INFECTIOUS DISEASES

Dr Muawia E A Idris
MD Clinical Paediatrics & Child
Health
Associate prof of Paediatrics
 Viral
7.1.
epstein-bar
measles virus
8.2.
cytomegalovirus
rubella
9.3.
HIV mumps
10.
4.poliomyelitis
herpes simplex
11.5.Influenza
varicella zoster
6. respiratory syncitial virus
 Bacterial

1. Diphtheria
2. Pertussis
3. Tetanus
4. Tuberculosis
 Protozoal & helminthic

1. Malaria
2. Leishmaniasis
3. Schistosomiasis
 Clinical infectious syndromes

1. Septicaemia
2. Meningitis
3. Viral hepatitis
4. Congenital infections
 Immunization
 EPI VACCINES: OPV, IPV, BCG,
Pentavaccine, Rota, pneumococcal,
measles, MenA
 Hib, HBV, MMR, yellow fever,
meningococcal
 Other vaccines
 Vaccines under development
Measles
 Measles
 Acute viral infection characterized by
maculopapular rash and accompanied by
fever
 Aetiology: measles virus- RNA- paramyxo-
one serotype
 Epidemiology: endemic- irregular epidemics-
similar to smallpox
 Measles
 Transmission: droplet spray- respiratory
tract- very contagious
 Infection occurs during prodromal stage- pt.
is infectious up to 5-7 days from appearance
of rash
 Disease confers life-long immunity
 Rare before 4-6 months of age
 Pathogenesis:
oEssential lesions → skin and mucosa
oLymphoid hyperplasia
oKoplik’s spots
oInterstitial pneumonitis (Hecht giant cell)
oEncephalomyelits-perivascular
demyelination
oSSPE- degeneration+ inclusion bodies
 Clinical picture
 Incubation period: 10-12 days to prodrome-
2-4 days to appearance of rash
 Prodromal stage: 3-5 days- low to moderate
grade fever- dry cough- coryza,
conjunctivitis & photophobia
Koplik’s spots pathognomonic: greyish white
dots on reddish base- opposite lower molars
in buccal mucosa- disappears rapidly 12-18
hours
 Clinical picture
 Rash phase: temperature rises abruptly as
rash appears- 40° or higher
 Rash: starts as faint macules in forehead,
upper lateral neck, hairline, behind ears→
maculopapular face downwards. When it
reaches feet it fades from face downwards
 Severity of measles is directly related to
extent and confluence of rash
 Severe: entire skin,palms,soles,swollen face
 Rash is slightly hemorrhagic- in severe
cases→ petechiae & ecchymoses
 Itching is absent or slight
 Ends by desquamation & brownish
discoloration
 Absence of rash is rare except in :
1. administration of immunoglobulins
2. HIV
3. Infants < 9 months
 Hemorrhagic (black measles)
 Atypical measles: recipients of killed
measles vaccine
 No prodrome except fever, Koplik rare
 Severe headache, abd pain, vomiting,
myalgia, pneumonia with pleural effusion
 Rash first on palms, wrist, soles, and
ankles- centripetal
 Rash maculopapular→ vesicular →purpuric
 Diagnosis
 Clinical
 Serology
 Tissue culture
 WBC ↓ with relative lymphocytosis
 Differential diagnosis
 Rubella
 Herpes simplex
 Infectious mononucleosis
 Kawsaki
 Drug rash
 Other viruses: echo- coxackie, adenovirus
 Treatment
 Supportive: bed rest, analgesics, fluids,
humidification-warm
 Antibiotics only for 2ry bacterial infections
eg conjunctivitis, staph pneumonia
 Encephalitis needs intensive supportive
care
 Vitamin A
 Complications
 Malnutrition
Otitis media
 Pneumonia
GBS- hemiplegia
 Encephalitis
Cerebral thrombophlebitis
1-2/1000
 Exacerbatesneuritis
Retrobulbar TB
 Myocarditis
Cancrum oris, gastroenteritis, appendicitis
 Purpura fulminans
Conjunctivitis, keratitis,
→ DIC corneal
→ gangrene
ulcers
 Myocarditis ECG changes
 Prevention
 Isolation from 7th d after exposure to 5 days
after rash disappears
 Vaccination
 Post-exposure prophylaxis: passive
immunization with immunoglobulins within 6
days after exposure
Poliomyelitis
 Poliomyelitis
 Aetiolgy: RNA enterovirus- 3 serotypes 1,2,3
 Transmission occurs from infected
individuals by pharyngeal secretions &
faeces
 Main lesions in ant horn cells of spinal cord
 Lesions occur in: spinal cord, medulla,
midbrain, thalamus & hypothal, pallidum,
motor cortex
 Areas spared: entire cerebral cortex except
for motor area & white matter of sp cord
 Poliovirus enters via oral route→ multiply in
tonsils & intestines→ LN → blood stream →
nervous system
 Incubation 1-3 weeks
 Clinical picture
 Inapparent infection 90-95%
 Abortive polio: fever, malaise, anorexia,
vomiting, headache, sore throat,
constipation
 Non-paralytic polio: as abortive but
more severe- meningeal signs: Kernig’s
sign, Brudzinski’s sign, tripod position,
kissing sign, head drop, bladder paralysis,
reflexes normal
 Paralytic polio: nonparalytic+ weakness
in one or more groups of muscles
o Asymmetrical flaccid paralysis
o Bladder can be affected
o Respiratory muscles, bulbar polio, arryhthmias,
BP instability
o Spinal, spinal resp, bulbar
o Meningitis, meningoencephalitis
 Diagnosis
 Clinical: asymmetrical acute flaccid
paralysis
 Stool culture, other body secretions
 Serology
 Differential diagnosis
 GBS
 Myasthenia gravis
 Polio-like: coxackie, echo, & other viruses
 Familial periodic syndrome
 Post-diphthritic neuropathy
 Lead toxicity
 Pseudoparalysis
 Complications
 Respiratory failure
Melena
 Acute gastric dilatation
Hypercalcaemia & nephrocalcinosis
 Mild hypertension
Pneumonia
 Cardiac retention
Urinary arrhythmias
 Pulmonary oedema
Constipation
 Pulmonary embolism
 Treatment & prevention
 Supportive
 Physiotherapy
 Orthopaedic care
 Respiratory care
 Isolation
 Vaccination: OPV or IPV
 https://polioeradication.org/
 https://www.who.int/home
 https://
www.who.int/home/search?indexCatalogue=
genericsearchindex1&searchQuery=poliomy
elitis&wordsMode=AnyWord
Mumps
 Mumps
 RNA- paramyxo- one serotype
 Endemic- all seasons esp late winter
 Transmission 24 hr before & 3 days after
swelling
 Resp tract→ blood → salivary glands &
other glands
 Clinical picture
 Incubation: 2-3 weeks
 30-40% subclinical
 Prodromal stage is rare in children
 Salivary glands swelling 25% unilateral- 10-
15% only submandibular
 Diagnosis: clinical, serology, viral culture,
increased serum amylase
 Δ /Δ:
HIV, influenza, parainfluenza
acute suppurative parotitis
calculs
 Complications
meningoencephalitis, arthritis
epididimitis, orchitis, oophoritis,
pancreatitis, thyroiditis, myocarditis,
deafness, ocular complications
 Treatment & prevention
 Supportive – avoid aspirin & sour liquids
 Steroids in case of orchitis
 Live-attenuated vaccine
Diphtheria
 Diphtheria
 Localized infection of mucosa or skin
caused by corynebacterium diphtheriae.
 A characteristic membrane may be present
 Aetiology: Corynebact. Species aerobic
non-encapsulated, non-sporeforming, non-
motile, G+ve bacilli
 3 biotypes: mitis, gravis, intermedius
 Toxinogenic (tox+) or nontoxinogenic(tox-)
 Exclusively human infection
 Disease transmitted by carriers-
contaminated milk & infected food-handlers
 Affects mainly children < 15 y- vaccination→
adolescents & adults
 Largest outbreak Soviet Union 1990-95
 In tropics cutaneous diph > resp diphth
usually tox-
 Pathogenesis: mucosa & skin- superficial
layers→ local infl reaction
 Virulence of bacteria: ability to produce
exotoxin → enz inhibitors+ tissue necrosis
 Pseudomembrane: necrotic coagulum of
organisms+ epith cells+ fibrin+ leucocytes +
erythrocytes. Greyish brown- adherent-
removal difficult → bleeding submucosa
 Clinical picture
 Incubation: 2-4 days
 Resp tract: affects tonsils, pharynx, nose, &
larynx
 Moderate fever
 Purulent nasal discharge, sore throat, dysphagia,
hoarse voice
 Tonsillar membrane, uvula, soft palate, oropharynx,
glottis → soft tissue oedema → bull neck
 Larynx, trachea, bronchi → hoarseness, stridor,
dyspnoea, croupy cough
 Toxic appearance
 Skin: indolent, non-progressive, non-
healing, superficial ulcer with membrane
 Other sites:
Otitis externa
Conjunctivitis
Vulvovaginitis
 Complications
 Toxic cardiomyopathy
10-25% of cases– 50-60% of deaths
2nd-3rd week
Tachycardia out of proportion to fever
↑PR interval- ST-T changes in ECG
Dilated & hypertrophic cardiomyopathy
Arrhythmias, HF
Recovery is usual- some conduction defects
 Toxic neuropathy
10%
1st 2 weeks
Bulbar dysfunction
Peripheral neuritis 1-3 months- proximal
Resp failure
Parasthesia – glove & stocking
 Resp obstruction
 Rarely: pneumonia, renal failure,
encephalitis, cerebral infarction, pulm
embolism, endocarditis
 Diagnosis
 Clinical
 Culture
Differential diagnosis
 Streptococcal pharyngitis, inf mono,
candidiasis, Vincent’s angina,
thrombophlebitis of jugular veins,
impetigo
 Treatment
 Antitoxin 20000-40000 units→ phrynx-larynx
40000-60000 → nasopharyngeal
80000-100000 → extensive disease
 Antibiotics: penicillin, erythromycin,
rifampicin, tetracyclin for 14 days
 Bed rest for at least 2 weeks
 Prevention
 Isolation- resp. or contact
 Vaccination DT or dT every 10 years for life
Pertussis
 Pertussis (whooping cough)
 Caused by Bordetella pertussis- small non-
motile G-ve coccobacillus
 Only humans
 No chronic carriers
 Endemic worldwide
 Extremely infectious
 Neither natural disease nor vaccination
provide lifelong immunity
 Clinical picture
 Incubation 3-12 days
 Catarrhal stage: congestion, rhinorrhoea,
low-grade fever, sneezing, conjunctivitis
 Paroxysmal stage: dry intermittent irritative
paroxysmal cough
 Whoop: forceful insp gasp- infrequent < 3
months
 Cough lasts days to weeks
 Convalescent stage: ↓ number & severity of
cough
 Children < 3 mo have apnoea, choking,
cyanosis, or gasping cough
 There may be conj haemorrhge or petechiae
on upper part of body
 Diagnosis
 Clinical: cough for > 14 days + one of the
following
o Paroxysmal nature
o Whoop
o Post-tussive emesis
 Culture
 Serology
 Treatment & prevention
 Supportive
 Antibiotics: erythromycin
 Vaccination: whole cell or acellular
 Complications
 Apnoea
 2ry infection- pneumonia, OM
 CNS haemorrhage
 Rectal prolapse
 Dehydration – malnutrition
 Seizures
Tetanus
 Tetanus
 Caused by Clostridium tetani- motile, G+ve,
spore forming, obligate anaerobic bacteria
 Worldwide, endemic in developing countries
 Neonatal tetanus- 500,000 deaths/yr
 spores→ wounds → proliferation → tetanus
toxins(tetanospasmin) → neuromuscular
junction of motor nerves
 Blocks normal inhibition of antag muscles →
sustained contraction
 Clinical picture
 Incubation 2-14 days → months
 Trismus, stiffness, difficulty chewing,
dysphagia, neck spasm
 Risus sardonicus
 Opisthotonus
 Laryngeal & resp spasm → airway
obstruction
 Patient is conscious
Trismus
Risus sardonicus
 Seizures: tonic- seconds to minutes evoked
by light, touch, or noise
 Tetanus neonatorum 3-12 days
 Localized tetanus
 Cephalic tetanus- bulbar muscles

Diagnosis
 clinical
 Treatment
 Quiet dark room
 Wound debridement
 Tetanus immunoglobulin (TIG) 500 U IM up
to 3000- 6000
 Tetanus antitoxin (TAT) 50,000-100,000
units
 Antibiotics
 Muscle relaxants & anticonvulsants
 Complications
 Aspiration pneumonia
 Muscular lacerations, rhabdomyolysis
 Renal failure
 Bone fractures, spine
 Autonomic dysfunction
 Venous thrombosis, pulmonary embolism,
 gastric ulceration with or without hemorrhage,
 Paralytic ileus,
 decubitus ulceration
 Prevention
 Vaccination
 Wound management
 Passive immunization
Malaria
 Plasmodium sp. ( falciparum, vivax,
malariae, ovale)
 Transmitted by bite of female anopheles
mosquito
 Life cycle: sporozoites→ liver → schizont →
merozoites → RBC → ring stage &
trophozoite →schizont & merozoites →
rupture →re-invasion of new RBCs
 Epidemiology
 Endemicity depends on spleen rates &
parasite rate as follows:
Hypoendemic < 10%
Mesoendemic 11-50%
Hyperendemic > 50%
Holoendemic >75%
 Stable & unstable
 Clinical picture
 Fever
 Non-specific symptoms: anorexia malaise
chills rigors sweating irritability
 Vomiting, cough, diarrhoea
 Febrile convulsions
 Liver, spleen
 Anaemia, jaundice
 Severe malaria→ P falciparum
 Severe malaria
 Severe anaemia
Change of behaviour,
Hb < confusion
6gm/dl
 Altered consciousness, coma
Shock
 Convulsions
Haemoglobinuria
 Hypoglycaemia
Jaundice
 Acidosis tendency
Bleeding
 Pulmonary oedema
Generalized weakness
 Oliguria or ARF
Hyperparasitaemia >10%
 Thrombocytopaenia
 Congenital malaria: fever, refusal of feeding,
anemia, jaundice, hepatosplenomegaly
 Rare in endemic areas
 Other manifestations:
– Nephrotic syndrome: P malariae recurrent or
prolonged- non-selective proteinuria,
unresponsive to steroids or cytotoxic drugs,
treatment with antimalarials does not reverse
the renal disease
– Hyperreactive malarial splenomegaly ( tropical
splenomegaly syndrome):
frequent P falciparum infections, massive
enlargement of spleen, ↑ IgM, ↑titres of malarial
antibodies, hepatic sinusoidal lymphocytosis
– Resolves slowly with prolonged antimalarial
treatment
 Diagnosis
 Peripheral blood smear thick & thin
 Hyperparasitemia is defined as a parasite
count of greater than 250,000 per microliter
(>250,000/µl), or as having greater than 5%
of red blood cells parasitized.
 Serology :ICT antigen detecting strips
 Clinical
 Treatment
 Chloroquine
 Pyrimethamine-sulfadoxine
 Quinine
 Mefloquine
 Halofantrine
 Artemther
 Primaquine
 Treatment
 Due to chloroquine resistance new protocol
 Combination artesunate-based
 1st line: Artesunate+ sulfadoxine-
pyrimethamine
 2nd line: artemether+ lumefantrine
 Treatment of severe malaria: quinine
10mg/kg 8 hourly for 7 days
 Artesunate inj.
Acute bacterial meningitis
 Aetiology
 1st 2 months of life: maternal flora
• Group B streptococci
• G-ve bacilli
• Listeria monocytogenes
• Occasionally bacteria of older children
 Thereafter:
• Haemophilus influenzae type b
• S pneumoniae
• N meningitidis
 Epidemiology
 Endemic in tropical countries (meningitis belt)- N
mening
 Sporadic throughout the year
 Transmission by resp tract
 Risk factors:
 Lack of immunity
 Close contact
 Crowding & poverty
 Absence of breast feeding
 Racial predilection- male sex
 Splenic dysfunction
 Pathology & pathogenesis
 Meningeal exudate around brain, cerebellum, sp
cord, & veins
 Ventriculitis, subdural effusion
 Inflammation of spinal nerves
 ↑ICP
 SIADH
 Distant site → bactremia → meninges
 Sinusitis, OM, mastoiditis, orbital cellulitis, cranial
or vertebral osteomyelitis, injuries,
meningomyelocoeles
 Clinical picture
 2 presentations:
1. Rapid, dramatic, fulminant with shock,
purpura, DIC
2. After several days of an URT or GIT
symptoms
Meningococcaemia
 Clinical picture
 Non-specific findings:
fever, anorexia, poor feeding, URTI,
myalgia, arthralgia, hypotension, petechiae
or purpura
 Meningeal irritation:
neck rigidity, back pain, Kernig’s sign,
Brudzinski’s sign
 Kernig’s sign:
flexion of hip 90° + leg extension→ pain
 Brudzinski’s sign:
passive flexion of neck→ involuntary
flexion of knees & hips
 These signs may absent in children < 12-18
months of age
 ICP→ headache, vomiting, bulging
fontanelle, widening of sutures, 3rd,6th cranial
nerves palsies, ↑BP, ↓PR, stupor, coma,
papilloedema
 Clinical picture

 Focal neurological signs: 10-20% but up to

30% in pneumococci
 Convulsions focal or generalized 20-30%
 ↓ level of consciousness
 There may be photophobia
 Diagnosis
 LP & CSF analysis: cells, protein, glucose,
Gram stain, culture
 Blood culture: 80-90%
 Contraindications for LP:
1. ↑ICP
2. Shocked critically ill child
3. Local skin infection at site of LP
4. Thrombocytopaenia
 Pressure Protein Glucose
Condition WBC/mm³
mmH2O mg/dl mg/dl

Normal 50-80 <5 20-45 >50

100- 100-
Bacterial ↑↑ ↓ G stain
10,000 N 500

Viral N or↑ <1000 L 50-200 N

100- ZN
TB ↑ 10-500 L ↓
3000 stain
 Differential diagnosis
 TB meningitis
 Syphilis
 Fungal, parasitic
 Cerebral malaria
 Brain abscess
 Malignancies
 Treatment
 Supportive care: control of convulsions,
fluids & electrolytes- fluids restricted to ½-⅓
maintenance
 Antibiotics according to susceptibility:
– Penicillin
– Chloramphenicol
– 3rd generation cephalosporins
– Other antibiotics
– 10-14 days
 Steroids: dexamethasone- 48-72 hours
 Complications
 Subdural effusion
Convulsions
 ↑ICP
SIADH
 Cranial
DIC- purpura
nervesfulminans
palsies
 Stroke palsy
Cerebral
 Cerebral or cerebellar herniation
Deafness
 Transverse myelitis
 Ataxia
Subdural effusion due to Hib meningitis
 Prognosis
 Early treatment 1-8% mortality
 Pnemococcal → highest mortality
 Poor prognosis< 6 mo
 10-20% → severe neurobehavioural
sequelae
 Neurological outcome: hearing loss, mental
retardation, visual impairment, convulsions,
speech delay, change of behaviour
 Prevention
 Vaccination
 Antibiotic prophylaxis: rifampicin in Hib &
meningococcus
Congenital infections
TORCHS
 Congenital toxoplasmosis
 Toxoplasma gondii- obligate intracellular
protozoa
 Clinical manifestations:
– Prematurity, jaundice, thrombocytopaenia, IU
death
– Triad of choriretinitis, hydrocephalus, cerebral
calcifications
– Skin rash, petechiae
 Diagnosis: culture, serology
 Treatment for one year by
– Pyrimethamine
– Sulfadizine
 Congenital rubella
 Affects almost all organs
 Common clinical manifestations:
– Eyes:
cataract, microphthalmia
– Heart:
myocarditis, PDA, pulmonary artery stenosis
– CNS
hearing loss, meingoencephalitis, motor &
mental retardation
Congenital rubella- microcephaly
Congenital rubella- microphthalmia& cataract
 Congenital CMV
 Cytomegalovirus- herpes virus
 Clinical manifestations:
– IUGR, Prematurity
– Hepatosplenomegaly, jaundice
– Thrombocytopaenia
– Microcephaly
– Cerebral calcifications
– Chorioretinitis, deafness
Congenital CMV- hepatosplenomegaly & skin rash
CMV chorioretinitis
 Diagnosis:
– Virus isolation
– PCR
– Serology
 Treatment:
– Ganciclovir
 Congenital syphilis
 Treponema pallidum- spirochete
 Transmission: sexual, transplacental
 Transmission rate 100% during pregnancy
 40% die
 Early congenital syphilis:
– 1st 2 years of life
– Hepatosplenomegaly
– Jaundice
 Congenital syphilis

– Lymphadenopathy
– Haemolytic anaemia
– Osteochondritis, periostitis
– Skin rash
– Rhinitis- snuffles
– Renal involvement
 Congenital syphilis
 Late congenital syphilis: 1st 2 decades
– Bone: frontal bossing
ant bowing of tibia ( sabre tibia)
– Dental: Hutchinson teeth
notching of teeth
– Saddle nose, depressed nasal bridge
– Mouth fissures
– Eye involvement
– Behaviour changes, convulsions
Hutchinson teeth
 Congenital syphilis
 Diagnosis: serology, microscopy
 Treatment: penicillin G