus Borrelia
o Lyme disease, or Lyme borreliosis, is an emerging infectious disease caused by at least

three species of bacteria belonging to the genus Borrelia: Borrelia burgdorferi sensu
stricto, Borrelia afzelii and Borrelia garinii.
The disease is named after the town of Lyme, Connecticut, USA, where a number of cases were
identified in 1975. Although Allen Steere realized Lyme disease was a tick-borne disease in
1978, the cause of the disease remained a mystery until 1981, when B. burgdorferi was identified
by Willy Burgdorfer.
2. ETIOLOGY
Lyme disease is caused by Gram-negative, spirochetal bacteria from the genus Borrelia. At
least 11 Borrelia species have been discovered, three of which are known to be Lyme-
related. The Borrelia species that cause Lyme disease are collectively known as Borrelia
burgdorferi sensu lato, and show a great deal of genetic diversity.
The group Borrelia burgdorferi sensu lato, made up of three closely related species, are probably
responsible for the large majority of cases: B. burgdorferi sensu stricto , B. afzelii, and B.
garinii. Some studies have also proposed B. bissettii and B. valaisiana may sometimes infect
humans, but these species do not seem to be important causes of disease.
3. TRANSMISSION
Lyme disease is a zoonosis, transmitted to humans from a natural reservoir among rodents
by ticks. Hard-bodied ticks of the genus Ixodes are the main vectors of Lyme disease. Most
infections are caused by ticks in the nymphal stage, as they are very small and may feed for long
periods of time undetected. Larval ticks are very rarely infected. Tick bites often go unnoticed
because of the small size of the tick in its nymphal stage, as well as tick secretions that prevent
the host from feeling any itch or pain from the bite. However, transmission is quite rare, with

only about 1% of recognized tick bites resulting in Lyme disease; this may be because an infected
tick must be attached for at least a day for transmission to occur.
4. PATHOPHYSIOLOGY
Borrelia burgdorferi can spread throughout the body during the course of the disease, and has
been found in the skin, heart, joint, peripheral nervous system, and central nervous system. Many
of the signs and symptoms of Lyme disease are a consequence of the immune response to the
spirochete in those tissues.
B. burgdorferi is injected into the skin by the bite of an infected Ixodes tick. Tick saliva, which
accompanies the spirochete into the skin during the feeding process, contains substances that
disrupt the immune response at the site of the bite. This provides a protective environment where
the spirochete can establish infection. The spirochetes multiply and migrate outward within
the dermis. The host inflammatory response to the bacteria in the skin causes the characteristic
circular EM lesion. Neutrophils, however, which are necessary to eliminate the spirochetes from
the skin, fail to appear in the developing EM lesion. This allows the bacteria to survive and
eventually spread throughout the body.
Days to weeks following the tick bite, the spirochetes spread via the bloodstream to joints, heart,
nervous system, and distant skin sites, where their presence gives rise to the variety of symptoms
of disseminated disease. The spread of B. burgdorferi is aided by the attachment of the host
protease plasmin to the surface of the spirochete. If untreated, the bacteria may persist in the body
for months or even years, despite the production of B. burgdorferi antibodies by the immune
system. The spirochetes may avoid the immune response by decreasing expression of surface
proteins that are targeted by antibodies, antigenic variation of the VlsE surface protein,
inactivating key immune components such as complement, and hiding in the extracellular
matrix, which may interfere with the function of immune factors.
In the brain, B. burgdorferi may induce astrocytes to undergo astrogliosis (proliferation

followed by apoptosis), which may contribute to neurodysfunction. The spirochetes may also
induce host cells to secrete products toxic to nerve cells, including quinolinic acid and
the cytokines IL-6 and TNF-alpha, which can produce fatigue and malaise. Both microglia and
astrocytes secrete IL-6 and TNF-alpha in the presence of the spirochete. This cytokine response
may contribute to cognitive impairment.

A developing hypothesis is that the chronic secretion of stress hormones as a result
of Borrelia infection may reduce the effect of neurotransmitters, or other receptors in the brain
by cell-mediated proinflammatory pathways, thereby leading to the dysregulation of
neurohormones, specifically glucocorticoids and catecholamines, the major stress hormones.
This process is mediated via the hypothalamic-pituitary-adrenal axis.
Additionally tryptophan, a precursor to serotonin, appears to be reduced within the central
nervous system (CNS) in a number of infectious diseases that affect the brain, including Lyme.
Researchers are investigating if this neurohormone secretion is the cause
of neuropsychiatric disorders developing in some patients with borreliosis.
5. SIGNS AND SYMPTOMS
Lyme disease can affect multiple body systems and produce a range of symptoms.
✔ The incubation period: (1 to 2 weeks), but can be much shorter (days), or much longer
(months to years). Asymptomatic infection exists, but occurs in less than 7% of infected
individuals.
✔ Early localized infection:
The classic sign of early local infection with Lyme disease is a circular, outwardly expanding rash
called erythema chronicum migrans (also erythema migrans or EM), which occurs at the site
of the tick bite three to thirty days after the tick bite.The rash is red, and may be warm, but is
generally painless. Classically, the innermost portion remains dark red and becomes indurated;
the outer edge remains red; and the portion in between clears, giving the appearance of a bull’s
eye.
Patients can also experience flu-like symptoms, such as headache, muscle soreness, fever, and
malaise. Lyme disease can progress to later stages even in patients who do not develop a rash.
✔ Early disseminated infection:
It is characterized by the spread of Borrelia through the bloodstream. EM may develop at sites
across the body that bear no relation to the original tick bite. Another skin condition
called borrelial lymphocytoma occurs.It is a purplish lump that develops on the ear lobe, nipple,
or scrotum. Other discrete symptoms include migrating pain in muscles, joint, and tendons,
and heart palpitations and dizziness caused by changes in heartbeat.

Various acute neurological problems, termed neuroborreliosis, appear in 10–15% of untreated
patients. These include facial palsy, meningitis, which involves severe headaches, neck
stiffness, and sensitivity to light. Radiculoneuritis causes shooting pains that may interfere
with sleep, as well as abnormal skin sensations. Mild encephalitis may lead to memory
loss, sleep disturbances, or mood changes.
✔ Late persistent infection:
After several months, untreated or inadequately treated patients may go on to develop severe and
chronic symptoms that affect many parts of the body, including the brain, nerves, eyes, joints
and heart. Many disabling symptoms can occur, including permanent paraplegia.
Chronic neurologic symptoms occur in up to 5% of untreated patients. A polyneuropathy that

involves shooting pains, numbness, and tingling in the hands or feet may develop. A neurologic
syndrome called Lyme encephalopathy is associated with subtle cognitive problems, such as
difficulties with concentration and short-term memory. These patients may also experience
profound fatigue. Depression and fibromyalgia are also possible. Chronic encephalomyelitis,
which may be progressive, can involve cognitive impairment, weakness in the legs, awkward
gait, facial palsy, bladder problems, vertigo, and back pain. In rare cases, untreated Lyme
disease may cause frank psychosis.
Lyme arthritis usually affects the knees.
Acrodermatitis chronica atrophicans (ACA) is a chronic skin disorder I sometimes

observed.ACA begins as a reddish-blue patch of discolored skin, often on the backs of the hands
or feet. The lesion slowly atrophies over several weeks or months, with the skin becoming first
thin and wrinkled and then, if untreated, completely dry and hairless.
NB: CHRONIC LYME DISEASE
The term "chronic Lyme disease" or "post-Lyme disease syndrome" is often applied to several
different sets of patients. One usage refers to people suffering from the symptoms of untreated
and disseminated late-stage Lyme disease: arthritis, peripheral
neuropathy and/or encephalomyelitis. The term is also applied to people who have had the
disease in the past and some symptoms remain after antibiotic treatment, which is also called
post-Lyme disease syndrome. A third and controversial use of the term applies to patients with

nonspecific symptoms, such as fatigue, who show no objective evidence they have been infected
with Lyme disease in the past, since the standard diagnostic tests for infection are negative.
6. DIAGNOSIS
Lyme disease is diagnosed clinically based on symptoms, objective physical findings (such
as erythema migrans, facial palsy or arthritis) or a history of possible exposure to infected
ticks, as well as serological blood tests.
⮚ Laboratory testing:
The most widely used tests are serologies. The serological laboratory tests most widely available
and employed are the Western blot and ELISA.
Polymerase chain reaction (PCR) tests for Lyme disease have also been developed to detect the
genetic material (DNA) of the Lyme disease spirochete.
⮚ Imaging:
Neuroimaging does not provide specific patterns unique to neuroborreliosis, but may aid
in differential diagnosis and in understanding the pathophysiology of the disease
7. PREVENTION
o Attached ticks should be removed promptly, as removal within 36 hours can reduce
transmission rates.
o Protective clothing includes a hat, long-sleeved shirts and long trousers tucked into socks
or boots.
o Light-colored clothing makes the tick more easily visible before it attaches itself.
o People should use special care in handling and allowing outdoor pets inside homes
because they can bring ticks into the house.
o A more effective, communitywide method of preventing Lyme disease is to reduce the
numbers of primary hosts on which the deer tick depends, such as rodents, other small
mammals, and deer.
o Reduction of the deer population may, over time, help break the reproductive cycle of the
deer ticks and their ability to flourish in suburban and rural areas.

⮚ Management of host animals
Lyme and all other deer tick-borne diseases can be prevented on a regional level by reducing the
deer population on which the ticks depend for reproductive success.
⮚ Vaccination
A recombinant vaccine against Lyme disease, based on the outer surface protein A (OspA) of B.
burgdorferi, was developed by GlaxoSmithKline was found to confer protective immunity
to Borrelia in 76% of adults and 100% of children with only mild or moderate and
transient adverse effects.
8. TREATMENT
o First line: According to the Infectious Diseases Society of America (IDSA) guidelines,
the antibiotics of choice are doxycycline (in adults), amoxicillin (in
children), erythromycin (for pregnant women) and ceftriaxone, with treatment lasting 10
to 28 days.
o Second line: Alternative choices are cefuroxime and cefotaxime. Treatment of pregnant
women is similar, but tetracyclines should not be used.
9. PROGNOSIS
For early cases, prompt treatment is usually curative. However, the severity and treatment of
Lyme disease may be complicated due to late diagnosis, failure of antibiotic treatment, and
simultaneous infection with other tick-borne diseases (coinfections), including ehrlichiosis,
, babesiosis, and immune suppression in the patient.

CHAPTER III. PARASITIC DISEASES
III.1 MALARIA
AA. DEFINITION
Malaria is a febrile parasitic disease caused by the pathogenic action of hematozoa of different
species of the genus Plasmodium transmitted to humans through the bite of a mosquito vector,
female anopheles.
B. ETIOLOGY AND TRANSMISSION
Four species of the genus Plasmodium are responsible for human malaria. These are P.
falciparum, the most prevalent agent of malaria, which kills; P. vivax; P. ovale; and P.
malariae.
Only female mosquitoes feed on blood while male mosquitoes feed on plant nectar, thus males
do not transmit the disease. The females of the Anopheles genus of mosquito prefer to feed at
night. They usually start searching for a meal at dusk, and will continue throughout the night until

taking a meal. Malaria parasites can also be transmitted by blood transfusions, although this is
very rare.
The geographical distribution of malaria depends on the climatic conditions necessary for the
survival of the vectors (the Anopheles mosquito) and the parasite. The vector needs a humid
climate, a warm average temperature, and suitable bleeding places. The development of
mosquitoes from eggs to larvae to adults is temperature dependent such that at 31 0 C it will take
7 days and at 20 0 C it will take 20 days. Malaria parasites develop successfully in the mosquito
at mean daily temperature of 160-210 C. Thus, the development of malaria parasites in the
mosquito is also temperature dependent such that at 30 0 C it will take 9 days, but below 16 0 C
the mosquito is likely to have died before the parasite is ready for transmission as a sporozoite.
Temperature and altitude are, therefore, important determinants of malaria transmission
C.LIFE CYCLE OF THE MALARIA PARASITE
Malaria develops via two phases: an exoerythrocytic and an erythrocytic phase. The
exoerythrocytic phase involves infection of the hepatic system, or liver, whereas the erythrocytic
phase involves infection of the erythrocytes, or red blood cells. When an infected mosquito pierces
a person's skin to take a blood meal, sporozoites in the mosquito's saliva enter the bloodstream
and migrate to the liver. Within minutes of being introduced into the human host, the sporozoites
infect hepatocytes, multiplying asexually and asymptomatically for a period of over 5-16 days
depending on the species. Once in the liver, these organisms differentiate to yield thousands of
merozoites, which, following rupture of their host cells, escape into the blood and infect red
blood cells, thus beginning the erythrocytic stage of the life cycle. Then, the merozoites infect red
blood cells, where they develop into ring forms, trophozoites and schizonts which in turn
produce further merozoites over 1-3 days depending on the species. . This asexual multiplication
can result in thousands of parasite-infected cells in the host bloodstream, leading to illness and
complications of malaria that can last for months if not treated.
Some of the merozoite-infected blood cells leave the cycle of asexual multiplication. Instead of
replicating, the merozoites in these cells develop into sexual forms of the parasite, called male
and female gametocytes, that circulate in the bloodstream which, if taken up by a mosquito, will
infect the insect and continue the life cycle. When a mosquito bites an infected human, it ingests
the gametocytes. In the mosquito gut, the infected human blood cells burst, releasing the

gametocytes, which develop further into mature sex cells called gametes. Male and female
gametes fuse to form diploid zygotes, which develop into actively moving ookinetes that burrow
into the mosquito midgut wall and form oocysts. Growth and division of each oocyst produces
thousands of active haploid forms called sporozoites. After 8-15 days, the oocyst bursts, releasing
sporozoites into the body cavity of the mosquito, from which they travel to and invade the
mosquito salivary glands. The cycle of human infection restarts when the mosquito takes a blood
meal, injecting the sporozoites from its salivary glands into the human bloodstream.
Some P. vivax and P. ovale sporozoites do not immediately develop into exoerythrocytic phase
(merozoites), but instead produce hypnozoites that remain dormant for periods ranging from
several months (6–12 months typically) to as long as three years. After a period of dormancy,
they reactivate and produce merozoites. Hypnozoites are responsible for long incubation and
late relapses in these two species of malaria.
The fever in malaria occurs at the end of erythrocytic phase. During this phase, the merozoites
lyse the RBCs and this hemolysis is accompanied by the release of HEMOZOIN pigment which
directly goes and disturbs the HYPOTHALAMIC functioning and causes the occurrence of fever.
The erythrocytic phase occurs every 48 h in cases of P. falciparum, P. vivax and P. ovale and 72
hours in case of P. malariae. Thus, P. falciparum, P. vivax and P. ovale are responsible for Tertian
fever (fever occurring at every 3rd day or after 2 days) and P. malariae is responsible for quatarn
fever (fever occurring at every 4th day or after 3 days). Then, the fever is intermittent (fever
occurring at regular intervals).
Note: Definitions of some terminologies that relates to lifecycle of malaria parasite
Diploid: Cells containing a full set of chromosomes.

Gametes: Reproductive elements, male and female.
Gametocytes: Precursors of the sexual forms of the malaria parasite, which release either male
or female gametes within the stomach of the mosquito.
Haploid: Cells containing a half set of chromosomes.
Merozoite: The form of the malaria parasite that invades red blood cells.
Oocyst: A stage of the malaria parasite within the mosquito which is produced when male and
female gametes combine.

Ookinete: The actively moving zygote of the malarial organism that penetrates the mosquito
stomach to form an oocyst under the outer gut lining.
Sporozoite: The infectious form of the malaria parasite, which is injected into people by
mosquitoes.
Zygote: The diploid cell resulting from union of a male and a female gamete.
❖ Sexual cycle happens in mosquito and is called SPOROGONY

❖ Asexual cycle happens in human and is called SCHIZOGONY
D. PHYSIOPATHOLOGY
The symptoms of malaria are directly or indirectly linked to the erythrocytic schizogonia, while
hepatic schizogonia is asymptomatic. The severity of the clinical picture depends on the parasite
species.
Fever results from the release of pyrogens (HEMOZOIN) during haemolysis.
Pallor of the mucous membranes or anaemia is due to lysis of red blood cells parasitized.

Hepatomegaly and splenomegaly occur after a certain period of evolution. This is related to
macrophage hyperactivity (phagocytosis of residue of RBCs) and congestion of these organs.
Severe forms of malaria are primarily due to P.falciparum which multiplies in the capillary
vascular organs. These mechanical phenomena cause a slowdown in the local circulatory flow,
plus the parasitized red blood cells lysis and release of cytokines by the activated macrophages.
The result will be a circulatory anoxia, anemic and cytotoxic effects responsible for the suffering
and the multi-organ failure, especially with cerebral coma and convulsions.
P.falciparum has a tropism to capillaries of deep organs, and its multiplication inside the
erythrocytes of those organs create the thrombosis (capillary obstruction) and cause cellular
anoxia.
E. CLINICAL FEATURES
The sporozoites and liver stages do not cause clinical symptoms. Illness only begins once the
invaded RBCs rupture to release new merozoites and vasoactive peptides which also activate the
immune system. Thereafter, late-stage trophozoites and schizonts are hidden in deep tissues
(spleen, brain, liver) where they may cause significant damage. This involves immune complex
formation, blockage of capillaries, breakdown of normal capillary lining and abnormal
metabolic activity (lactic acidosis) which may lead to severe illness. The merozoites of P.
Falciparum are able to invade erythrocytes of all ages (young and old). The merozoites of other
plasmodia prefer young erythrocytes. P.falciparum infections also multiply more efficiently,
resulting in a higher parasite density and hence more severe clinical illness.
Note that the signs and symptoms of malaria are non-specific and can mimic those of many other
infections
Therefore, according to clinical manifestations, malaria is classified into three forms:

● Simple malaria
● Simple malaria with minor digestive symptoms and
● Severe malaria
1. SIMPLE MALARIA

The incubation varies according to plasmodial species. But generally it is about 15 days.
● Onset or prodromal phase: headache, anorexia, nausea, fatigue, arthralgia, lombalgia,
myalgia, herpes labialis. These signs are the same for each patient. This phase lasts 1
to 2 hours, then suddenly occurs overwhelming phase.
● Overwhelming phase; access is done in 3 stages, easily identifiable: Chills, Fever and
Sweating.
I. STAGE OF CHILLS (cold stage): Marked by feeling of cold with tremors throughout the
body, slam of the teeth, the patient seeks coverage, vibrating bed by intense chills. The fever
rises to 39oC, and digestive signs may occur such as nausea, vomiting and diarrhea. This stage
lasts 1 to 2 hours.
II. STAGE OF HEAT: Shivering stops, the patient rejects blankets claimed earlier, the skin
is dry and hot, the fever reaches 40oC or more, the earlier signs are functional at their maximum
( headache , vomiting). The pulse is often rapid in connection with temperature and sometimes
it is slower. The patient is thirst. This stage lasts 3 to 4 hours.
III. STAGE OF PROFUSE SWEATING: bathing the sick, the temperature suddenly
collapses with a hypothermic phase (36.5oC), BP rises. This stage lasts 2 to 4 hours. It is
sometimes followed by a feeling of euphoria or well being.
This is an illness characterized by axillary temperature superior or equal to 37.5°C (hot body)
or history of fever in the last 24 hours with or without the following signs: headache, weakness,
chills, loss of appetite, stiffness, joints pain and muscular pains.
Laboratory confirmation using either a blood smear or a rapid diagnostic test is compulsory
in all cases without exception. Signs of severity and other illnesses must be looked for and
excluded systematically.
In endemic areas of malaria, moderate pallor of the palms without an obvious cause in a
pregnant woman and children under 5 years, or isolated splenomegaly in a child less than 5
years with history of fever orient to clinical simple malaria.
2. SIMPLE MALARIA WITH MINOR DIGESTIVE SYMPTOMS

This is an illness characterized by signs of simple malaria where the patient presents also with
vomiting that prevents oral medication, with or without associated moderate diarrhea.
The signs of gravity as well as other differential diagnosis must be excluded. The
parasitological confirmation of plasmodium by either blood smear or rapid test is obligatory
without any exception.
3. SEVERE MALARIA
Severe malaria is marked by the presence of severe/danger signs. This form of malaria is an
extreme emergency and requires hospitalization in a district or in referral hospital.
It is characterized by positive parasitaemia due to plasmodium falciparum, and the presence
of one or more of the following signs of severity or danger signs:
Clinical signs (gravity signs of malaria) Frequency

Children Adults
Prostration (extreme weakness, failure to be upright or Very Very frequent
walk ) frequent
Altered level of consciousness (somnolence, Very Very frequent
unconsciousness or deep coma) frequent
Respiratory distress (difficulties of respiration, rapid Very Rare
respiration ) frequent
Acute pulmonary oedema(radiological) Rare Rare
Repeated convulsions (≥ 2 convulsions in 24 hours) Very Rare
frequent
Cardiovascular collapse or shock(weak pulse, cold Rare Rare
extremities)
Spontaneous haemorrhages Rare Rare
Jaundice (yellow colouration of the conjunctival Rare Frequent

membranes)
Haemoglobinuria (coca cola or dark urine) Rare Rare

Paraclinical signs (gravity signs of malaria) Frequency
Children Adults
Severe anaemia (haemoglobin < 6 g/dl) ; Very Rare
frequent
Hypoglycaemia (Blood glucose < 40 mg/dl ) Frequent Rare
Renal failure (little or dark urine) Rare Frequent

Hyperparasitaemia (over 200 000 parasites/μl or over Frequent Rare
5% RBC containing parasites);
Acidosis( Ph <7.25) Very Frequent
frequent
Note: There may be a case of severe malaria with negative blood smear due to P.falciparum
tropism to deep capillaries.
● General danger signs for children
✔ Incapacity of breastfeeding or drinking

✔ Vomiting every thing
✔ Convulsions
✔ Lethargy or unconsciousness
● Vulnerable groups to severe malaria
✔ Children less than 5 years old in highly endemic zones

✔ People in zones of low endemicity
✔ Pregnant women
✔ Splenectomised patients
● Factors influencing the gravity of the disease
1. Type of plasmodium: P.falcipparum that causes severe malaria while also it is the
commonly cause of simple malaria.

2. Age: it is probable that very earlier infection during the first three months of life, where
maternal antibodies are still protecting the infant, reduce the gravity of the disease for infants.
3. Intensity of transmission: adults and old children in endemic zones of malaria are less
sensible for severe malaria.
4. Degree of drug resistance to parasite
● Complications of severe malaria
1. Anemia: the most common complication

2. Coma
3. Convulsions: beyond 2 times/ day
4. Hypoglycaemia: glycaemia < 0,45g/l due to parasite and quinine therapy
5. Hypovolemia
6. Respiratory difficulties: APO (Acute Pulmonary Oedema)
7. Renal failure, abortion
● Types of severe malaria
Severe malaria can have different forms:
● Severe malaria associated or complicated with anaemia

● Cerebral malaria
● Severe malaria complicated with hemoglobinuria
Other forms of malaria are:
● Evolutive visceral malaria
● Splenomegalic malaria
1. Cerebral malaria
It is due to P.falciparum. It occurs in young children between 4 months and 4 years, but it
is described in adults who are not immunized, recently submitted to the malaria infection
The beginning is often progressive, following simple malaria no or poorly treated. It is the
most sudden in a child in apparent good health. The overwhelming phase is reached in a
few hours and involves fever (40oC), neurological disorders (coma or convulsions,
abnormal reflexes, meningeal signs).

Anemia is always present, sometimes jaundice, signs of pulmonary edema, cardiovascular
collapse with hypothermia, signs of hypoglycemia, bleeding. It is really a medical
emergency.
2. Evolutive visceral malaria
It is a chronic form observed for individual living in endemic zones and undergoing
repeated infections with irregular and insufficient treatment and favoured by malnutrition.
It is characterized by:
● Anemia sometimes intense

● Moderate splenomegaly for children between 2-5 years old
● Irregular fever
● Alteration of general state; asthenia, anorexia, weight loss
3. Splenomegalic form of malaria
This splenomegaly is seen for some individuals who live in endemic zones of malaria.
These people present abnormal immunological response to the infection caused by malaria.
This abnormal immunological response results in;
● Splenomegaly
● Hepatomegaly
● Increasing of immunoglobulin in the blood (IgM, Anti-malaria)
● Increasing of lymphocytes
Symptoms:
✔ The presence of abdominal mass

✔ Abdominal pain (peri-splenic, due to inflammation of tissue surrounding the spleen)
✔ Anemia
✔ The lab doesn’t show the presence of parasites in the blood
F. GUIDELINES FOR THE MANAGEMENT OF DIFFERENT FORMS OF

MALARIA

I. Guidelines of management of simple malaria
*At family level
Strengthening information, education and communication (IEC):

● Knowledge of the mode of transmission of malaria in Rwanda
● Utilization of long lasting insecticide treated nets (LLINs) as the principle means of
prevention and utilization of other preventive measures
● Membership to the community health insurance scheme (mutuelle de sante) as means
of ensuring earl access to health care
● Recognition by the family members of the signs of simple malaria, simple malaria
with minor digestive symptoms and severe malaria;
● Seeking care in a timely manner from a community health worker or the nearest
health facility, after reducing fever, if present by using sponging.
*At community level (Community health workers)

The role of the community health worker is to:
● Sensitize the population on the mode of transmission of malaria in Rwanda;

● Sensitize the population on the recognition of the signs of the simple malaria, malaria
with minor digestive symptoms and severe malaria;
● Sensitize the population on seeking care in a timely manner from a community health
worker or the nearest health facility, after reducing fever, if present by using tepid
sponging.
● Manage cases of children under five with malaria in accordance with the national
guidelines after confirmation using a rapid diagnostic test (RDT), under the framework
of CCM(community case management ), and when necessary refer to a health facility
● Orient the population to the health facility for appropriate management;
● Sensitize the population to the use of the long lasting insecticide treated nets as principle
means of prevention, environment hygiene and sanitation as well as other preventive
measures;
● Participate in other malaria control activities at the community level such as indoor
residual spraying campaigns, application of larvicides, etc;

*At the level of the health facility.
It is indicated to prescribe the first line of treatment only after obtaining a positive blood
smear or positive rapid diagnostic test. A negative blood smear or rapid diagnostic test
excludes the diagnosis of malaria and the administration of an antimalarial. Another cause of
the fever should be sought systematically and treated accordingly.
The first line treatment recommended is an artemisinin combination therapy (ACT) of 2
molecules in one tablet. That is: Artemether 20 mg and Lumefantrine 120 mg to be taken
preferably during meals.
The combination of artemether – lumefantrine (COARTEMR) is administered orally, twice a
day for 3 days. Total dose=6 doses
Important instructions to follow:

● Respect the dose prescribed by the health provider;
● Directly observe the administration of the first dose;
● Do not exceed the prescribed dose;
Table 1. Posology of artemether-lumefantrine (COARTEMR) in function of body weight
Weight(kg) Age Number of tablets/ intake

5-14 3months-3years 1
15-24 3-8 years 2
25-34 9-14 years 3
≥ 35 >14years 4
First dose: at x time

DAY 1 Second dose: 8 hours after the first dose
Third dose: 24 hours after the first dose
DAY 2 Fourth dose: 36 hours after the first dose
Fifth dose: 48 hours after the first dose
DAY 3 Sixth dose: 60 hours after the first dose

NB: From May 2012 a formulation of Dispersible Coartem is available for use in the
pediatric age. This formulation is dissolved in water (1/3 standard glass of water).The
formulation is used for both 6*1 tablets for infants and children weigh 5 to <15 kg bodyweight
and 6*2 tablets children weigh 15 to <25 kg bodyweight .The same formulation will be used
respectively at the community level by CHWs as Red and Yellow Primo.
● Artemether-lumefantrine is contraindicated :
-In children weighing less than 5 kg;

-During first trimester of pregnancy,
-In case of allergy to one of the two drugs in the combination and
-In cases of severe liver or renal disease.
In such cases, oral quinine sulphate is indicated as 10 mg per kg body weight per dose,
taken three times a day over seven consecutive days.
Table 2. Posology of oral quinine in function of weight

Body weight of patient in kg Number of tablets of
quinine 300 mg per dose
Weight ≤10 kg ¼ tablet
10 kg < weight ≤ 15 kg ½ tablet
15 kg < weight ≤ 21 kg ¾ tablet
21 kg < weight ≤ 31 kg 1 tablet
31 kg < weight ≤ 36 kg 1+ ¼ tablet
36 kg < weight ≤ 47 kg 1+ ½ tablet
Weight > 48 kg 2 tablets
Note: Syrup Quinine is not recommended
N.B. If there is no improvement after 48 hours of treatment, verify if the patient swallowed the
drugs correctly, re-examine the patient carefully and do another peripheral blood smear. If the

test is positive, change the treatment to oral quinine sulphate as 10 mg per kg body weight per
dose, taken three times a day over seven consecutive days. If the peripheral blood smear is
negative, exclude and treat other causes of illness and/or refer the patient to the nearest district
hospital;
If there is no improvement after 48 hours of treatment with quinine, refer the patient to the
nearest District hospital because there is suspicion of other associated pathologies other than
malaria. Monotherapy using artemisinine derivatives is not allowed for the management of
simple malaria in Rwanda.
II. Guidelines for the management of simple malaria with minor digestive symptoms
● At health facility level
The minimum requirements are:
● Qualified and trained staff;

● The existence of a continuous system of clinical and paraclinical monitoring of
patients, 24 out of 24 hours;
● A laboratory with the capacity to diagnose malaria with microscopy, rapid diagnostic
tests and measure haemoglobin level.
● The management of simple malaria with minor digestive symptoms is done at the health
centre, or when not possible in the district hospital.
● The patient must be admitted in the health centre where he/she will receive treatment
for at least 24 hours.
After this period, a clinical and paraclinical re-evaluation is done to assess if the patient can be
discharged to go home (if there has been improvement and transition towards simple malaria),
or can be transferred to the district hospital (in cases where there has been no improvement)
⮚ Modes of administration of the antimalarials
It is indicated to administer antimalarial treatment only after obtaining a positive blood smear
or positive rapid diagnostic test

Depending on the general status and level of hydration of the patient, drugs may be
administered as follows:
1. Artesunate in intramuscular or intravenous administration: ARTESUNATE: Drug of

the 1st choice
For all patients (except for pregnant mothers in 1 st trimester), Artesunate 2.4mg/kg of body
weight in IV or IM given at 0Hour, then 12hours after the first dose and at 24Hours, then once
a day is the recommended treatment.
If the patient’s condition does not improve within 24 hours of treatment, refer the patient to the
nearest district hospital. If the patient’s condition improves, change to oral Artemether-
lumefantrine (COARTEM) twice a day for three consecutive days.
2. Quinine dihydrochloride (Salt) intra-rectal (for children): 15mg per kg body weight
diluted in 4 ml of distilled water or physiological saline and administered rectally with a 5 ml
syringe every eight hours. This dose is justified by the slow absorption of quinine by the rectal
mucosa. The drug is administered slowly through the anus, and the buttocks are held together
for 5 minutes to prevent a premature reflex ejection of the drug. If the patient’s condition does
not improve after 24 hours of treatment, refer the patient to the nearest hospital.
If the patient’s condition improves, change to oral Arthemether-Lumefantrine, twice a day

for three consecutive days, or in the case of contraindications to AL, administers oral quinine.
Note:
● If the drug is ejected during the first 10 minutes following its administration,
administer another half dose;
● Diarrhoea and anal lesions limit the utilisation of this route of administration.
3. Quinine dihydrochloride (salt) intravenous administration (Children and adults) in

infusion:
Administered as 10 mg per kg body weight per dose, diluted in 5% or 10% glucose (500ml),
every 8 hours. Rapid administration of Quinine is unsafe. Each dose of parenteral Quinine
must be administered as a slow rate-controlled infusion. The infusion rate should not exceed 5
mg/kg body weight per hour.

If the patient’s condition does not improve within 24 hours of treatment, refer the patient to the
nearest district hospital. If the patient’s condition improves, change to oral AL twice a day for
three consecutive days, or to oral quinine in case of contraindications to AL.
NB: Whatever the medicine and the mode of administration used, (IM/IV Artesunate, IR/IV
perfusion quinine), if the state of health of the patient doesn't improve in 24 hours, do a rapid
diagnostic test and refer the patient with the referral note or treatment file, giving detailed
information on the treatment provided so far, to the nearest hospital.
In this case of transfer, the loading dose won't be administered at hospital.
Choice of antimalarial drugs for the treatment of simple malaria with minor digestive
symptoms
Young children Older children and Adults
No diarrhoea Has diarrhoea or Pregnant woman Other Adults and

anal lesions older children
2nd and 3rd

Artesunate IV 1 Trimester
st
Trimesters
Or Quinine IR Artesunate IV
Or Quinine IV infusion Or Quinine IV
Quinine IV infusion
infusion
Artesunate
IM/IV or Quinine
IV infusion
Quinine IV
Artemether- Quinine tablets infusion
Lumefantrine
Artemether-
Lumefantrine

III. Guidelines for the management of severe malaria
In all patients with suspected severe malaria with or without fever or history of fever, the use
of parasitological diagnosis is recommended.
The treatment must be initiated based on malaria positive blood smear or rapid diagnostic test
results..
Antimalarial treatment should not be withheld if parasitological diagnosis is not feasible but
the lab confirmation is still an obligation. In that case, presumptive treatment will be started
immediately while efforts to confirm diagnosis are ongoing (to make a blood smear for reading
later).
Meanwhile, other investigations to determine severity and prognosis should be undertaken.
The management of severe malaria must be done in either district hospital or the national
referral hospital (private or public) as recommended by the Ministry of Health.
1. Pre-transfer treatment at the health centre
or positive rapid diagnostic test.
While preparing for the transfer of the patient, urgently administer IM/IV artesunate or quinine
IR or IV (IV infusion) if there is a contra indication to artemesinine derivates(artesunate) and
depending on the general condition of the patient (weak pulse or not, dehydration or none), the
health centre staff will administer, either:
- Artesunate 2.4 mg per kg body weight IV or I M administered as a single dose before

transferring the patient.
- Quinine(for contra indication to Artesunate or non availability of Artesunate),
preferably by intravenous infusion as a loading dose of 20 mg per kg body weight to
run in 4 hours (not exceeding a total dose of 1200 mg for the loading dose); or
- Quinine by intrarectal route in children; as 20mg per kg body weight diluted in 4ml
of distilled water of physiological saline, administered with a 5 ml syringe without a

needle. The drug is gently guided through the anus and the buttocks are held together
for 5 minute to prevent the premature reflex expulsion of the drug. If the drug is
expelled within the first 10 minutes following its administration, administration is
repeated using half the original dose. Diarrhoea and anal lesion limit the utilization of
this route for the administration of drugs.
Note:
Regardless of the pre-transfer treatment that is given (Artesunate or Quinine), at the hospital
the treatment is continued as follows:
● For all patients, artesunate 2.4 mg/kg BW IV or IM is given then at 12h and 24h, then
once a day is the recommended treatment. , quinine, is an acceptable alternative if
parenteral artesunate is not available: then quinine 10 mg salt/kg BW diluted in 10ml of
5% or 10% Glucose per kg body weight every 8 h; infusion rate should not exceed 5 mg
salt/ kg BW per hour. Give parenteral antimalarials in the treatment of severe malaria for a
minimum of 24h, once started (irrespective of the patient’s ability to tolerate oral
medication earlier), and, thereafter, complete treatment by giving a complete course of:
– Artemether plus lumefantrine per os (COARTEM) twice /day in three consective days
For cerebral malaria, associate with the first dose of antibiotics if transfer is not direct:
o For children: Ampicillin 50 mg/kg body weight per dose, four times a day accompanied
by chloramphenicol 25 mg/ kg body weight per dose, four times a day.
o For adults: Ampicillin 1.5 g four times a day and chloramphenicol 1 g four times a day
;
In case of hypovolaemia (severe anemia, rapid breathing, coma or systolic BP < 80 mm Hg),
start with normal saline or Ringer’s lactate infusion in a dose of 20 ml/kg to run for 30 minutes
to move the patient out of shock.
For malnourished children (kwashiorkor or marasmus), give the loading dose of quinine in IV
perfusion without fluid replenishment (as it is difficult to assess hypovolaemia and dehydration,
this increases the risk of circulatory overload).
Note: The intramuscular use of Quinine is prohibited in all health facilities in Rwanda.
⮚ Supportive treatment

If the temperature is higher or equal to 38°C:
● Do tepid sponging ;
● Give Paracetamol 15 mg /kg body weight by oral route or suppository form, or any other
antipyretic that may be indicated.
● Paracetamol 500 mg per dose not exceed 3 gram per day
To prevent hypoglycemia (characterized by lack of consciousness, severe weakness):
● Or administration of water with 10% sugar per mouth or with nasogastric tube, at a rate
of 5 ml/kg for children and 50 -100 ml for the adults;
Water with 10% sugar is readily prepared in the following way: take 100 ml of boiled clean
water and add 10 g of sugar or measure of 2 coffee spoons.
In case of convulsions:
● Administer Diazepam 0.5 mg/kg body weight Intra-rectal for children and 10 mg IV
slow for adults; and
● Treat or prevent hypoglycaemia;
● Treat the fever if necessary.
Refer the patient to the nearest district hospital or national reference hospital.
⮚ Treatment of the severe malaria in the hospital

Criteria required for a health facility to do clinical management of severe malaria
The minimum requirements are:
- Qualified staff, trained in the clinical management of malaria by Malaria Division;
- The existence of a continuous system of 24 hours clinical and paraclinical follow-up

of patients;
- A laboratory with the capacity to do at least:

● peripheral blood smear,
● rapid diagnostic tests
● hemoglobin and/or hematocrit,
● blood sugar and
● proteinuria;
- Capacity to do a lumbar puncture, (recommended in cerebral malaria form);
- Possibility to transfuse in case of severe anaemia;
- Possibility to provide oxygen;
- Availability of the drugs and consumables required for the treatment of severe malaria (IV
Artesunate ,IV quinine, 50% and 5% glucose, phenobarbital, diazepam, antipyretics
and furosemide).
⮚ Mode of administration of antimalarial drugs
For all patients, artesunate 2.4 mg/kg BW IV or IM given on admission (time = 0), then at
12h and 24h, then once a day is the recommended treatment. ARTESUNATE is the drug of the
first choice in this case of severe malaria
Quinine is an acceptable alternative if parenteral artesunate is not available:
Administer a loading dose of 20 mg/kg body weight of quinine dihydrochloride infusion

(do not exceed 1200 mg) diluted in an isotonic solution or 5 or 10% glucose on the basis of 5
to 10 ml/kg body weight to run for 4 hours in IV perfusion. Then run IV glucose 5 or 10% for
4 hours as maintenance drip. Thereafter, i.e. 8 hours after the beginning of the administration
of the loading dose or 4 hours after the beginning of the maintenance drip, administer a
maintenance dose of 10 mg/kg body weight of quinine dihydrochloride, to run for 4 hours.
This maintenance dose of quinine will be repeated every 8 hours until the patient can swallow,
at the most within 48 hours.
After 48 hours, if the patient's state does not permit the patient to take quinine orally, one may
continue the drip of quinine by reducing the doses to 7 mg/kg every 8 hours to run for 4 hours.
Give parenteral antimalarials in the treatment of severe malaria for a minimum of 24h, once
started (irrespective of the patient’s ability to tolerate oral medication earlier), and, thereafter,
complete treatment by giving a complete course of:

– Oral Artemether 20 mg and Lumefantrine 120 mg (COARTEM), as recommended for the
treatment of simple malaria.
-Or oral quinine 10 mg/kg of quinine sulphate every 8 hours as soon as the patient can
swallow; to complete the 7 days of treatment in case of contraindication to artemesinin
derivates (COARTEM).
Artesunate powder 60 mg will be diluted in 1 ml 5% sodium bicarbonate (provided in the

package), and then further diluted with 5% dextrose or 0.9% normal saline to a total volume
of 10 ml, making a final concentration of 6 mg/ml.
Once reconstituted, the artesunate solution is not stable and should be administered within
half an hour. Also the solution that is not given to patient should be discared, and not kept for
use for the next patient. Administration is by slow intravenous injection through an
indwelling IV catheter. Alternatively it can be administered by intramuscular injection in 2
separate doses in the anterior thighs . At least 2 I.V doses should be given before switching to
oral therapy can be considered i.e.: stop I.V artesunate and give oral antimalarial. When the
patient is improving and able to take oral tablets a switch to Co-artem should be considered.
NB:
- For the patient with over 60kg body weight give the loading dose, and decrease the dose
from 1200mg to 800mg divided in two doses not to exceed 2000mg per day,
- The loading dose of quinine is not administered if the patient received quinine the past
12 hours or Mefloquine in the 7 past days.
- Never exceed 2 g of daily dose of quinine.
- For the cerebral form of severe malaria (cerebral malaria or neurological malaria),
the association of IV antibiotherapy is recommended or not after evaluation of patient
from the health center based on laboratory results:
- Children : (ampicilline 50mg/kg /dose 4x/jour +Chloramphénicol 25 mg/kg/dose
4x/jour)
- Adults : (ampicilline 1.5g 4x/jour +Chloramphénicol 1g 4x/jour)
- For the anaemic form of severe malaria antibiotherapy is not indicated.

- The recommended dose for oral quinine is 10 mg Quinine salt per kg body weight
every 8 hours for 7 days;
Note: Syrup Quinine is not recommended
Diagram showing dosage of intravenous quinine in the treatment of severe malaria.

Maintenance Maintenance Maintenance
period period period
Start of
(With or (With or (With of
treatment:
without without without
Loading
G 5% - G 10% G 5% - G 10% G 5% - G 10%
dose QNN 20 End of
infusion) infusion) infusion) hours o
mg per kg QNN 10 mg QNN 10 mg
treatm
during 4 WITHOUT per kg over WITHOUT per kg over WITHOUT
hours QNN 4 hours QNN 4 hours QNN
ex: 10 h 14 h 18h 22h 02 h 06h

(With or (With or (With of
G 5% - G 10% G 5% - G 10% G 5% - G 10%
infusion) infusion) infusion)
QNN 10 mg QNN 10 mg QNN 10 mg
per kg over WITHOUT per kg over WITHOUT per kg over WITHOUT End of 4
of treatm
4 hours QNN 4 hours QNN 4 hours QNN
10 h 14 h 18h 22h 02 h 06h

(With or (With or (With or
G 5% - G 10% G 5% - G 10% G 5% - G 10%
infusion) infusion) infusion)
QNN 7 mg QNN 7 mg QNN 7 mg
per kg over WITHOUT per kg over WITHOUT per kg over WITHOUT End of
of trea
4 hours QNN 4 hours QNN 4 hours QNN
10 h 14 h 18h 22h 02 h 06h
⮚ The management of severe malaria complications
1. Hypovolaemia
In the presence of hypovolaemia, (rapid breathing, coma or systolic BP < 80 mmHg), do

replenishment with normal saline or Ringer’s lactate 20 ml/kg to run for 30 minutes to
stabilize the patient. For malnourished children (kwashiorkor or marasmus), give normal
saline or Ringer’s lactate 10 ml/kg plus 5 ml/kg of 5% glucose solution. This solution is
given over an hour.
2. Hyperthermia
Administer oral Paracetamol 15 mg/kg body weight, 4 times per day or any other available
antipyretic. Physical means, such as tepid sponging, ventilation and wearing of light clothing
are also recommended.
3. Convulsions

For children with cerebral malaria, diazepam 0.5 mg/kg is recommended. For repeated
convulsions, intramuscular Phenobarbital at a dose of 15 mg/kg for infants, 10 mg/kg for
children and 5 mg/kg for adults is recommended. The maintenance dose of Phenobarbital is 5
mg/kg for children, 48 hours after the loading dose. Diazepam is administered as slow
Intravenous dose or IntraRectal, 10 mg for adults. Because of its side effects, strict monitoring
of the respiration is required during the administration of this drug.
4. Severe anaemia
Transfusion must be considered if the haematocrit of a patient who is normally hydrated falls
below 18 % or the concentration of haemoglobin is < 6 g/dl or in presence of the clinical signs
of cardio respiratory distress (pallor, tachypnoea, and tachycardia). Transfusion with packed
cells is recommended, 10 ml/kg body weight to run for 2 hours for children. The height of the
stand should be raised to increase the speed of flow. In case of lack of packed cells, transfuse
with whole blood at a rate of 20 ml/kg body weight. For children with severe malnutrition,
whole blood is preferable to correct anaemia, administered as 10 ml/kg body weight and it is
recommended to prolong the transfusion for at least 3 hours.
For the regulating of the speed of flow, 1 ml of whole blood corresponds to 20 drops and 1 ml
of the concentrated globules corresponds to 15 drops.
If signs of respiratory distress appear during the transfusion, stop the transfusion and administer
Frusemide slowly at the rate of 1mg per kg body weight in children and 40 mg in adults.
After transfusion, continue to monitor the appearance of any signs of anaemia (that may signify
continued haemolysis).
5. Hypoglycaemia
Hypoglycaemia must be ruled out in all patients with severe malaria. It is defined as levels of
blood sugar (< 2.5 mmol/l or 45 mg/dl) in a well fed child and < 40 mg/dl in adult: severe
hypoglycaemia).
When measuring blood sugar is not possible, for children it is recommended to give 3 ml/kg of
10 % glucose or if not available, 1 ml/kg of 50 % glucose IV slow (over 5 minutes)

For adults in coma, a test dose of 20 ml of 50% dextrose by intravenous injection is
administered over 5 minutes. Monitoring of the clinical status and blood sugar must continue
even when the hypoglycaemia is corrected.
If patient is receiving Quinine, in order to prevent hypoglycaemia in children, it is advisable to

maintain a drip of 5 ml/kg of 5% glucose or 3-4 ml/kg body weight of 10%, (between the two
doses of quinine infusion).
10 % glucose is obtained from the solutions of 50 % glucose and 5 % (i.e. 56 ml of Glucose 50

% + 444 ml of Glucose 5 % = 500 ml of Glucose 10%). Or from 50 % glucose and distilled
water (i.e. 1 volume 50 % glucose + 4 volume of distilled water: 100 ml of 50 % glucose+400
ml of water distilled = 500 ml of glucose 10 %)...
6. Respiratory distress
In cases of respiratory distress, undertake the following measures:

● Clear the respiratory tract;
● Administer oxygen, 5 litres per minute continuously until the patient’s respiratory status
improves;
● Verify the level of hemoglobin and treat anaemia if necessary. Treat possible cardiac
insufficiency or pulmonary oedema;
● If the respiratory distress persists despite a good replenishment, think about an
associated infection, then it may necessitate to administer antibiotics:
o If renal function is normal (urea and creatinine are normal) administer
Ampicillin IV 75 mg/kg/dose 3x/day and IM Gentamycine, 7,5mg/kg body
weight, once a day for 5 days;
o If renal function is unknown, administer penicillin G IV 50 mg/kg/dose, 4 times
a day and chloramphenicol 25 mg/kg/dose, 4 times a day for 5 days.
● In the immunocompromised adult with HIV whose respiratory distress persists, think
about a lung infection due to Pneumocystis jiroveci (opportunistic infection) or
pulmonary tuberculosis.
7. Coma

● Clear the respiratory airways;
● Put the patient in lateral decubitus position;
● If the peripheral blood smears (GE) and the rapid diagnostic test (RDT) are negative or
if the coma persists after 48 hours,monitor the comatose patient:
o Evaluate the level of coma regularly, at least twice a day;
o Monitor blood sugar and treat accordingly;
o Monitor temperature and treat accordingly;
o Treat convulsions if any;
o Put the patient in the lateral decubitus position;
o Aspirate if necessary;
o Monitor the quantity of inputs and outputs (fluids);
o Change the position at least 4 times in 24 hours;
o Mark all these elements on the patient’ s monitoring card/chart
If no improvement and no clear diagnosis transfer the patient in three days to the next high
level.
8. Renal Insufficiency
It is important to monitor the daily diuresis in order to detect possible renal insufficiency in
time. For children, the diuresis in this case is lower than 12ml / kg/24 hours. For the adults, it
is lower than 400 ml/24 hours; blood creatinine is > 265 µmols (3mg/dl )
It is recommended that this complication be managed in next high level .
IV. Management of malaria in pregnant women
⮚ At the family level
Strengthen IEC on:
● Knowledge of the mode of transmission of malaria

● Utilisation of long lasting insecticide treated mosquito nets as principle means of
prevention and other preventive measures
● Membership to the community health insurance schemes (mutuelle) as a way of
ensuring better access to care
● Recognition of the signs of simple malaria, simple malaria with minor digestive
symptoms and severe malaria by the family members;
● Seeking timely care from the community health care worker or the nearest health
facility after lowering fever, if any, using tepid sponging.
⮚ At the Community level (Community Health Workers)
The role of the community health worker is to educate the pregnant woman on:
● The mode of transmission of malaria (mosquito bites);

● The effects of malaria on pregnancy (on the mother and the baby)
● Recognition of the signs of the simple malaria, malaria with minor digestive symptoms
and severe malaria, and the ill effects of fever during pregnancy;
● The benefits of sleeping under long lasting insecticide treated nets
● Removal or treatment of breeding sites (stagnant water)
● Seeking health care from the health facility as soon as they feel signs of malaria
● The importance of taking all the drugs as prescribed by the health worker;
● The benefits of 4 ANC visits
⮚ At the level of the Health center
To educate the pregnant woman on the preventive measures of malaria in pregnancy during the
antenatal consultations:
● What causes malaria and its transmission;

● The effects of malaria on the mother and the baby;
● The advantages of sleeping under long lasting insecticide treated mosquito nets;
● The danger signs of severe malaria;
● The importance of seeking medical care when the symptoms of malaria occur ;

● The importance of taking a complete dose of antimalarials when sick,
● The benefits of 4 ANC visits.
⮚ Antenatal care
During antenatal care, the health facility staff must do the following to the pregnant woman:
● Give her a long lasting insecticide treated mosquito net;
● Give other components of antenatal care : vaccination, iron and folic acid, vitamin A and
Mebendazole;
● Discuss with her the program of the ANC visits;
● Record on the ANC card, her ANC appointment card and the register all the drugs
prescribed and given as well as LLINs;
● Register all illness relate to the pregnancy in the ANC register.
⮚ Mode of administration of antimalarials
or positive rapid diagnostic test.
❖ Simple malaria
Because malaria during pregnancy can aggravate latent anaemia, it is recommended to do a

complete clinical exam.
● The first line treatment of malaria in pregnancy is quinine sulphate per os 10

mg/kg/dose, 3 times a day for 7 days during the first trimester of pregnancy.
AL is indicated during the 2nd and 3rd trimesters of pregnancy as is the case for the non
pregnant adults;
NB:
● In case of fever, administer paracetamol tablets, 500 mg three times per day;
● Directly observe the woman as she swallows the first dose of antimalarials;

● Record all the information on the ANC card, ANC register and the hospitalization file;
● Give advice on the prevention of the malaria and the necessity to consult in time in case
of illness;
● Recommend to the pregnant woman to come back any time if the symptoms persist
and/or she develops signs of severe malaria.
❖ Simple malaria with minor digestive symptoms
The symptomatology of this type of malaria is similar to the one described earlier in children
and adults. The alteration of the general status can be accentuated by the vomiting and other
symptoms related to the pregnancy.
⮚ Curative treatment
First trimester
Administer Quinine dihydrochloride (salt) in intravenous infusion: 10 mg/kg/dose diluted in

10 ml of 5% or 10% glucose/kg BW, eight hours until patient is able to take drugs orally
making sure the treatment does not exceed 24 hours. Once the patient can take orally, complete
the remaining quinine 3 X10 mg/kg/day to make 7 days by oral route of drug administration.
Second and third trimester
Depending on the general status and level of hydration of the patient, drugs may be
administered as follows:
1. Artesunate intravenous or intramuscular injection : administered as dose of:

- Artesunate 2.4mg/kg BW IV or IM on admission (time=0), then at 12h and 24h, then once a
day the recommended treatment. Quinine is an alternative if parentaral Artesunate is not
available
2. Quinine dihydrochloride (salt) intravenous administration:
Administered as 10 mg per kg bodyweight per dose, diluted in 5 to 10 ml/kg BW of 5% or 10%

glucose, every eight hours.

If the patient’s condition does not improve within 24 hours of treatment, refer patient to the
nearest district hospital. If the patient’s condition improves, change to oral Arthemether-
Lumefantrine, twice a day for three consecutive days, or to oral quinine in case of
contraindications to Arthemether-Lumefantrine. .
NB: Whatever the medicine and the mode of administration used, (IM/IV Artesunate, IV
quinine infusion), if the state of health of the patient doesn't improve in 24 hours, do a rapid
diagnostic test or blood smear and refer the patient with the referral note or treatment file,
giving detailed information on the treatment provided so far, to the nearest hospital. If the
patient’s condition improves, change to oral Arthemether-Lumefantrine, twice a day for three
consecutive days, or to oral quinine in case of contraindications to Arthemether-Lumefantrine.
.
In this case of transfer after quinine, the loading dose won't be administered at hospital.
⮚ Supportive treatment
In case of diarrhoea or vomiting:

● Evaluate and monitor the state of hydration;
● Rehydrate with ORS or other available liquids and even introduce nasogastric tube if
necessary ;
● Anti-emetics are not recommended.
In case of fever, administer paracetamol 15 mg/kg orally or any other antipyretic that may be
indicated.
❖ Severe malaria in the pregnant woman
At the health centre

- Severe malaria in the pregnant woman is characterized by the same signs as those
described earlier for adults and children.

- During the first quarter while organizing an emergency transfer, administer loading
dose by intravenous infusion of quinine 20 mg/kg body weight in 10 ml/ kg BW of 5%
or 10 % dextrose to run for 4 hours (without exceeding 1200 mg);
- Artesunate, 2.4 mg/ kg can be administered by intramuscular/intravenous route during

the 2nd and 3rd quarter as pre- transfer treatment.
- It is important to do a complete clinical examination of the woman and to regularly

check the vitality of the fœtus.
Supportive treatment
If the axillary temperature is ≥ 38°C, give paracetamol 500 mg 3 times per day if able to
swallow, or any other antipyretic as may be indicated.
For the prevention of hypoglycaemia that may manifest as loss of consciousness, severe
asthenia):
● Give 20-50 ml of 50 % of dextrose by intravenous injection to run for 5-10 minutes; or

administer water with 10 % sugar orally or by NGT (50 -100 ml).
Preparation of water with 10% sugar: To make 100 ml of water with 10%
sugar: you take 100 ml of clean water and add to it 10 g (also equivalent to 2
teaspoons) of sugar.
In case of convulsions:
● Administer diazepam, 10 mg IV slow; and if convulsions persist, administer

diazepam, 10 mg in 500 ml of 5 % glucose to run slowly.
● Treat or prevent hypoglycaemia;
● Treat the fever if necessary;
● Fill in the transfer card correctly and clearly,
● Record all the necessary information in the register and the ANC card;
● Refer the patient immediately to the nearest district or national reference hospital.
At the hospital

The treatment of severe malaria in pregnant women at the hospital level is the same as in others
adults. Some complications are more frequent in pregnant women and require a particularly
close monitoring. These include hypoglycaemia, respiratory distress (APO) and severe
anaemia.
NB: It is important to do close obstetrical follow-up in general and monitoring of the fatal
vitality in particular.
LABORATORY DIAGNOSIS OF MALARIA
The parasitological confirmation of malaria is obligatory for all patients without any
exceptions, before initiating antimalarial treatment. Two types of tests are possible: microscopy
(blood smear/BS) or the rapid diagnostic tests (RDTs) .
In the health facilities, microscopic examination of a blood drop after coloration using the
Giemsa stain to look for malaria parasites is recommended. The blood slide allows the counting
of parasites.
Table: Comparison of the cross system and that of counting of parasites per microlitre
The plus system Number of parasites per microlitres
+ :1-10 parasites per 100 fields of BS 4-40 parasites per µl
++ : 11-100 parasites per 100 fields of BS 40-400 parasites per µl
+++ : 1-10 parasites per 1 field of BS 400-4.000 parasites per µl
++++ : 11-100 parasites per 1 field of BS 4.000-40.000 parasites per µl
Number of Number of parasites X 8 000 white blood cells
parasites =
At the per microlitre

level Number of leucocytes counted
of the community (Community health worker), rapid diagnostic tests are
recommended before initiating antimalarial treatment under the framework of CCM or HBMF.
Other indications for the rapid diagnostic tests are:
● Microscopy not available or not feasible

● Confirmation and monitoring of malaria epidemic situation.

Rapid diagnostic tests are not recommended for the follow up of patients on treatment because
they remain positive even after clinical cure.
CHEMOPROPHYLAXIS OF MALARIA
⮚ Indications
It is intended for:
● Travellers coming from malaria free zones;
● Expatriates and other nationals coming from non malaria endemic countries;
● Splenectomised patients;
● Patients with Sickle cell disease.
For these people it is necessary to begin the chemoprophylaxis at least one week before the
journey, maintain it for all their period of stay in the endemic zone of malaria, and to continue
it for 4 weeks after having left the zone (international travellers).
The recommended medicines are the following below
⮚ Recommended drugs
Mefloquine 250 mg
The recommended prophylactic dose is 250 mg per week for adults and 5 mg/kg for children
of more than 5 kg. In case of intolerance to Mefloquine and if the intended period of stay is
short, Doxycline is prescribed.
Mefloquine is also recommended for treatment of splenomegaly (of malaria origin) at the same
dose and preferably in an institution where a haematological follow-up is possible

Table: Dosing scheme for prophylaxis using mefloquine
Body weight of patient in kg Number of tablets of mefloquine 250 mg
< 5 kg Contraindicated
5 kg ≤ weight < 12 kg ¼ tablet
13 kg ≤ weight < 24 kg ½ tablet
25 kg ≤ weight < 35 kg ¾ tablet
≥ 36 kg 1 tablet
Doxycycline
The adult prophylactic dose is 100 mg per day (or 1.5 mg per kg body weight). It is
contraindicated for people weighing below 25 kg (or below 8 years), pregnant and
breastfeeding mothers.
Table: Dosing scheme for prophylactic Doxycycline
Body weight of the patient in kg Number of tablets of Doxycycline 100 mg
< 25 kg Contraindicated

25 kg ≤ weight < 35 kg ½ tablet
36 kg ≤ weight < 50 kg ¾ tablet
≥ 50 kg 1 tablet
⮚ Score for the evaluation of coma due to cerebral malaria
Score for the assessment of coma due to cerebral malaria in adults using the "Glasgow Coma
Scale" and for the children using the "Blantyre coma scale” developed by M. Molyneux.
Adults Children
Eye opening Ocular movements
● Spontaneous, voluntary……….4 ● Well adapted ……………………1

● To command …………………..3 (e.g. follows mother’s face)
● To pain …………………………..2
● Non adapted ……………………0
● No response ……………………1
Verbal response
Verbal response
● Screaming …………………….…2
● Oriented ……………….…….…5
● Moaning or screaming………...1
● Confused ……………………… 4
● No response ……………………..0
● Raving patient …….……….. 3
Motor response
● Unintelligible …………………..2
● No response………………….…1 ● Localises pain stimulus * ……....2
Motor response (lower extremities) ● Extension of legs due to pain
**………………………….1
● To command ………….. ……..6
● No response ……………………..0
● To pain ……………………….…5
● Retraction……………………... 4
● Flexion…………………………..3
● Maladjusted extension …..…2
● No response …………………..1

Total Score : minimum 3, maximum 15 Total Score : minimum 0, maximum 5
Normal or nearly normal =……13-15 Normal = ………..................... 5
Obnubilation Stage I =…………..8-12 Obnubilation =…...................................4
Coma Stage II =………….....6-7 Coma Stage II = ………..…. …….....3-2
Coma Stage III =……………....4-5 Coma Stage III = …………....………..1
Coma Stage IV =........................3 Coma Stage IV = ...................................0
* Rubbing the finger joint on patient’s sternum.
** Firm pressure on patient’s nails with a pencil placed horizontally.
III.2. AMOEBIASIS
A. DEFINITION
Also known as amebiasis, amoebiasis is an infection with the intestinal protozoa Entamoeba
histolytica. Entamoeba histolytica belongs to the protozoa of the genus Entamoeba.
About 90% of infections are asymptomatic, and the remaining 10% produce a spectrum of
clinical syndromes ranging from dysentery to abscesses of the liver or other organs.
Thus the parasite has been shown to give rise to two very differing clinical presentations:
1. The commensal or non-invasive luminal form where the parasite causes no signs or
symptoms of disease.

2. The pathogenic or invasive form where the parasite invades the intestinal mucosa and
produces dysentery or amebiasis and may give rise to extra-intestinal lesions via the
blood, mainly to the liver.
The genus Entamoeba contains other many species such as Entamoeba dispar, Entamoeba coli,
Entamoeba hartmanni, etc and some of them can reside in the human interstitial lumen.
E.histolytica is, thus far, the only Entamoeba species definitely associated with disease; the
other species are in general considered as nonpathogenic.
B. RISK FACTORS
● In developing countries
o Inadequate sanitation
o Crowding
● In developed countries
o History of travel to areas where amebiasis is endemic
o Recent immigration
o Male homosexual activity
o Residence in institutions, prisons, etc
● The following are the risk factors for severe amebiasis:
o Alcoholism
o Cancer
o Malnutrition
o Older or younger age
o Pregnancy
o Prolonged use of corticosteroid medication and other states of
immunosuppression
C. EPIDEMIOLOGY AND TRANSMISSION
The reservoir is a human and the parasite is eliminated through the faeces. The transmission is
interhuman either directly by dirty hands or indirectly by water and food contaminated by the
cysts. Lack of hygienic measures is an important factor and the role of flies cannot be neglected.
Infection is spread through ingestion of the cyst form of the parasite, a semi-dormant and hardy
structure found in feces. Any non-encysted amoebae, or trophozoites, die quickly after leaving

the body but may also be present in stool: these are rarely the source of new infections. The
parasite can also be transmitted directly by ano-genital or oro-anal sexual contact (but this is a
rare transmission mode). Amoebiasis results from infection with E. histolytica and is the third
most common cause of death from parasitic disease (after schistosomiasis and malaria).
D. PATHOGENESIS AND PATOPHYSIOLOGY
In asymptomatic infections the amoeba lives by eating and digesting bacteria and food particles
in the gut. It does not usually come in contact with the intestine itself due to the protective layer
of mucus that lines the gut. Disease occurs when amoeba comes in contact with the cells lining
the intestine. It then secretes the same substances it uses to digest bacteria, which include
enzymes that destroy cell membranes and proteins. This process can lead to penetration and
digestion of human tissues, resulting first in flask-shaped ulcers in the intestine. The initial
lesion is in colonic mucosa, most often in the cecum or sigmoid colon. The slow transit of the
intestinal contents in these two locations seems an important factor in invasion of the mucosa,
both because it affords the ameba greater mucosal contact time and because it permits changes
in the intestinal milieu that may facilitate invasion. The initial superficial ulcer may deepen
into the submucosa and muscularis to become the characteristic flask-shaped, chronic amebic
ulcer. Spread may occur by direct extension, by undermining of the surrounding mucosa until
it sloughs, or by penetration that can lead to perforation or fistulous communication to other
organs or the skin. If the amebas gain access to the vascular or lymphatic circulation, metastases
may occur first to the liver and then by direct extension or further metastasis to other organs,
including the brain. Entamoeba histolytica ingests the destroyed cells by phagocytosis and is
often seen with red blood cells inside when viewed in stool samples.
Note: If amebas pass down the colon they encyst under the stimulus of desiccation, and then
are evacuated with the stool.
In about 10% of invasive cases the amoebae enter the blood stream. If the parasite reaches the
blood stream it can spread through the body, most frequently ending up in the liver where it
causes amoebic liver abscesses. Liver abscesses can occur without previous development of
amoebic dysentery. When no symptoms are present, the infected individual is still a carrier,
able to spread the parasite to others through poor hygienic practices.
E. CLINICAL MANIFESTATIONS
1. INTESTINAL AMOEBIASIS

Intestinal amoebiasis has 2 forms.
1.1. Acute form: Amoebic dysentery
a. Symptoms
Symptoms develop 2–6 weeks after the ingestion of infectious cysts.

✔ Lower abdominal pain and mild diarrhea is followed by malaise, weight loss, and
diffuse lower abdominal or back pain.
✔ Patients may pass 10 to12 stools per day. The stools are less abundant but repeated and
contain little fecal material and consist mainly of blood and mucus, tenesmus.
✔ More fulminant intestinal infection, with severe abdominal pain, high fever, and
profuse diarrhea, is rare and occurs predominantly in children.
b. Diagnosis
Direct exam of the fresh stool to search for hematophage amoeba.
1.2. Chronic form
a. Definition: Patients may develop a chronic form of amoebic colitis, which can be confused
with inflammatory bowel disease. It is due to the presence of cysts in the colon.
b. Symptoms: It is manifested by abdominal pain, alternance of diarrhea and constipation.
c. Diagnosis: Direct exam of the stool (cysts can be seen)
⮚ COMPLICATIONS OF INTESTINAL AMOEBIASIS
● Digestive hemorrhage
● Intestinal perforation
● Amoebomas: parasitic tumor or mass that leads to intestinal obstruction
● Tissue amoebiasis
2. HEPATIC AMOEBIASIS (AMOEBIC LIVER ABSCESS)
Extra intestinal infection by E. histolytica most often involves the liver.

a. Signs and symptoms
o Most patients are febrile and have right-upper-quadrant pain and may radiate to the
shoulder.
o Point tenderness over the liver.
o Hepatomegaly
o Jaundice is rare.
o Weight loss
N.B. For tissular amoebiasis, the diagnosis is done by detecting anti-amoebian antibodies.
For hepatic abscess; ultrasonography is also necessary.
b. Complications of amebic liver abscess
1. Pleuropulmonary involvement is the most frequent complication of amoebic liver abscess.

Pulmonary amoebiasis can occur from hepatic lesion by haemotagenous spread and also by
perforation of pleural cavity and lung. It can cause lung abscess, pulmopleural fistula,
empyema of lung and broncho- pleural fistula.
2. Subdiaphragmatic abscess, perforation of diaphragm to pericardium and pleural cavity,

perforation to abdominal cavity (amoebic peritonitis) and perforation of skin (amoebic cutis).
N.B. Other Extra intestinal Sites
The genitourinary tract may become involved by direct extension of amoebiasis from the
colon or by hematogenous spread of the infection. Urogenital tract amoebiasis derived from
intestinal lesion can cause amoebic vulvovaginitis (May's disease), rectovaginal fistula, etc.
Cerebral involvement: It can also reach brain through blood stream and cause amoebic brain
abscess and amoebic meningoencephalitis.
F. DIFFERENTIAL DIAGNOSIS
● Intestinal amebiasis

o Bacterial diarrheal disease : Caused by Campylobacter species; enteroinvasive
Escherichia coli; or Shigella, Salmonella, and Vibrio species, etc
o Inflammatory bowel disease
o Ischemic colitis
o Diverticulitis
o Cancer: Amebiasis occasionally presents with only an asymptomatic or tender
abdominal mass caused by an ameboma. Therefore, ameboma may easily be
confused with cancer on barium studies.
● Extraintestinal amebiasis
o Fever of unknown origin

o Pulmonary disease
o Gallbladder disease
o Malaria
o Typhoid fever
o Pyogenic liver abscess
o Echinococcal cyst (rare).
G. TREATMENT
✔ Drugs used to treat amebiasis can be classified according to their primary site of action.
❖ Luminal amebicides such as iodoquinol and paromomycin. Their features are:
▪ They are poorly absorbed and reach high concentrations in the bowel
▪ Their activity is limited to cysts and trophozoites close to the mucosa
❖ Tissue amebicides such as nitroimidazole compounds (Metronidazole,
tinidazole, ornidazole) characterized by:
▪ They reach high concentrations in blood and tissue after oral or
parenteral administration
▪ They must be used in conjunction with luminal agents, as these drugs do
not eradicate intestinal cysts
✔ Remarkable note: Asymptomatic cyst carriage should be treated to:

❖ Prevent progression to invasive disease

❖ Prevent spread to family members
⮚ Specific Treatments
1. Asymptomatic carriers (luminal agents)
✔ Iodoquinol
❖ Dosage: 650 mg PO tid for 20 days
✔ Paromomycin
❖ Dosage: 500 mg PO tid for 10 days
2. Acute colitis
✔ Metronidazole
❖ Dosage: 500-750 mg PO or IV tid for 7–10 days, plus a luminal agent
3. Amebic liver abscess
✔ Medical therapy
❖ Metronidazole 750mg PO or IV tid, plus a luminal amebicide
❖ Alternative treatment:
▪ Tinidazole 2 g PO qd for 3 days (for moderate disease) or 5 days (for
severe disease) plus a luminal amebicide
✔ Aspiration of liver abscess
❖ Usually does not accelerate healing
❖ Its indications are:
▪ Need to rule out pyogenic abscess, particularly in patients with multiple
lesions
▪ Lack of response to treatment after 3–5 days
▪ Imminent threat of abscess rupture
▪ Need to prevent left-lobe abscess rupture into pericardium
✔ Surgical therapy
❖ Reserved for bowel perforation and rupture into pericardium
H.PREVENTION
To help prevent the spread of amoebiasis around the home:

● Wash hands thoroughly with soap and hot running water for at least 10 seconds after
using the toilet or changing a baby's diaper, and before handling food.
● Clean bathrooms and toilets often; pay particular attention to toilet seats and taps.
● Avoid sharing towels.
● Early screening and treatment of carriers of the cysts
To help prevent infection:
● Avoid uncooked vegetables when in endemic areas, as they may have been fertilized
using human feces.
● Boil water or treat with sûr ’eau or iodine tablet.
● Avoid eating street foods especially in public places
● Avoid flies and use of latrines
III.3 GIARDIASIS (LAMBLIASIS)
Giardiasis is one of the most common parasitic diseases in both developed and developing
countries worldwide, causing both endemic and epidemic intestinal disease and diarrhea. It is
caused by Giardia lamblia (also known as G. intestinalis) which is a cosmopolitan protozoal
parasite that inhabits the small intestines of humans and other mammals.
2. TRANSMISSION
Transmission is by dirty hands, food and water contaminated by the cysts which are eliminated
in faeces (Feco-oral transmission).
● Often asymptomatic.
● Disease manifestations of giardiasis range from asymptomatic carriage to fulminant
diarrhea and malabsorption.
● Most infected persons are asymptomatic, but in epidemics the proportion of
symptomatic cases may be higher.

● Symptoms may develop suddenly or gradually. In persons with acute giardiasis,
symptoms develop after an incubation period that lasts at least 5–6 days and usually 1–
3 weeks. Prominent early symptoms include diarrhea made of soft stool alternating with
constipation or normal stools, abdominal pain or epigastric pain, abdominal bloating,
nausea, and vomiting.
● The duration of acute giardiasis is usually >1 week, although diarrhea often subsides.
4. DIAGNOSIS
Direct exam of the stool permits to identify the cysts or trophozoites

Biopsy of intestinal wall (very rare)
5. TREATMENT
o Metronidazole (Flagyl) 500 mg three times a day in 5-7 days for adults
and for children: 30 mg/kg per os three times a day
o or Tinidazole 2 gr single dose for adults and 50mg/ kg for children
6. PREVENTION
✔ Although Giardia is extremely infectious, disease can be prevented by consumption of

noncontaminated food and water and by personal hygiene when caring for infected
children.
✔ Handwashing
✔ Boiling or filtering potentially contaminated water
✔ Using latrines
III.4.ASCARIASIS
1. DEFINITION
It is a parasitic disease caused by Ascaris lumbricoides.
Ascaris lumbricoides is the largest intestinal nematode parasite of humans. It inhabits in small

intestines where it takes intestinal content as its food. Clinical disease arises from larva
migration in the lungs or effects of the adult worms in the intestines.
2. LIFE CYCLE
Adult worms live in the lumen of the small intestines (12 to 18 months). Adult A . lumbricoides
are white or yellow and 15-35 cm long. Mature female produces up to 240,000 eggs a day,
which pass in the faeces and develop in external environment where they can also be ingested
through food and water contaminated by the faeces. After ingestion, the larva in the developed
egg is released in intestine, travels the intestinal wall and gains blood stream where it is
disseminated to the liver, heart and to the pulmonary capillaries. The larva penetrates the
alveolar wall, ascends the respiratory airways and reaches the pharynx where it is swallowed
and invades again the intestine and becomes adult and produces the eggs which will be apparent
in faeces.
Note: During movement through the lungs the larvae may produce an uncommon form of
pneumonia called eosinophilic pneumonia
The disease can be asymptomatic

The migration of the larva through the lungs results in pulmonary symptomatology called
LOEFFLER’S SYNDROME.
This syndrome is the result of allergic reaction of the lung and is manifested by dry cough,
sometimes dyspnea, wheezing or hemoptysis. Also characterized by radiologic signs and
increased eosinophils in the blood.
● Abdominal pain, nausea, vomiting or diarrhea
● In case of heavy intestinal infestation: Severe abdominal pain, fatigue , weight loss,
a worm in vomit or stool
4. COMPLICATIONS
Ascariasis can complicate in:
✔ Intestinal occlusion due to a package of ascaris

✔ Ascardian appendicitis due to migration of worms in the appendix
✔ Pancreas inflammation due to engagement of worm in the pancreatic canal
✔ Intestinal perforation
✔ Peritonitis due to intestinal perforation
✔ Biliary tract obstruction
5. DIAGNOSIS
● Adult worms can be seen in stool or in vomit

● Stool exam to search for eggs
● In severe cases , the larvae are ejected in sputum ( in case of pulmonary complication)
6. DIFFERENTIAL DIAGNOSES
● Biliary colic
● Colonic obstruction
● Acute pancreatitis
● Community-acquired pneumonia
● Other intestinal worms
7. TREATMENT
o Mebendazole (Vermox):100mg twice a day for 3 consecutive days for adults and
children
Or Albendazol (Zentel) 400mg as a single dose
o Surgical intervention to treat complications caused by obstruction or perforation
8. PREVENTION
✔ Hand washing and food hygiene

✔ Latrines use
✔ Avoid the use of human faeces to fertilize vegetables.
III.5. HOOKWORM DISEASE (ANKYLOSTOMIASIS)

1. DEFINITION AND CAUSE
Hookworm is a parasitic intestinal infection. A disease resulting from infestation in the

duodenum with Ancylostoma duodenale or Necator americanus.
2. TRANSMISSION
Both forms of hookworm disease are transmitted to humans through direct skin penetration
(usually in the foot) by hookwonn larvae in soil contaminated with faeces that contain
hookworm ova. These ova develop into infectious larvae in 1 to 3 days.
3. PHYSIOPATHOLOGY
✔ The larvae attach to the cell surface of the mucosa of the small intestine. There, the
larvae nourish the blood, causing minor bleeding from the wounds caused by their bite
in the mucosa. This results in anemia. On the other hand, the larvae secrete substances
that destroy the RBCs resulting in hemolysis.
✔ The larvae (immature form of the worm) penetrate the skin, where an itchy rash called
ground itch may develop. This itchy rash consists of what is called preanemic phase
of ancylostomiasis. The larvae migrate to the lungs via the bloodstream, enter the
airways and cause coughing.
4. LIFE CYCLE OF HOOKWORM
Infection of the host is by the larvae, not the eggs. While A. duodenale can be ingested, the
usual method of infection is through the skin; this is commonly caused by walking barefoot
through areas contaminated with fecal matter. The larvae are able to penetrate the skin of the
foot, and once inside the body, they migrate through the vascular system to the lungs, and from
there up the trachea, and are swallowed. They then pass down the esophagus and enter the
digestive system, finishing their journey in the intestine, where the larvae mature into adult
worms. The adult worms inhabit the intestine and produce eggs. The eggs are eliminated in the
feces and embyonate in external environment to give the larvae. These, will undergo maturation
and become infestant.
Once in the host gut, Necator tends to cause a prolonged infection, generally 1–5 years (many
die within a year or two of infecting), though some adult worms have been recorded to live for

15 years or more. On the other hand, Ancylostoma adults are short lived, surviving on average
for only about 6 months. However, infection can be prolonged because dormant larvae can be
"recruited" sequentially from tissue "stores” over many years, to replace expired adult worms.
Infective larvae of Necator americanus can survive at higher temperatures, whereas those of
Ancylostoma duodenale are better adapted to cooler climates. Generally, they live for only a
few weeks at most under natural conditions, and die almost immediately on exposure to direct
sunlight or desiccation
✔ Sign due to skin penetration: Itching called the ground itch

✔ The migration of the larvae to the respiratory system causes the irritation of the airways
that is manifested by dry cough
✔ Installation of adult worms in the digestive tract causes the inflammation of the
duodenum that is manifested by epigastric pain, diarrhea (sometimes muco-purulent),
nausea and vomiting.
✔ Anemia for prolonged infestation
6. DIAGNOSIS
Stool examination to search for the eggs
7. TREATMENT
Albendazole or Mebendazole
8. PREVENTION
✔ To prevent hookworm, it is advisable not to walk barefoot or contact the soil with bare
hands in areas where hookworm is common or where feces are more likely to be found
in the soil or sand.
✔ Latrines use
✔ To advise people against the use of human faeces to fertilize
9. COMPLICATIONS

● Anemia
● Pneumonitis
III.6 TRICHOMONIASIS
1. DEFINITION
Trichomoniasis is a sexually transmitted infection caused by a protozoan, usually found in

the vagina and urethral tissues. Trichomonas is in general the common cause of vaginal
infections. Trichomoniasis is also known as trichomonas vaginitis.
Although this condition is most often treated in women, men can also be infected. The latter
often have no symptoms.
2. AETIOLOGY (ETIOLOGY)
Trichomoniasis is caused by Trichomonas vaginalis, a flagellated motile protozoan.
3. TRANSMISSION
The human genital tract is the only reservoir for this species. Trichomonas is transmitted
through sexual or genital contact. Transmission from objects (e.g. toilet seats, towels) is also
possible but very rare.
4. SYMPTOMS
⮚ For Women:
● Discomfort with intercourse

● Itching of the inner thighs
● Vaginal discharge (thin, greenish-yellow, frothy or foamy)
● Vaginal itching
● Vulvar itching or swelling of the labia
● Vaginal odor (foul or strong smell)
For Men: usually the disease is asymptomatic in men, but there may be:
● Burning after urination or ejaculation

● Itching of urethra
● Slight discharge from urethra
● Occasionally, some men with trichomoniasis may develop prostatitis or epididymitis
from the infection.
5. DIAGNOSIS
⮚ In women:
A pelvic examination shows red blotches on the vaginal wall or cervix. A wet
prep (microscopic examination of discharge) shows the infection-causing organisms in vaginal
fluids. A pap smear may also diagnose the condition.
⮚ In men:
The disease can be hard to diagnose in men. Men are treated if the infection is diagnosed in
any of their sexual partners. Men may also be treated if they have ongoing symptoms of urethral
burning or itching despite treatment for gonorrhea and chlamydia.
6. TREATMENT
✔ The treatment of choice is metronidazole (Flagyl) 2 gr single dose, except in the

first trimester of pregnancy, when clotrimazole is used topically or metronidazole for
vaginal use. It is important not to drink alcohol while taking this drug (the combination
can lead to disulfiram-like effect).
✔ Clotrimazole (Gyne-Lotrimin, Mycelex-7) if pregnant and having symptoms.
Medicine is inserted into the vagina at night for 14 days. This will decrease symptoms,
but the cure rate is only 20%.
7. PREVENTION
Because trichomoniasis is a sexually transmitted disease, the following must be considered:

⮚ Abstinence is the preferred method to avoid contraction of this disease.
⮚ Safe sex and hygiene practices may also help prevent trichomonas infection.
⮚ Use of condoms.
⮚ Washing before and after intercourse.

⮚ Avoid sharing swimsuits or towels. (Trichomonads survive for up to 45 minutes
outside the body).
⮚ Shower immediately after swimming in a public pool.
8. COMPLICATIONS
▪ Trichomoniasis is associated with increased risk of transmission of HIV.

▪ Trichomoniasis may cause a woman to deliver a low-birth-weight
or premature infant.
▪ Trichomoniasis is also associated with increased risk of cervical cancer
▪ Evidence implies that infection in males potentially raises the risks of prostate
cancer development and spread due to inflammation.
Remark: Note that Trichomonas intestinalis rarely causes intestinal trichomoniasis

specifically in high risk groups (people with immunocompromised state). It is characterized
by a chronic colitis. Easily detectable by direct stool examination, trichomonas intestinalis is
very motile. The treatment of choice is metronidazole or alternatively tinidazole.
III.7 TAPEWORM OR TAENIASIS
1. DEFINITION
Teniasis is a form of tapeworm infection which is caused by tapeworms of the genus Taenia.
It is an infestation with or disease caused by tapeworms.
2. ETIOLOGY
Tapeworm infection is caused by eating the raw or undercooked meat of infected animals. Beef
generally carry Taenia saginata (T. saginata ) whereas pigs carry Taenia solium (T. solium).
Cestodes include the following:
• Taenia solium
• Taenia saginata
• Taenia asiatica
• Diphyllobothrium

• Hymenolepis
• Dipylidium caninum
• Echinococcus
• Spirometra
• Taenia multiceps
The following table shows cestodes and their respective hosts:
Cestode Primary Host Intermediate Host
T. solium Humans Pigs, humans, dogs, cats, sheep
T. saginata Humans Cattle
Diphyllobothrium Humans Fish
Hymenolepis Humans Hymenolepis nana: None; Hymenolepis diminuta:

Rodents
D. caninum Humans, dogs, cats Fleas on dogs/cats
Echinococcus Dogs Humans, sheep, cattle, goats, horses, camel
Spirometra Humans -
T. multiceps Hares, rabbits, squirrels, humans (rarely)
3. TRANSMISSION
Transmission of tapeworm can occur by:

✔ Ingestion of eggs:
Eggs are generally ingested through food, water or soil contaminated with human or animal
(host) faeces.
Tapeworms have many segments (proglottides). Each segment is able to produce eggs. Eggs
are spread individually or in groups, and can pass out with the stool or through the anus. Adults
and children with pork tapeworm can infect themselves if they have poor hygiene. They can
ingest eggs from tapeworm they pick up on their hands while wiping or scratching their anus
or the surrounding skin. Those who are infected can expose other people to T. solium eggs,
usually through food handling.
N.B: Once the eggs have been ingested, they develop into larvae, which can migrate out of the
intestines and form cysts in other tissues such as the lungs or liver. This type of infection is not
common with beef or fish tapeworms, but can occur with the pork tapeworm (where it is called
CYSTICERCOSIS) and can also occur with dog and sheep tapeworms (where it is called
ECHINOCOCCOSIS).
✔ Ingestion of larvae cysts in meat or muscle tissue:
Tapeworm infection can also be caused by eating raw or undercooked meat from an animal or
a fish that has the larval form of the tapeworm cysts in its muscle tissue. Once ingested, the
larvae then develop into adult tapeworms in the intestines. Adult tapeworms can measure up to
50 feet (15 m) long and can survive as long as 20 years.
4. RISK FACTORS
Factors that may put someone at greater risk of tapeworm infection include:
⮚ Poor hygiene: infrequent washing and bathing increases the risk of accidental transfer
of contaminated matter to the mouth.
⮚ Exposure to livestock: this is especially problematic in areas where human and animal
feces are not disposed of properly.
⮚ Frequent travel to developing countries: infection occurs more frequently in areas

with poor sanitation practices.
⮚ Eating raw or undercooked meats: improper cooking may fail to kill tapeworm eggs
and larvae contained in contaminated pork or beef.

5. PATHOGENESIS
In most cestode infestations (ie, T.solium, T.saginata, Diphyllobothrium species,

Hymenolepis species, and D. caninum), humans are the primary hosts. Adult worms survive
inside their human hosts, where they are limited to the intestinal tract. Human fecal
contamination of the environment is needed to sustain these life cycles. In the remaining
cestodes (ie, Echinococcus species, Spirometra species, and T multiceps), humans function as
the intermediate hosts. Larvae exist within the tissues and migrate through different organ
systems. Hymenolepis species and T.solium are the only cestodes for which humans can
function as both primary hosts and intermediate hosts. Hymenolepis diminuta is primarily a
cestode of rodents, although humans can be a rare and accidental hosts in the life cycle. Humans
are infected by swallowing insects that contain cysticercoid larvae, most often by ingesting
mealworms or grain beetles that infest dried grains, cereals, flour, and dried fruit. A tapeworm
infection starts after ingestion of tapeworm eggs or larvae. Some tapeworms attach themselves
to the walls of the intestine, where they cause irritation or mild inflammation, while others may
pass through stool and exit the body.
6. SYMPTOMS
Tapeworm infection usually does not cause any symptoms. People often realize they are
infected when they pass segments of the worm in their stool, especially if the segments are
moving. Invasive tapeworm infection symptoms vary depending on where the larvae have
migrated.
⮚ Intestinal infection
Signs and symptoms of intestinal infection include:
✔ Nausea
✔ Weakness
✔ Loss of appetite
✔ Abdominal pain
✔ Diarrhea
✔ Weight loss
✔ Inadequate absorption of nutrients from food
✔ Proglottides in the faeces
⮚ Invasive infection
If tapeworm larvae have migrated out of intestines and formed cysts in other tissues, they can
eventually cause organ and tissue damage, resulting in:
✔ Fever
✔ Cystic masses or lumps
✔ Allergic reactions to the larvae
✔ Bacterial infections
✔ Neurological symptoms or seizures
7. COMPLICATIONS
The consequences of tapeworm infection can vary, depending on what species of tapeworm
someone has got.
✔ Intestinal infection complications

Generally, intestinal tapeworm infections have little or no complications. But if the tapeworms
grow large enough, they can block the bile duct, appendix or pancreatic duct, causing
problems for those organs.
✔ Invasive infection complications

Invasive infections have a greater likelihood of developing complications, including:
o Brain and central nervous system impairment: Called neurocysticercosis, this

dangerous complication of invasive pork tapeworm infection can result in headaches
and visual impairment, as well as seizures, meningitis, hydrocephalus or dementia.
Death can occur in severe cases of infection.
o Organ function disruption: When larvae migrate to tissues or organs in the body, they
develop into lesions or cysts. Over time, they grow larger, and sometimes their size can
disrupt organ function, or they can grow so large that they rupture. In other cases, cysts
put pressure on nearby blood vessels, hindering circulation or causing blood vessels to
rupture. Surgery or organ transplantation may be needed in severe cases.

8. DIAGNOSIS
✔ Intestinal infections
When there is an intestinal tapeworm infection, eggs and sometimes tapeworm segments are
passed in the stool, where they can be identified as a tapeworm infection. However, they are
released irregularly and the segments may be broken down by the time they pass through the
digestive system. A laboratory may use microscopic identification techniques to check for eggs
or tapeworm segments in the feces.
✔ Invasive infections
For tissue-invasive infections, the blood is tested for antibodies. Certain types of imaging, such
as CT or MRI scans, X-rays or ultrasounds of cysts may also suggest the diagnosis. These
exams may be helpful for the diagnosis.
9. TREATMENT
⮚ Medications for intestinal tapeworm
The most common treatment for tapeworm infection involves oral medications that are toxic
to the tapeworm. The drug of choice is niclozamide (yomesan).Praziquantel (Biltricide) and
Albendazole (Albenza) are sometimes used.
Niclosamide should be given in the morning on an empty stomach (either 1 hour before or 2
hours after a meal). The tablets should be thoroughly chewed or crushed and then swallowed
with a small amount of water.
Dosage: T.saginata, T.solium, and Diphyllobothrium latum: A single 2 g dose.
⮚ Treatments for invasive tapeworm infection
Treating an invasive infection depends on the location and effects of the infection:
✔ Anthelmintic or anthelminthic drugs: Niclosamide, Albendazole (Albenza) can

shrink some tapeworm cysts.

✔ Antiinflammatories: If tapeworm cysts are causing swelling or inflammation in the
tissues or organs, an anti-inflammatory medication can help.
✔ Anti-epileptic therapy: If the disease is causing seizures, anti-epileptic medications

can stop them.
✔ Shunt placement: One type of invasive infection can cause too much fluid on the brain,
called hydrocephalus. The doctor may recommend placing a permanent shunt, or tube,
in the head to drain the fluid.
✔ Surgery: Whether cysts can be removed surgically depends on their location and
symptoms. Those that develop in the liver, lungs and eyes are typically removed, since
they can eventually threaten organ function.
10. PREVENTION
To prevent tapeworm infection, the following guidelines are crucial:
✔ Proper hand washing before eating or handling food and after using the toilet.
✔ Wash and cook all fruits and vegetables with safe water before eating.
✔ Eliminate livestock exposure to tapeworm eggs by properly disposing of animal and
human feces.
✔ Thoroughly cook meat at temperatures of at least 125 F (52 C) to kill tapeworm eggs
or larvae.
✔ Freeze meat for at least 12 hours and fish for at least 24 hours to kill tapeworm eggs
and larvae.
✔ Avoid eating raw or undercooked meat of pork, beef and fish.
✔ Promptly treat dogs infected with tapeworm.
III.8 TRICHURIASIS (HUMAN WHIPWORM) OR TRICHOCEPHALIASIS OR

TRICURIASIS
1. DEFINITION
Trichuriasis is a parasitic infection primarily in the tissue of the caecum, appendix, colon and
rectum that is caused by Trichuris trichiura (whipworm), an intestinal parasitic nematode
(roundworm).

2. ETIOLOGY
Trichocephaliasis is caused by Trichirus trichiura (whipworm), an intestinal parasitic

nematode.
Adult worms are usually 3–5 cm long, with females being larger than males as is typical of
nematodes. The thin, clear majority of the body (the anterior, whip-like end) is the esophagus,
and it is the end that the worm threads into the mucosa of the colon. The widened, pinkish gray
region of the body is the posterior, and it is the end that contains the parasite’s intestines and
reproductive organs. Trichuris trichiura has characteristic football-shaped eggs, which are
about 50-54 um long and contain polar plugs (also known as refractile prominences) at each
end.
3. TRANSMISSION
Humans can become infected with the parasite due to ingestion of infective eggs by mouth
contact with hands or food contaminated with egg-carrying soil. However, there have also been
rare reported cases of transmission of trichuris trichiura by sexual contact. Some major
outbreaks have been traced to contaminated vegetables (due to presumed soil contamination).
4. LIFE CYCLE
Unembryonated eggs (unsegmented) are passed in the feces of a previous host to the soil. In
the soil, these eggs develop into a 2-cell stage (segmented egg) and then into an advanced
cleavage stage. Once at this stage, the eggs embryonate and then become infective, a process
that occurs in about 15 to 30 days. Next, the infective eggs are ingested by way of soil-
contaminated hands or food and hatch inside the small intestine, releasing larvae into the
gastrointestinal tract. These larvae burrow into a villus and develop into adults (over 2–3 days).
They then migrate into the cecum and ascending colon where they thread their anterior portion
(whip-like end) into the tissue mucosa and reside permanently for their year-long life span.
About 60 to 70 days after infection, female adults begin to release unembryonated eggs
(oviposit) into the cecum at a rate of 3,000 to 20,000 eggs per day, linking the life cycle to the
start.
✔ Most infected individuals have no symptoms and no eosinophilia.

✔ Heavy infestations may result in abdominal pain, anorexia, and bloody or mucoid diarrhea
resembling inflammatory bowel disease.
✔ Rectal prolapse can result from massive infestations in children, who often suffer from
malnutrtion and other diarrheal illnesses.
✔ Moderately heavy Trichuris burden also contributes to growth retardation, weight loss,
nutritional deficiencies, and anemia (due to long-standing blood loss), and these symptoms
are more prevalent and severe in children.
6. DIAGNOSIS
✔ Direct exam of the stool: Trichuris trichiura eggs are readily detected in stool
examination.
✔ Adult worms are occasionally seen on proctoscopy.
7. TREATMENT
o Albendazole (ZENTEL): 400mg as a single dose
o Vermox 100mg: 1 tablet twice a day for 3days or Mebendazole (vermox) 500 mg:2
tablets as single dose
o Diarrheic patients may be treated with Imodium (loperamide hydrochloride) to increase

the amount of drug contact with the parasites.
1. PREVENTION
● Improved facilities for feces disposal

● Handwashing before food handling, and avoiding ingestion of soil by thorough washing
of food that may have been contaminated with egg-containing soil.
● Mass Drug Administration (preventative chemotherapy) especially among children,
who are at highest risk for infection.
● Control of soil fertilizers
● Early detection and treatment
● Hand, food and water hygiene
III.9 PINWORM (ENTEROBIASIS, OXYUROSE)

1. DEFINITION
A pinworm infection or enterobiasis is a human parasitic disease and one of the most
common childhood parasitic worm infections in the developed world.
2. ETIOLOGY
It is caused by infestation with the parasitic roundworm Enterobius vermicularis

(human pinworm).
3. TRANSMISSION
Infection usually occurs through the ingestion of pinworm eggs, either through contaminated
hands, food, or water.
4. LIFE CYCLE AND EPIDEMIOLOGY
Enterobius adult worms are 1 cm long and inhabit in the coecum. Gravid female worms migrate
nocturnally into the perianal region and release up to 10,000 immature eggs each. The eggs
become infective within hours and are transmitted by hand-to-mouth passage. From ingested
eggs, larvae hatch and mature into adults. This life cycle takes 1 month, and adult worms
survive for 2 months. Self-infection results from perianal scratching and transport of infective
eggs on the hands or under the nails to the mouth. Because of the ease of person-to-person
spread, pinworm infections are common among family members.
o Most pinworm infections are asymptomatic and often attack children
o Anal and perianal pruritus is the cardinal symptom.
o The itching, which is often worse at night as a result of the nocturnal migration of the
female worms, may lead to excoriation and bacterial surinfection.
o Heavy infestations have been claimed to cause abdominal pain, intermittent diarrhea
and weight loss.
o In rare occasions, pinworms invade the female genital tract, causing vulvovaginitis.
6. DIAGNOSIS

● Since pinworm eggs are not released in feces. Eggs are detected by the application of
clear cellulose acetate tape to the perianal region in the morning. After the tape is
transferred to a slide, microscopic examination will detect pinworm eggs
● See the worm itself on the faeces (adult female worm was discovered in diarrheic stool)
N.B. The eggs are rare in the faeces.
7. TREATMENT AND CONTROL

⮚ Drugs:
o ALBENDAZOLE (Zentel) 400mg as a single dose
o MEBENDAZOLE(Vermox) 100 mg:2X100 mg/day for 3 days or 500 mg as single

dose
o Treatment of family members is compulsory to eliminate asymptomatic reservoirs

responsible of potential reinfestation.
N.B.: The above mentioned drugs are to kill the pinworms (not the eggs).
⮚ To control the eggs:
● Clean toilet seats daily

● Keep fingernails short and clean
● Wash all bed linens twice a week
● Wash hands before meals and after using the toilet
● Avoid scratching the infected area around the anus. This can contaminate your fingers
and everything else that you touch afterwards.
● Keep the hands and fingers away from the nose and mouth unless they are freshly
washed.
8. PROGNOSIS
Pinworm infection is fully treatable.
2. COMPLICATIONS
● Pelvic inflammatory disease

● Repeated infection with the parasite (re-infestation)
● Vaginitis
3. PREVENTION
o Hygiene measures
o Treat family members
o Repeat the treatment after 8 days
o Hand hygiene and hygiene of the bed sheets
III.10 STRONGYLOIDIASIS
Strongyloidiasis: A parasitic infectious disease involving the intestines and caused by the
nematode Strongyloides stercoralis.
Infection usually occurs in crowded, unsanitized populations. People catch the infection when
their skin comes in contact with soil contaminated with the worms. The tiny worm is barely
visible to the naked eye. Young roundworms can move through a person's skin and into the
bloodstream to the lungs and airways. They then move up to the throat, where they are
swallowed into the stomach. The worms then move to the small intestine, where they attach to
the wall. Later, they produce eggs, which hatch into tiny larvae and pass out of the body. Unlike
other worms, these larvae can reenter the body through the skin around the anus, which allows
an infection to grow. Areas where the worms go through the skin may become red and painful.
3. SYMPTOMS
The list of signs and symptoms mentioned in various sources for Strongyloidiasis includes
the 16 symptoms listed below:
✔ Stage 1: initial infestation from exposure: No specific symptoms

✔ Stage 2: worm larvae temporarily in the lungs, characterized by:
o Coughing

o Wheezing
✔ Stage 3: intestinal infestation whose features are:

o Nausea and vomiting
o Diarrhea or constipation
o Anemia
o Weight loss
o Chronic diarrhea
o Epigastric pain
o Epigastric tenderness
4. DIAGNOSTIC TESTS
The possible diagnostic tests are:
✔ Worm larvae in stool

✔ Strongyloides antibody blood test
5. DIFFERENTIAL DIAGNOSIS
The other diseases that make differential diagnosis with Strongyloidiasis are:
o Ascariasis
o Diabetic diarrhea
o Hookworm
o Pinworm
o Whipworm
6. COMPLICATIONS
The following complications may arise from strongyloidiasis:
✔ Anemia
✔ Weight loss

✔ Malabsorption syndrome
✔ Pruritus
✔ Pulmonary eosinophilia
✔ Ascites
✔ Visceral larva migrans
✔ Gastrointestinal bleeding
✔ Bronchospasm
✔ Severe diarrhoea can lead to dehydration
7. TREATMENT
✔ Thiabendazole (Mintezol)
✔ Ivermectin
✔ Albendazole
✔ Intravenous fluids if volume replacement is required
✔ Blood transfusion if anemia
✔ Mechanical ventilation if severe lung complication
8. PROGNOSIS
With good treatment, people should make a full recovery and the parasites should be removed.
Sometimes treatment needs to be repeated. Infections that are severe or widespread often have
a poor outcome, especially in people with a weakened immune system.
9. PREVENTION
o Good personal hygiene

o Public health services and sanitary facilities provide good infection control.
III.11 TRYPANOSOMIASIS
1. INTRODUCTION AND EPIDEMIOLOGY
Trypanosomiasis, also called sleeping sickness, endemic, and sometimes epidemic, chronic
disease caused by a protozoan blood parasite, genus Trypanosoma. In cattle and other animals,
which serve as the reservoir for the protozoa, the disease is called nagana. Two variations of
the disease occur in central and western Africa, both of them transmitted in the salivary glands

of infected tsetse flies. The most common is caused by T. brucei gambiense, whereas a more
local version is caused by T. brucei rhodesiense. In South America, another version of the
protozoan, T. cruzi, is transmitted by the triatoma bug and is called Chagas' disease.
The disease is found in two forms, depending on the parasite, either Trypanosoma brucei
gambiense or Trypanosoma brucei rhodesiense. Humans are the main reservoir
for Trypanosoma brucei gambiense, but this species can also be found in pigs and other
animals. Wild game animals and cattle are the main reservoir of T. b. rhodesiense. T. b.
gambiense is found in central and western Africa; it causes a chronic condition that can remain
in a passive phase for months or years before symptoms emerge. T. b. rhodesiense is
the acute form of the disease, but has a much more limited geographic range. It is found in
southern and eastern Africa and symptoms of infection emerges in a few weeks and is more
virulent and faster developing than T. b. gambiense. According to recent estimates, the
disability adjusted life years (9 to 10 years) lost due to sleeping sickness are 2.0 million. Recent
estimates indicate that over 60 million people living in some 250 locations are at risk of
contracting the disease, and there were under 10,000 cases reported in 2009 according to WHO
figures which represents a huge decrease from the estimated 300,000 new cases in 1998. The
disease has been recorded as occurring in 36 countries, all in sub-Saharan Africa. It is endemic
in southeast Uganda and western Kenya, and killed more than 48,000 Africans in 2008.
Horse-flies (Tabanidae) and stable flies (Muscidae) possibly play a role in transmission
of nagana (the animal form of sleeping sickness) and the human disease form.
III.11.1 HUMAN AFRICAN TRYPANOSOMIASIS (SLEEPING SICKNESS,

AFRICAN LE THARGY, CONGO TRYPANOSOMIASIS)
1. DEFINITION
Human african trypanosomiasis is a parasitic disease of people and animals, caused

by protozoa of the species Trypanosoma brucei and transmitted by the tsetse fly.
Four major epidemics have occurred in recent history: one from 1896–1906 primarily in
Uganda and the Congo Basin, two epidemics in 1920 and 1970 in several African countries,
and a recent 2008 epidemic in Uganda.

2. ETIOLOGY
The most common is caused by T. brucei gambiense, whereas a more local version is caused
by T. brucei rhodesiense.
3. TRANSMISSION
In addition to the bite of the tsetse fly (of the genus glossina), the disease can be transmitted in
the following ways:
⮚ Mother to child infection: the trypanosome can sometimes cross the placenta and infect
the fetus.
⮚ Laboratories: accidental infections, for example, through the handling of blood of an
infected person and organ transplantation, although this is uncommon.
⮚ Blood transfusion
⮚ Possibly by sexual contact ( but this is rare)
4. TRYPANOSOMA LIFE CYCLE
The tsetse fly (genus Glossina) is a large, brown biting fly that serves as both a host and vector
for the Trypanosome parasites. While taking blood from a mammalian host, an infected tsetse
fly injects metacyclic trypomastigotes into skin tissue. From the bite, parasites first enter the
lymphatic system and then pass into the bloodstream. Inside the mammalian host, they
transform into bloodstream trypomastigotes, and are carried to other sites throughout the body,
reach other blood fluids (e.g., lymph, spinal fluid), and continue to replicate by binary
fission.The entire life cycle of African trypanosomes is represented by extracellular stages. A
tsetse fly becomes infected with bloodstream trypomastigotes when taking a blood meal on an
infected mammalian host. In the fly's midgut, the parasites transform into procyclic
trypomastigotes, multiply by binary fission, leave the midgut, and transform into epimastigotes.
The epimastigotes reach the fly's salivary glands and continue multiplication by binary fission.
The entire life cycle of the fly takes approximately 3 weeks.
African trypanosomiasis symptoms occur in two stages:

⮚ The first stage is known as the haemolymphatic phase and is characterized by fever,
headaches, joint pains, and itching. Invasion of the circulatory and lymphatic system
by the parasites is associated with severe swelling of lymph nodes, often to tremendous
sizes. Winterbottom's sign, the tell-tale swollen lymph nodes along the back of the
neck, may appear. If left untreated, the disease overcomes the host's defenses and can
cause more extensive damage, broadening symptoms to include anemia, endocrine,
cardiac, and kidney dysfunctions.
⮚ The second stage, called the neurological phase, begins when the parasite invades
the central nervous system by passing through the blood-brain barrier. The term
'sleeping sickness' comes from the symptoms of the neurological phase. The symptoms
include confusion, reduced coordination, and disruption of the sleep cycle, with bouts
of fatigue punctuated with manic periods leading to daytime slumber and night-
time insomnia. Without treatment, the disease is invariably fatal, with progressive
mental deterioration leading to coma and death. Damage caused in the neurological
phase is irreversible. Tryptophol is a chemical compound that induces sleep in
humans. It is produced by the trypanosomal parasite in sleeping sickness.
6. DIAGNOSIS
✔ Identification of trypanosomes in a patient sample by microscopic examination.

Patient samples that can be used for diagnosis include chancre fluid, lymph node
aspirates, blood, bone marrow, and, during the neurological stage, cerebrospinal
fluid.
✔ Detection of trypanosome-specific antibodies (but it is less accurate).
7. TREATMENT
✔ First line, first stage
The current standard treatment for first stage (haemolymphatic) disease is:
▪ Intravenous or intramuscular pentamidine (for T.b. gambiense); or

▪ Intravenous suramin (for T.b. rhodesiense)
According to a treatment study of Trypanosoma gambiense caused by human African

trypanosomiasis, use of eflornithine (DMFO) resulted in fewer adverse events than treatment
with melarsoprol.
✔ First line, second stage
The current standard treatment for second stage (neurological phase) disease is:
▪ Intravenous melarsoprol 2.2 mg/kg daily for 12 consecutive days.
Alternative first line therapies include:

▪ Intravenous melarsoprol 0.6 mg/kg on day 1, 1.2 mg/kg IV melarsoprol on day 2, and
1.2 mg/kg/day IV melarsoprol combined with oral 7.5 mg/kg nifurtimox twice a day
on days 3 to 10; or
▪ Intravenous eflornithine 50 mg/kg every six hours for 14 days.
8. PREVENTION
Two alternative strategies can be used in the attempts to reduce the African trypanosomiases:
o Eradication of the tsetse fly, which disrupts transmission rates by reducing the number
of flies (the use of the sterile insect technique).
o The second tactic is primarily medical or veterinary and tries to reduce spread of the
parasite by monitoring, prophylaxis, treatment, and surveillance to reduce the number of

people/animals that carry the disease
III.11.2 CHAGAS DISEASE OR AMERICAN TRYPANOSOMIASIS
Chagas disease also called American trypanosomiasis is a tropical parasitic disease caused
by the flagellate protozoan Trypanosoma cruzi. T. cruzi is commonly transmitted to humans
and other mammals by an insect vector, the blood-sucking insects of the subfamily
Triatominae (family Reduviidae) most commonly species belonging to the

Triatoma, Rhodnius, and Panstrongylus genera. The disease was first identified by Carlos
Chagas in 1909.
2. TRANSMISSION
The disease is spread by insects but T. cruzi can also be transmitted through blood
transfusions. With the exception of blood derivatives (such as fractionated antibodies), all
blood components are infective. The parasite remains viable at 4 °C for at least 18 days or up
to 250 days when kept at room temperature. It is unclear whether T. cruzi can be transmitted
through frozen-thawed blood components. Other modes of transmission include organ
transplantation, through breast milk, and by accidental laboratory exposure. Chagas disease
can also be spread congenitally (from a pregnant woman to her baby) through the placenta, and
accounts for approximately 13% of stillborn deaths in parts of Brazil. In 1991, farm workers in
the state of Paraíba, Brazil, were infected by eating contaminated food; transmission has also
occurred via contaminated açaí palm fruit juice and sugar cane juice. A 2007 outbreak in 103
Venezuelan school children was attributed to contaminated guava juice.
The insects that spread the disease are known by various local names, including vinchuca in
Argentina, Bolivia, Chile and Paraguay, barbeiro (the barber) in Brazil, pito in
Colombia, chinche in Central America, chipo in Venezuela, chupança,chinchorro, and "the
kissing bug".
Rhodnius prolixus is the principal vector in Colombia, Venezuela, Guatemala, Honduras and
some parts of Nicaragua and El Salvador.
3. PATHOGENESIS
In Chagas-endemic areas, the main mode of transmission is through an insect vector called a
triatomine bug. A triatomine becomes infected with T. cruzi by feeding on the blood of an
infected person or animal. During the day, triatomines hide in crevices in the walls and roofs.
The bugs emerge at night, when the inhabitants are sleeping. Because they tend to feed on
people’s faces, triatomine bugs are also known as “kissing bugs.” After they bite and ingest
blood, they defecate on the person. Triatomines pass T. cruzi parasites
(called trypomastigotes) in feces left near the site of the bite wound. Scratching the site of the
bite causes the trypomastigotes to enter the host through the wound, or through intact mucous
membranes, such as the conjunctiva. Once inside the host, the trypomastigotes invade cells,

where they differentiate into intracellular amastigotes. The amastigotes multiply by binary
fission and differentiate into trypomastigotes, which are then released into the bloodstream.
This cycle is repeated in each newly infected cell. Replication resumes only when the parasites
enter another cell or are ingested by another vector.
The human disease occurs in two stages: An acute stage, which occurs shortly after an
initial infection, and a chronic stage that develops over many years.
✔ The acute phase lasts for the first few weeks or months of infection.
It usually occurs unnoticed because it is symptom free or exhibits only mild symptoms that are
not unique to Chagas disease. These symptoms are general to many infectious diseases and can
include:
o Fever,
o Fatigue,
o Body aches,
o Headache,
o Rash,
o Loss of appetite,
o Diarrhea and vomiting.
The signs on physical examination can include mild enlargement of the liver or spleen, swollen
glands, and local swelling (a chagoma) where the parasite entered the body. The most
recognized marker of acute Chagas disease is called Romaña's sign, which includes swelling
of the eyelids on the side of the face near the bite wound or where the bug feces were deposited
or accidentally rubbed into the eye. Rarely, young children, or adults may die from the acute
disease due to severe inflammation/infection of the heart muscle (myocarditis) or brain
(meningoencephalitis). The acute phase also can be severe in people with weakened immune
systems.
If symptoms develop during the acute phase, they usually resolve spontaneously within 3–8
weeks in approximately 90% of individuals. Although the symptoms resolve, even with
treatment the infection persists and enters a chronic phase. Of individuals with chronic Chagas

disease, 60–80% will never develop symptoms (called indeterminate chronic Chagas disease),
while the remaining 20–40% will develop life-threatening heart and/or digestive disorders
during their lifetime (called determinate chronic Chagas disease). In 10% of individuals the
disease progresses directly from the acute form to a symptomatic clinical form of chronic
Chagas disease.
✔ The symptomatic (determinate) chronic stage affects the nervous system, digestive
system and heart.
About two thirds of people with chronic symptoms have cardiac damage, including dilated
cardiomyopathy, which causes heart rhythm abnormalities and may result in sudden death.
About one third of patients go on to develop digestive system damage, resulting in dilation of
the digestive tract (megacolon and megaesophagus), accompanied by severe weight loss.
Swallowing difficulties (secondary achalasia) may be the first symptom of digestive
disturbances and may lead to malnutrition. Twenty to fifty percent of individuals with
intestinal involvement also exhibit cardiac involvement. Up to 10% of chronically infected
individuals develop neuritis that results in altered tendon reflexes and sensory impairment.
Isolated cases exhibit central nervous system involvement, including dementia, confusion,
chronic encephalopathy and sensitivity and motor deficits.
The clinical manifestations of Chagas disease are due to cell death in the target tissues that
occurs during the infective cycle, by sequentially inducing an inflammatory response,
cellular lesions, and fibrosis. For example, intracellular amastigotes destroy the intramural
neurons of the autonomic nervous system in the intestine and heart, leading to megaintestine
and heart aneurysms, respectively. If left untreated, Chagas disease can be fatal, in most cases
due to heart muscle damage.
5. DIAGNOSIS
o The presence of T. cruzi is diagnostic of Chagas disease.

o It can be detected by microscopic examination of fresh anticoagulated blood, or
its buffy coat, for motile parasites; or by preparation of thin and thick blood smears
stained with Giemsa, for direct visualization of parasites.

o Microscopically, T. cruzi can be confused with Trypanosoma rangeli, which is not
known to be pathogenic in humans.
o Immunoassay tests include:
▪ Detecting complement fixation, indirect hemagglutination, indirect
fluorescence assays, radioimmunoassays, and ELISA. Alternatively, diagnosis and strain
identification can be made using polymerase chain reaction (PCR).
6. PREVENTION
o There is currently no vaccine against Chagas disease

o Fighting the vector Triatoma by using sprays and paints containing insecticides
(synthetic pyrethroids)
o Improving housing and sanitary conditions in rural areas.
o Sleeping in a mosquito net is recommended, specifically in endemic area.
o Blood bank screening tests
7. TREATMENT
There are two approaches to treating Chagas disease:
▪ Antiparasitic treatment
▪ Symptomatic treatment
Medication:
▪ Antiparasitic treatment is most effective early in the course of infection
▪ Drugs of choice include azole or nitro derivatives such as benznidazole or

nifurtimox. Both agents are limited in their capacity to effect parasitologic cure (a
complete elimination of T. cruzi from the body), especially in chronically infected
patients
▪ Treatment of chronic infection in women prior to or during pregnancy does not appear
to reduce the probability the disease will be passed on to the infant. Likewise, it is
unclear whether prophylactic treatment of chronic infection is beneficial in persons who

will undergo immunosuppression (for example,, organ transplant recipients) or in
persons who are already immunosuppressed (for example,, those with HIV infection).
8. COMPLICATIONS AND SEQUELAE
If Chagas disease progresses to the chronic phase, serious heart or digestive complications may
occur. These may include:
● Heart failure and myocaritis
● Enlargement of the esophagus (megaesophagus)

● Enlargement of the colon (megacolon)
● Abdominal distension with severe constipation
● Lymphadenopathy
● Aseptic meningitis
● Alopecia
● Oedema
● Intrauterine death
● Localized edema
● Pyrexia
● Cranial nerve disorder
● Intrauterine growth retardation
III.12 SCHISTOSOMIASIS (BILHARZIASIS OR BLOOD FLUKES)
1.
DEFINITION
Schistosomiasis or Bilharziasis, is a widespread disease caused by the infestation of the human

body by flukes commonly called blood flukes, of the genus Schistosoma.
2. ETIOLOGY

Three species produce serious diseases. These are S. haematobium, S. mansoni, and S.
japonicum, found in the Tropics and in the Orient. About eight other species are known to
produce irritations of the skin, commonly called swimmer's itch, of bathers in the lakes of the
north-central U.S., especially Michigan and Wisconsin, and of Canada, especially Manitoba.
Only those species that produce serious disease are described here.
The Egyptian blood fluke, S. haematobium, was first described by the German physician
Theodor Bilharz in 1851. The cercariae of the Egyptian blood fluke pierce the skin or mucous
membranes when a human bathes in infested water. Eventually the flukes reach the venules
and capillaries of the bladder. They mate and deposit eggs that, acting as foreign proteins, give
rise to a severe inflammatory reaction in the walls of the bladder and find their way to the
interior of the bladder; during their course, hemorrhages are produced, causing bloody urine
and pain during urination. Eggs can be found in the urine on microscopic examination. The
rectal blood fluke, S. mansoni, and the Japanese blood fluke, S. japonicum, concentrate in the
blood vessels of the large intestine and liver. Some are carried up the portal veins to the liver
where they cause inflammation and scarring, with enlargement of liver and spleen. Because of
obstruction to blood flow through the liver, enlargement of veins ensues, particularly in the
esophagus (esophageal varices). These veins often rupture, causing serious hemorrhage.
Untreated schistosomiasis often results in death
⮚ Clinical features of schistosomiasis
Symptoms
Hematuria, painful and frequent urination for S.heamatobium
Referred pain to hinder part for S.haematobium.
Cardiac disturbances and mental weakness
Abdominal pain for S. mansoni and S. japonicum
Affection of anus and rectum for S. mansoni and S. japonicum
Diarrhea and sanguinous stools for Mansoni and Japonicum

4. DIAGNOSIS
● Urine and stool examinations
5. TREATMENT
o Praziquantel (Biltricide) is the drug of choice. PRAZIQUANTEL is active against all

schistosomal species. The current recommended dosage is 2 Oral Doses of 40 mg/kg in
1 day for either S. haematobium or S. mansoni.
o Surgery when the treatment is unresponsive for S.heamatobium.
6. PREVENTATIVE MEASURES
As there is no available vaccine, the best way to prevent schistosomiasis is to take the
following steps areas where schistosomiasis is common:
● Avoid swimming or wading in freshwater. Nevertheless, swimming in the ocean and

in chlorinated swimming pools is safe.
● Drink safe water: Although schistosomiasis is not transmitted by swallowing
contaminated water, the mouth or lips come in contact with water containing the
parasites, there is a risk of getting the infection, specifically when the membranes
have a cut.
● Water used for bathing should be brought to a rolling boil for 1 minute to kill any
cercariae, and then cooled before bathing to avoid scalding
● Vigorous towel drying after an accidental, very brief water exposure may help to
prevent the Schistosoma parasite from penetrating the skin in some circumstances
● Reducing the number of infections in people by screening and treatment: Control
measures can include mass drug treatment of entire communities and targeted
treatment of school-age children.
● Eliminating the snails that are required to maintain the parasite’s life cycle by using
molluscicides
Note:

1. Chemicals used to eliminate snails in freshwater sources may harm other species of
animals in the water and, if treatment is not sustained, the snails may return to those
sites afterwards.
2. For certain species of the parasite, such as S. japonicum, animals such as cows or
water buffalo can also be infected. Runoff from pastures (if the cows are infected) can
contaminate freshwater sources.
⮚ URINARY SCHISTOSOMIASIS
A. AETIOLOGY
It is due to S.haematobium
B. PATHOGENESIS
Egg laying (oviposition) by adult S. haematobium normally occurs in vesical and pelvic
venules; these vessels are tributaries of the caval system but are connected to the portal venous
system through hemorrhoidal collateral vessels. They produce and deposit approximately 200
to 500 eggs per day. Thus, during its estimated mean life span of 3 to 6 years, a single worm
pair spawns 250,000 to 600,000 eggs; moreover, occasional worm pairs may persist as long as
30 years. They mate and deposit eggs that, acting as foreign proteins, give rise to a severe
inflammatory reaction in the walls of the bladder and find their way to the interior of the
bladder; during their course, hemorrhages are produced, causing bloody urine and pain during
urination. The spectrum of serious disease ascribed to S . haematobium results from the
interaction of 4 factors: intensity, duration, activity and focality.
C. CLINICAL MANIFESTATIONS
Schistosomiasis haematobium infection progresses through 3 clinical stages:

1. Swimmers' itch (schistosomal dermatitis), which relates to cercarial skin penetration.
2. Acute schistosomiasis (also known as Katayama fever), which relates to the onset of
oviposition characterized by haematuria and pain when urinating.
3. Chronic urinary schistosomiasis.
D. CHRONIC URINARY SCHISTOZOMIASIS

The infection enters a patent "active" stage, in which eggs are deposited in tissues, traverse the
bladder or rectosigmoid mucosa, and are excreted in the urine (and less regularly in the feces).
This prepatent period is usually 2 to 3 months but may last over 7 months. The classic clinical
presentation of "active" schistosomiasis, hematuria and terminal dysuria, has been
recognized for over 3000 years. After some years, egg deposition and excretion continue at a
lower rate and symptoms are diminished. Over 30% of light infections "resolve" spontaneously
in some endemic areas. However, although symptoms are absent, silent obstructive uropathy
develops throughout this phase, as sandy patches and fibrosis replace polypoid patches and
the bladder and ureters undergo irreversible damage. Patients finally enter a chronic inactive
phase, in which viable eggs are no longer detected in urine or tissues. Signs and symptoms at
this stage are caused by Sequelae & Complications rather than by the schistosomal infection
itself. Inactive urinary schistosomiasis, which occurs after adult worms have died, is
characterized by the absence of viable eggs in tissues or urine and the presence of "sandy
patches”.
Diagnosis means include urine test, radiological studies, ultrasound.
E. COMPLICATIONS
✔ Cystitis
✔ Bladder ulcers
✔ Bladder stones
✔ Leukoplasia
✔ Carcinoma of ureter
✔ Contracted bladder.
III.13 FILARIASIS OR PHILARIASIS
1. DEFINITION
Filariasis (Philariasis) is a parasitic disease and is considered an infectious tropical disease,

which is caused by thread-like filarial nematodes (roundworms) in the superfamily Filarioidea,
also known as "filariae".
There are 9 known filarial nematodes which use humans as their definitive hosts. These are
divided into 3 groups according to the niche within the body that they occupy: 'lymphatic
filariasis', 'subcutaneous filariasis', and 'serous cavity filariasis'.

⮚ Lymphatic filariasis is caused by the worms Wuchereria bancrofti, Brugia malayi,
and Brugia timori. These worms occupy the lymphatic system, including the lymph
nodes, and in chronic cases these worms lead to the disease elephantiasis.
⮚ Subcutaneous filariasis is caused by loa loa (the African eye worm), Mansonella
streptocerca, Onchocerca volvulus, and Dracunculus medinensis (the Guinea worm).
These worms occupy the subcutaneous layer of the skin, in the fat layer.
⮚ Serous cavity filariasis is caused by the worms Mansonella perstans and Mansonella
ozzardi, which occupy the serous cavity of the abdomen.
Those which are interesting are:
✔ Wuchereria bancrofti,
✔ Loa loa,
✔ Onchocerca volvulus,
✔ Dracunculus medinensis and
✔ Brugia malayi
2. CHARACTERISTICS OF FILARIAE
Organism Periodicity Distribution Vector Location of Microfilarial

adult location
Wuchereria Nocturnal Cosmopolitan Culex Lymphatic Blood

bancrofti areas worldwide, (mosquitoes) tissue
including South Anopheles
America and (mosquitoes)
Africa Mainly Aedes
India China, (mosquitoes)
Indonesia

Brugia Nocturnal Southeast Asia, Mansonia, Lymphatic Blood
malayi Indonesia, India Anopheles tissue
(mosquitoes)
Loa loa Diurnal West and Central Chrysops Subcutaneous Blood

Africa (deer flies) tissue
Onchocerca None South and Central Simulium Subcutaneous Skin, eye

volvulus America, Africa (black flies) tissue
In all cases, the transmitting vectors are either bloodsucking insects (flies or mosquitoes),
or copepod crustaceans in the case of Dracunculus medinensis.
Individuals infected by filarial worms may be described as either "microfilaraemic" or

"amicrofilaraemic," depending on whether or not microfilaria can be found in their peripheral
blood. Filariasis is diagnosed in microfilaraemic cases primarily through direct observation of
microfilaria in the peripheral blood. Occult filariasis is diagnosed in amicrofilaraemic cases
based on clinical observations and, in some cases, by finding a circulating antigen in the blood.
3. LIFE CYCLE AND TRANSMISSION
Human filarial nematode worms have a complicated life cycle, which primarily consists of five
stages. After the male and female worms mate, the female gives birth to live microfilariae by
the thousands. The microfilariae are taken up by the vector insect (intermediate host) during a
blood meal. In the intermediate host, the microfilariae molt and develop into 3 rd stage
(infective) larvae. Upon taking another blood meal, the vector insect injects the infectious
larvae into the dermis layer of the skin. After about one year, the larvae molt through 2 more
stages, maturing into the adult worms.
4. TYPES OF FILARIASIS
A. WUCHERERIASIS OR LYMPHATIC FILARIASIS OF BANCROFT
⮚ Clinical Manifestations
Clinical signs are due to the presence of live or dead adult worms in lymphatic vessels. This
results in lymphatic stasis which is also accompanied by secondary infection.

Consequently, the following will occur:
● Lymphangitis which is manifested by sensible and palpable lymphatic cord,

erythematous and hot, often accompanied by fever. This lymphangitis is frequent on
lower limbs. Later, lymphatic varices can occur
● Obstruction of lymphatic vessels (especially for lower limbs and genital organs) often
results in lymphoedema. This lymphoedema is localized at the level of subcutaneous
tissue and causes a firm edema which becomes chronic and creates elephantiasis. The
edema can creates hydrocele which contains a liquid in which the microfilariae can be
identified. Deep lymphatic vessels obstruction often leads to ascites.
● The rupture of lymphatic vessels in urinary tract leads to lymphuria
N.B. ELEPHANTIASIS is the thickening of the skin and tissue, its frequent localization is
lower limbs and genital organs (scrotum for males, labia majora for females). It can also be
located on arms and breasts.
⮚ Diagnosis
✔ Nocturnal blood smear because the microfilaria have nocturnal blood periodicity
(22h00 to 2h00)
✔ Examine fluids from hydrocele and ascites
✔ Full blood count shows hypereosinophilia
✔ Identification of antifilarian antibodies
B. LOASIS
⮚ Etiology
It is caused by Loa loa. The adult worms actively circulate in subcutaneous tissues.
⮚ Clinic Manifestations
● Oedema of Calabar: It is a subcutaneous oedema, itchy and migrant

● Intense itching resulting in lesions due to scratching

● Superficial migration of adult worm which can be seen where the mucus is less
adherent and where the adipose tissue is reduced, especially at the conjunctiva. There
is irritation of the conjunctiva without causing blindness
⮚ Complications
✔ Cardiac and ocular complications: they are benign in general

✔ Neurologic complications: filarian encephalopathy with the presence of microfilaria
in CSF. This complication is very severe. It can also happen as allergic accident during
the treatment due to abrupt lysis of microfilaria in case of intense microfilaremia.
⮚ Diagnosis
✔ Diurnal blood smear because the microfilaria have diurnal blood periodicity
✔ Hypereosinophilia (FBC)
C. ONCHOCERCIASIS
⮚ Etiology
Onchocerciasis is caused by the filarial nematode Onchocerca volvulus, which infects an

estimated 13 million individuals. Onchocerciasis is the second leading cause of infectious
blindness worldwide.
Onchocerciasis primarily affects the skin, eyes, and lymph nodes.
⮚ Clinical Features
The adult worms live in subcutaneous tissue where they form the nodules.
✔ Skin: Pruritus and rash are the most frequent manifestations of onchocerciasis. The
pruritus can be debilitating; the rash is typically a papular eruption that is generalized
rather than localized to a particular region of the body.
✔ Superficial subcutaneous nodules (Onchocercomata): These are subcutaneous
nodules, which can be palpable and/or visible, contain the adult worm. Nodules tend to
develop preferentially in the upper part of the body (at the thorax) and can also be
localized at the pubic symphysis.

✔ Ocular lesions: they occur very late but they make the gravity of the disease because
they lead to decreased visual acuity and finally to blindness. The reason why
onchocericiasis is called “river blindness” is that the disease is transmitted by small
black flies called SIMULIUM which live near the rivers.
✔ Lymph nodes: Mild to moderate lymphadenopathy is common, particularly in the
inguinal and femoral areas, where the enlarged nodes may hang down in response to
gravity ("hanging groin").
✔ Systemic manifestations: Some heavily infected individuals develop cachexia with
loss of adipose tissue and muscle mass.
⮚ Diagnosis
● Definitive diagnosis depends on the detection of an adult worm in an excised nodule

or, more commonly, of microfilariae in a skin snip.
● Eosinophilia and elevated serum IgE levels are common but, because they occur in
many parasitic infections, are not diagnostic in themselve.
5. TREATMENT OF FILARIASIS
o Old drug: DIETHYL CARBAMAZINE or Carbilazine

o Actual drug: IVERMECTINE (Mectizan) a single dose
o The combination of albendazole with ivermectin or albendazole with
diethylcarbamazine is also effective
o Associate also with a corticoid or antihistamine
6. PREVENTION AND CONTROL OF FILARIASIS
✔ Avoidance of mosquito bites by using insecticide-treated mosquito bed nets

(impregnated mosquito nets)
✔ DIETHYL CARBAMAZINE (DEC) can kill developing forms of filarial parasites and
is useful as a prophylactic agent in humans.
✔ Community-based intervention is the current approach to elimination of lymphatic
filariasis as a public health problem: mass annual distribution of antimicrofilarial
chemotherapy by albendazole with either DEC or ivermectin

✔ Community education and clinical care for persons already suffering from the chronic
sequelae of lymphatic filariasis are important components of filariasis control and
elimination
CHAPTER IV. VIRAL DISEASES

IV.1. INTRODUCTION TO VIRUSES
In 1898, Friedrich Loeffler and Paul Frosch found evidence that the cause of foot-and-mouth
disease in livestock was an infectious particle smaller than any bacteria. This was the first clue
to the nature of viruses, genetic entities that lie somewhere in the grey area between living and
non-living states.
The virus particles are 100 times smaller than a single bacteria cell. The bacterial cell alone is
more than 10 times smaller than a human cell and a human cell is 10 times smaller than the
diameter of a single human hair.
Viruses cannot grow or multiply on their own and need to enter a human or animal cell and
take over the cell to help them multiply.
Viruses are not simply taken into cells. They must ﬁrst attach to a receptor on the cell surface.
Each virus has its speciﬁc receptor, usually a vital component of the cell surface. It is the
distribution of these receptor molecules on host cells that determines the cell-preference of
viruses. For example, the cold and flu virus prefers the mucus lining cells of the lungs and the
airways.
Viruses depend on the host cells that they infect to reproduce. When found outside of host cells,
viruses exist as a protein coat or capsid, sometimes enclosed within a membrane. The capsid
encloses either DNA or RNA which codes for the virus elements. While in this form outside
the cell, the virus is metabolically inert. When it comes into contact with a host cell, a virus
can insert its genetic material into its host, literally taking over the host's functions. An infected
cell produces more viral protein and genetic materials instead of its usual products. Some
viruses may remain dormant inside host cells for long periods, causing no obvious change in
their host cells (a stage known as the lysogenic phase). But when a dormant virus is stimulated,
it enters the lytic phase: new viruses are formed, self-assemble, and burst out of the host cell,
killing the cell and going on to infect other cells.
Viruses do not have the chemical machinery needed to survive on their own. They, thus seek
out host cells in which they can multiply. These viruses enter the body from the environment
or other individuals.

⮚ LIFE CYCLE OF A BASIC VIRUS
There are a few basic steps that all infecting viruses follow and these are called the lytic
cycle. These include:
1. The adsorption process where a virus particle attaches to a host cell

2. The particle injects its DNA or RNA into the host cell, the step known as entry.
3. The invading DNA or RNA takes over the cell and recruits the host’s enzymes
4. The cellular enzymes start making new virus particles and this process is called
replication
5. The particles of the virus created by the cell come together to form new viruses, the
process known as assembly
6. The newly formed viruses kill the cell so that they may break free and search for a
new host cell: this is a release process.
⮚ THE CLASSIFICATION OF VIRUSES
In 1995, the international committee on taxonomy of viruses had organized more than 4000
animal and plant viruses into 71 families, 11 subfamilies, and 164 genera, with hundreds of
viruses still unassigned. Currently 24 families contain viruses that infect humans and animals.
According to the type of nucleic acid, viruses are classified into DNA and RNA viruses:
✔ DNA viruses:
o Polyomaviruses
o Papillomaviruses
o Adenoviruses
o Herpesviruses
o Poxviruses
o Hepadnaviruses
✔ RNA viruses:
o Picornaviruses
o Flaviviruses
o Arboviruses

o Togaviruses
o Viroids
o Caliciviruses
o Orthomyxoviruses
o Prions
o Retroviruses
o Paramyxoviruses
o Rhabdoviruses
o Bunyaviruses
⮚ PATHOGENESIS AND CONTROL OF VIRAL DISEASES
More than 300 viruses are known to infect humans and to cause as many as 50 different
syndromes. Viral diseases are known to have no curative treatment but most of them can be
prevented. The immune system plays a major role in fighting against viral diseases.
o Host Immune Response:
a. Both humeral immunity and cellular immunity are involved in control of viral infection.
b. Cytotoxic T lymphocytes lyse virus infected cells.
c. Secretory IgA antibody is important against viral infections of the respiratory or
gastrointestinal tract.
⮚ PREVENTION AND TREATMENT OF VIRAL DISEASES
Viruses are obligate intracellular parasites, antiviral drugs must have to be of selectively
inhibiting viral functions without damaging the host. Furthermore an ideal drug would reduce
disease symptoms without modifying the viral infection so much as to prevent an immune
response in the host. There is a need for antiviral drugs active against viruses for which
vaccines are not available or not highly effective.
IV.2. VIRAL DISEASES
IV.2.1. HIV INFECTION AND AIDS

IV.2.1.1. DEFINITION
HIVstands for Human Immunodeficiency Virus, the virus that causes AIDS.
AIDS stands for Acquired Immunodefiency Syndrome. It is a disease of the human immune
system caused by the human immunodeficiency virus (HIV)
IV.2.1.2. CAUSE
There are two types of HIV:

o HIV-1 and
o HIV-2.
Both types are transmitted by sexual contact, through blood, and from mother to child, and they
appear to cause clinically indistinguishable AIDS. However, it seems that HIV-2 is less easily
transmitted, and the period between initial infection and illness is longer in the case of HIV-2.
Worldwide, the predominant virus is HIV-1, and generally when people refer to HIV without
specifying the type of virus they will be referring to HIV-1. The relatively uncommon HIV-2
type is concentrated in West Africa and is rarely found elsewhere.
IV.2.1.3 ORIGIN OF HIV /AIDS AND THE FIRST CASES
The first recognized cases of AIDS occurred in the USA in the early 1980s. A number
of gay men in New York and California suddenly began to develop rare opportunistic
infections and cancers that seemed stubbornly resistant to any treatment. At this time, AIDS
did not yet have a name, but it quickly became obvious that all the men were suffering from a
common syndrome.
The discovery of HIV, the Human Immunodeficiency Virus, was made soon after. While some
were initially resistant to acknowledge the connection (and indeed some remain so today), there
is now clear evidence to prove that HIV causes AIDS. So, in order to find the source of AIDS,
it is necessary to look for the origin of HIV, and find out how, when and where HIV first began
to cause disease in humans.
✔ WHERE?
In February 1999 a group of researchers from the University of Alabama announced that they
had found a type of SIVcpz that was almost identical to HIV-1. This particular strain was
identified in a frozen sample taken from a captive member of the sub-group of chimpanzees

known as Pan troglodytes troglodytes (P. t. troglodytes), which were once common in west-
central Africa.
The researchers (led by Paul Sharp of Nottingham University and Beatrice Hahn of the
University of Alabama) made the discovery during the course of a 10-year long study into the
origins of the virus. They claimed that this sample proved that chimpanzees were the source of
HIV-1, and that the virus had at some point crossed species from chimps to humans.
Their final findings were published two years later in Nature magazine . In this article, they
concluded that wild chimps had been infected simultaneously with two different simian
immunodeficiency viruses which had "viral sex" to form a third virus that could be passed on
to other chimps and, more significantly, was capable of infecting humans and causing AIDS.
These two different viruses were traced back to a SIV that infected red-capped mangabeys and
one found in greater spot-nosed monkeys. They believe that the hybridisation took place inside
chimps that had become infected with both strains of SIV after they hunted and killed the two
smaller species of monkey.
They also concluded that all three 'groups' of HIV-1 - namely Group M, N and O- came from
the SIV found in P. t. troglodytes, and that each group represented a separate crossover 'event'
from chimps to humans.
✔ HOW?
HIV is a lentivirus, and like all viruses of this type, it attacks the immune system. Lentiviruses
are in turn part of a larger group of viruses known as retroviruses. The name 'lentivirus' literally
means 'slow virus' because they take such a long time to produce any adverse effects in the
body. They have been found in a number of different animals, including cats, sheep, horses and
cattle. However, the most interesting lentivirus in terms of the investigation into the origins of
HIV is the Simian Immunodeficiency Virus (SIV) that affects monkeys, which is believed to
be at least 32,000 years old.
It is now generally accepted that HIV is a descendant of a Simian Immunodeficiency Virus

because certain strains of SIVs bear a very close resemblance to HIV-1 and HIV-2, the
two types of HIV.

HIV-2 for example corresponds to SIVsm, a strain of the Simian Immunodeficiency Virus
found in the sooty mangabey (also known as the White-collared monkey), which is indigenous
to western Africa.
The more virulent, pandemic strain of HIV, namely HIV-1, was until recently more difficult to
place. Until 1999, the closest counterpart that had been identified was SIVcpz, the SIV found
in chimpanzees. However, this virus still had certain significant differences from HIV.
It has been known for a long time that certain viruses can pass between species. Indeed, the
very fact that chimpanzees obtained SIV from two other species of primate shows just how
easily this crossover can occur. As animals ourselves, we are just as susceptible. When a viral
transfer between animals and humans takes place, it is known as zoonosis.
Below are some of the most common theories about how this 'zoonosis' took place, and how
SIV became HIV in humans:
1. The 'hunter' theory
The most commonly accepted theory is that of the 'hunter'. In this scenario, SIVcpz was
transferred to humans as a result of chimps being killed and eaten or their blood getting into
cuts or wounds on the hunter. Normally the hunter's body would have fought off SIV, but on a
few occasions it adapted itself within its new human host and became HIV-1. The fact that
there were several different early strains of HIV, each with a slightly different genetic make-
up (the most common of which was HIV-1 group M), would support this theory: every time it
passed from a chimpanzee to a man, it would have developed in a slightly different way within
his body, and thus produced a slightly different strain.
An article published in The Lancet in 2004, also shows how retroviral transfer from primates
to hunters is still occurring even today. In a sample of 1099 individuals in Cameroon, they
discovered ten (1%) were infected with SFV (Simian Foamy Virus), an illness which, like SIV,
was previously thought only to infect primates. All these infections were believed to have been
acquired through the butchering and consumption of monkey and ape meat. Discoveries such
as this have led to calls for an outright ban on bush meat hunting to prevent simian viruses
being passed to humans.
2. The oral polio vaccine (OPV) theory

Some other rather controversial theories have contended that HIV was transferred
iatrogenically (i.e. via medical interventions). One particularly well-publicised idea is that
polio vaccines played a role in the transfer.
In his book, The River, the journalist Edward Hooper suggests that HIV can be traced to the
testing of an oral polio vaccine called Chat, given to about a million people in the Belgian
Congo, Ruanda and Urundi in the late 1950s. To be reproduced, live polio vaccine needs to be
cultivated in living tissue, and Hooper's belief is that Chat was grown in kidney cells taken
from local chimps infected with SIVcmz. This, he claims, would have resulted in the
contamination of the vaccine with chimp SIV, and a large number of people subsequently
becoming infected with HIV-1.
Many people have contested Hooper's theories and insist that local chimps were not infected
with a strain of SIVcmz that is closely linked to HIV. Furthermore, the oral administration of
the vaccine would seem insufficient to cause infection in most people (SIV/HIV needs to get
directly into the bloodstream to cause infection because the lining of the mouth and throat
generally act as good barriers to the virus).
In February 2000 the Wistar Institute in Philadelphia (one of the original manufacturers of the
Chat vaccine) announced that it had discovered in its stores a phial of polio vaccine that had
been used as part of the program. The vaccine was subsequently analysed and in April 2001 it
was announced that no trace had been found of either HIV or chimpanzee SIV. A second
analysis confirmed that only macaque monkey kidney cells, which cannot be infected with SIV
or HIV, were used to make Chat. While this is just one phial of many, it means that the OPV
theory remains unproven.
The fact that the OPV theory accounts for just one (group M) of several different groups of
HIV also suggests that transferral must have happened in other ways too, as does the fact that
HIV seems to have existed in humans before the vaccine trials were ever carried out. More
about when HIV came into being can be found below.
3. The contaminated needle theory
This is an extension of the original 'hunter' theory. In the 1950s, the use of disposable plastic
syringes became commonplace around the world as a cheap, sterile way to administer

medicines. However, to African healthcare professionals working on inoculation and other
medical programmes, the huge quantities of syringes needed would have been very costly. It is
therefore likely that one single syringe would have been used to inject multiple patients without
any sterilisation in between. This would rapidly have transferred any viral particles (within a
hunter's blood for example) from one person to another, creating huge potential for the virus to
mutate and replicate in each new individual it entered, even if the SIV within the original person
infected had not yet converted to HIV.
4. The colonialism theory
The colonialism or 'Heart of Darkness' theory is one of the more recent theories to have
entered into the debate. It is again based on the basic 'hunter' premise, but more thoroughly
explains how this original infection could have led to an epidemic. It was first proposed in 2000
by Jim Moore, an American specialist in primate behavior, who published his findings in the
journal AIDS Research and Human Retroviruses.
During the late 19th and early 20th century, much of Africa was ruled by colonial forces. In
areas such as French Equatorial Africa and the Belgian Congo, colonial rule was particularly
harsh and many Africans were forced into labour camps where sanitation was poor, food was
scarce and physical demands were extreme. These factors alone would have been sufficient to
create poor health in anyone, so SIV could easily have infiltrated the labor force and taken
advantage of their weakened immune systems to become HIV. A stray and perhaps sick
chimpanzee with SIV would have made a welcome extra source of food for the workers.
5. The conspiracy theory
Some say that HIV is a 'conspiracy theory' or that it is 'man-made'. A recent survey carried out
in the US for example, identified a significant number of African Americans who believe HIV
was manufactured as part of a biological warfare programme, designed to wipe out large
numbers of black and homosexual people. Many say this was done under the auspices of the
US federal 'Special Cancer Virus Program' (SCVP). Linked into this theory is the belief that
the virus was spread (either deliberately or inadvertently) to thousands of people all over the
world through the smallpox inoculation programme, or to gay men through Hepatitis B vaccine
trials. While none of these theories can be definitively disproved, the evidence given to back

them up is usually based upon supposition and speculation, and ignores the clear link between
SIV and HIV or the fact that the virus has been identified in people as far back as 1959.
✔ WHEN
Studying the subtype of virus of some of the earliest known instances of HIV infection can
help to provide clues about the time it first appeared in humans and its subsequent evolution.
Four of the earliest known instances of HIV infection are as follows:
1. A plasma sample taken in 1959 from an adult male living in what is now the Democratic
Republic of the Congo.
2. A lymph node sample taken in 1960 from an adult female, also from the Democratic
Republic of the Congo.
3. HIV found in tissue samples from an American teenager who died in St. Louis in 1969.
4. HIV found in tissue samples from a Norwegian sailor who died around 1976.
A 1998 analysis of the plasma sample from 1959 suggested that HIV-1 was introduced into
humans around the 1940s or the early 1950s
In January 2000, the results of a new study suggested that the first case of HIV-1 infection
occurred around 1931 in West Africa. However, a study in 2008 dated the origin of HIV to
between 1884 and 1924, much earlier than previous estimates. The researchers compared the
viral sequence from 1959 (the oldest known HIV-1 specimen) to the newly discovered
sequence from 1960. They found a significant genetic difference between them, demonstrating
diversification of HIV-1 occurred long before the AIDS pandemic was recognised.
The authors suggest a long history of the virus in Africa and call Kinshasa the “epicentre of the
HIV/AIDS pandemic” in West Africa. They propose the early spread of HIV was concurrent
with the development of colonial cities, in which crowding of people increased opportunities
for HIV transmission. If accurate, these findings imply that HIV existed before many scenarios
(such as the OPV and conspiracy theories) suggest.
NOTE: WHAT ABOUT HIV-2? WHEN DID THAT GET PASSED TO HUMANS?
Until recently, the origins of the HIV-2 virus had remained relatively unexplored. HIV-2 is
thought to come from the SIV in Sooty Mangabeys rather than chimpanzees, but the crossover
to humans is believed to have happened in a similar way (i.e. through the butchering and

consumption of monkey meat). It is far rarer, significantly less infectious and progresses more
slowly to AIDS than HIV-1. As a result, it infects far fewer people, and is mainly confined to
a few countries in West Africa. By analysing samples of the two different subtypes of HIV-2
(A and B) taken from infected individuals and SIV samples taken from sooty mangabeys, Dr
Vandamme concluded that subtype A had passed into humans around 1940 and subtype B in
1945 (plus or minus 16 years or so). Her team of researchers also discovered that the virus had
originated in Guinea-Bissau and that its spread was most likely precipitated by the
independence war that took place in the country between 1963 and 1974 (Guinea-Bissau is a
former Portuguese colony).
It is likely that we will never know who the first person was to be infected with HIV, or exactly
how it spread from that initial person.
IV.2.1.4. TRANSMISSION
HIV is transmitted through direct contact of a mucous membrane or the bloodstream with a
bodily fluid containing HIV, such as blood, semen, vaginal fluid, preseminal fluid, and
breast milk.
This transmission can involve anal, vaginal or oral sex, blood transfusion, contaminated
hypodermic needles, exchange between mother and baby during pregnancy, childbirth,
breastfeeding or other exposure to one of the above mentioned bodily fluids.
o Sexual transmission
Sexual transmission occurs with the contact between sexual secretions of one person with the
rectal, genital or oral mucous membranes of another. Unprotected sexual acts are riskier for
the receptive partner than for the insertive partner. Other sexually transmitted infections (STI)
increase the risk of HIV transmission and infection, because they cause the disruption of the
normal epithelial barrier by genital ulceration and/or microulceration; and by accumulation of
pools of HIV-susceptible or HIV-infected cells (lymphocytes and macrophages) in semen and
vaginal secretions.Women are more susceptible to HIV-1 infection due to hormonal changes,
vaginal microbial ecology and physiology, and a higher prevalence of sexually transmitted
diseases. People who have been infected with one strain of HIV can still be infected later on in
their lives by other strains.

o Exposure to blood-borne pathogens
This transmission route is particularly relevant to intravenous drug users, hemophiliacs and
recipients of blood transfusions and blood products. Sharing and reusing syringes
contaminated with HIV-infected blood represents a major risk for infection with HIV.
The risk of transmitting HIV to blood transfusion recipients is currently low.
o Perinatal transmission
The transmission of the virus from the mother to the child can occur in utero during the last
weeks of pregnancy and at childbirth. In the absence of treatment, the transmission rate
between a mother and her child during pregnancy, labor and delivery is 25%. However, when
the mother takes antiretroviral therapy and gives birth by caesarean section, the rate of
transmission is just 1%. The risk of infection is influenced by the viral load of the mother at
birth, with the higher the viral load, the higher the risk. Breastfeeding also increases the risk
of transmission by about 4 %.
IV.2.1.5. PATHOPHYSIOLOGY
o The Pathophysiology of AIDS is complex. HIV causes AIDS by depleting CD4+ T

helper lymphocytes. This weakens the immune system and allows opportunistic
infections. T lymphocytes are essential to the immune response and without them; the
body cannot fight infections or kill cancerous cells. The mechanism of CD4+ T cell
depletion differs in the acute and chronic phases.
o During the acute phase, HIV-induced cell lysis and killing of infected cells by cytotoxic
T cells accounts for CD4+ T cell depletion, although apoptosis may also be a factor.
During the chronic phase, the consequences of generalized immune activation coupled
with the gradual loss of the ability of the immune system to generate new T cells appear
to account for the slow decline in CD4+ T cell numbers.
o Although the symptoms of immune deficiency characteristic of AIDS do not appear for
years after a person is infected, the bulk of CD4+ T cell loss occurs during the first
weeks of infection, especially in the intestinal mucosa, which harbors the majority of
the lymphocytes found in the body. The reason for the preferential loss of mucosal
CD4+ T cells is that a majority of mucosal CD4+ T cells express the CCR5 co receptor,
whereas a small fraction of CD4+ T cells in the bloodstream do so.

o HIV seeks out and destroys CCR5 expressing CD4+ cells during acute infection. A
vigorous immune response eventually controls the infection and initiates the clinically
latent phase. However, CD4+ T cells in mucosal tissues remain depleted throughout the
infection, although enough remain to initially ward off life-threatening infections.
o Continuous HIV replication results in a state of generalized immune activation
persisting throughout the chronic phase. Immune activation, which is reflected by the
increased activation state of immune cells and release of pro inflammatory cytokines,
results from the activity of several HIV gene products and the immune response to
ongoing HIV replication. Another cause is the breakdown of the immune surveillance
system of the mucosal barrier caused by the depletion of mucosal CD4+ T cells during
the acute phase of disease.
o This results in the systemic exposure of the immune system to microbial components
of the gut’s normal flora, which in a healthy person is kept in check by the mucosal
immune system. The activation and proliferation of T cells that results from immune
activation provides fresh targets for HIV infection. However, direct killing by HIV
alone cannot account for the observed depletion of CD4+ T cells since only 0.01–0.10%
of CD4+ T cells in the blood are infected.
o A major cause of CD4+ T cell loss appears to result from their heightened susceptibility
to apoptosis when the immune system remains activated. Although new T cells are
continuously produced by the thymus to replace the ones lost, the regenerative capacity
of the thymus is slowly destroyed by direct infection of its thymocytes by HIV.
Eventually, the minimal number of CD4+ T cells necessary to maintain a sufficient
immune response is lost, leading to AIDS.
✔ Cells affected by HIV :
The virus, entering through whichever route, acts primarily on the following cells:
● Lymphoreticular system:
o CD4+ T-Helper cells
o Macrophages
o Monocytes
o B-lymphocytes

● Certain endothelial cells
● Central nervous system:
o Microglia of the nervous system
o Astrocytes
o Oligodendrocytes
o Neurons: indirectly by the action of cytokines and the gp-120
IV.2.1.6. SYMPTOMS
HIV infection can present no clinical symptoms, cause a spectrum of conditions, or appear as
full-blown AIDS. A unique virus, HIV continually reproduces after it enters the body,
eventually overwhelming the immune system and weakening the body’s ability to fight lethal
infections and cancers.
Most people infected with HIV are not ill. It is common to develop a brief flu-like illness 2 to
6 weeks after being infected. These symptoms are similar to many other diseases and may not
be recognized as HIV infection.These symptoms include fever, headache, sore throat, swollen
lymph glands and a rash. Some are without symptoms for more than 10 years. A “carrier” can
host the virus and pass it on to other people without knowing it, because during this time the
virus continues to multiply and destroy the immune cells.
The symptoms of AIDS are primarily the result of conditions that do not normally develop in
individuals with healthy immune systems. Most of these conditions are infections caused by
bacteria, viruses, fungi and parasites that are normally controlled by the elements of the
immune system that HIV damages.
People with AIDS also have an increased risk of developing various cancers such as Kaposi's
sarcoma, cervical cancer and cancers of the immune system known as lymphomas. The
specific opportunistic infections that AIDS patients develop depend in part on the prevalence
of these infections in the geographic area in which the patient lives. The following are the
common opportunistic infections for AIDS patients:
✔ Pulmonary infections
1. Pneumocystis pneumonia: originally known as Pneumocystis carinii pneumonia, and still

abbreviated as PCP, which now stands for Pneumocystis pneumonia, it is relatively rare in

healthy, immunocompetent people, but common among HIV-infected individuals. It is caused
by Pneumocystis jirovecii.
2. Tuberculosis: Pulmonary TB is unique among infections associated with HIV because it is

transmissible to immunocompetent people via the respiratory route. It is not easily treatable
once identified due to its multidrug resistance which is a common and serious problem.
Tuberculosis with HIV co-infection (TB/HIV) is a major world health problem according to
the WHO, in 2007, 456,000 deaths among incident TB cases were HIV-positive, a third of all
TB deaths and nearly a quarter.
TB incidence is high in developing countries where HIV is most prevalent. In advanced HIV
infection, TB often presents atypically with extrapulmonary disease a common feature.
Symptoms are usually constitutional and are not localized to one particular site, often affecting
bone marrow, bone, urinary and gastrointestinal tracts, liver, regional lymph nodes, and the
central nervous system.
✔ Gastrointestinal infections
1. Esophagitis: it is an inflammation of the lining of the lower end of the esophagus. In HIV
infected individuals, this is normally due to fungal (candidiasis) or viral (herpes simplex-1 or
cytomegalovirus) infections. In rare cases, it could be due to mycobacteria.
2. Unexplained chronic diarrhea: in HIV infection, it is due to many possible causes,

including common bacterial (Salmonella, Shigella, Listeria or Campylobacter) and parasitic
infections; and uncommon opportunistic infections such as cryptosporidiosis,
microsporidiosis, Mycobacterium avium complex (MAC) and viruses (E.g.:
cytomegalovirus).
In some cases, diarrhea may be a side effect of several drugs used to treat HIV, or it may simply
accompany HIV infection, particularly during primary HIV infection. It may also be a side
effect of antibiotics used to treat bacterial causes of diarrhea (common for Clostridium
difficile). In the later stages of HIV infection, diarrhea is thought to be a reflection of changes
in the way the intestinal tract absorbs nutrients, and may be an important component of HIV-
related wasting.

✔ Neurological and psychiatric involvement
1. Toxoplasmosis: it is a disease caused by the single-celled parasite called Toxoplasma gondii.

It usually infects the brain, causing toxoplasma encephalitis, but it can also infect and cause
disease in the eyes and lungs. Cryptococcal meningitis is an infection of the meninx or
meninges by the fungus called Cryptococcus neoformans.
2. Progressive multifocal leukoencephalopathy (PML) is a demyelinating disease, in which

the gradual destruction of the myelin sheath covering the axons of nerve cells impairs the
transmission of nerve impulses. It is caused by a virus called JC virus.
3. AIDS dementia complex (ADC): it is a metabolic encephalopathy induced by HIV infection

and fueled by immune activation of HIV infected brain macrophages and microglia. These cells
are productively infected by HIV and secrete neurotoxins of both host and viral origin. Specific
neurological impairments are manifested by cognitive, behavioral, and motor abnormalities
that occur after years of HIV infection and are associated with low CD4+ T cell levels and high
plasma viral loads.
✔ Tumors and malignancies
1. Kaposi's sarcoma: As HIV is thought to be cytotoxic and even oncogenic, patients with
HIV infection have substantially increased incidence of several cancers, which is primarily due
to co-infection with an oncogenic DNA virus, especially Epstein-Barr virus (EBV), Kaposi's
sarcoma-associated herpesvirus (KSHV) (also known as human herpesvirus-8 [HHV-8]), and
human papillomavirus (HPV).
Caused by a gammaherpes virus called Kaposi's sarcoma-associated herpes virus (KSHV), it

often appears as purplish nodules on the skin, but can affect other organs, especially the mouth,
gastrointestinal tract, and lungs.
2. High-grade B cell lymphomas such as Burkitt's lymphoma, Burkitt's-like lymphoma,

diffuse large B-cell lymphoma (DLBCL), and primary central nervous system lymphoma
present more often in HIV-infected patients. These particular cancers often foreshadow a poor
prognosis. Epstein-Barr virus (EBV) or KSHV cause many of these lymphomas. In HIV-
infected patients, lymphoma often arises in extra nodal sites such as the gastrointestinal tract.

When they occur in an HIV-infected patient, KS and aggressive B cell lymphomas confer a
diagnosis of AIDS.
3. Invasive cervical cancer in HIV-infected women is also considered AIDS-defining. It is

caused by human papillomavirus (HPV).
4. Other tumours: in addition to the AIDS-defining tumors listed above, HIV-infected patients
are at increased risk of certain other tumors, notably Hodgkin's disease, anal and rectal
carcinomas, hepatocellular carcinomas, head and neck cancers, and lung cancer. Some of
these are causes by viruses, such as Hodgkin's disease (EBV), anal/rectal cancers (HPV), head
and neck cancers (HPV), and hepatocellular carcinoma (hepatitis B or C). Other contributing
factors include exposure to carcinogens (cigarette smoke for lung cancer), or living for years
with subtle immune defects..
✔ Other infections
AIDS patients often develop opportunistic infections that present with non-specific symptoms,
especially low-grade fevers and weight loss. These include opportunistic infection with
Mycobacterium avium-intracellulare and cytomegalovirus (CMV). CMV can cause colitis, and
CMV retinitis can cause blindness. An infection that often goes unrecognized in AIDS patients
is Parvovirus B19. Its main consequence is anemia, which is difficult to distinguish from the
effects of antiretroviral drugs used to treat AIDS itself.
IV.2.1.7. DIAGNOSIS
The diagnosis of AIDS in a person infected with HIV is based on the presence of certain signs
or symptoms. Since June 5, 1981, many definitions have been developed for epidemiological
surveillance such as the Bangui definition and the 1994 expanded World Health Organization
AIDS case definition. However, clinical staging of patients was not an intended use for these
systems as they are neither sensitive, nor specific. Both World Health Organization staging
system for HIV infection and disease, using clinical and laboratory data, and the Center for
Disease Control (CDC) Classification System are used.

✔ CDC Classification System for HIV Infection
The CDC categorization of HIV/AIDS is based on the lowest documented CD4 cell count
(Table 1) and on previously diagnosed HIV-related conditions (Tables 2 and 3). For example,
if a patient had a condition that once met the criteria for Category B but now is asymptomatic,
the patient would remain in Category B. Additionally, categorization is based on specific
conditions, as indicated below. Patients in categories A3, B3, and C1-C3 are considered to have
AIDS.
CDC Classification System for HIV-Infected Adults and Adolescents

Key to abbreviations: CDC = Centers for Disease Control and Prevention; PGL = persistent
generalized lymphadenopathy.
CD4 Cell Categories Clinical Categories
A B C
Asymptomatic, Acute Symptomatic AIDS-
HIV, or PGL Conditions, not A Indicator
or C Conditions
(1)≥500 cells/µL A1 B1 C1
(2)200-499 cells/µL A2 B2 C2
(3)<200 cells/µL A3 B3 C3

❖ CDC Classification System: Category B : Symptomatic Conditions
Category B symptomatic conditions are defined as symptomatic conditions occurring in an

HIV-infected adolescent or adult that meets at least 1 of the following criteria:
a) They are attributed to HIV infection or indicate a defect in cell-mediated immunity.
b) They are considered to have a clinical course or management that is complicated by HIV
infection.
Examples include, but are not limited to, the following:
● Bacillary angiomatosis
● Oropharyngeal candidiasis (thrush)
● Vulvovaginal candidiasis, persistent or resistant
● Pelvic inflammatory disease (PID)
● Cervical dysplasia (moderate or severe)/cervical carcinoma in situ
● Hairy leukoplakia, oral
● Idiopathic thrombocytopenic purpura
● Constitutional symptoms, such as fever (>38.5°C) or diarrhea lasting >1 month
● Peripheral neuropathy
● Herpes zoster (shingles), involving ≥2 episodes or ≥1 dermatome
❖ CDC Classification System: Category C : AIDS-Indicator Conditions
● Bacterial pneumonia, recurrent (≥2 episodes in 12 months)

● Candidiasis of the bronchi, trachea, or lungs
● Candidiasis, esophageal
● Cervical carcinoma, invasive, confirmed by biopsy
● Coccidioidomycosis, disseminated or extrapulmonary
● Cryptococcosis, extrapulmonary
● Cryptosporidiosis, chronic intestinal (>1-month duration)
● Cytomegalovirus disease (other than liver, spleen, or nodes)
● Encephalopathy, HIV-related
● Herpes simplex: chronic ulcers (>1-month duration), or bronchitis, pneumonitis, or
esophagitis

● Histoplasmosis, disseminated or extrapulmonary
● Isosporiasis, chronic intestinal (>1-month duration)
● Kaposi sarcoma
● Lymphoma, Burkitt, immunoblastic, or primary central nervous system
● Mycobacterium avium complex (MAC) or M kansasii , disseminated or
extrapulmonary
● Mycobacterium tuberculosis , pulmonary or extrapulmonary
● Mycobacterium , other species or unidentified species, disseminated or
extrapulmonary
● Pneumocystis jiroveci (formerly carinii ) pneumonia (PCP)
● Progressive multifocal leukoencephalopathy (PML)
● Salmonella septicemia, recurrent (nontyphoid)
● Toxoplasmosis of brain
● Wasting syndrome due to HIV (involuntary weight loss >10% of baseline body weight)
associated with either chronic diarrhea (≥2 loose stools per day ≥1 month) or chronic
weakness and documented fever ≥1 month
✔ WHO Clinical Staging of HIV/AIDS and Case Definition
The clinical staging and case definition of HIV for resource-constrained settings were
developed by the WHO in 1990 and revised in 2007. Staging is based on clinical findings that
guide the diagnosis, evaluation, and management of HIV/AIDS, and does not require a CD4
cell count. This staging system is used in many countries to determine eligibility for
antiretroviral therapy, particularly in settings in which CD4 testing is not available. Clinical
stages are categorized as 1 through 4, progressing from primary HIV infection to advanced
HIV/AIDS (Table 4). These stages are defined by specific clinical conditions or symptoms. For
the purpose of the WHO staging system, adolescents and adults are defined as individuals aged
≥15 years.
WHO Clinical Staging of HIV/AIDS for Adults and Adolescents
Primary HIV Infection
● Asymptomatic
● Acute retroviral syndrome

Clinical Stage 1
● Asymptomatic
● Persistent generalized lymphadenopathy
Clinical Stage 2
● Moderate unexplained weight loss (<10% of presumed or measured body weight)

● Recurrent respiratory infections (sinusitis, tonsillitis, otitis media, and pharyngitis)
● Herpes zoster
● Angular cheilitis
● Recurrent oral ulceration
● Papular pruritic eruptions
● Seborrheic dermatitis
● Fungal nail infections
Clinical Stage 3
● Unexplained severe weight loss (>10% of presumed or measured body weight)

● Unexplained chronic diarrhea for >1 month
● Unexplained persistent fever for >1 month (>37.6°C, intermittent or constant)
● Persistent oral candidiasis (thrush)
● Oral hairy leukoplakia
● Pulmonary tuberculosis (current)
● Severe presumed bacterial infections (eg, pneumonia, empyema, pyomyositis, bone or
joint infection, meningitis, bacteremia)
● Acute necrotizing ulcerative stomatitis, gingivitis, or periodontitis
● Unexplained anemia (hemoglobin <8 g/dL)
● Neutropenia (neutrophils <500 cells/µL)
● Chronic thrombocytopenia (platelets <50,000 cells/µL)
Clinical Stage 4
● HIV wasting syndrome, as defined by the CDC (see Table 3, above)

● Pneumocystis pneumonia
● Recurrent severe bacterial pneumonia

● Chronic herpes simplex infection (orolabial, genital, or anorectal site for >1 month or
visceral herpes at any site)
● Esophageal candidiasis (or candidiasis of trachea, bronchi, or lungs)
● Extrapulmonary tuberculosis
● Kaposi sarcoma
● Cytomegalovirus infection (retinitis or infection of other organs)
● Central nervous system toxoplasmosis
● HIV encephalopathy
● Cryptococcosis, extrapulmonary (including meningitis)
● Disseminated nontuberculosis Mycobacteria infection
● Progressive multifocal leukoencephalopathy
● Candida of the trachea, bronchi, or lungs
● Chronic cryptosporidiosis (with diarrhea)
● Chronic isosporiasis
● Disseminated mycosis (eg, histoplasmosis, coccidioidomycosis, penicilliosis)
● Recurrent non typhoidal Salmonella bacteremia
● Lymphoma (cerebral or B-cell non-Hodgkin)
● Invasive cervical carcinoma
● Atypical disseminated leishmaniasis
● Symptomatic HIV-associated nephropathy
● Symptomatic HIV-associated cardiomyopathy
● Reactivation of American trypanosomiasis (meningoencephalitis or myocarditis)
IV.2.1.8. HIV TEST
Many people are unaware that they are infected with HIV.
HIV tests are usually performed on venous blood. Many laboratories use fourth generation
screening tests which detect anti-HIV antibody (IgG and IgM) and the HIV p24 antigen. The
detection of HIV antibody or antigen in a patient previously known to be negative is evidence
of HIV infection. Individuals whose first specimen indicates evidence of HIV infection will
have a repeat test on a second blood sample to confirm the results.HIV antibody tests are the
most appropriate test for routine diagnosis of HIV among adults. Antibody tests are
inexpensive and very accurate.

The window period (the time between initial infection and the development of detectable
antibodies against the infection) can vary since it can take 3-6 months to seroconvert and to
test positive. Detection of the virus using polymerase chain reaction (PCR) during the window
period is possible, and evidence suggests that an infection may often be detected earlier than
when using a fourth generation EIA screening test.
Positive results obtained by PCR are confirmed by antibody tests. Routinely used HIV tests
for infection in neonates and infants (i.e., patients younger than 2 years), born to HIV-positive
mothers, have no value because of the presence of maternal antibody to HIV in the child's
blood. HIV infection can only be diagnosed by PCR, testing for HIV pro-viral DNA in the
children's lymphocytes.
There are several tests that are used in HIV testing.
IV.2.1.9. PREVENTION
a. Preventive measures regarding sexual contact
✔ The abstinence, faithfulness among couples, one sexual partner

✔ Correct use of condom (male and female condoms)
✔ Randomized controlled trials have shown that male circumcision lowers the risk of HIV
infection among heterosexual men by up to 60%.
b. Preventive measures regarding exposure to infected bodily fluids
✔ Health care workers can reduce exposure to HIV by employing precautions to reduce
the risk of exposure to contaminated blood. These precautions include barriers such as
gloves, masks, protective eyewear or shields, and gowns or aprons which prevent
exposure of the skin or mucous membranes to blood borne pathogens.
✔ Frequent and thorough washing of the skin immediately after being contaminated with
blood or other bodily fluids can reduce the chance of infection.
✔ Sharp objects like needles, scalpels and glass, are carefully disposed of to prevent
needles tick injuries with contaminated items.
✔ Single use of some matrials such as needles and syringes,gloves, etc
✔ Avoid sharing sharp objects

c. Mother-to-child transmission (MTCT)
✔ When replacement feeding is acceptable, feasible, affordable, sustainable and safe,

HIV-infected mothers should avoid breast-feeding their infant.
✔ If not feasible, exclusive breast-feeding is recommended during the first months of life
(about 6 months) and discontinued as soon as possible.
d. Education, health literacy and cognitive ability
✔ The most important way to change risky behavior is health education.

✔ Education itself does not work, only if it leads to higher health literacy and general
cognitive ability. This ability is relevant to understand the relationship between own
risky behavior and possible outcomes like HIV-transmission.
IV.2.1.10. IMPACT OF HIV ON THE COUNTRY (RWANDA)
HIV and AIDS are having a widespread impact on many parts of African society such as:
a. The effect on life expectancy: In many countries of sub-Saharan Africa including

Rwanda, AIDS has erased decades of progress made in extending life expectancy.
b. The effect on households: The effect of the AIDS epidemics on households can be
very severe, especially when families lose their income earners. In other cases, people
have to provide home based care for sick relatives, reducing their capacity to earn
money for their family. Many of those dying from AIDS have surviving partners who
are themselves infected and in need of care. They leave behind orphans, who are often
cared for by members of the extended family.
c. The effect on healthcare: In all affected countries, the epidemic is putting strain on
the health sector. As the epidemic develops, the demand for care for those living with
HIV rises, as does the number of health care workers affected.
d. The effect on schools: Schools are heavily affected by AIDS. This a major concern,
because schools can play a vital role in reducing the impact of the epidemic,
through HIV education and support.
e. The effect on productivity: The HIV and AIDS epidemic has dramatically affected
labour, which in turn slows down economic activity and social progress.

f. The effect on economic growth and development: The HIV and AIDS epidemic has
already significantly affected Africa's/contry economic development, and in turn, has
affected Africa/country's ability to cope with the epidemic.
IV.2.1.11. HIV/AIDS ASSOCIATED STIGMA AND DISCRIMINATION
a. Definition
AIDS-related stigma and discrimination refers to prejudice, negative attitudes, abuse and
maltreatment directed at people living with HIV and AIDS. They can result in being shunned
by family, peers and the wider community; poor treatment in healthcare and education settings;
an erosion of rights; psychological damage; and can negatively affect the success of HIV testing
and treatment.
b. Why is there stigma related to HIV/AIDS?
Fear of contagion coupled with negative, value-based assumptions about people who are
infected leads to high levels of stigma surrounding HIV and AIDS
c. Factors that contribute to HIV/AIDS-related stigma include:
● HIV/AIDS is a life-threatening disease, and therefore people react to it in strong ways.

● HIV infection is associated with behaviors (such as homosexuality, drug addiction,
prostitution or promiscuity) that are already stigmatized in many societies.
● Most people become infected with HIV through sex which often carries moral baggage.
● There is a lot of inaccurate information about how HIV is transmitted, creating irrational
behavior and misperceptions of personal rise.
● HIV infection is often thought to be the result of personal irresponsibility.
● Religious or moral beliefs lead some people to believe that being infected with HIV is
the result of moral fault (such as promiscuity or 'deviant sex') that deserves to be
punished.
d. Consequences of HIV related stigma
Research by the International Centre for Research on Women (ICRW) found the possible
consequences of HIV-related stigma to be:
● Loss of income/livelihood
● Loss of marriage & childbearing options
● Poor care within the health sector
● Withdrawal of caregiving in the home
● Loss of hope & feelings of worthlessness
● Loss of reputation
IV.2.1.12. HIV/AIDS TREATMENT AND APPROACH IN RWANDA
A. DEFINITIONS
✔ What is HIV antiretroviral drug treatment?
This is the main type of treatment for HIV or AIDS. It is not a cure, but it can stop people from
becoming ill for many years. The treatment consists of drugs that have to be taken every day
for the rest of a person’s life.
The aim of antiretroviral treatment is to keep the amount of HIV in the body at a low level.
This stops any weakening of the immune system and allows it to recover from any damage that
HIV might have caused already.
The drugs are often referred to as:
o Antiretrovirals
o ARVs
o Anti-HIV drugs or
o anti-AIDS drugs
✔ What is combination therapy?
Taking two or more antiretroviral drugs at a time is called combination therapy. Taking a
combination of three or more anti-HIV drugs is sometimes referred to as Highly Active
Antiretroviral Therapy (HAART).
Taking 2 or more HIV drugs combined into one pill refers to fixed dose combination.
✔ Why do people need to take more than one drug at a time?

If only one drug was taken, HIV would quickly become resistant to it and the drug would stop
working. Taking two or more antiretrovirals at the same time vastly reduces the rate at which
resistance would develop, making treatment more effective in the long term.
✔ How many HIV and AIDS drugs are there?
There are more than 20 approved antiretroviral drugs but not all are licensed or available in
every country.
✔ First and second line therapy
At the beginning of treatment, the combination of drugs that a person is given is called first
line therapy. If after a while HIV becomes resistant to this combination, or if side effects are
particularly bad, then a change to second line therapy is usually recommended.
✔ Adherence
The term adherence means taking the drugs exactly as described. This includes taking all of
the medication at the right time and exactly as the directions state. It also means ensuring that
there will be no interactions with other drugs being taken.
✔ Viral load
Viral load refers to the amount of HIV in the blood. If the viral load is high, T-helper cells tend
to be destroyed more quickly. Therefore, the aim of antiretroviral treatment is to keep the viral
load as low as possible.
✔ Structured Treatment Interruptions (STIs)
A Structured Treatment Interruption (STI) or 'drug holiday' is when someone stops taking
antiretroviral treatment temporarily.
✔ Immune Reconstitution Inflammatory Syndrome (IRIS)
IRIS is a syndrome that occurs for a small number of patients soon after ARV treatment is
started. It is caused by an excessive response by the recovering immune system to opportunistic
infections that were already present, but were previously dormant and not producing
symptoms. Although the symptoms of IRIS are often mild, occasionally they can be life

threatening. Generally those who have a severely damaged immune system before starting
antiretroviral treatment are more at risk of developing IRIS. IRIS does not indicate that
treatment is failing. Usually the best response to IRIS is to continue treatment; the symptoms
normally disappear within a few weeks
✔ Switching treatment
A change of treatment is needed when the antiretrovirals fail to slow down the replication of
the virus in the body. This can occur as a result of drug resistance, poor adherence, poor drug
absorption or a weak combination of drugs. Substitution refers to replacement of some ARVS
but not all the entire regimen.
✔ Salvage treatment
Salvage therapy is the term often used to describe the treatment for those who are resistant to
drugs in the three original drug classes. In this situation it may be difficult to find a drug
regimen that suppresses the viral load to undetectable.
B.HOLISTIC MANAGEMENT OF PERSONS LIVING WITH HIV/AIDS
1. Definition
Holistic Management (HM) is the medical, psychological and social care that takes into
consideration all of the problems of the patient so as to be able to lead him/her towards a normal
family, social and professional life (TRAC, 2009).
2. Its aims
✔ Ensuring an adequate level of care to the concerned patient
✔ Reducing the mortality and morbidity related to HIV/AIDS
✔ Increasing the quality of life of the concerned patients
✔ Promoting prevention through increasing access to screening
3. Principles of holistic management (HM)
HM is a product of team work among many different professionals who must work together in
a complementary and synergistic manner so as to meet the different needs of every patient.

The work of the different providers must be carried out with the highest degree of
confidentiality. HM must ensure a continuum of care within the health facility as well as
beyond the boundaries of that structure.
4. Why psychosocial care in the holistic management of persons living with HIV/AIDS?
Three reasons justify the provision of psychosocial care:
1. HIV/AIDS affects different aspects of person‘s life.

2. Handling problems related to stigma and discrimination related to HIV/AIDS.
3. Ensuring adequate adherence to antiretroviral treatment and other drugs.
Therefore its objectives are:
✔ Provide support to the affected person regarding stress and psychosocial disturbances.
✔ Assist the affected person to adopt safe behavior for prevention and control of infection.
✔ Give correct information on HIV infection.
✔ Sensitize the community of the affected person to avoid stigmatization.
✔ Contribute to the prevention of HIV infection by making the patient responsible for its
control.
✔ Educate the patient’s neighbors and family to support the adherence to ARVs
Activities of psychosocial care include:
✔ Psychosocial consultation
✔ Education and treatment initiation sessions
✔ Individual follow-up
✔ Group counseling or support groups
✔ The pharmacy and distribution of drug
✔ Data entry and filling
✔ Follow up at home and
✔ Providing care to multidisciplinary team.
C. PROTOCOL OF PROPHYLAXIS FOR OPPORTUNISTIC INFECTIONS IN

RWANDA
1. Introduction

Regarding cotrimoxazole (CTZ) prophylaxis, the Rwanda national protocol recommends
universal access. That is systematically put all HIV- infected patients (adults or infants) on
cotrimoxazole without taking into account the CD4 Count (TRAC, 2009). Thus CTZ
prophylaxis is maintained among patients on ARVs regardless of the trend in CD4 count level.
2. General preventative measures
Every patient who has been diagnosed with an OI must have health education on the following
facts:
o Information on the mode of transmission for HIV/AIDS

o Hygiene especially to avoid the diseases transmitted by oral-fecal route
o The environment: the work environment can constitute a risk especially the risk
for TB
o Nutrition: boiled water and a balanced diet are recommended for all
immunosuppressed patients. the consumption of alcohol and cigarette is
discouraged
o Antiretroviral drugs and good adherence
3. Specific preventive measures
CTZ (cotrimoxazole or bactrim): protects against infections by toxoplasmosis, pneumocystis

pneumonia, isospora belli and nocardia infections. The dosage is 960mg once a day orally. In
case of allergy Dapsone 100 mg once a day PO is given.
IHN (izoniazide): currently systematic IHN is not recommended in Rwanda and should only
be used in the reference hospital for selected cases where active TB has been excluded.
Azithromycin: 1200mg PO once a week for protection against mycobacterium avium complex
(MAC). It should be stopped if the CD4 count is above 200 for more than 6 months and there
are no signs suggestive of MAC. It should particularly be considered for patients that have
IRIS.
Ganciclovir: 1000mg TID PO. For patient with cytomegalovirus (CMV) retinitis
Albendazole: 400MG once a year PO for intestinal helminths

Fluconazole: 200 mg once a day PO in case of prevention against fungal infection such as
Cryptococcus neoformans, oral and esophageal candidiasis.
4. Vaccination
Vaccination should be postponed until CD4 increases; otherwise there may be insufficient
immunological response. The live attenuated vaccines are contraindicated in symptomatic HIV
patients and all persons whose CD4 count is below 200. Pneumococcal , hepatitis B ,tetanus
and diphtheria vaccines are recommended.
D. THE PRINCIPLES OF ANTIRETROVIRAL TREATMENT
1. Introduction
ARV treatment is an essential element of the care for persons or people living with HIV/AIDS
(PLWHA) and it changes the natural evolution of HIV infection. It results in reduced morbidity
and mortality.
2. Key factors in treatment
There 3 factors that will influence the treatment success:
● The virus which may be more or less aggressive

● The patient who will determine the success of the treatment
● The ARV which should be ideally efficacious over a long time with minimum side
effects.
3. Mechanism of action of ARVs: the multiplication cycle of HIV
HIV is a RNA virus that must penetrate a CD4 cell in order to replicate inside the cell it
undergoes a series of transformation to give rise to new viruses. Therefore the ARVs act by
blocking one of the stages during the replication cycle of HIV within the CD4 cell.
The key stages of the replication cycle are:
i. Entry and fusion: entry through the membrane of the CD4 cell by fusion with the aid of co-
receptors for eg.CCR5 or CXCR4.
ii. Transcription: transformation of viral RNA into DNA carried out by enzyme reverse
transcriptase

iii. Integration of DNA formed above into foci of DNA within the CD4 nucleus under the
action of an enzyme named integrase enzyme
iv. Replication: manufacture of viral RNA from DNA. Formation of new viruses from that
RNA and synthesized proteins in the CD4 cell under the influence of the protease enzyme.
v. Release of reconstituted particles.
The main ARVs currently in use in Rwanda block the action of the two enzymes: reverse
transcriptase and protease. Drugs able to block entry of the virus into CD4 cells (coreceptor
antagonists) and integrase inhibitors are newly available in other countries.
4. The aims of the ARV treatment are:
✔ Suppress the viral load to undetectable

✔ Increase the number of CD4 cells so as to improve the immune reconstitution
✔ Reduce the transmission of HIV
✔ Minimize the risk of cross resistance
✔ Minimize long term toxicity
✔ Improve the clinical status of the patient
✔ Improve the quality of life of the patient
✔ Minimize the cost of care
Hence to meet those aims, the quality of a good treatment regimen that can result in good
adherence, is one that combines drugs that are:
✔ Potent (powerful): capable of adequately blocking replication of HIV.

✔ With prolonged action: the association must block the replication of HIV as long as
possible.
5. Supporting a patient on ART
✔ Adequately prepare the patient before initiation of treatment.

✔ Prescribe to the patient the drugs that are most suited to him/her mode of life.
✔ Adequately inform the patient on how he needs to take his/her drugs and any possible
side effects.
✔ Ensure the patient has people around to support throughout the treatment

E. ANTIRETROVIRAL TREATMENT
I. HIV in Rwanda
• Prevalence 3% (3.6% women and 2.3% men) to be reduced to less than 1% from 2008-
2012 (EDPRS)
• More than 200,000 PLWHA(RBC,2009)
• Patient on ARV 31,379 ad. &2,757 children (Dec.,2006), 56,153 people on ARV in
2008 and 72,539 in 2009(from cnls report). Currently 76,726 people on ARVs (CNLS
report,2011)
II. Evolution
Reflecting on 100 patients on ARV treatment:

o 60% remain on treatment
o 15% die
o 25% lost (TRAC ,2008)
III. HIV life cycle
a. Binding and fusion: HIV begins its life cycle when it binds to a CD4 receptor and one of
two co-receptors on the surface of a CD4+ T- lymphocyte. The virus then fuses with the host
cell. After fusion, the virus releases RNA, its genetic material, into the host cell.
b. Reverse transcription: An HIV enzyme called reverse transcriptase converts the single-
stranded HIV RNA to double-stranded HIV DNA.
c. Integration: The newly formed HIV DNA enters the host cell's nucleus, where an HIV
enzyme called integrase "hides" the HIV DNA within the host cell's own DNA. The integrated
HIV DNA is called provirus. The provirus may remain inactive for several years, producing
few or no new copies of HIV.
d. Assembly: An HIV enzyme called protease cuts the long chains of HIV proteins into smaller
individual proteins. As the smaller HIV proteins come together with copies of HIV's RNA
genetic material, a new virus particle is assembled.

e. Budding: The newly assembled virus pushes out ("buds") from the host cell. During
budding, the new virus steals part of the cell's outer envelope. This envelope, which acts as a
covering, is studded with protein/sugar combinations called HIV glycoproteins. These HIV
glycoproteins are necessary for the virus to bind to CD4 and co- receptors. The new copies of
HIV can now move on to infect other cells.
IV. Principles for selection of a regimen
a. It is necessary to: either block replication at several levels (combination of NRTI and PI),
or block at the same level but through different but complementary mechanisms (NRTI with
NNRTI).
b. Main associations are:
• 2NRTIs+1NNRTI (1st line regimen)

• 2NRTIs+1PI(2nd line regimen)
The association of 3 NRTIs is possible in extreme necessity or after expert opinion.
c. Initiate HIV treatment in adult
✔ Initial assessment:
• Full clinical examination

• Exclusion of active tuberculosis
• CD4,FBC,ALAT &CREATININE
✔ Eligibility criteria:
Criteria for clinical & immunological eligibility are:
HIV+ and one or two of the following criteria:
✔ Any patient with WHO clinical stage 4,regargless of CD4 count

✔ Any patient with WHO clinical stage 1,2 or 3 whose CD4 count <350/mm3
The table below shows class of ARVs and their mechanism of action

CLASS APPROVAL EXAMPLES MECHANISM OF
ACTION
NUCLEOSIDE 1987 Zidovudine (azt), Interfere with reverse

REVERSE lamivudine transcriptase
TRANSCRIPTASE
INHIBITORS
(NRTI)
NON NUCLEOSIDE 1997 Nevirapine (nvp) Interfere with reverse

REVERSE transcriptase
Efavirenz (efv)
TRANSCRIPTASE
INHIBITORS Delavirdine (dlv)
(NnRTI)
PROTEASE 1995 Lopinavir/ritonavir Interfere with protease by

INHIBITORS (PI) (kaletra) stopping from replication
within cell
Nelfinavir (nfv)
Indinavir, ritonavir
FUSION/ENTRY 2003 Enfivirtine T20 Prevent from binding/entry

INHIBITORS (fuseon)
INTEGRASE 2007 - Interfere with integrase

INHIBITORS
✔ Recommended first line treatment
1. TDF (TENOFOVIR) +3TC/FTC (LAMIVUDINE) OR EMITRICITABINE+ NVP

(NEVIRAPINE)
2. TDF (TENOFOVIR) +3TC/FTC (LAMIVUDINE) OR EMITRICITABINE+ EFV

(EFAVIRENZ)
3. ABC (ABACAVIR) +3TC (LAMIVUDINE) + EFV(EFAVIRENZ)

4. ABC (ABACAVIR)+3TC (LAMIVUDINE) + NVP(NEVIRAPINE)
NB:
1. Give EFV in case of allergy to NVP or patient on TB drugs, or patient with less than
9gr/dl of hemoglobin. In HIV-tuberculosis co-infection, the first line treatment
can be for e.g.: TDF (TENOFOVIR) + 3TC/FTC(LAMIVUDINE) or
EMITRICITABINE+ EFAVIRENZ NVP(NEVIRAPINE) plus ANTI-TB
2. Give ABC in case where TDF is CI (renal failure)
3. Give ABC instead of TDF when initiating ART in pregnant women
V. HIV-tuberculosis coinfection
✔ Consequences of HIV on TB control
• Increases the number of Tuberculosis linked to HIV

• Late diagnosis: due to fear of the stigma attached to both TB-HIV
• Difficult in treating a 1 patient with two diseases at the same time in two separate clinics
• Difficult in diagnosis due to different clinical presentation of TB linked to HIV which
increases EXTRAPULMONARY TB
• High rate of relapse
• Risk of nosocomial infection/transmission
• Heavy workload in the TB and HIV clinics
NB: The treatment of TB is a priority and must be supervised (DOTS)
✔ Treatment of TB in HIV/AIDS patients
SITUATION RECOMMENDATION
Pulmonary TB&CD4<500/mm3 or Extra Start anti-TB

Pulmonary tuberculosis 2-8 weeks after the start of anti-TB, start one
of the following regimen:
✔ TDF+3TC/FTC+EFV or
✔ ABC+3TC+EFV

For pregnant women in 1st trimester:
AZT/D4T+3TC+ABC
2nd trimester: ABC/AZT+3TC+EFV
Pulmonary TB &CD4 >500/mm3 Anti-TB treatment
Do CD4 Test after 2 months of anti TB

treatment.
If >500/mm3, continue anti-TB only
If <500/mm3, start ARV treatment
VI. Clinical and biological follow up of patient on treatment
DATE CLINICAL FOLLOW UP LABORATORY
Pre ARV The client is starting the CD4,FBC,CREAT,GPT,X-RAY if

treatment clinical indication
D15 +adherence None
M1 +adherence None
M2 +adherence None
M3 +adherence FBC IF AZT, CREAT IF TDF,GPT if

indicated
M4 +adherence None
M5 +adherence None
M6 +adherence CD4,FBC,CREAT,if on TDF,GPT if

indicated
Monthly for 1 year ❖ CD4 every 6 months

❖ VL every 12 months

+adherence ❖ FBC
❖ Creatinine if on TDF
❖ GPT if clinically indicated
VII. Treatment failure
● Clinical failure: occurrence of new opportunistic infection or malignancy reveals

progession of disease to next stage (new WHO stage 4 condition) or reocurence of previous
opportunistic infection.
● Immunological failure: return of CD4 to pretreatment baseline or below (in absence
of any concomitant infection that is liable to cause transient reduction of CD4),a fall to >50%
● Virological failure: detectable VL (40 copies/ml) after 12 months on treatment
VIII. Immune reconstitution inflammatory syndrome (IRIS)
Inflammatory response in first 1-2 months following initiation of ARV among patient with
latent TB (non active TB) which becomes active.
It is due to decreased CD4 and exaggerated host response to ARVS
Its features are fever, adenopathy, pulmonaly and neurologic disorders

Common in infection with Mycobacterium tuberculosis
When it appears, don’t stop ARVs BUT adjust.
IX. Post exposure prophylaxis (PEP)
Accidental exposure to bloody /body fluids or rape (sex violence)

It has shown that initiating the prophylaxis early diminishes the risk of HIV infection by about
80%.
1. Criteria for prophylactic ARV treatment
✔ The severity of the exposure (r/t to depth of the wound and the type of wound).
✔ Venapuncture needle type.
✔ Less with skin contact than with blood being higher than other body secretions.
2. Treatment
Always clean the area immediately with clean water, rince with antiseptic: Dakin, povidone,
70% alcohol at least 5 minutes.
ARVs depends on HIV serostatus of the source and degree of exposure
3. Evaluation of degree of exposure
• Massive exposure: deep penetration with intravenous devices(IV)

• Moderate exposure: cut with a lancet through gloves, superficial with IV or
IAN(intraartery needle)
• Minimum exposure: superficial bruise with a plain needle(suture) or a small caliber
needle(SC/IM),contact with mucosa or skin
4. Maximum delay in implementing prophylaxis
• Given within 6 hours following the exposure without following the lab results of the
source
• A limit of 48 hours is reasonable in seeking maximum efficacy.
5. Treatment duration

4 weeks (28 days) without interruption
6. Choice of drugs
• TDF+3TC/FTC+KALETRA
• TDF+3TC/FTC+EFV
If no TDF or a Contraindication: AZT+3TC+KALETRA
7. Followup
Person should be informed of
• Side effects
• Adherence
• Need for prevention
IV.2.2. ACUTE CORYZA (COMMON COLD OR COLD)
Also known as nasopharyngitis, acute viral rhinopharyngitis, acute coryza, or a cold), the
common cold is is a viral infectious disease of the upper respiratory system, caused primarily
by rhinoviruses and coronaviruses.
The common cold generally involves a runny nose, nasal congestion and sneezing.There may
be also a sore throat, cough, headache, or other symptoms.
IV.2.2.2. ETIOLOGY
The most commonly implicated virus is a rhinovirus, a type of picornavirus with 99

known serotypes. Others include: coronavirus, influenza, human parainfluenza
viruses, human respiratory syncytial virus, adenoviruses, enteroviruses,
and metapneumovirus.

A cold virus spreads through tiny air droplets that are released when the sick person sneezes,
coughs, or blows his nose (both saliva and nasal secretions can be contagious). A cold can be
caught if:
● A person with a cold sneezes, coughs, or blows his nose near a healthy person
● A person touches his nose, eyes, or mouth after he has touched something contaminated
by the virus.
N.B.: People are most contagious for the first 2 to 3 days of a cold.
IV.2.2.4. PATHOGENESIS
The major entry point for the virus is normally the nose, but can also be the eyes (in this case
drainage into the nasopharynx would occur through the nasolacrimal duct). From there, it is
transported to the back of the nose and the adenoid area. The virus then attaches to a
receptor, ICAM-1, which is located on the surface of cells of the lining of the nasopharynx.
The receptor fits into a docking port on the surface of the virus. Large amounts of virus receptor
are present on cells of the adenoid. After attachment to the receptor, virus is taken into the cell,
where it starts an infection, and increases ICAM-1 production, which in turn helps the immune
response against the virus. Rhinovirus colds do not generally cause damage to the
nasal epithelium.
Macrophages trigger the production of cytokines which, together with bradykinin, play a major
role in causing the local symptoms such as sore throat and nasal irritation.
The common cold is self-limiting, and the host's immune system effectively deals with the
infection, specific antibodies, and leukocytes destroy the virus through phagocytosis and
destroy infected cells to prevent further viral replication. In healthy, immunocompetent
individuals, the common cold resolves in seven days on average.
IV.2.2.5. SIGNS AND SYMPTOMS
Cold symptoms usually occur within 2 to 3 days after a person came in cpontact with the virus,
although it could take up to a week.
The most common symptoms are:
✔ cough
✔ sore throat (scratchy throat)

✔ runny nose
✔ nasal congestion
✔ sometimes conjunctivitis
✔ muscle aches
✔ fatigue
✔ headaches
✔ shivering
✔ loss of appetite
✔ sneezing
✔ Fever is often present thus creating a symptom picture which overlaps with influenza.
The symptoms of influenza however are usually more severe.
IV.2.2.6. PROGNOSIS
The common cold is generally mild and self-limiting. Pneumonia is a possible severe
complication
IV.2.2.7. COMPLICATIONS
There are numerous complications such as
o Sinusitis
o Laryngitis
o Tonsillitis
o Bronchitis
o Pneumonia
o Otitis
o Sacculitis
IV.2.2.8. DIAGNOSIS
✔ A presumptive diagnosis can be rendered on the history, progress of the disease and
the lesions.
✔ The organism can be demonstrated in a gram-stained smear of the nasal exudates.

✔ Cultures should be made from nostrils, eye, cleft and trachea plus lung or air sacs if
lesions are present.
Note: Treatment should be started based on presumptive diagnosis
IV.2.2.9. MANAGEMENT
There are currently no medications or herbal remedies which have been conclusively
demonstrated to shorten the duration of infection in all people with cold symptoms.
✔ Symptomatic treatment
✔ Aanalgesics and antipyretics such as ibuprofen and acetaminophen / paracetamol

✔ Symptoms of a runny nose can be reduced by a first generation antihistamine
✔ Getting plenty of rest, drinking fluids to maintain hydration, gargling with warm salt water,
saline nasal drops may help alleviate nasal congestion.
✔ Zinc supplements inhibit rhinovirus replication and reduce inflammation
✔ Vitamin C supplements may reduce the duration of illness and causing symptoms to
be milder
✔ Antibiotics and antiviral should be used when suspecting surinfection especially after
7 days of unimprovement.
Preventative measures include:
o Isolation
o Regular hand washing is recommended to reduce transmission via direct contact.
o Cleaning contaminated surfaces reduce risk of transmission via direct contact
o Avoid the exposure to cold temperatures and wet weather whenever possible
o Healthy behaviours (proper nutrition,drink plenty of water, etc)
IV.2.3. INFLUENZA OR FLU
Influenza, commonly referred to as the flu, is an infectious disease caused by RNA viruses of
the family Orthomyxoviridae (the influenza viruses), that affects the respiratory tract of

many birds and mammals. The flu (or common flu) is a very contagious viral infection which
is raised as epidemic. The disease is generally benign but it can become serious at the old
person or debilated person.
IV.2.3.2. ETIOLOGY
The flu or Influenza is caused by the virus of the family the Orthomyxoviridae: myxovirus
ABC (influenza virus A, B, and C)
Influenza can be spread by:
● Direct transmission (when an infected person sneezes mucus directly into the eyes,
nose or mouth of another person);
● Through hand-to-eye, hand-to-nose, or hand-to-mouth transmission, either from

contaminated surfaces or from direct personal contact such as a hand-shake.
The influenza is a very polymorphic affection. The most usual form is the respiratory form.
The disease is usually most severe in very young children (under 5 years of age) and the elderly.
N.B.: Unlike symptoms of common cold, flu symptoms usually come on suddenly!!! It often
starts with the abrupt (brutal) onset with:
● Fever (with temperature of 400c with), shills and aches

● Severe diffuse headache, irradiated to the frontal sinuses and jawbones.
● Severe aches and pains in the joints and muscles and around the eyes
● Fatigue (generalized weakness)
● Ill appearance with warm, flushed skin and red, watery eyes
● Dry cough (fitfull), oculo-nasal catarrh (watery discharge from nose)
● Sore throat
● The raucousness of the voice testifying the Laryngo-Tracheal attack
● Gastrointestinal symptoms can sometimes accompany influenza infection such as
nausea, vomiting, and diarrhea
IV.2.3.5. DIAGNOSIS

It is based on the history, physical examination and, in some instances, laboratory testing before
treatment is initiated. However, it is very difficult to distinguish influenza from viral (including
common cold) and bacterial causes of respiratory illness on the basis of symptoms alone.
TABLE: Comparison of Influenza and the Common Cold
Features Influenza Common cold

Onset Abrupt More gradual
Fever Common: 37.7°C to 40.0°C (100°F to Uncommon or only 0.5°C

104°F) (1°F) increase
Myalgia Severe and common Uncommon
Arthralgia Severe and common Uncommon
Anorexia Common Uncommon
Headache Severe and common Mild, uncommon
Cough (dry) Common and severe Mild to moderate
Malaise Severe Mild
Fatigue, More common than with the common cold; Very mild, short lasting
weakness lasts 2 to 3 weeks
Chest Common and severe Mild to moderate

discomfort
Stuffy nose Occasional Common
Sneezing Occasional Common
Sore throat Occasional Common
IV.2.3.6. EVOLUTION

It is of short duration in few days, the symptoms attenuate, cough becomes loose and is
accompanied by a purulent expectoration. At the end of the influenza, the patient remains
asthenic and convalescence is often long.
IV.2.3.7. PROGNOSIS
Influenza's effects are much more severe and last longer than those of the common cold. Most
people will recover completely in about one to two weeks, but others will develop life-
threatening complications (such as pneumonia). Influenza, thus, can be deadly, especially for
the weak immune system, young and old, or chronically ill.
IV.2.3.8. CLINICAL FORMS
o Respiratory or thoracic form

o Gastro-intestinal form with vomiting and diarrhea
o Nervous form pseudo-meningitis which is malignant form resulting in death in a few
days
A. Pulmonary complications
• Upper respiratory tract infection (URTI)

o otitis media
o sinusitis
• Lower respiratory tract infection (LRTI)
o exacerbation of asthma/chronic obstructive pulmonary disease (COPD)
o croup, bronchiolitis or Acute laryngotracheobronchitis in young
children
o primary viral pneumonia
o secondary bacterial pneumonia
B. Non-pulmonary complications of influenza
• myositis
• cardiac complications: pericardiatis,myocarditis

• liver and NS complications
C. Others influenza related complications
• Decompensation of chronic diseases such as pulmonary disease, heart disease, renal

insufficiency, metabolic disease, gastrointestinal bleeding in children, etc
D. Influenza complicatios in pregnancy : Increased vulnerability during the second and third
trimester, possible consequences are :
• Severe pulmonary complications and death for pregnant woman

• Foetal loss and abortion
• Other risks
o foetal complications (growth, weight, etc.)

o brain damage
o neural tube defects
IV.2.3.10. GROUPS AT HIGHER RISK OF COMPLICATIONS
• Elderly (> 60 years of age)

• Children and teenagers Pregnant women belonging to high-risk groups
• Patients with chronic respiratory disease, chronic heart disease, chronic metabolic
disease, immunosuppression due to treatment or disease, haematological disorders,
chronic renal failure
IV.2.3.11. TREATMENT AND PREVENTION
People with the flu are advised to get plenty of rest, drink plenty of liquids, avoid
using alcohol and tobacco and, if necessary, take medications such as paracetamol) to relieve
the fever and muscle aches associated with the flu. Children and teenagers with flu symptoms
should avoid taking aspirin during an influenza infection (especially influenza type B), because
doing so can lead to Reye's syndrome. Since influenza is caused by a virus, antibiotics have no
effect on the infection; unless prescribed for secondary infections such as bacterial pneumonia.

⮚ Neuraminidase inhibitors
Antiviral drugs such as Tamiflu and zanamivir (trade name Relenza) are neuraminidase
inhibitors that are designed to halt the spread of the virus in the body. These drugs are often
effective against both influenza A and B and therefore were concluded that they reduce
symptoms and complications.
Managing Influenza with Tamiflu
According to the CDC, antiviral medications can also be effective at treating and preventing
influenza.
Treatment Prevention
Antiviral treatment should be started within 48 As an adjunct to vaccination, antivirals are

hours of influenza illness onset 68% to 89% effective in preventing influenza
●
Treatment should not be delayed while the Post exposure chemoprophylaxis is typically
results of diagnostic testing are awaited administered for a total of no more than 10
● days after the most recent known exposure
●
Antiviral treatment also can be considered for
any previously healthy, non-high-risk, Generally, post exposure chemoprophylaxis
symptomatic outpatient with confirmed or for persons should be only used when
suspected influenza based upon clinical antivirals can be started within 48 hours of the
judgment, if treatment can be initiated within most recent exposure
48 hours of illness onset
⮚ Indications and limitations of use
TAMIFLU is indicated in patients 1 year and older for the treatment of uncomplicated influenza
caused by viruses types A and B who have been symptomatic for no more than 2 days and for
the prophylaxis of influenza.
⮚ Vaccination
✔ Vaccination against influenza with an influenza vaccine is often recommended

for high-risk groups, such as children and the elderly, or in people who have
asthma, diabetes, heart disease, or are immuno-compromised.

✔ In Rwanda, the influenza vaccine is include in immunization schedule for
children
⮚ Infection control
✔
Good personal health and hygiene habits such as: not touching your eyes, nose
or mouth
✔
Frequent hand washing (with soap and water, or with alcohol-based hand rubs)
✔
Covering coughs and sneezes
✔
Avoiding close contact with sick people
✔
Staying home yourself if you are sick and Avoiding spitting is recommended
IV.2.4. CHICHENPOX
Also known as varicella, chickenpox or chicken pox is a highly contagious illness caused by
primary infection with varicella zoster virus (VZV). It usually starts with vesicular skin rash
mainly on the body and head rather than at the periphery and becomes itchy, raw pockmarks,
which mostly heal without scarring.
IV.2.4.2. ETIOLOGY
Chickenpox is caused by the varicella-zoster virus (VZV), also known as human herpes virus
3 (HHV-3), one of the eight herpes viruses known to affect humans.
Chickenpox is an airborne disease spread easily through coughing or sneezing of ill

individuals or through direct contact with secretions from the rash. A person with chickenpox
is infectious one to two days before the rash appears. The contagious period continues for 4 to
5 days after the appearance of the rash, or until all lesions have crusted over. Immuno-
compromised patients are probably contagious during the entire period new lesions keep
appearing. Crusted lesions are not contagious.
IV.2.4.4. EPIDEMIOLOGY
Primary varicella is a disease that is endemic to all countries worldwide.

Exposure to VZV in a healthy child initiates the production of antibodies that can persist for
life and confer immunity. Cell-mediated immune responses are also important in limiting the
scope and the duration of primary varicella infection. After primary infection, VZV is
hypothesized to spread from mucosal and epidermal lesions to local sensory nerves. VZV then
remains latent in the dorsal ganglion cells of the sensory nerves. Reactivation of VZV results
in the clinically distinct syndrome of herpes zoster (i.e., shingles), and sometimes Ramsay Hunt
syndrome type II. In pregnant women, antibodies produced as a result of immunization or
previous infections are transferred via the placenta to the fetus. Women who are immune to
chickenpox cannot become infected and do not need to be concerned about it for themselves
or their infant during pregnancy. Varicella infection in pregnant women could lead to viral
transmission via the placenta and infection of the fetus. If infection occurs during the first 28
weeks of gestation, this can lead to fetal varicella syndrome (also known as congenital varicella
syndrome). While a late infection in gestation or immediately following birth is referred to as
“neonatal varicella”. Effects on the fetus can range in severity from underdeveloped toes and
fingers to severe anal and bladder malformation.
Healthy children (and adults) generally experience one to two days of fever, sore throat and
malaise approximately two weeks following exposure to VZV. Other symptoms may include
myalgia, nausea, headache, pain in both ears, complaints of pressure in head or swollen face.
Within 24 hours of these symptoms, a characteristic rash develops initially on the torso and
then spreads over the next 7 to 10 days outward to the head, arms, and legs. The rash progresses
through a predictable evolution from a red papule (“beg bite” appearance) to blister (vesicle)
then to pustule and finally scabs over. The vesicle and pustular fluids are highly concentrated
with infectious virus particles.New lesions characteristically come in “waves” over the skin
surface. The patient may thus have newly formed papules, middle-aged vesicles and pustules,
and crusted lesions all at the same time. Once all lesions are scabbed over and no new lesions
are developing, the person is no longer contagious. The lesions rarely cause permanent
scarring, unless secondary infection develops. Lesions may commonly be found in the mouth
and may also involve the genitalia.
Note: The most common late complication of chickenpox is shingles, caused by reactivation
of the varicella zoster virus decades after the initial episode of chickenpox.
In healthy children, chickenpox is a mild disease. In adults, the disease is more severe, though
the incidence is much less common.
Common complications affecting both children and adults are:
✔ Skin infection: secondary bacterial infections can be caused by either staphylococcus

or streptococcus (E.g.: impetigo, cellulitis, and erysipelas).
✔ Pneumonia
✔ Neurologic complications suchas encephalitis
✔ Reye’s syndrome: this rare childhood complication of chickenpox (and influenza) is
most commonly associated with the administration of aspirin.
✔ Rare complications: Hepatatis, kidney disease, ulcers of the intestinal tract, and
orchitis.
Note that the immune system keeps the virus at bay, but later in life, usually as an adult, it can
be reactivated and cause a different form of the viral infection called shingles (herpes zoster).
Chickenpox and pregnancy
If infection occurs during the first 28 weeks of gestation, this can lead to fetal varicella
syndrome (also known as congenital varicella syndrome). Effects on the fetus can range in
severity from underdeveloped toes and fingers to severe anal and bladder malformation.
Possible problems include:
● Damage to brain: encephalitis, microcephaly, hydrocephaly, aplasia of brain

● Damage to the eye: optic stalk, optic cup, and lens vesicles, microphthalmia, cataracts,
chorioretinitis, optic atrophy
● Other neurological disorders: damage to cervical and lumbosacral spinal cord,
motor/sensory deficits, absent deep tendon reflexes, anisocoria/Horner's syndrome
● Damage to body: hypoplasia of upper/lower extremities, anal and bladder sphincter
dysfunction
● Skin disorders: (cicatricial) skin lesions, hypopigmentation
● Neonatal varicella

● Newborns who develop symptoms are at a high risk of pneumonia and other serious
complications of the disease.
IV.2.4.8. DIAGNOSIS
The diagnosis of varicella is primarily clinical, with typical early "prodromal" symptoms, and
then the characteristic rash. Confirmation of the diagnosis can be sought through either
examination of the fluid within the vesicles of the rash, or by testing blood for evidence of an
acute immunologic response
IV.2.4.9. TREATMENT
o Local antiseptic
o Antibiotherapy when cutaneous surinfection
o Antihistamine and acyclovir may be used
⮚ Hygiene measures
o Isolating affected individuals.

o The chicken pox virus (VZV) is susceptible to disinfectants, notably chlorine
bleach (i.e., sodium hypochlorite).
o Also, like all enveloped viruses, VZV is sensitive to desiccation, heat and
detergents. Therefore these viruses are relatively easy to kill.
IV.2.5. HERPES ZOSTER
Also called shingles, zoster or zona, herpes zoster is a viral disease characterized by a painful
skin rash with blisters in a limited area on one side of the body, caused by the varicella zoster
virus, which is the virus that causes chickenpox.
IV.2.5.2. ETIOLOGY
The causative agent for herpes zoster is varicella zoster virus (VZV).

IV.2.5.3. TRANSMISSION /REACTIVATION
Varicella zoster virus (VZV) has a high level of infectivity and has a worldwide prevalence.
Herpes zoster is a re-activation of latent VZV infection: this means that zoster can only occur
in someone who has previously had chickenpox (varicella). It has a relationship with some risk
factors such as increasing age, immunocompromised state (E.g.: HIV), psychological stress,
etc.
Herpes zoster occurs only in people who have had chickenpox, and although it can occur at
any age, the majority of sufferers are more than 50 years old. Most people are infected with
this virus as children, and suffer from an episode of chickenpox. The immune system
eventually eliminates the virus from most locations, but it remains dormant (or latent) in the
ganglia adjacent to the spinal cord (called the dorsal root ganglion) or the ganglion semilunare
(ganglion Gasseri) in the base of the skull. Repeated attacks of herpes zoster are rare, and it is
extremely rare for patients to suffer more than three recurrences. The disease results from the
virus reactivating in a single sensory ganglion. Unless the immune system is compromised, it
suppresses reactivation of the virus and prevents herpes zoster. It is more likely to occur in
people whose immune system is impaired due to aging, immunosuppressive therapy,
psychological stress, or other factors. Upon reactivation, the virus replicates in the nerve cells,
and virions are shed from the cells and carried down the axons to the area of skin served by
that ganglion. In the skin, the virus causes local inflammation and blisters. The short- and long-
term pain caused by herpes zoster comes from the widespread growth of the virus in the
infected nerves, which causes inflammation.
The first symptom is usually burning or shooting pain and tingling or itching, usually on one
side of the body or face. The pain and burning may be severe and is usually present before any
rash appears.
Red patches on the skin, followed by small blisters, form in most people.
● The blisters break, forming small ulcers that begin to dry and form crusts. The crusts
fall off in 2 to 3 weeks. Scarring is rare.

● The rash usually involves a narrow area from the spine around to the front of the belly
area or chest.
● The rash may involve face, eyes, mouth, and ears.
Additional symptoms may include: abdominal pain, chills, difficulty moving some of the
muscles in the face, drooping eyelid (ptosis), fever and chills, general ill-feeling, genital
lesions, headache, hearing loss, joint pain, loss of eye motion, swollen glands (lymph nodes),
taste problems, vision problems
Patient may also have pain, muscle weakness, and a rash involving different parts of face if
shingles affects a nerve in the face.
Complications of shingles are common. About one in five patients develops a painful condition
called postherpetic neuralgia, which is often difficult to manage.
Other possible complications are:
• polyneuritis
• myelitis
• aseptic meningitis
• facial paralysis (usually temporary)
• ear damage with hearing difficulties or even deafness
• encephalitis or sepsis due to secondary infection
• during pregnancy, first infections with VZV, causing chickenpox, may lead to infection
of the fetus and complications in the newborn
• secondary bacterial infection
• eye involvement trigeminal nerve involvement may lead to blindness
IV.2.5.7. DIAGNOSIS
o It is based on clinical diagnosis and medical history taking. If the rash has appeared,
identifying this disease only requires a visual examination, since very few diseases
produce a rash in a dermatomal pattern.

o The Tsanck smear is helpful for diagnosing acute infection with a herpes virus, but does
not distinguish between HSV and VZV.
o The most popular test detects VZV-specific IgM antibody in blood; this only appears
during chickenpox or herpes zoster and not while the virus is dormant. In larger
laboratories, lymph collected from a blister is tested by polymerase chain reaction for
VZV DNA, or examined with an electron microscope for virus particles.
IV.2.5.8. TREATMENT AND CONTROL OF DISEASE
• The aims of treatment are to limit the severity and duration of pain, shorten the duration
of a shingles episode, and reduce complications because there is no cure for shingles.
Symptomatic treatment is often needed for the complication of postherpetic neuralgia.
• Strong anti-inflammatory medicines (corticosteroids, such as prednisone)
• Antihistamines to reduce itching (taken by mouth or applied to the skin)
• Pain medicines such as paracetamol, ibuprofen,
• Topical antibiotics can be used
• Cool wet compresses can be used to reduce pain
• Soothing baths and lotions may help to relieve itching and discomfort
• Resting in bed until the fever goes down is recommended.
• The skin should be kept clean, and contaminated items should not be reused
• Nondisposable items should be washed in boiling water or otherwise disinfected before
reuse
• The person may need to be isolated while lesions are oozing to prevent infecting other
people who have never had chickenpox especially pregnant women.
IV.2.5.9. PROGNOSIS
The rash and pain usually subside within three to five weeks, but about one in five patients
develops a painful condition called postherpetic neuralgia, which is often difficult to manage.
In regards to prognosis also, note that complications can arise.
IV.2.6. VIRAL HEMORRHAGIC FEVERS
The viral hemorrhagic fevers (VHFs) are a diverse group of animal and human illnesses that
are caused by four distinct families of RNA viruses: the Arenaviridae, Filoviridae,

Bunyaviridae, and Flaviviridae. All types of VHF are characterized by fever and bleeding
disorders and all can progress to high fever, shock and death in extreme cases.
A. ETIOLOGIC AGENTS
● The Arenaviridae include the viruses responsible for Lassa fever and Argentine,
Bolivian, Brazilian and Venezuelan hemorrhagic fevers.
● The Bunyaviridae include the members of the Hantavirus genus that cause hemorrhagic
fever with renal syndrome (HFRS), the Crimean-Congo hemorrhagic fever (CCHF)
virus from the Nairovirus genus, and the Rift Valley fever (RVF) virus from the
Phlebovirus genus.
● The Filoviridae include Ebola and Marburg viruses.
● Finally, the Flaviviridae include dengue, yellow fever, and two viruses in the tick-borne
encephalitis group that cause VHF: Omsk hemorrhagic fever virus and Kyasanur Forest
disease virus.
The most recently recognized virus capable of causing hemorrhagic fever is Lujo virus, a new
member of the arenaviruses described in 2009 and found in South Africa.
B. PATHOPHYSIOLOGY
The diversity of clinical features seen among the VHF infections probably originates from
varying mechanisms of pathogenesis. An immunopathogenic mechanism, for example, has
been identified for dengue hemorrhagic fever, which usually occurs among patients previously
infected with a heterologous dengue serotype. An influential theory explaining this
phenomenon is called “antibody-dependent enhancement.” In contrast, disseminated
intravascular coagulation (DIC) is thought to underlie the hemorrhagic features of Rift Valley,
Marburg and Ebola fevers. In most VHFs, however, the etiology of the coagulopathy is most
likely multifactorial (e.g., hepatic damage, consumptive coagulopathy, primary marrow
dysfunction, etc).
The reasons for variation among patients infected with the same virus are unknown but stem
from a complex system of virus-host interactions. Moreover, why some infected persons
develop full-blown VHF while others do not also remains an unresolved issue. Virulence of
the infecting agent clearly plays an important role. Characteristically, the overall vascular

system is damaged, and the body’s ability to regulate itself is impaired. The “VHF
syndrome” (capillary leak, bleeding diathesis and hemodynamic compromise leading to shock)
occurs in a majority of patients manifesting disease from filoviruses, CCHF and the South
American hemorrhagic fever viruses, while it occurs in a small minority of patients with
dengue, RVF and Lassa fever.
C. TRANSMISSION
Bats drop partially eaten fruits and pulp, terrestrial mammals such as gorillas and duikers feed
on these fallen fruits. This chain of events forms a possible indirect means of transmission from
the natural host to animal populations, which have led to research towards viral shedding in the
saliva of bats. Fruit production, animal behavior, and other factors vary at different times and
places which may trigger outbreaks among animal populations. Transmission between natural
reservoirs and humans is rare, and outbreaks are usually traceable to a single index case where
an individual has handled the carcass of gorilla, chimpanzee, or duiker. The virus then spreads
person-to-person, especially within families, hospitals, and during some mortuary rituals where
contact among individuals becomes more likely.
The virus has been confirmed to be transmitted through body fluids. Transmission through oral
exposure and through conjunctiva exposure is likely, which have been confirmed in non-human
primates. Filoviruses are not naturally transmitted by aerosol. They are, however, highly
infectious as breathable 0.8-1.2 micron droplets in laboratory conditions; because of this
potential route of infection, these viruses have been classified as Category A biological
weapons.
All epidemics of Ebola have occurred in sub-optimal hospital conditions, where practices of
basic hygiene and sanitation are often either luxuries or unknown to caretakers and where
disposable needles and autoclaves are unavailable or too expensive. In modern hospitals with
disposable needles and knowledge of basic hygiene and barrier nursing techniques, Ebola has
never spread on a large scale. In isolated settings such as a quarantined hospital or a remote
village, most victims are infected shortly after the first case of infection is present. The quick
onset of symptoms from the time the disease becomes contagious in an individual makes it
easy to identify sick individuals and limits an individual's ability to spread the disease by
traveling. Because bodies of the deceased are still infectious, some doctors had to take measures
to properly dispose dead bodies in a safe manner despite local traditional burial rituals.

IV.2.6.1. EBOLA
Ebola is the virus Ebolavirus (EBOV), a viral genus, and the disease is Ebola hemorrhagic
fever (EHF), a type of viral hemorrhagic fever (VHF).
IV.2.6.1.1. SIGNS AND SYMPTOMS
The incubation period ranges from 2–21 days, although it is generally 5–18 days. Illness is
characterized by the rapid onset of fever, malaise, muscle pain, headache, and the inflammation
of the pharynx. Six days following vomiting and bloody diarrhea, individuals may develop
maculopapular rash with bleeding at needle sites and bodily orifices.
Reston ebolavirus is non-pathogenic to humans and individuals often do not show any
symptoms, although it is fatal in monkeys. There is only one known case of Ivory Coast
ebolavirus. There has been only one outbreak of Bundibugyo ebolavirus Zaire virus, then
Sudan ebolavirus, is the most common. Symptoms include:
• abdominal pain
• Fever, headache and myalgia
• Bloody vomit (vomiting [59%])
• Maculopapular rash
• Malaise
• Joint and muscle pain
• Inflammation of the pharynx
• Blood fails to clot
• Chest pain
• CNS involvement (rare)
• Dry and sore throat
• Hemorrhagic diathesis (71%-78%), hiccups
• Non-bloody diarrhea occurs in 81%
• Purpura, petechia, sclerotic arterioles, and low blood-pressure are characteristic as the
disease progresses.
IV.2.6.1.2. DIAGNOSIS

Before outbreaks are confirmed in areas of weak surveillance on the local or regional levels,
ebola is often mistaken for malaria, typhoid fever, dysentery, influenza, or various bacterial
infections which may be endemic to the region. Learning from the failure response such as the
2000 Uganda outbreak, public health measures such as the WHO's Global Outbreak and
Response Network were instituted in areas at high risk. Field laboratories were established in
order to confirm cases as to shipping samples to South Africa.
Methods of diagnosis of Ebola include testing saliva and urine samples. Ebola is diagnosed
with an Enzyme-Linked ImmunoSorbent Assay (ELISA) test.
IV.2.6.1.3. PREVENTION
In the early stages, Ebola may not be highly contagious. Contact with someone in early stages
may not even transmit the disease. As the illness progresses, bodily fluids from diarrhea,
vomiting, and bleeding represent a hazard.
In such conditions:
o Immediately cease all needle-sharing or use without adequate sterilization procedures

o Isolate patients, and observe strict barrier nursing procedures with the use of a medical
rated disposable face mask, gloves, goggles, and a gown at all times. This should be
strictly enforced for all medical personnel and visitors.
IV.2.6.1.4. TREATMENT
There is no standard treatment for Ebola hemorrhagic fever. Treatment is primarily supportive
and includes:
o Minimizing invasive procedures

o Balancing electrolytes, replacing lost coagulation factors to help stop bleeding,
o Maintaining oxygen and blood levels,
o Treating any complicating infections.
IV.2.6.1.5. PROGNOSIS

Ebola hemorrhagic fever is potentially lethal and encompasses a range of symptoms including
fever, vomiting, diarrhea, generalized pain or malaise, and sometimes internal and external
bleeding. The span of time from onset of symptoms to death is usually between 2 and 21 days.
IV.2.6.2. MARBURG VIRUS
IV.2.6.2.1. DEFINITION
Marburg virus or simply Marburg is the common name for the genus of viruses Marburgvirus,
which contains one species, Lake Victoria marburgvirus. The virus causes the disease Marburg
Hemorrhagic Fever (MHF), also referred to as Marburg Virus Disease, and previously also
known as green monkey disease due to its primate origin. Marburg originated in Central and
East Africa, and infects both human and nonhuman primates. The Marburg Virus is in the same
taxonomic family as Ebola, and both are identical structurally although they elicit different
antibodies.
IV.2.6.2.2. TRANSMISSION
The disease is spread through bodily fluids, including blood, excrement, saliva, and vomit.
Early symptoms are often non-specific, and usually include fever, headache and myalgia after
an incubation period of three to nine days. After five days, a maculopapular rash is often
present on the torso. Later-stage Marburg infection is acute and can include jaundice,
pancreatitis, weight loss, delirium and neuropsychiatric symptoms, haemorrhaging,
hypovolemic shock and multi-organ dysfunction, with liver failure most common. Accounts of
external haemorrhaging from bodily orifices are pervasive in popular references to the disease
but are in fact rare. Time course varies but symptoms usually last for one to three weeks until
the disease either resolves or kills the infected host. The fatality rate is from 23% to over 90%.
IV.2.6.2.3. SYMPTOMS
Many of the symptoms of Marburg hemorrhagic fever are similar to those of other infectious
diseases, such as malaria or typhoid, but are most similar to those of Ebola strains.

Diagnosis of Marburg is similar to Ebola using the Enzyme-Linked ImmunoSorbent Assay

(ELISA) test.
If a patient survives, recovery is usually prompt and complete, though it may be prolonged in
some cases, with inflammation or secondary infection of various organs, including: orchitis,
hepatitis, transverse myelitis, uveitis, and parotitis. Recovered patients often have little or no
memory of being sick, though only 10-40% survives.
✔ There is no specific antiviral therapy indicated for treating Marburg, and hospital care
is usually supportive in nature.
✔ Hypotension and shock may require early administration of vasopressors and
hemodynamic monitoring with attention to fluid and electrolyte balance, circulatory
volume, and blood pressure. Viral hemorrhagic fever (VHF) patients tend to respond
poorly to fluid infusions and may develop pulmonary edema.
Caregivers require barrier infection control measures including double gloves, impermeable
gowns, face shields, eye protection, and leg and shoe coverings. Precautions are very needed.
IV.2.6.3. LASSA FEVER
IV.2.6.3.1. DEFINITION
Lassa fever is an acute viral hemorrhagic fever first described in 1969 in the town of Lassa, in
Borno State, Nigeria located in the Yedseram river valley at the south end of Lake Chad.
IV.2.6.3.2. PATHOGENESIS
Lassa virus will infect almost every tissue in the human body. It starts with the mucosa,
intestine, lungs and urinary system, and then progresses to the vascular system.

IV.2.6.3.3. EPIDEMIOLOGY
Lassa virus is zoonotic (transmitted from animals), in that it spreads to man from rodents,
specifically multi-mammate rats (Mastomys natalensis).
IV.2.6.3.4. SYMPTOMS
In 80% of cases the disease is inapparent, but in the remaining 20% it takes a complicated
course. It is estimated that the virus is responsible for about 5,000 deaths annually. The fever
accounts for up to one third of deaths in hospitals within the affected regions and 10 to 16% of
total cases.
After an incubation period of six to twenty-one days, an acute illness with multiorgan
involvement develops. Non-specific symptoms include fever, facial swelling, and muscle
fatigue, as well as conjunctivitis and mucosal bleeding. Other symptoms arising from the
affected organs are:
● Gastrointestinal tract: Nausea, vomiting (bloody), diarrhea (bloody), stomach ache,

constipation, dysphagia, hepatitis
● Cardiovascular system: pericarditis, hypertension, hypotension, tachycardia
● Respiratory tract: cough, chest pain, dyspnoea, pharyngitis, pleuritis
● Nervous system: encephalitis, meningitis, unilateral or bilateral hearing deficit, seizures
Clinically, Lassa fever infections are difficult to distinguish from other viral hemorrhagic
fevers such as Ebola and Marburg, and from more common febrile illnesses such as malaria.
The virus is excreted in urine for three to nine weeks and in semen for three months.
There is a range of laboratory investigations that are performed to diagnose the disease and
assess its course and complications.
✔ ELISA test for antigen and IgM antibodies gives 88% sensitivity and 90% specificity
for the presence of the infection.

✔ Other laboratory findings in Lassa fever include lymphopenia (low white blood cell
count), thrombocytopenia (low platelets), and elevated aspartate aminotransferase
(AST) levels in the blood.
About 15%-20% of hospitalized Lassa fever patients will die from the illness. It is estimated
that the overall mortality rate is 1%, however during epidemics mortality can climb as high as
50%. The mortality rate is greater than 80% when it occurs in pregnant women during their
third trimester; fetal death also occurs in nearly all those cases. Abortion decreases the risk of
death to the mother.
o All persons suspected of Lassa fever infection should be admitted to isolation facilities
and their body fluids and excreta properly disposed of.
o Ribavirin is a drug which appears to interfere with viral replication by inhibiting RNA-
dependent nucleic acid synthesis, although the precise mechanism of action is disputed.
Control of the Mastomys rodent population is impractical, so measures are limited to keeping
rodents out of homes and food supplies, as well as maintaining effective personal hygiene.
Gloves, masks, laboratory coats, and goggles are advised while in contact with an infected
person.
IV.2.7. YELLOW FEVER
IV.2.7.1 DEFINITION
Yellow fever is an acute viral hemorrhagic disease transmitted by infected mosquitoes. The
“yellow” in the name refers to the jaundice that affects some patients.
IV.2.7.2. CAUSE
Yellow fever is caused by the yellow fever virus of the Flaviviridae family (arbovirus).

The yellow fever virus is usually passed between monkeys and mosquitoes
A person may be infected if he is bitten by an infected mosquito in the jungle (jungle yellow
fever).
If an infected Monkey, mosquito or a person comes to a town the diseases can then be
passed between people and mosquitoes in the town (urban yellow fever).
People who live in an area where yellow fever is common and do not die from an attack
usually become immune or only suffer only mild attacks.
Severe attacks occur usually and especially when people from other areas go to an
infected area or the diseases spread to a new area.
IV.2.7.4 SIGNS AND SYMPTOMS
1) At first there are severe general symptoms and signs of viral type infection similar
to dengue fever:
✔ Fever
✔ Headache
✔ Painful eyes
✔ Backaches
✔ Joints pain
✔ Red watery eyes
✔ Nausea and vomiting
✔ Watery diarrhea
✔ The pulse is usually slow, not fast
2) After few days the temperature falls and the patient may improve.
3) After some hours or a day or so, however the patient may get much worse.
o He develops a higher fever ( although the pulse is still slow)
o Jaundice and a tender liver and bile in the urine
o A lot of proteins in the urines
o Bleeding into the skin
o Hemorrhagic manifestations including gastro-intestinal, renal, vaginal, nasal, and
conjunctival hemorrhage

o Bleeding from the mouth and the lungs are also found
4) Death occurs from liver or kidney failure or bleeding.
If these can be successfully treated and the patient lives for about 12 days, the patient usually
recovers. The mortality rate is from 10- 60 %
IV.2.7.5. DIAGNOSIS
o Yellow fever is clinically diagnosed.

o A direct confirmation can be obtained by Reverse transcription polymerase chain
reaction where the genome of the virus is amplified.
o Another direct approach is the isolation of the virus and its growth in cell culture using
blood plasma; this can take one to four weeks.
o Serologically an enzyme linked immunosorbent assay during the acute phase of the
disease using specific IgM against yellow fever or an increase in specific IgG-titer
(compared to an earlier sample) can confirm yellow fever.
IV.2.7.6. DIFFERENTIAL DIAGNOSIS
In a differential diagnosis, infections with yellow fever have to be distinguished from other
feverish illnesses like malaria; viral hemorrhagic fevers such as Ebola virus, Lassa virus,
Marburg virus or Junin virus.
Personal prevention of yellow fever includes vaccination as well as avoidance of mosquito

bites in areas where yellow fever is endemic. Institutional measures for prevention of yellow
fever include vaccination programmes and measures of controlling mosquitos as they are all
known.
IV.2.7.8. TREATMENT
✔ For yellow fever there is, like for all diseases caused by Flaviviruses, no etiological
treatment
✔ Hospitalization is advisable and intensive care may be necessary because of rapid
deterioration in some cases.

✔ Different methods for acute treatment of the disease have been shown to not be very
successful; passive immunisation after emergence of symptoms is probably without
effect.
✔ Ribavirin and other antiviral drugs as well as treatment with interferons do not have a
positive effect in patients.
✔ A symptomatic treatment includes rehydration and pain relief with drugs like
paracetamol. Acetylsalicylic acid (for example Aspirin) should not be given because of
its haemodiluting effect, which can be devastating in the case of inner bleeding that can
occur with yellow fever.
IV.2.8. HERPES SIMPLEX VIRUS (HSV) INFECTIONS
IV.2.8.1. DEFINITION AND ETIOLOGY
Herpes simplex is a viral disease caused by both herpes simplex viruses type 1 (HSV-1) and
type 2 (HSV-2).
Herpes simplex is most easily transmitted by direct contact with a lesion or the body fluid of
an infected individual. Transmission may also occur through skin-to-skin contact during
periods of asymptomatic shedding.
IV.2.8.3. CLASSIFICATION
Herpes simplex is divided into two types HSV type 1 and HSV type 2. HSV1 primarily causes
mouth, throat, face, eye, and central nervous system infections while HSV2 primarily causes
anogenital infections. However each may cause infections in all areas.
HSV infection causes several distinct medical disorders. Common infection of the skin or
mucosa may affect the face and mouth (orofacial herpes), genitalia (genital herpes), or hands
(herpes whitlow). More serious disorders occur when the virus infects and damages the eye
(herpes keratitis), or invades the central nervous system, damaging the brain (herpes
encephalitis). Patients with immature or suppressed immune systems, such as newborns,

transplant recipients, or AIDS patients are prone to severe complications from HSV infections.
HSV infection has also been associated with cognitive deficits of bipolar disorder, and
Alzheimer's disease, although this is often dependent on the genetics of the .infected person.
⮚ Oral herpes (herpetic gingistomatitis) is characterized by:
o Ulceration of the mouth, tongue, gums and fauces.

o The patient experiences pain and bleeding of the gums.
⮚ Herpes of genitals: when symptomatic, the typical manifestation of a primary HSV-1

or HSV-2 genital infection is clusters of inflamed papules and vesicles on the outer
surface of the genitals resembling cold sores.
IV.2.8.5. DIAGNOSIS
Essentially clinical. Laboratory tests include: culture of the virus, direct fluorescent antibody
(DFA) studies to detect virus, skin biopsy, and polymerase chain reaction (PCR) to test for
presence of viral DNA.
✔ Barrier methods
o The use of condoms limits the transmission of herpes from the genitals.
o When one partner has a herpes simplex infection and the other does not, the use of
antiviral medication, such as valaciclovir, in conjunction with a condom
o All preventive measures of STI should be considered for genital herpes
✔ Pregnancy
o To prevent neonatal infections, seronegative women are recommended to avoid

unprotected oral-genital contact with an HSV-1 seropositive partner and conventional
sex with a partner having a genital infection during the last trimester of pregnancy.
o Mothers infected with HSV are advised to avoid procedures that would cause trauma
to the infant during birth (e.g., forceps, etc); caesarean section is advisable.

o The use of antiviral treatments, such as acyclovir, given from the 36th week of
pregnancy, limits HSV recurrence and shedding during childbirth, thereby reducing the
need for caesarean section.
IV.2.8.7. TREATMENT
✔ There is no method to eradicate herpes virus from the body, but antiviral medications
can reduce the frequency, duration, and severity of outbreaks.
✔ Analgesics such as ibuprofen and acetaminophen can reduce pain and fever.
✔ Topical anesthetic treatments such as prilocaine, lidocaine, to relieve itching and pain.
IV.2.8.8. PROGNOSIS
Many HSV-infected people experience recurrence within the first year of infection. The causes
of reactivation are uncertain.
IV.2.9. RABIES
This is an acute viral disease of central nervous system of animals, accidentally transmitted to
human being by the bite of a rabid animal. Rabies is a deadly viral infection that is mainly
spread by infected animals.
IV.2.9.2. ETIOLOGY
The virus of rabies is in the group of rhabdovirus. This virus is fragile and is quickly destroyed
by the soap, the ether, and the ammonium derivatives. It is sensitive to heat, the light and the
desiccation.
It is zoonotic, most commonly by a bite (saliva) from an infected animal but occasionally by
other forms of contact (aerosol droplets, ingestion of infected tissues, transplantation of
infected tissue). The main route of transmission is the bites of rabid animal, most often dogs.
The disease is transmitted to domestic animals and humans through exposure to infected saliva.
Humans also become infected with rabies through the bite of infected cats, wild carnivorous

species like foxes, raccoons, skunks, jackals and wolves. Cattle, horses, deer and other
herbivores can become infected with rabies.
People at risk
● Poor people, especially children, are at highest risk of dog rabies. Children often play
with animals and are less likely to report bites or scratches.
● In areas known for rabies, professionals with frequent exposure to animals (e.g.
veterinarians), or who spend a lot of time outdoors (e.g. wildlife specialists or
researchers), particularly in rural areas, should be vaccinated preventively.
Virulence depends
■ Depends on severity of bites

■ If treatment is given and when
■ Once the disease manifests in CNS: ultimate death
Vehicle of transmission
■ Saliva
■ Mucous membranes
■ Aerosol transmission
■ Corneal transplantations
The pathogenesis begins when infected saliva of host is passed to uninfected animal by
scratches or bites. Virus replicates in muscle cells near site of bite for most of incubation time.
Incubation time 30-90 days. Latency up to 7 years. Then ascends along motor and sensory
axons at rate of 12-100mm/day and has predilection for brainstem and medulla. It enters
salivary glands after replication in CNS where it undergoes the perivascular infiltration
throughout entire central nervous system that causes cytoplasmic eosinophilic inclusion bodies
(Negri bodies) in neuronal cells which will be defined by encephalitis and myelitis. Several
factors may affect outcome of rabies exposure such as rabies variant, dose, route, location of
exposure and individual host factors.

Incubation: The incubation period of the disease is usually a few months in humans,
depending on the distance the virus must travel to reach the central nervous system.
Invasion: Once the rabies virus reaches the central nervous system and symptoms begin to
show: The first symptoms of rabies are flu-like, including fever, headache and fatigue, and then
progress to state phase which involves the respiratory, gastrointestinal and/or central nervous
systems.
State phase: Two clinical forms which are critical stages are possible translating the
encephalitis:
● The furious rabies or spastic or encephalitic rabies:
There are signs of hyperactivity (psychomotor excitation) with hallucination and convulsions,
pain, violent movements, uncontrolled excitement, depression, and hydrophobia very
characteristic of the human rabies, and finally, the patient may experience periods of mania
and lethargy, eventually leading to coma. Vitals abnormal: tachycardia, tachypnea, fever.
Other characteristic features are:
Hydrophobia: Patient cannot swallow because violent jerky contraction of diaphragm and
accessory muscles of inspiration when patient attempts to swallow liquids. Patients will be
terrified during this reaction and may even experience this at the sight of water or if water
touches their face.
Aerophobia: an extreme fear of air in motion can be elicited from some patients. This can
also cause violent muscle spasms in the neck and pharynx.
● Paralytic rabies or dumb rabies:

It is less frequent. It realizes an ascending paralytic syndrome (reach of lower limbs then
sphincters and after cranial nerves).
In both furious and dumb rabies, some paralysis eventually progresses to complete paralysis,
followed by coma and death in all cases, usually due to respiratory failure. Without intensive
care, death occurs during the first seven days of illness.
IV.2.9.6. DIAGNOSIS

✔ Essentially done by assessing patient history and clinical features.
✔ Saliva can be tested by virus isolation or reverse transcription by polymerase chain
reaction (RT-PCR).
✔ Serum and spinal fluid are tested for antibodies to rabies virus.
✔ Skin biopsy specimens are examined for rabies antigen in the cutaneous nerves at the
base of hair follicles.
✔ It is possible to make the diagnosis by viral culture of saliva, urine and cerebrospinal
fluid samples
✔ Inclusion bodies called Negri bodies are of certain diagnostic (100%) for rabies
infection, but are found in only about 80% of cases.
IV.2.9.7. TREATMENT
TREATMENT AFTER EXPOSURE
✔ To check if the anti-rabid vaccination is update

✔ Wound cleansing and immunizations, done as soon as possible after suspect contact
with an animal and following WHO recommendations, can prevent the onset of rabies
in virtually 100% of exposures. Recommended treatment to prevent rabies depends on
the category of the contact:
● Category I: touching or feeding suspect animals, licks on intact skin
● Category II: nibbling of uncovered skin, minor scratches or abrasions without
bleeding
● Category III: single or multiple transdermal bites or scratches, licks on broken
skin, contamination of mucous membranes with saliva from licks, exposure to
bats.
✔ Post-exposure care to prevent rabies includes cleaning and disinfecting a wound, or

point of contact, and then administering anti-rabies immunizations as soon as possible.
● Anti-rabies vaccine is given for Category II and III exposures.

● Anti-rabies immunoglobin, or antibody, should be given for Category III
contact, or to people with weaker immune systems.
● They give one dose of human rabies immunoglobulin (HRIG) and four doses
of rabies vaccine over a fourteen day period.

● The immunoglobulin dose should not exceed 20 units per kilogram body
weight.
● As much as possible of this dose should be infiltrated around the bites and other
is given by deep intramuscular injection at a site distant from the vaccination
site.
● The first dose of rabies vaccine is given as soon as possible after exposure, with
additional doses after. Patients who have previously received pre-exposure
vaccination do not receive the immunoglobulin, only the post-exposure
vaccinations on day 0 and 2.
✔ When humans are exposed to suspect animals, attempt to identify, capture or humanely
sacrifice the animal involved should be undertaken immediately. Post-exposure
treatment should start right away and only be stopped if the animal (dog or cat) remains
healthy after 15 days.
N.B.: Once the signs and symptoms of rabies start to appear, there is no treatment and the
disease is almost always fatal!!
a. Eliminating rabies in dogs through animal vaccinations.

b. Anti-rabic vaccination for human uses the inactivated vaccine in subcutaneous or in intra
muscular according to the protocols below:
- WHO Protocol: injection on day 0, 3, 7, 14, 30 and day 90
- Short Protocol: injection with on day 0, 7, and 21
IV.2.10. POLIOMYELITIS
Poliomyelitis, often called polio or infantile paralysis, is an acute viral infectious

disease spread from person to person, primarily via the fecal-oral route, caused by poliovirus.
IV.2.10.2. ETIOLOGY

Three serotypes of poliovirus have been identified: poliovirus type 1 (PV1), type 2 (PV2), and
type 3 (PV3), each with a slightly different capsid protein. All three are extremely virulent and
produce the same disease symptoms. PV1 is the most commonly encountered form, and the
one most closely associated with paralysis.
Poliomyelitis is highly contagious via the oral-oral (oropharyngeal source) and fecal-oral
(intestinal source) routes. In endemic areas, wild polioviruses can infect virtually the entire
human population.
The disease is transmitted primarily via the fecal-oral route, by ingesting contaminated food
or water. It is occasionally transmitted via the oral-oral route, a mode especially visible in areas
with good sanitation and hygiene. Polio is most infectious between 7–10 days before and 7–10
days after the appearance of symptoms, but transmission is possible as long as the virus remains
in the saliva or feces. Although the virus can cross the placenta during pregnancy, the fetus
does not appear to be affected by either maternal infection or polio vaccination.
The virus is ingested with fecally contaminated food or water. The initial
multiplication occurs in the lymphatic tissue of the oropharynx (tonsils) and
intestine (appendix). Dissemination to the regional lymphatics is followed by
viremia. The mechanism by which circulating viruses cross the blood- brain barrier
is probably by transcapillary diffusion.
The term poliomyelitis indicates that:
i. The gray matter (polio) of the spinal cord (myel) is inflamed (itis).
ii. Motor neurons are involved, but the lesions are not usually confined to the anterior horns of
the cord.
iii. In fatal cases, destruction is found in the cerebral ganglia, reticular formation,
cerebellar nuclei, hypothalamus, thalamus and cerebral cortex.
When the brain is cut during postmortem examination, damage is grossly evident as
swelling, softening, congestion and petechial hemorrhage.

The non-neural aspects of poliomyelitis, so critical to the pathogenesis of the disease,
are reflected not only in the lymph nodes but also in the spleen, liver, kidneys and
other viscera.
IV.2.10.5. CLASSIFICATION AND CLINICAL FEATURES
Two basic patterns of polio infection are described: a minor illness which does not involve
the central nervous system (CNS), sometimes called abortive poliomyelitis, and a major
illness involving the CNS, which may be paralytic or non-paralytic. In most people with
a normal immune system, a poliovirus infection is asymptomatic. Rarely the infection produces
minor symptoms. These may include upper respiratory tract infection (sore throat and
fever), gastrointestinal disturbances (nausea, vomiting, abdominal pain, constipation or, rarely,
diarrhea), and influenza-like illness.
The virus enters the central nervous system in about 3% of infections. Most patients with CNS
involvement develop non-paralytic aseptic meningitis, with symptoms of headache, neck,
back, abdominal and extremity pain, fever, vomiting, lethargy and irritability. Approximately
1 to 5 in 1000 cases progress to paralytic disease, in which the muscles become weak, floppy
and poorly controlled, and finally completely paralyzed; this condition is known as acute
flaccid paralysis.
Depending on the site of paralysis, paralytic poliomyelitis is classified as spinal, bulbar,

or bulbospinal.
o Paralytic polio
In around 1% of infections, poliovirus spreads along certain nerve fiber pathways,

preferentially replicating in and destroying motor neurons within the spinal cord, brain stem,
or motor cortex. This leads to the development of paralytic poliomyelitis, the various forms of
which (spinal, bulbar, and bulbo spinal) vary only with the amount of neuronal damage and
inflammation that occurs, and the region of the CNS that is affected.
The destruction of neuronal cells produces lesions within the spinal ganglia; these may also
occur in the reticular formation, vestibular nuclei, cerebellar vermis, and deep cerebellar
nuclei. Inflammation associated with nerve cell destruction often alters the color and
appearance of the gray matter in the spinal column, causing it to appear reddish and

swollen. Other destructive changes associated with paralytic disease occur in
the forebrain region, specifically the hypothalamus and thalamus.
The molecular mechanisms by which poliovirus causes paralytic diseases are poorly
understood.
Early symptoms of paralytic polio include high fever, headache, stiffness in the back and neck,
asymmetrical weakness of various muscles, sensitivity to touch, difficult swallowing, muscle
pain, loss of superficial and deep reflexes, paresthesia (pins and needles), irritability,
constipation, or difficulty urinating. Paralysis generally develops one to ten days after early
symptoms begin, progresses for two to three days, and is usually complete by the time the fever
breaks.
In children under five years of age, paralysis of one leg is most common; in adults, extensive
paralysis of the chest and abdomen also affecting all four limbs (quadriplegia) is more
likely. Paralysis rates also vary depending on the serotype of the infecting poliovirus; the
highest rates of paralysis (1 in 200) are associated with poliovirus type 1, the lowest rates (1 in
2,000) are associated with type 2.
1. Spinal polio (The location of motor neurons in the anterior horn cells of the spinal column).
Spinal polio is the most common form of paralytic poliomyelitis; it results from viral invasion
of the motor neurons of the anterior horn cells, or the ventral (front) gray matter section in
the spinal column, which are responsible for movement of the muscles, including those of
the trunk, limbs and the intercostal muscles. Virus invasion causes inflammation of the nerve
cells, leading to damage or destruction of motor neuron ganglia. When spinal neurons
die,Wallerian degeneration takes place, leading to weakness of those muscles
formerly innervated by the now dead neurons. With the destruction of nerve cells, the muscles
no longer receive signals from the brain or spinal cord; without nerve stimulation, the
muscles atrophy, becoming weak, floppy and poorly controlled, and finally completely
paralyzed. Progression to maximum paralysis is rapid (two to four days), and is usually
associated with fever and muscle pain. Deep tendon reflexes are also affected, and are usually
absent or diminished; sensation (the ability to feel) in the paralyzed limbs, however, is not
affected. The extent of spinal paralysis depends on the region of the cord affected, which may
be cervical, thoracic, or lumbar. The virus may affect muscles on both sides of the body, but
more often the paralysis is asymmetrical. Any limb or combination of limbs may be affected;

one leg, one arm, or both legs and both arms. Paralysis is often more severe proximally (where
the limb joins the body) than distally (the fingertips and toes).
2. Bulbar polio (The location and anatomy of the bulbar region)
Making up about 2% of cases of paralytic polio, bulbar polio occurs when poliovirus invades
and destroys nerves within the bulbar region of the brain stem. The bulbar region is a white
matter pathway that connects the cerebral cortex to the brain stem.
The destruction of these nerves weakens the muscles supplied by the cranial nerves, producing
symptoms of encephalitis, and causes difficulty breathing, speaking and swallowing. Critical
nerves affected are the glossopharyngeal nerve, which partially controls swallowing and
functions in the throat, tongue movement and taste; the vagus nerve, which sends signals to the
heart, intestines, and lungs; and the accessory nerve, which controls upper neck movement.
Due to the effect on swallowing, secretions of mucus may build up in the airway causing
suffocation. Other signs and symptoms include facial weakness, caused by destruction of
the trigeminal nerve and facial nerve, which innervate the cheeks, tear ducts, gums, and
muscles of the face, among other structures; double vision; difficulty in chewing; and abnormal
respiratory rate, depth, and rhythm, which may lead to respiratory arrest. Pulmonary
edema and shock are also possible, and may be fatal.
3. Bulbospinal polio
Approximately 19% of all paralytic polio cases have both bulbar and spinal symptoms; this
subtype is called respiratory polio or bulbospinal polio. Here, the virus affects the upper part
of the cervical spinal cord (C3 through C5), and paralysis of the diaphragm occurs. The critical
nerves affected are the phrenic nerve, which drives the diaphragm to inflate the lungs, and those
that drive the muscles needed for swallowing. By destroying these nerves this form of polio
affects breathing, making it difficult or impossible for the patient to breathe without the support
of a ventilator. It can lead to paralysis of the arms and legs and may also affect swallowing and
heart functions.
IV.2.10.6. DIAGNOSIS

Paralytic poliomyelitis may be clinically suspected in individuals experiencing acute onset of
flaccid paralysis in one or more limbs with decreased or absent tendon reflexes in the affected
limbs that cannot be attributed to another apparent cause, and without sensory or cognitive loss.
A laboratory diagnosis is usually made based on recovery of poliovirus from a stool sample or
a swab of the pharynx. Antibodies to poliovirus can be diagnostic, and are generally detected
in the blood of infected patients early in the course of infection. Analysis of the
patient's cerebrospinal fluid (CSF), which is collected by a lumbar puncture ("spinal tap"),
reveals an increased number of white blood cells (primarily lymphocytes) and a mildly
elevated protein level. Detection of virus in the CSF is diagnostic of paralytic polio, but rarely
occurs.
IV.2.10.7. PROGNOSIS
Patients with abortive polio infections recover completely. In those that develop only aseptic
meningitis, the symptoms can be expected to persist for two to ten days, followed by complete
recovery. In cases of spinal polio, if the affected nerve cells are completely destroyed, paralysis
will be permanent. The degree of both acute paralysis and residual paralysis is likely to be
proportional to the degree of viremia, and inversely proportional to the degree of immunity.
Spinal polio is rarely fatal.
✔ Muscle paresis and paralysis can sometimes result in skeletal deformities,

tightening of the joints and movement disability.
✔ Deformities of the spine (such as scoliosis).
✔ Osteoporosis and increased likelihood of bone fractures may occur.
✔ Extended use of braces or wheelchairs may cause compression neuropathy, as

well as a loss of proper function of the veins in the legs, due to pooling of blood
in paralyzed lower limbs.
✔ Complications from prolonged immobility involving

the lungs, kidneys and heart include pulmonary edema, aspiration

pneumonia, urinary tract infections, kidney stones, paralytic
ileus, myocarditis and cor pulmonale.
N.B.: Post-polio syndrome
Between 25% and 50% of individuals who survive paralytic polio in childhood develop
additional symptoms, notably new muscle weakness and extreme fatigue. This condition is
known as post-polio syndrome (PPS) or post-polio sequelae. The symptoms of PPS are thought
to involve a failure of the over-sized motor units created during recovery from paralytic
disease. Factors that increase the risk of PPS include the length of time since acute poliovirus
infection. Post-polio syndrome is not an infectious process, and persons experiencing the
syndrome do not shed poliovirus.
IV.2.10.9. TREATMENT
There is no specific therapy. Supportive treatment includes:

❖ BP monitoring: bulbar damage may produce either hypertension or shock
❖ Aid in ventilation
❖ Examination for vocal cord weakness - vagal paralysis can produce respiratory
obstruction
❖ Monitoring ability to handle secretions
❖ Monitoring of ability to swallow
❖ Examination of breath sounds for evidence of pulmonary edema, atelectasis
(incomplete expansion or collapse of pulmonary alveoli) or pneumonitis.
❖ Monitoring of ability to void
❖ Examination for evidence of thrombophlebitis.
❖ Rest and close observation are essential. Once the acute phase has passed,
physical therapy and orthopedic surgery are required.
❖ Supportive measures include antibiotics to prevent infections in weakened
muscles, analgesics for pain, moderate exercise and a nutritious diet
Two vaccines are used:

1. Inactivated (parenteral) virus vaccine (Salk)

2. Attenuated (oral) virus vaccine (Sabin): do not give to immunosuppressed patients.
The oral polio vaccine is used in Rwanda.
IV.2.11. INFECTIOUS MONONUCLEOSIS/EPSTEIN-BARR VIRUS INFECTION/

“THE KISSING DISEASE”
Infectious mononucleosis is a disease caused by the Epstein-Barr virus (EBV). It is often called
simply mono or “the kissing disease” because the virus is usually transmitted in saliva.
IV.2.11.2. ETIOLOGY
The disease is caused by Epstein Barr Virus (EBV) in 90% of Herpes Family
✔ Two subtypes
EBV-1 (type A): Western countries and EBV-2 (type B): less virulent
◆ In immunocompromised persons : co-infection both type 1 and type 2 strains
◆ No one subtype is responsible for specific lymphoproliferative diseases

(geographic differences)
◆ Other Herpesviruses :
❖ Cytomegalovirus (CMV)
❖ Herpes simplex 1 and simplex 2
❖ Human herpesvirus 6
◆ Other viruses :
❖ Adenovirus
❖ Hepatitis A, hepatitis B, or hepatitis C
❖ Rubella
❖ Primary human immunodeficiency virus in adolescents or young adults.

Kissing is only one means of transmission; sneezing, coughing, or drinking from a glass used
by an infected person can also spread it. This disease is sometimes known as glandular fever
because fever and swollen lymph nodes are among its symptoms.
❖ In children and infants the time of onset is usually vague and the duration of prodromal
symptoms is difficult to determine.
❖ Anorexia, sometimes accompanied by nausea and vomiting, is a common and non-
specific early symptom of this infection.
❖ The most important and most characteristic symptom of IM is a sore throat. This
usually develops a few days after the onset of the illness, increases in severity during
the first week, and then rapidly subsides during the next five to seven days.
❖ In many young adults sore throat is the first indication of sickness and in some it is the
only major symptom throughout the entire illness.
❖ Although anorexia may persist for as long as there is fever, its intensity and duration
are more directly related to the severity of sore throat and dysphagia.
❖ Gross tonsillar and pharyngeal edema may cause virtually complete pharyngeal
obstruction with harsh-sounding breathing and complete inability to swallow either
food or fluids.
❖ In some patients the soreness of the throat is so severe that swallowing even a few sips
of water is extremely painful.
❖ The headaches of early IM are often retro-orbital in location but have no
characteristic features. They may be moderately severe for one or two days but
usually they are mild and rarely last for more than three or four days.
❖ Ocular symptoms may be in the form of photophobia, ocular muscle aching or the
awareness of puffiness
❖ Lymphadenopathy, disease of the lymph nodes, is sometimes accidentally discovered
or detected during self-examination following the development of systemic symptoms.
❖ In about 3 percent of all cases of IM, the gross cervical lymphadenopathy imparts a
“bull neck” appearance. Enlargement of lymph nodes usually begins two or three days
after the onset of the first symptoms and, by the end of the week, palpable
lymphadenopathy is present in 70-80 percent of all patients.

❖ Jaundice is a moderately important symptom of infectious mono as 8-10 percent of
patients eventually become visibly jaundiced. In most instances, however, it is not
noticed since it consists of only a transient icteric tint to the sclerae and mucous
membranes, lasting for a few days.
✔ Meningitis/Encephalitis (<1%)
✔ Hepatitis : > 90% of patients
✔ Hemolytic anemia
✔ Upper airway obstruction
o 0.1-1%, due to hypertrophy of tonsils and other lymph nodes of Waldeyer ring
o treatment with corticosteroids may be beneficial
✔ Splenic rupture : 0.1-0.2%
✔ Hematologic complications
o Hemophagocytic syndrome.
o Immune thrombocytopenic purpura occurs and may evolve to aplastic anemia.
o Accelerate hemolytic anemia in congenital spherocytosis or hereditary
elliptocytosis.
o Disseminated intravascular coagulation associated with hepatic necrosis has
occurred
✔ Neurologic complications : < 1%
o During the first 2 weeks.

o Negative for the heterophile antibody.
o Severe (fatal), complete recovery
o Aseptic meningitis, acute viral encephalitis, coma, meningitis, and
meningoencephalopathy.
o Hypoglossal nerve palsy, Bell palsy, hearing loss, brachial plexus neuropathy,
multiple cranial nerve palsies, Guillain-Barré syndrome, autonomic neuropathy,
gastrointestinal dysfunction secondary to selective cholinergic dysautonomia,
acute cerebellar ataxia, transverse myelitis.
✔ Cardiac and pulmonary complications
o Chronic interstitial pneumonitis.

o Myocarditis and pericarditis
✔ Autoimmune complications
o Autoimmune diseases and Reye syndrome have been associated with EBV
infection.
o Infectious mononucleosis stimulates production of many antibodies not directed
against EBV. These include autoantibodies, anti-I antibodies, cold hemolysins,
antinuclear antibodies, rheumatoid factors, cryoglobulins, and circulating
immune complexes. These antibodies may precipitate autoimmune syndromes.
✔ Miscellaneous complications
o Renal disorders: immune deposit nephritis, renal failure, paroxysmal nocturnal
hemoglobinuria.
o After cardiac bypass or transfusion, an infectious mononucleosis–like
syndrome: primary CMV infection > EBV.
o A syndrome of chronic fatigue, myalgias, sore throat, and mild cognitive
dysfunction occurring primarily in young adult females initially was attributed
to EBV. Current data suggest that EBV is not the etiologic agent.
The 3 classic criteria for laboratory confirmation are the following:
1) lymphocytosis
2) the presence of at least 10% atypical lymphocytes on peripheral smear
3) a positive serologic test for Epstein-Barr virus (EBV).
IV.2.11.7. PROGNOSIS
❖ Immunocompetent: full recovery in several months.

❖ The common hematologic and hepatic complications resolve in 2-3 months.
❖ Neurologic complications
o Children : resolve quickly
o Adults : neurological deficits
❖ All individuals develop latent infection: asymptomatic.

A. Medical Care:
◆ Self-limited illness: not require specific therapy.

◆ Inpatient therapy of medical and surgical complications may be required.
◆ Acyclovir (10 mg/kg/dose IV every 8h for 7-10 d)
◆ Short-course corticosteroids : prednisolone (1 mg/kg/d, max 60 mg/d for 7 days
and tapered over another 7 for:
o Marked tonsillar inflammation with impending airway obstruction
o Massive splenomegaly
o Myocarditis
o Hemolytic anemia
o Hemophagocytic syndrome
o Seizure and meningitis
B. Surgical Care for splenic rupture.
Activity:
◆ Depends on severity of the patient's symptoms.
◆ Extreme fatigue: bed rest for 1-2 weeks.
◆ Malaise may persist for 2-3 months.
◆ Patients should not participate in contact sports or heavy lifting for at least 2-3 weeks
◆ Some authors recommend avoiding activities that may cause splenic trauma for 2
months.
✔ Isolation is not required: low transmission.

✔ Avoid contact with saliva.
✔ Do not kiss children on the mouth.
✔ Maintain clean conditions: day care, avoid sharing toys.
✔ EBV can be transmitted by blood transfusion and by bone marrow transplantation.
✔ Vaccine development is proceeding, although the role of a vaccine is unclear.
IV.2.12. CYTOMEGALOVIRUS INFECTION

Cytomegalovirus (from the Greek cyto-, "cell", and -megalo-, "large") is a herpes viral genus
of the Herpesviruses group: in humans it is commonly known as HCMV or Human Herpesvirus
5 (HHV-5).
Transmission of HCMV occurs from person to person through bodily fluids. Infection requires
close, intimate contact with a person excreting the virus in their saliva, urine, or other bodily
fluids. CMV can be sexually transmitted and can also be transmitted via breast milk,
transplanted organs, and rarely from blood transfusions.
IV.2.12.3. CMV DISEASES
The most common types of infections by CMV can be grouped as follows:

● Fetus/Infant:
o Congenital CMV infection
o Perinatal CMV infection
● Immunocompetent patient:
o CMV mononucleosis
o Post-transfusion CMV - similar to CMV mononucleosis
● Immunocompromised patient:
o CMV pneumonitis
o CMV GI disease
o CMV retinitis
o Polyradiculopathy, transverse myelitis, and subacute encephalitis
Pregnancy and congenital infection
HCMV is one of the TORCH infections that lead to congenital abnormalities. These are:
toxoplasmosis, rubella, cytomegalovirus, and herpes simplex. Congenital HCMV infection
occurs when the mother suffers a primary infection (or reactivation) during pregnancy. Due to
the lower seroprevalence of HCMV in industrialized countries and higher socioeconomic
groups, congenital infections are actually more common in poorer communities, where more
women of child-bearing age are already seropositive. Healthy pregnant women are not at

special risk for disease from CMV infection. When infected with CMV, most women have no
symptoms and very few have a disease resembling infectious mononucleosis. It is their
developing fetuses that may be at risk for congenital CMV disease. HCMV is the most common
cause of congenital infection in humans and intrauterine primary infections are second only to
Down's syndrome as a known cause of mental retardation.
For infants who are infected by their mothers before birth, two potential adverse scenarios
exist:
● Generalized infection may occur in the infant, and can cause complications such as low
birth weight, microcephaly, seizures, petechial rash similar to the "blueberry muffin"
rash of congenital rubella syndrome, and moderate hepatosplenomegaly (with
jaundice). Though severe cases can be fatal, with supportive treatment most infants with
CMV disease will survive. However, from 80% to 90% will have complications within
the first few years of life that may include hearing loss, vision impairment, and varying
degrees of mental retardation.
● Another 5% to 10% of infants who are infected but without symptoms at birth will
subsequently have varying degrees of hearing and mental or coordination problems.
Recommendations for pregnant women with regard to CMV infection:
● Throughout the pregnancy, practice good personal hygiene, especially hand washing
with soap and water, after contact with diapers or oral secretions (particularly with a
child who is in day care).
● Women who develop a mononucleosis-like illness during pregnancy should be
evaluated for CMV infection and counseled about the possible risks to the unborn child.
● Laboratory testing for antibody to CMV can be performed to determine if a woman has
already had CMV infection.
● Recovery of CMV from the cervix or urine of women at or before the time of delivery
does not warrant a cesarean section.
● The demonstrated benefits of breast-feeding outweigh the minimal risk of acquiring
CMV from the breast-feeding mother.
Recommendations for individuals providing care for infants and children:

● Employees should be educated concerning CMV, its transmission, and hygienic
practices, such as hand washing, which minimize the risk of infection.
● Susceptible non pregnant women working with infants and children should not
routinely be transferred to other work situations.
● Pregnant women working with infants and children should be informed of the risk of
acquiring CMV infection and the possible effects on the unborn child.
Immunocompromised patients
CMV hepatitis may cause fulminant liver failure. Specific disease entities recognised in those
people are cytomegalovirus retinitis (inflammation of the retina, characterised by a "pizza pie
appearance" on ophthalmoscopy) and cytomegalovirus colitis (inflammation of the large
bowel).
Exposing immunosuppressed patients to outside sources of CMV should be minimized to avoid

the risk of serious infection. Whenever possible, patients without CMV infection should be
given organs and/or blood products that are free of the virus.
Patients without CMV infection who are given organ transplants from CMV-infected donors
should be given prophylactic treatment with valganciclovir (ideally) or ganciclovir and require
regular serological monitoring to detect a rising CMV titre, which should be treated early to
prevent a potentially life-threatening infection becoming established.
Potential role in vascular disease and hypertension
CMV infection may be linked to the development of arterial hypertension. CMV infection
stimulated cytokines – IL6, TNF, and MCP1 – in the infected mice indicating that the infection
led to an inflammatory response in vessels and other tissues. Further, renin and angiotensin II
release were increased in these animals as additional factors to lead to hypertension. In humans
CMV infection has been demonstrated in the aortic smooth muscle cells from patients with
abdominal aortic aneurysms suggesting that CMV infection contributes to vascular disease.
Most infections with CMV are not diagnosed because the virus usually produces few, if any,
symptoms and tends to reactivate intermittently without symptoms. Laboratory tests that detect

CMV antibodies have been developed. In addition, the virus can be cultured from specimens
obtained from urine, throat swabs, bronchial lavages and tissue samples to detect active
infection. Both qualitative and quantitative polymerase chain reaction (PCR) testing for CMV
are available as well, allowing physicians to monitor the viral load of CMV-infected patients.
A virus culture can be performed at any time the patient is symptomatic. Laboratory testing for
antibody to CMV can be performed to determine if a woman has already had CMV infection.
ELISA is the most commonly available serologic test for measuring antibody to CMV.
Cytomegalovirus Immune Globulin Intravenous (Human) (CMV-IGIV) is an immunoglobulin

G (IgG) containing a standardized amount of antibody to Cytomegalovirus (CMV). It may be
used for the prophylaxis of cytomegalovirus disease associated with transplantation of kidney,
lung, liver, pancreas, and heart.
Alone or in combination with an antiviral agent, it has been shown to:
● Reduce the risk of CMV-related disease and death in some of the highest-risk transplant
patients
● Provide a measurable long-term survival benefit
● Produce minimal treatment-related side effects and adverse events.
Ganciclovir (Cytovene®) treatment is used for patients with depressed immunity who have
either sight-related or life-threatening illnesses. Valganciclovir (Valcyte®) is an antiviral drug
that is also effective and is given orally.
Vaccine
Cytomegalovirus vaccines are still in the research and development stage.
CHAPTER V. FUNGAL DISEASES
INTRODUCTION

Fungal infections are infections caused by a fungus, a type of microorganism. Two common
causes of fungal infections are a fungus called tinea and yeast infections caused by the fungus
Candida albicans.
The incidence of fungal infections is increasing greatly, mostly due to opportunistic fungal
infections related weakened immune systems (due to HIV, cancer, and other diseases; and to
modern medical practices such as the use of intensive chemotherapy and drugs that suppress
the immune system). However, fungal infections like vaginal yeast infections and athlete's
foot are common even in healthy people.
Many kinds of fungi live inside the human body in peaceful equilibrium with it. When the
body's immune system is weakened, the balance can be disturbed, and the disease occurs.
V.1. CANDIDIASIS
V.1.1 DEFINITION
Candidiasis or thrush or candidosis or yeast infection is a fungal infection (mycosis) of any of

the Candida species, of which Candida albicans is the most common. Candidiasis
encompasses infections that range from superficial, such as oral thrush and vaginitis, to
systemic and potentially life-threatening diseases. Candida infections of the latter category are
also referred to as candidemia and are usually confined to severely immunocompromised
persons, such as cancer, transplant, and AIDS patients.
Superficial infections of skin and mucosal membranes by Candida causing local inflammation
and discomfort are however common in many human populations. While clearly attributable
to the presence of the opportunistic pathogens of the genus Candida, candidiasis describes a
number of different disease syndromes that often differ in their causes and outcomes.
Commonly referred to as a yeast infection, it is also technically known as candidosis,
moniliasis, and oidiomycosis.
V.1.2 CAUSE
Candida albicans is the cause of candidiasis
A weakened or undeveloped immune system or metabolic illnesses such as diabetes are

significant predisposing factors of candidiasis. Diseases or conditions linked to candidiasis

include HIV/AIDS, mononucleosis, cancer treatments, steroids, stress, and nutrient deficiency.
In penile candidiasis, the factors include sexual intercourse with an infected individual, low
immunity, antibiotics, and diabetes. Male genital yeast infection is less common, and incidence
of infection is only a fraction of that in women; however, yeast infection on the penis from
direct contact via sexual intercourse with an infected partner is not uncommon. Candida
species are frequently part of the human body's normal oral and intestinal flora. Treatment with
antibiotics can lead to eliminating the yeast's natural competitors for resources, and increase
the severity of the condition.
V.1.3 CLASSIFICATION
Candidiasis may be divided into the following types:
● Oral candidiasis (Thrush)

● Perlèche (Angular cheilitis)
● Candidal vulvovaginitis
● Candidal intertrigo
● Diaper candidiasis
● Congenital cutaneous candidiasis
● Perianal candidiasis
● Erosio interdigitalis blastomycetica
● Chronic mucocutaneous candidiasis
● Systemic candidiasis
● Antibiotic candidiasis (Iatrogenic candidiasis)
V.1.4 SIGNS AND SYMPTOMS
Most candidial infections are treatable and result in minimal complications such as redness,
itching and discomfort, though complication may be severe or fatal if left untreated in certain
populations. In immunocompetent persons, candidiasis is usually a very localized infection of
the skin or mucosal membranes, including the oral cavity (thrush), the pharynx or esophagus,
the gastrointestinal tract, the urinary bladder, or the genitalia (vagina, penis).
Candidiasis is a very common cause of vaginal irritation, or vaginitis, and can also occur on
the male genitals. In immunocompromised patients, Candida infections can affect the

esophagus with the potential of becoming systemic, causing a much more serious condition, a
fungemia called candidemia.
Children, mostly between the ages of three and nine years of age, can be affected by chronic
mouth yeast infections, normally seen around the mouth as white patches. However, this is not
a common condition.
Symptoms of candidiasis may vary depending on the area affected. Infection of the vagina or
vulva may cause severe itching, burning, soreness, irritation, and a whitish or whitish-
gray cottage cheese-like discharge, often with a curd-like appearance. These symptoms are
also present in the more common bacterial vaginosis. Symptoms of infection of the male
genitalia include red patchy sores near the head of the penis or on the foreskin, severe itching,
or a burning sensation. Candidiasis of the penis can also have a white discharge, although
uncommon.
V.1.5 DIAGNOSIS
In addition to clinical manifestations, the diagnosis of a yeast infection is done either via
microscopic examination or culturing.
V.1.6 TREATMENT
In clinical settings, candidiasis is commonly treated with antimycotics. The antifungal drugs
commonly used to treat candidiasis are topical clotrimazole, topical nystatin, fluconazole,
and topical ketoconazole. For example, a one-time dose of fluconazole (as Diflucan 150-mg
tablet taken orally) has been reported as being 90% effective in treating a vaginal yeast
infection.
In severe infections (generally in hospitalized patients), amphotericin B, caspofungin, or

voriconazole may be used. Local treatment may include vaginal suppositories or medicated
douches.
C. albicans can develop resistance to antimycotic drugs, such as fluconazole, one of the drugs
that are often used to treat candidiasis. Recurring infections may be treatable with other anti-
fungal drugs, but resistance to these alternative agents may also develop.

V.2. PITYRIASIS VERSICOLOR OR TINEA VERSICOLOR
2.2.1 DEFINITION
A common chronic, noninflammatory and usually symptomless disorder, characterized by the

occurrence of multiple macular patches of all sizes and shapes, and varying in pigmentation
from fawn-colored to brown. It is seen most frequently in hot, humid, tropical regions. The
term “versicolor” refers to the fact that it causes the affected skin to change color and become
either lighter or darker than surrounding skin. Tinea versicolor is a chronic fungal infection of
the skin.
V.2.2 CAUSE
Tinea versicolor is relatively common. It is caused by yeast called Malassezia furfur, a type of
yeast that is normally found on human skin without causing problems and therefore, becomes
pathogenic under certain circumstances. The condition is most common in adolescent and
young adult males. It typically occurs in hot climates.
V.2.3 SYMPTOMS
The main symptom is patches of discolored skin with sharp borders (edges) and fine scales.
The patches are often dark reddish-tan in color. The most common sites are the back, shoulders,
underarms, upper arms, chest, and neck. Affected areas do not darken in the sun (skin may
appear lighter than surrounding healthy skin)
In African Americans, there may be loss of skin color (hypopigmentation) or an increase in

skin color (hyperpigmentation).
Other symptoms include: increased sweating, itching
V.2.4 DIAGNOSIS
A skin scraping that is examined under a microscope should show the yeast.
2.2.5 TREATMENT
Treatment consists of applying antifungal medicines to the skin including: clotrimazole,

ketoconazole, miconazole, etc

V.2.6 PROGNOSIS
Though tinea versicolor is easily treated, pigment changes may last for months after treatment.
The condition may come back during the warm months.
V.2.7 PREVENTION
People with a history of tinea versicolor should try to avoid excessive heat or sweating.
V.3. DERMATOPHYTIES
V.3.1 DEFINITION
Dermatophytosis or ringworm is a clinical condition caused by fungal infection of the skin in

humans, pets such as cats, and domesticated animals such as sheep and cattle. It is caused by
fungi of several different species. The dermatophytes feed on keratin, the material found in the
outer layer of skin, hair, and nails. These fungi thrive on skin that is warm and moist, but may
also survive directly on the outsides of hair shafts, or in their interiors. In pets, the fungi
responsible for the disease survive in skin and on the outer.
Misdiagnosis and treatment of ringworm with a topical steroid, a standard treatment of the
superficially similar pityriasis rosea, can result in tinea incognito, a condition where ringworm
fungus will grow without typical features like a distinctive raised border.
V.3.2 CLASSIFICATION
A number of different species of fungi are involved. Dermatophytes of the genera Trichophyton
and Microsporum are the most common causative agents. These fungi attack various parts of
the body and lead to the following conditions:
● Dermatophytosis
o Tinea pedis (athlete's foot) affects the feet
o Tinea unguium affects the fingernails and toenails
o Tinea corporis affects the arms, legs, and trunk with ringworm
o Tinea cruris (jock itch) affects the groin area
o Tinea manuum affects the hands and palm area
o Tinea capitis affects the scalp

o Tinea barbae affects facial hair
o Tinea faciei (face fungus) affects the face
● Other superficial mycoses
o Tinea versicolor caused by Malassezia furfur
o Tinea nigra caused by Hortaea werneckii
V.3.3 SIGNS AND SYMPTOMS
Infections on the body may give rise to typical enlarging raised red rings of ringworm, infection
on the skin of the feet may cause athlete's foot and in the groin jock itch. Involvement of the
nails is termed onychomycosis, and they may thicken, discolour, and finally crumble and fall
off. Dermatophytosis tends to get worse during summer, with symptoms alleviating during the
winter. Animals such as dogs and cats can also be affected by ring worm and the disease can
be transmitted between animals and humans (zoonotic disease).
V.3.4 DIAGNOSIS
Microscopic test: Hairs are taken from around the infected area and places them in a staining
solution to view under the microscope. Fungal spores may be viewed directly on hair shafts.
This technique identifies a fungal infection in about 40%-70% of the infections but cannot
identify the species of dermatophyte.
Culture Test: This is the most effective but also the most time-consuming way to determine if
there is ringworm on a pet.
V.3.5 TREATMENT
✔ Antifungal treatments include topical agents such as Miconazole, Terbinafine,

Clotrimazole, Ketoconazole, or Tolnaftate applied twice daily until symptoms resolve
usually within one or two weeks. Topical treatments should then be continued for a
further 7 days after resolution of visible symptoms to prevent recurrence. The total
duration of treatment is therefore generally two weeks, but may be as long as three.
✔ In more severe cases or where there is scalp ringworm, systemic treatment with oral
medications may be given.
✔ To prevent spreading the infection, lesions should not be touched, and good hygiene
maintained with washing of hands and the body. Treatment in pets requires both

systemic and oral treatment with most of the same drugs used in humans (Terbinafine,
Fluconazole, or Itraconazole) plus topical therapy.
V.3.6 PREVENTION
● Avoidance of sharing clothing, sports equipment, towels, or sheets.

● Washing clothes in hot water with fungicidal soap after suspected exposure to
ringworm.
● Avoidance of walking barefoot, instead wearing appropriate protective shoes to the
beach and flip-flops in locker rooms.
● After being exposed to places where the potential of being infected is great, one should
wash with an antibacterial and anti-fungal soap or one that contains tea tree oil
● Avoid touching pets with bald spots as they are often carriers of the fungus.
V.4. CRYPTOCOCCOSIS
V.4.1 DEFINITIONS
Also called cryptococcal disease, cryptococcosis is a potentially fatal disease caused by

Cryptococcus neoformans.
V.4.2 CAUSES
Cryptococcosis is a defining opportunistic infection for AIDS. Other conditions which pose an
increased risk include certain lymphomas (E.g.: Hodgkin’s lymphoma), patients on long-term
corticosteroid therapy, etc
Cryptococcus neoformans, the fungus that causes this disease, is ordinarily found in soil.
V.4.3 PATHOGENESIS
It enters and infects the body through the lungs. Once inhaled, infection with cryptococcosis
may go away on its own, remain in the lungs only, or spread throughout the body (disseminate).
Most cases are in people with a weakened immune system, such as those with HIV infection,
taking high doses of corticosteroid medications, cancer chemotherapy, or who have Hodgkin's
disease. In people with a normal immune system, the lung form of the infection may have no
symptoms. In people with impaired immune systems, the cryptococcus organism may spread

to the brain. Neurological (brain) symptoms begin gradually. Most people with this infection
have meningoencephalitis (swelling and irritation of the brain and spinal cord) when they are
diagnosed. Cryptococcosis is one of the most common life-threatening fungal infections in
people with AIDS.
V.4.4 SYMPTOMS
In humans, C.neoformans causes three types of infections:
1) Wound or cutaneous cryptococcosis

2) Pulmonary cryptococcosis
3) Cryptococcal meningitis
Most symptoms in cryptococcal disease are the following:
● Blurred vision or double vision (diplopia)

● Bone pain or tenderness of the breastbone (sternum)
● Chest pain
● Confusion
● Cough (Often dry)
● Fatigue
● Fever
● Headache
● Nausea
● Skin rash {pinpoint red spots (petechiae)}
● Sweating (unusual, excessive at night)
● Swollen glands
● Unintentional weight loss and weakness
Note: People with a normal immune system may have no symptoms at all.
V.4.5 DIAGNOSIS
● Sputum culture and stain

● Lung biopsy
● Bronchoscopy

● Cerebrospinal fluid culture and stain for Cryptococcus
● Chest x-ray
● Cryptococcal antigen test (looks for a certain molecule that the Cryptococcus fungus
can shed into the blood)
● Blood culture may be positive in heavy infections
V.4.6 TREATMENT
Some infections require no treatment. Even so, there should be regular check-ups for a full year
to make sure the infection has not spread. If there are lung lesions or the disease spreads,
antifungal medications are prescribed. These drugs may need to be taken for a long time.
Medications include:
● Intravenous Amphotericin B combined with oral Flucytosine

● Fluconazole
V.4.7 PROGNOSIS
Central nervous system involvement often causes death or leads to permanent damage.
V.4.8 POSSIBLE COMPLICATIONS
● Relapse of infection
● Meningitis
● Hydrocephalus
● Encephalitis
● Damage to the optic nerve
● Inflammation of the blood vessels in the brain (brain-stem vasculitis)
● Permanent brain or nerve damage
● Side effects of medications (such as Amphotericin B) can be severe
V.4.9 PREVENTION
o Take the lowest doses of corticosteroid medications possible.

o Practice safe sex to reduce the risk of getting HIV and the infections associated with a
weakened immune system.

V.5. ASPERGILLOSIS
V.5.1 DEFINITION
Aspergillosis is an infection, growth, or allergic response due to the Aspergillus fungus.

It is the name given to a wide variety of diseases caused by fungi of the genus Asergillus. And
the most common forms are allergic bronchopulmonary aspergillosis, pulmonary
aspergilloma and invasive aspergillosis.
V.5.2 CAUSE
Aspergillosis is caused by a fungus (Aspergillus), which is commonly found growing on dead

leaves, stored grain, compost piles, or in other decaying vegetation. It can also be found on
marijuana.
Although most people are frequently exposed to aspergillus, infections caused by the fungus
rarely occur in people with a normal immune system. The rare infections caused by aspergillus
include pneumonia and fungus ball (aspergilloma).
There are several forms of aspergillosis:
● Pulmonary aspergillosis: allergic bronchopulmonary type which is an allergic reaction

to the fungus that usually develops in people who already have lung problems (such as
asthma or cystic fibrosis).
● Pulmonary aspergilloma: is a growth (fungus ball) that develops in an area of previous
lung disease or lung scarring (such as tuberculosis or lung abscess).
● Pulmonary aspergillosis invasive type which is a serious infection with pneumonia
that can spread to other parts of the body. This infection occurs almost exclusively in
people with weakened immune systems due to cancer, AIDS, leukemia, organ
transplantation, chemotherapy, or other conditions or medications that lower the
number of normal white blood cells or weaken the immune system.
V.5.3 SYMPTOMS
Symptoms depend on the type of infection. For symptoms of aspergillosis-related growth, see
aspergilloma.

Symptoms of allergic bronchopulmonary aspergillosis may include:
● Cough
● Coughing up blood or brownish mucous plugs
● Fever and chills
● Generalized ill feeling (malaise)
● Wheezing
● Weight loss
● Recurrent episodes of lung airway obstruction
Additional symptoms seen in invasive aspergillosis depend on the part of the body affected,
and may include:
● Bone pain
● Blood in the urine
● Chest pain
● Chills
● Decreased urine output
● Endocarditis
● Headaches
● Increased sputum production, which may be bloody
● Meningitis
● Shortness of breath
● Sinusitis
● Skin sores (lesions)
● Vision problems
V.5.4 DIAGNOSIS
Tests to diagnose Aspergillus infection include:
● Aspergillosis antibody test

● Chest x-ray
● Complete blood count

● CT scan
● Galactomannan (a molecule derived from the fungus, which is sometimes found in the
blood)
● Sputum stain and culture for Aspergillus
● Tissue biopsy (see bronchoscopy with transtracheal biopsy)
V.5.5 TREATMENT
o A fungus ball is usually not treated (with antifungal medicines) unless there is bleeding
into the lung tissue. In that case, surgery is required.
o Invasive aspergillosis is treated with several weeks of an antifungal drug called
voriconizole. It can be given orally or in an IV. Amphotericin B, or itraconazole can
also be used.
o Endocarditis caused by Aspergillus is treated by surgically removing the infected heart
valves. Long-term amphotericin B therapy is also needed.
o Antifungal drugs do not help people with allergic aspergillosis. Allergic aspergillosis is
treated with immunosuppressive drugs (most often prednisone taken by mouth).
V.5.6 PROGNOSIS
✔ People with allergic aspergillosis usually get better gradually, with treatment.
✔ It is common for the disease to come back (relapse) and need repeat treatment.
✔ If invasive aspergillosis may eventually leads to death.
V.5.7 POSSIBLE COMPLICATIONS
● Amphotericin B can cause kidney impairment and unpleasant side effects such as fever
and chills
● Bronchiectasis (permanent scarring of the small sacs in the lungs)
● Invasive lung disease can cause massive bleeding from the lung
● Mucous plugs
● Permanent airway obstruction
● Respiratory failure
V.5.8 PREVENTION

o Be careful when using medications that suppress the immune system.
o Prevention of AIDS prevents certain diseases, including aspergillosis, that are
associated with a damaged or weaken immune system.

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COLLEGE OF MEDICINE AND HEALTH SCIENCES

SCHOOL OF NURSING AND MIDWIFERY

MODULE NAME: FUNDAMENTALS OF COMMUNITY HEALTH

UNIT NAME: COMMUNICABLE DISEASES

YEAR OF STUDY: 1ST YEAR NURSING AND MIDWIFERY

ACADEMIC YEAR: 2015-2016

4.1. General Information

4.1.8 Resistance to infectious diseases (immunity)

FCH-- Communicable Diseases (2015-2016≈>2020)/j.p poly-. 1

4.3. Parasitic diseases

4.4. Viral diseases

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4.5. Fungal diseases

CHAPTER I. INTRODUCTION TO COMMUNICABLE DISEASES

I.1 DEFINITIONS OF KEY TERMS

Infection: Invasion by and multiplication of pathogenic microorganisms (bacteria, fungi,

Symptom: A symptom is a change in body function felt by the patient.

FCH-- Communicable Diseases (2015-2016≈>2020)/j.p poly-. 3

Syndrome: A collection of signs and symptoms characterizing a disease or an abnormality.

Etiology: the cause of a disease or abnormal condition; or a branch of medical science

Koch's postulates (as addressed in 1800s):

✔ The functional changes associated with or resulting from disease or injury.

Pathogenecity: The ability of a microbe to cause disease.

Virulence: The degree of pathogenicity in a microorganism.

Chronic infection: An infection characterized by delayed onset and slow progression.

FCH-- Communicable Diseases (2015-2016≈>2020)/j.p poly-. 4

Opportunistic infection: An infection caused by microorganisms that are commonly found in

Direct mechanisms of disease transmission: Directly from person to person

Indirect mechanisms of disease transmission: By the intermediate agents or objects.

FCH-- Communicable Diseases (2015-2016≈>2020)/j.p poly-. 5

Parasitology: The study of parasitic diseases

I.2 FACTORS NECESSARY FOR THE EXISTENCE OF A COMMUNICABLE

The presence of a particular communicable disease in an area at a certain time depends on

The three factors interact in a triangular manner as follows:

FCH-- Communicable Diseases (2015-2016≈>2020)/j.p poly-. 6

I.3 THE HOST AND INFECTION

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I.4 PHASES OF AN INFECTIOUS ILLNESS EVOLUTION

A. THE INCUBATION PHASE

✔ The amount of absorbed or inoculated germs

C.THE STATE PERIOD OR PHASE

D. DEFERVESCENCE PHASE OR PERIOD

FCH-- Communicable Diseases (2015-2016≈>2020)/j.p poly-. 8

E. THE CONVALESCENT PHASE OR PERIOD

I.5 CARRIER OF INFECTION

⮚ TYPES OF CARRIERS OF DISEASES

I.6 EPIDEMIOLOGY OF THE INFECTIOUS AND PARASITIC DISEASES

A. TRANSMISSION CYCLE OF AN INFECTIOUS AGENT

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1. SOURCES OF INFECTIOUS DISEASES

● The sick person or healthy carriers

On the basis of routes of transmission, common communicable diseases can be conveniently

FCH-- Communicable Diseases (2015-2016≈>2020)/j.p poly-. 10

B. MODES OF TRANSMISSION OF AN INFECTIOUS DISEASE

There are two modes of transmission:

✔ Indirect transmission: in indirect transmission an agent is carried from a reservoir to a

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C.CHAIN OF SPREAD OF COMMUNICABLE DISEASES