Lecture 2.

Diseases of the
immune system. Principles of
immunodiagnosis,
immunotherapy, immuno-
reabilitation and
immunoprophylactics.
Lecturer: professor, DM V. Babadzhan.
 Immune deficiencies

Occur when one or more components of the

immune system are defective.

Immune defects can be inherited or acquired.

The immune defects can involve the T cell, the B

cell or both compartments of the immune system,
the Complement or the APC.
 Immunodeficiency
 Can involve the different parts of the
immune system either alone or together
 May involve a deficiency in cell-mediated or
humoral immunity
 May involve deficiency in phagocytosis
 Divided into
 Primary immunodeficiency of genetic origin
 Secondary immunodeficiency from another
underlying disorder
 Immunodeficiency Diseases

Primary: Usually congenital, Secondary: (Acquired):

resulting from genetic defects as a result of other
in some components of the diseases or conditions
immune system. such as:
»HIV infection
»malnutrition
»immunosuppression

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Primary Immunodeficiency Diseases
occur when there is a defect
in any one of the many steps
during lymphocyte development

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 Classification of Primary IDDs
• Primary B cell immunodeficiency:
 X-linked Agammaglobulinaemia (Bruton,s disease)
 Selective IgA deficiency

• Primary T cell immunodeficiency:

 Di George syndrome
 Ataxia – telangiectasia
 Wiskott – Aldrich syndrome
 Acquired immunodeficiency
 Chemotaxis deficiency
 Chronic granulomatous disease
 Chediak – Higashi syndrome
 Leukocyte adhesion deficiency

• Complement system deficiency

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 Primary B Cell Immunodeficiency
 Common variable immunodeficiency associated
with
 Mature B cells failure to differentiation
into mature plasma secreting cells
(antibody forming cells).

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 X-linked Agammaglobulinaemia
(XLA)/Bruton’s Disease:
 Deficiency of B cell tyrosine kinase causing failure in
the development of pre-B cell maturation to B cells.

 Majority of XLA patients show:

 Profound hypogammaglobulinaemia involving all
immunoglobulin classes with <1% B cells in normal
peripheral blood.
 Patients suffer mainly from infectious diseases with
bacteria and viruses that require antibodies for their
disposal.

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 Bacterial Infections
1.Impetigo: This is typified by dermal lesions on face or extremities
and often affects groins and axillae. Lesions, which may be either
bullous (blisters which rupture) or non-bullous (smaller and encrusted)
are highly contagious. The causative agent of bullous lesions is
Staphylococcus aureus and of non-bullous lesions is Group A,
hemolytic streptococcus. Topical or systemic antibiotics are the
customary treatment.

2.Scarlet fever: Scarlet fever is an infection by group A streptococci

(Streptococcus pyogenes) and is characterized by a bright red papular
rash on the trunk. In the oral cavity “strawberry tongue” is common
which is a red tongue covered by a removable coating and presence of
distinctive swollen papilla. Treatment consists of systemic antibiotic
regimens and complications include rheumatic fever, arthritis and
glomerulonephritis.
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 BACTERIAL INFECTIONS

Impetigo:

The ruptured blister, encrusted

lesions are caused by beta hemolytic
Group A streptococci.

The bullous lesions are

caused by Staphylococcus
aureus

impetigo
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 Selective IgA deficiency (IgA D)
 Patients with IgA deficiency have:
 IgA levels < 5mg/dL with normal levels of other Igs and
 50% have chronic otitis, sinusitis or pneumonia.

 IgA committed B lymphocytes:

 Fail to mature into IgA-secreting plasma cells caused by
intrinsic B cell defect.
 Patients of IgA deficiency are susceptible to:
 Allergic conjunctivitis, urticaria and asthma.
 Autoimmune and neurological disorders.
 Various gastrointestinal diseases (food allergy).
 recurrent sinopulmonary infections.

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Severe Combined Immunodeficiency
Disease (SCID)
Disorder characterized by:
 Deficiency in both B and T lymphocyte functions
with markedly low IgG, IgA and IgE levels.

 SCID associated with:

 Children failure to thrive.
 chronic respiratory infections.
 Gastrointestinal and/or cutaneous infections
particularly recurrent viral, bacterial, fungal and
protozoan infections in 6 months' infants.

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 SCID manifests early with:
Persistent and recurrent diarrhoea,
otitis, thrush and respiratory
infections in the first few months of
life.
 T cell defects associated with:
 Candidiasis, CMV infection, measles and varicella
leading to life threatening pneumonia, meningitis and
sepsis.
 SCID managed through Ig infusion, stem cell
transplantation and gene replacement.

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T Cell Immunodeficiency Diseases

 T cell congenital disorders display:

 Littleor no cell mediated immunity and may
involve B cell deficiencies.

 Patients particularly susceptible to:

 Repeated fungal (Candida) infection.
 Protozoan and viral infections.

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 Primary T cell immunodefiency
includes:
 Di-George syndrome
 Wiskott-Aldrich syndrome
 Cartilage hair hypoplasi,
 Ataxia - telangiectasia
 Defective expression of class II MHC
molecules
 Defective expression of CD3-T cell receptor
(TCR) complex

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Di George Syndrome (Thymic Aplasia)
Congenital disorder characterized by:

 Lack of embryonic development or

underdevelopment of the 3rd and 4th
pharyngeal pouches.

 Thymic hypoplasia, hypothyroidism and

congenital heart disease.
 Patients susceptible to uncontrolled
opportunistic infections.
 Impaired in cellular mechanisms.
 Profound lymphopenia (T cell <1200L).

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 Ataxia Telangiectasia (AT)
Autosomal recessive progressive
neurodegenerative childhood disorder
associated with:

 Lack of coordination (cerebella ataxia) and dilation of

facial blood vessels (telangiectasis) and slurred speech.

 Patients have defective mechanisms of DNA repair and
are predisposed to leukaemias and lymphomas.

 Extremely sensitive to radiation exposure and

susceptible to chronic respiratory infections.

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 Wiskott-Aldrich Syndrome (WAS)
An X-linked recessive disorder associated
with thyrombocytopenia and eczema.
 Patients have
 Elevated IgA and IgE
 Low IgM
Variable T cell dysfunctionsT cell dysfunction
manifested by:
 Severe herpex virus and Pneumocystis carinii infections
 Increased lymphomas and autoimmune diseases.
 Recurrent pyogenic bacterial infections.
 Usually affecting ears, sinuses and lungs.

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 Mixed Immunodeficiencies

Inherited defects of phagocytic function.

Inherited defects of complement: Loss of

specific complement components. Inability to
form the MAC and/or to produce anaphylatoxins.
 Viral Infections
1.Acute herpetic gingivo-stomatitis (primary herpes infection): Primary herpes is
a viral infection of the oral mucosa caused by Type I herpes simplex virus (HSV-
1). It affects young children (usually under 5 years) who have not developed
resistance to the virus. Clinically, patients present with multiple painful ulcers, 1
to 2mm in diameter surrounded by erythematous tissue on all mucosal surfaces
of the oral cavity. Pain upon eating, especially salty or acidic foods, is common
and tooth-brushing is painful if ulcers appear on gingivae. Low fever and
malaise also are present and patients often become under-nourished or
dehydrated from insufficient food or liquids. The infection which sheds viruses
from ulcers, is highly contagious and can spread to other mucous membranes
such as eye tissue. The condition is self-limiting and will subside within 10 to 14
days.
 VIRAL INFECTIONS
Primary herpes infection:

Symptoms:
1. Painful generalized ulcers
on oral mucosa.
Sometimes it appears
extra-orally.
2. Low fever and malaise.
Patients often are under-
nourished due to pain
upon eating.
3. Self-limiting. Will last 10
to 14 days.

4. Differential diagnosis
must rule out
candidaisis (thrush)
which is not painful
and produces a white
membranous patches
on mucosal surfaces. Occurs frequently in
young children
 VIRAL INFECTIONS
Primary herpes infection:
Treatment:

1. Palliative treatment

2. Viscous topical anesthetic

xylocaine or benadryl elixir plus
kaopectate (to relieve for pain,
especially upon eating) and
Pedelite.

3. A balanced nutrient drink to

compensate for insufficient diets.

4. Anti-viral agent Acylovir (Zovirax;

400mg q3h for 10 days) may be
administered in extreme cases to
inhibit the virus.

5. (Note: steroids should not be used

as the inflammatory reaction
constitutes the first line of defense
against the virus.)
VIRAL INFECTIONS

Recurrent herpes labialis:

After a primary infection HSV-1 travels

up a sensory nerve and remains
dormant in a ganglion (trigeminal).

It can revert to the lytic form upon

certain stimulation and usually erupts
at the vermillion border of the lips.
 Viral Infections
2.Recurrent herpes labialis (cold sore): This is a HSV-1 infection which occurs in
individuals who previously experienced a primary herpes infection. The virus
remains dormant in sensory nerve ganglia after the first infection, but can erupt
following episodes of emotional stress, excessive exposure to sunlight, trauma,
dental procedures or intake of certain foods to form single ulcerated lesions on
the vermilion border of the lips and mouth (usually). The common occurrence
during “cold seasons” when resistance is often compromised accounts for the
name (cold sore). In addition, foods containing high levels of arginine such as
cereals, nuts and chocolate can activate the virus. The limited manifestation,
versus primary herpes, is due to immunity developed after the first exposure to
the virus. The condition is self-limiting, lasting 10 to 14 days. Remedies which
may enhance resolution of the ulcer are alloe or acyclovir which inhibit HSV-1.
Foods high in lysine such dairy products and yeast may alleviate the condition
by counteracting the effect of arginine.
 Viral Infections
3.Herpangina: This is caused by the cocksackie A virus and is evidenced by
multiple painful ulcers on oral mucosa similar to primary herpes infections. The
susceptible age is similar to that of primary herpes, being before age 5, but it is
less common and affects mainly the distal portion of the mouth or throat.
Treatment and progress of the condition is similar to that of primary herpes.
4.Hand, foot and mouth disease: The causative agent is cocksackie A virus and
clinical appearance is herpetic-like multiple ulcers on the hard palate, tongue and
buccal mucosa. The susceptible ages are 1 to 10 years and the condition is less
common than primary herpes. In addition, characteristic ulcerative lesions
appear on soles of feet and plams. Treatment and course of the disease are
similar to primary herpes.
5.Herpes zoster infection (varicella zoster virus, Type 3 Herpes Simplex virus):
This is commonly known as chicken pox when it affects school age children and
first appears as papular lesions on the skin which form encrusted ulcers. If the
virus infects adults, shingles, a painful dermal condition, will develop. In chicken
pox oral lesions appear on oral mucosa secondarily to skin lesions and resemble
herpetic ulcers, but are not painful (usually). The disease confers immunity and is
self-limiting within 14 days.
 VIRAL INFECTIONS

Varicella (chicken pox) – Coxsackie A virus:

zoster (shingles). Human
Herpes Virus-3; HHV-3:

Herpangina
chickenpox

shingles Hand foot and mouth disease

 Fungal Infections

Candidosis (thrush) is the most common oral fungal infection and

frequently affects young children. It appears as white patchy lesions
on the oral mucosa. When the white patches are removed a bright red
tissue surface is seen which is usually non-painful. Sometimes a
distinctive yeasty oral odor is present. Occurrence frequently follows
broad spectrum antibiotics, but it may also be transmitted from vaginal
yeast infections. Diagnosis may be confirmed by identification of
Candida albicans in mucosal specimens and treatment consists of
topical anti-fungal ointment such as Nystatin.
FUNGAL INFECTIONS

Candidosis (Thrush):

“thrush”, “acute pseudomembraneous”

 TREATMENT

Cell wall with no

peptidoglycan

Yeast cell
Cell membrane
POLYENES
ergosterol • nystatin
• Amphotercin B
AZOLES
These adsorb to
• miconazole
cell membranes
• fluconazole
and disrupt
• ketoconazole
ergosterols
These inhibit
synthesis of
ergosterols
 Recurrent Aphthous Ulcer (canker sore)

This appears as single (usually) painful erythematous ulcers on oral

mucous membranes which are slightly larger than herpetic lesions. The
condition is self-limiting within 14 days, but contains no virus. The
etiology has not been definitively established, but may involve
autoimmune reactions to antigens from Streptococcus sanguis.
Several palliative non-prescription remedies are available including
kenalog in orabase (a steroid anti-inflammatory agent; Note: steroids
may be used since viral etiology is not suspected.)
 RECURRENT APHTHOUS ULCER (CANKER SORE)

The condition is self-limiting and is

treated by palliative measures.

A definitive cause is not known.

SYSTEMIC DISORDERS WITH ORAL
MANIFESTATIONS

AID
S:

Parotid
swelling
thrush

gingivitis

periodo
ntitis Herpetic
ulceration
 SIGNS, ALLOWING TO SUSPECT IMMUNODEFICIENCY
Recidivic bacterial-viral infections which are characterized:
a) chronic curse;
b) incomplete reconvalescence;
c) unsteady remissions;
d) unusual microflora (opportunistic infection, with multiresistence stability
to the antibiotics).
Unusual reactions on vaccines.
Information of physical investigation:
delay of development; decline of body mass; subfebril tempereture; increase,
excalation or complete absence of lymphatic knots, amygdales, thymus;
dermatitises, skin abscesses; candidosis of mucous membrane of mouth
cavity.
Haematological changes: leukocitopenia, thrombocitopenia, anaemia.
Paratherapeutic interferences:
chemotherapy; splenectomy; irradiation.
Protracted stress.
Autoimmune diseases.
Tumour.
33
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Acquired immune deficiency is violation of the immune
system, developing in a postneonatal period (in adults)
and not subsequent upon genetic defects.
Acquired immune deficiency is dysimmunity, which
arise up as a result of somatic and other diseases,
and also other factors and have clinical symptoms.
Acquired immune deficiency
a) develops on a background before normally
functioning immune system;
b) characterized the proof decline of quantitative and
functional indexes of immune status;
c) it is the area of risk development of chronic infectious
diseases, autoimmune pathology, allergic diseases and
tumor formations.
(Dranik G.N., 2005)
 Forms of acquired (secondary) immunodeficiency
The squared secondary immunodeficiency is a syndrome of
AIDS, developing as a result of defeat of the immune system the
human immunodeficiency virus (HIV).
The inducting (specified) secondary immunodeficiency (ICD-10,
code D.84.8) arises up as a result of concrete reasons, causing
its appearance: x-ray radiation, cytostatic therapy, application of
corticosteroids, traumas and surgical intervention,
dysimmunities, developing the secondary in relation to a basic
disease (diabetes, disease of liver, kinds, malignant tumors).
The spontaneous (unspecified) secondary immunodeficit (ICD-
10, code D.84.9) is characterized absence of reason, causing
violation of immune reactivity. Clinically shows up as chronic,
recidivate infectiously-inflammatory processes of bronchial tree,
additional bosoms of nose, urogenital and gastroenteric system,
35
eyes, skin, soft tissues, caused opportunistic microorganisms.
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 CLASSIFICATION OF SECONDARY IMMUNODEFICITES
 By the rates of development:
 Acute immunodeficiency (conditioned an acute infectious disease, trauma,
intoxication and other).
 Chronic immunodeficiency (develops on a background of chronic
festering-inflammatory diseases, autoimmunity, tumors, persistent viral
infection).
 II. By the level of breakage:
 Violation of cellular (Т-cells) immunity.
 Violation of humeral (B-cells) immunity.
 Violation of phagocytes.
 Violation of complement system.
 Combined defects.
 III. By prevalence:
 «Local» immunodeficiency.
 Systemic immunodeficiency.
 IV. By the degree of severity:
 Compensated (mild).
 Subcompensated (moderate).
36
 Decompensated (severe).
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 Psychological aspects
 beta-endorfins
 during exams
lymphopenia
 activity of NK cells
 production of IFN-gamma

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Secondary Immunodeficiencies

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 Secondary Immunodeficiencies
 Occur as the result of an underlying
disorder
 May be malnutrition, viral infection, cancer,
renal disease and Hodgkin’s disease
 May occur with immunosuppressive drugs,
drugs used along with radiation, chemotherapy

Oral Manifestations of Therapy for

Oral Cancer
 Radiation Therapy
 Chemotherapy

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 Consequences of immunodeficiencies in
dental patients

Increased incidence of infections in the oral cavity

(Herpes virus), even with organisms that are usually non-
pathogenic such as Candida species (candidiasis):
In AIDS patients
In cancer patients undergoing chemotherapy, and in
immunosuppressed transplant recipients:
Increased plaque formation
Ulcerations
Xerostomia
Sialadenitis
Periodontal disease, bone loss
Osteomyelitis
Papillary atrophy of the tongue
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 Radiation Therapy
 The patient often experiences
mucositis during radiation therapy.
 Mucositis begins about the second
week of therapy and subsides a few
weeks after its completion.
 It is painful and appears as an
erythematous and ulcerated mucosa.
 The patients may have difficulty
eating, pain on swallowing, and loss
of taste.

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 Radiation Therapy (cont.)
 Destruction of major salivary glands may result in
xerostomia
 The patient is prone to rampant caries and oral
candidiasis.
 They also are prone to osteoradionecrosis.

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 Radiation Therapy (cont.)
 Patients should have an oral evaluation
before radiation therapy of the head and
neck.
 Potential sources for oral infection and teeth
with a questionable prognosis should be
removed.
 The hygienist can help with
 Fluoride application
 Patient education
 Frequent follow-up appointments

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 Chemotherapy
 Drugs used for cancer chemotherapy
affect basal cells of the epithelium.
 Mucositis and oral ulceration are common
complications.
 A decrease in all blood cells may occur
 Lowered RBC counts can lead to anemia.
 Lowered WBC counts can lead to infections.
 Lowered platelets can lead to bleeding
problems.

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Effects of Drugs on the Oral Cavity
 Blood pressure drugs, antianxiety
medications, antipsychotic medications,
and antihistamines can cause xerostomia.
 Prednisone suppresses the immune
system and can lead to candidiasis and
oral infections.
 Antibiotics may increase risk of
candidiasis.

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Effects of Drugs on the Oral Cavity
(cont.)

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Effects of Drugs on the Oral Cavity
(cont.)
 Tetracycline can cause tooth discoloration.
 Phenytoin and nifedipine can cause
gingival enlargement.
 Cyclosporine may cause gingival
enlargement.

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 Immunotropic preparations
 Immunostimulators (immunomodulators)
 Biological (human, animal origin):
 - Immunoglobulins
 - Erbisol
 - Thymalin
 - Tactivin

 Immunosupressive
 Glucocorticosteroids
 Citostatics
 Monoclonal antibodies
 Ciclosporin A

48
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Immunoprophilactic and immunoreabilitation
preparations

 Vegetable
 Bacterial
 Mycotic
 Antiviral vaccines
 Allergovaccintion

49
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 Immunostimulators
Clinical criteria: chronic infection, low efficiency of
treatment of inflammatory process; treatment of
cytostatics, glucocorticosteroids, antibacterial and
radial therapy.
Immunological criterias: decrease of amount and
functional activity of lymphocytes, decline level of
immunoglobulines, complement, phagocytic activity
(uncompleted phagocytosis) no less what on 30-
50%.
Immunosupressive therapy
Clinical criteria: heavy forms of allergy with the
defeat of kinds, transplantation of organs and
tissues, connecting system diseases.
Immunological criteria: appearance high 50
titles of
autoantibodyes in blood.
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 Classification of immune drugs
at the point of application
Affecting primarily Affecting mainly on Affecting influencing
on a cellular link humoral predominantly on
(NK-cells, T-killer (B-lymphocytes, Ig) macrophage- interferon status
cells) monocytic link

•timalin • immunoglobulins •polioksidony • Interferon

•Imunofan •Interferons (reduce the •sodium nucleinate preparations:
•immunomaks synthesis of •immunomaks (laferon, viferon,
•Galavit ® (100 mg) immunoglobulins) Laferobion, etc.)
•derinat
• Bacterial • Interferon inducers
•Galavit ® (amiksin, Lavomax,
Immunopreparat
(ribomunil, bronhomunal) tsikloferon, Kagocel
• Galavit ® proteflazid)
(200 mg - reduced the • Galavit ®
synthesis of low avidity (100 mg -
antibody in a dose of 100 increases the
mg - improves the synthesis of
specificity of the antibody) interferon)

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 IMMUNOCORRECTION (I)
(ID, lymphocyte type)
CRITERIA
1. Decline of maintenance of CD3, CD4, CD25.
2. Decline of immunoregulatory index of CD4/CD8.
3. Decline of production IL-2, gamma-INF.
4. Increase of production IL-4, 5, 6.

 STIMULATION of SYNTHESIS ILT-2 (IZOPRINOZIN,

GROPRINOZIN)
 THYMIC PEPTIDS:

- old are THYMALIN, TAKTIVIN, THYMOPTIN

- new are ZADAKSIN, IMMUNOFAN
 METABOLIC ROW - GALAVIT.

52
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The patient 37 years old. Diagnosis: chronic recurrent herpes viral infection in the area
of ​the face and lips. Oropharyngeal candidiasis. Immune deficiency in T-
limfotsytopenichnomu type (D 84.9).
Causal and Immunotropic therapy:
1) Zovirax (acyclovir ) 400 mg is
inside the 4 times a day for 1
month ; Gerpevir (ointment )
lubricate the affected
skin and mucous membranes of
the lips 4 times a day 7 days;
3) viferon 500 thousand IU 1 per
day in candlelight for 1 month ;
virohel -
lubricate the affected skin and
mucous membranes of the lips , 2
times a day, 5 - 7 days;
- Interferon inductor - cyclopheron -
12.5 % injection - 2 ml , dose of
0.25 g / m at 1, 2, 4, 6, 8, 11, 14,
17, 20 , 23, 26, 29 days. After
interferon ;
4) imunofan 1 ml / m in a day , №
10;
5) Polyoxidonium 12 mg (
suppository) 1 every 3 days , № 10;
6) amiksin 125 mg (1 cap. ) Day
after breakfast , № 20;
7) intrakonazol ( intrunhar ) 100 mg
1 time a day for 2 weeks .
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 IMMUNOCORRECION (II)
(ID, interferonone type)
CRITERIA
1. Decline of alfa- and gamma-INF production.
2. Decline of CD4 and CD16 levels .
3. Decline of immunoregulatory index of CD4/CD8.
4. Increase of IL-4, 5, 6 production.

 INTERFERONS (VIFERON, LAFERON);

 INDUCTORS of ENDOGENOUS INTERFERON and NK-
CRLLS:
 NEOVIR, CYCLOFERON);
 AMIXIN;
 Antiagregants (CURANTYL);
54
 NEW (with the protracted
Elsevier items and derived items effect) - KAGOCEL.
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 PRINCIPLES of INTERFERONTERAPY
in the syndrome of chronic fatigue and immunodeficits

1. Local and systemic application of viferon (laferon).

2. High or middle doses of viferon (laferon) from the
beginning of treatment, since 2-3 millions, rarer - with 4-6
million - during 1,5-2 months, further, -
3. The doses of Viferon go down «step by step» in 1,5-
time each 2-3 weeks, rarer, - each month.
4. In the relapse of infection to return to former, more high
dose on 2-3 weeks, further, is an attempt of decline of dose.
5. Duration of course treatment of viferon (laferon) - no less
than 3,5-4,5 months.
6. If necessary courses repeat in critical periods.

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 IMMUNOCORRECTION (III)
(ID, humoral type)
CRITERIA
Diminishing of amount of CD19.
Decline levels of immunoglobulins classes A, M, G.
Seronegativ forms of infection (specific IGM-, IGG-, DNA+)

SPECIFIC IMMUNOGLOBULINS:
 antistaphylococcal ( 3 ml IM, 3 - 5 inj. 1 time per 3 days ).
 antiherpetic (1 or 2 types) (amp. for 1,5 ml, use for 4,5 ml IM
1 time per 3 days of 5 inj.);
 anticitomegalovirus;
 IG against the virus of Ebshtain-Barr;
 antichamidial (1,5 ml one time per 3 days IM of 6 inj.),
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The patient 58 years old. Diagnosis: chronic obstructive pulmonary disease, II c.,
Exacerbation. Diffuse fibrosis. Emphysema. LW II c. Immunodeficiency by B-cell type (D
84.9).
Immunotropic therapy:
1) causal antibiotic therapy -
levofloxacin 500 mg / in drip-
Lynn 1 time a day 7 days
dimexyd 5 ml per 200 ml of 0.9%
sodium chloride in / drip 1 per
day 5 days azithromycin 500 mg
1 time a day, 3 days;
2) Polyoxidonium 6 mg / m 2
twice a week, for 10 days;
3) halavit 100 mg 1 time a day /
m, 10 days;
4) laktophiltrum 2 MSA. 2 times
a day for 14 days.
5) fluconazole 100 mg a day, 10
days.
immunorehabilitation:
6) IRS-1 19 inhalations once a
day, 20 days;
7) timalin 1 ml subcutaneously
in a day, 10 days.

57
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 INTRAVENOUS IMMUNOGLOBULINS

Intravenous immunoglobulins prescribes in day's dose 400

mg/kg IV dropes 1 ml/kg/h for premature born and 4-5
ml/kg/h for worn children.
IVG prescribes for prophylaxis of infections to the prematurely
born children with mass of body less than 1500 g and by the
level of IGG 3 g/l and below.
IVG use to achievement the concentration of IGG in blood not
below than 4-6 g/l in immunodeficit with the low level of IGG in
blood.
IVG prescribes for treatment of heavy festering-inflammatory
diseases 1th daily 3-5 injections to reach the dose of IVG 1-2,5
g/kg.

58
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 IMMUNOCORRECION (IV)
(ID, phagocytic type)
CRITERIA
Decline of phagocyte number and index.
Decline of NBT-test.

POLIOXSYDONIY - 6 mg of preparation before injection

dissolve in 1-1,5 ml of phys. sol., dist. water or 0,25% sol.
of Novocain, IM or SC injection.
Acute inflammatory process: 6 mg daily, course is 3-5
injections;
Chronic inflammatory process 6 mg daily, 5 injections,
then 2 times per a week, course 10-15 injections.

METHYLURACIL - prescribes in pills for 0,5 g 3 times per

59
a day duringElsevier
3-4 itemsweeks or
and derived items by
© 2009 more
by Saunders, protracted
an imprint of Elsevier Inc. courses. 59
The patient 28 years old. Diagnosis: chronic recurrent furunculosis. By phagocytic
immunodeficiency type (D 84.9)
Immunotropic therapy:
1) specific antibiotic therapy
(normal human immunoglobulin
4.5 ml / m in a day for 10 days);
2) causal antibiotic therapy -
spiramycin 500 mg 2 times a
day;
3) locally - triderm lesions in
areas 2 times a day - 2 weeks;
4) Polyoxidonium 6 mg / m 2
twice a week, 20 days or 100 mg
halavit a day / m, 20 days;
5) probiotic Linex 2 MSA. 3
times a day, 20 days.
immunorehabilitation:
6) viferon 150 thousand IU, a day
in the candlelight, 10 entries;
7) Sodium Nucleinat 0.1 g 3
times a day 30 days

60
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 Vaccination against flu
Autumn (better October)
Possibly simultaneously with other vaccines (in different places)
To utillize the exceptionally registered vaccines
INFLUVAK subunit vaccine
- antigen composition answers annual recommendations of WHO

Doses: - children from 6 month to 3 years - 0,25 ml

- to the children more senior than 3 years - 0,50 ml
- adults - 1,0ml
Patients, never before getting an inoculation from flu, must get the
second dose of preparation in 4-6 weeks.
Introduction:
- intramuscular
- deeply subcutaneously

before introduction to warm a vaccine to the room temperature.

61
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 HIV/AIDS Info & History
 In 1981,1 the first cases of AIDS were identified among gay men
in the US. However, scientists later found evidence that the
disease existed in the world as early as 1959.

 The first documented case of HIV was traced back to 1959 using
preserved blood samples, which were analyzed in 1998.

 In first-world countries, AIDS is now a chronic disease, but this

was not the case in the past.

 AIDS is 100% preventable, and yet there were 56,300 new

infections in 2006 in the US alone.2

1. 1. Advert.org
2. 2. Centers for Disease Control and Prevention
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc. 62
 Definitions
 H - Human  A - Acquired

 I - Immune
 I - Immunodeficiency
 D - Deficiency

 S - Syndrome
 V - Virus

Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc. 63
 Normal Immune Response

Virus binds to T-cells

Antibodies
Virus T-cells bind to virus

Antibodies
Normal response: Virus invades blood kill virus
Virus
stream and binds to lymphocytes.
Lymphocytes make antibodies to the virus.
Antibodies bind to the virus and destroy
the virus.

Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc. 64
 Immune Response to HIV

HIV HIV destroys T-

cells (CD4 cells)

T-cells cannot
produce antibodies

Cannot destroy virus

Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc. 65
 Immunopathological Mechanisms of HIV
infection
HIV infected patients progress to AIDS disease in three
phases:
Early phase: lasts about 2 weeks accompanied by:
Fever, aches and flue-like symptoms with high levels of virus in
blood.
Middle phase: lasting months or several years (latent) with:
 Anti-HIV antibodies
 Continuous depletion of CD4 T cells
Late phase (AIDS): characterized by:
 Rapid decline in CD4 T cells,
 Opportunistic infections including viral (herpes simplex,
herpes varicella zoster, EBV), bacterial (M. tuberculosis),
fungi (Candida-thrush) and protozoan (Microsporidia) .
 Cancers (lymphoma; Kaposi’s sarcoma).
Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc. 66
What’s the difference between
HIV and AIDS?
 HIV, a virus, eventually causes AIDS,
a syndrome.

Spectrum of HIV

Infection

Possible Minor Symptoms

Blood tests Healthy, HIV+ Symptomatic

can last for years HIV/AIDS
positive

Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc. 67
 T-Cell Count

 If 1,200 or higher, the individual has a normal

immune system.
 If 800 or less, the immune system is weakened
and individual is susceptible to infection.
 If 200 or less, AIDS is diagnosed.
 Once a person is diagnosed with AIDS, she or
he is always categorized as having AIDS, even if
her or his T-cell count increases.

Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc. 68
 Symptoms of HIV
 Recurring fever  White, thick spots
 Night sweats on the tongue
 Rapid weight loss  Dry cough
 Diarrhea lasting  Shortness of
several weeks breath
 Purple bumps on
the skin, inside the
mouth, and rectum

Elsevier items and derived items © 2009 by Saunders, an imprint of Elsevier Inc. 69
 Criteria for Diagnosing AIDS

 A CD4 cell (type of T-cell) count of 200

or less,
or

 One opportunistic infection.

• An opportunistic infection is an infection
that typically does not affect individuals with
normal immune systems.

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 Opportunistic Infections
 Mycobacterium Avium Complex  Herpes Simplex
 Salmonellosis  Herpes Zoster
 Syphilis and Neurosyphilis  Human Papillomavirus
 Tuberculosis  Molluscum Contagiosum
 Bacillary angiomatosis  Oral Hairy Leukoplakia
 Aspergillosis  Progressive Multifocal
Leukoencephalopathy
 Candidiasis
 AIDS Dementia Complex
 Coccidioidomycosis
 Peripheral Neuropathy
 Cryptococcal Meningitis
 Apthous Ulcers
 Histoplasmosis
 Malabsorption
 Kaposi’s Sarcoma
 Depression
 Systemic Non-Hodgkin’s
Lymphoma  Diarrhea
 Primary CNS Lymphoma  Thrombocytopenia
 Cryptosporidiosis  Wasting Syndrome
 Isosporiasis  Idiopathic Thrombocytopenic
Purpura
 Microsporidiosis
 Listeriosis
 Pneumocystis Carinii
Pneumonia  Pelvic Inflammatory Disease
 Toxoplasmosis  Burkitt’s Lymphoma
 Cytomegalovirus  Immunoblastic Lymphoma
 Hepatitis  Valley Fever
Source: AIDS Education Global Information System
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 MRSA 71
 HIV Infection/AIDS Staging System
Clinical Stages& Major Clinical Features:
Stage 1: Asymptomatic; persistent generalized
lymphodenopathy (PGL) and acute retroviral infection (ARI).
Stage 2: Loss of weight (< 10% of body weight); minor
mucocutaneous infections; herpes zoster and recurrent upper
respiratory tract infections (URTI).
Stage 3: Loss of weight (>10% of body weight); chronic
diarrhoea(> 1 month); prolonged fever; oral candidiasis; oral
hairy leukoplakia; pulmonary tuberculosis; severe bacterial
infections and vulvovaginal candidiasis.
Stage 4: HIV wasting syndrome; extrapulmonary tuberculosis;
Pneumocystis carinii pneumoniae, Candidiasis of the
oesophagus, trachea, bronchi or lungs; toxoplasmosis of the
brain, cryptosporidiasis with mycobacteriosis; lymphoma;
Kaposi’s sacoma (KS) and HIV encephalopathy.

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 Oral Candidiasis
 This is a fungal
infection that occurs
in nearly all patients
with AIDS.
 It commonly precedes
other OI’s.
 Untreated, it
progresses to the
esophagus and
stomach.
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SYSTEMIC DISORDERS WITH ORAL MANIFESTATIONS

AIDS:

AIDS periodontitis

AIDS gingivitis
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 Pulmonary Infections:
M. Tuberculosis and Pneumocystis pneumonia common
when CD4 T cells <200/μl.

 TB in advanced HIV infection often presents atypically

with extrapulmonary diseases affecting:

 Bone marrow, bone,

 Urinary and gastrointestinal tracts:

 Liver, regional nodes and the central nervous system.

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 Gastrointestinal illness:

 Inflammation of the lining of the oesophagus

(oesophagitis).

 Fungal (candidiasis) or viral (herpex simplex or

cytomegalovirus) infections.

 Chronic diarrhoea also occurs that may be caused

by bacteria (Salmonella, Shigella, Listeria or
Escherichia coli).

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 Major neurological illnesses:
 Toxoplasma encephalitis of the brain caused by
Toxoplasma gondii, progressive multifocal
leukoencephalopathy (PML), demyelinating
disease.

 Crytococcal meningitis caused by fungus

Cryptococcus neoformans.

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 Malignancies:
AIDS-defining malignancies include:

 Kaposi’s sarcoma presenting as purplish nodules

of the skin, mouth, gastrointestinal tract and
lungs.

 Hodgkin’s disease, anal and rectal carcinomas.

 High grade B cell lymphomas (Burkitt’s

lymphoma).

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 Diagnosis of HIV

 Elisa test
 Western Blot test
 Oraquick test
 Home HIV tests
• Home Access Express

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Fluids that can transmit HIV

Fluids that DO Fluids that DO NOT

transmit HIV: transmit HIV:

 Blood  Saliva
 Semen  Tears
 Vaginal Fluid  Mucus
 Breast Milk  Urine
(in order of the highest  Sweat
concentration of HIV)
 Feces
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 Universal Precautions

 Wash your hands!

 Disinfect utensils and living space.
 Use barriers—preferably latex.

HIV cannot be spread through casual contact,

but these are good practices for preventing
opportunistic infections.

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 Barriers include:

 Latex Gloves
 Latex Dental Dams
 Anything that protects your skin from a fluid

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 Testing
 The test is for antibodies against HIV, not for the
virus itself.

 It can take up to three months for the body to

produce antibodies against HIV.

 A negative test result may mean recent infection.

It is possible to infect others during this stage.

 An individual should be tested three months after

possible exposure to guarantee an accurate result.

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 Timeline

Test Date New Test Date

Three-month
window from
first exposure
Three-month
First Second
window from
exposure exposure
second
exposure

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 Treatment

 Today, in the US, HIV/AIDS is a chronic disease.

 Anti-retroviral drugs are used in combination, known
as Highly Active Anti-Retroviral Therapy (HAART).
 Side effects can be severe, but the risks of not being
treated are more severe.
 Cornell University estimates the monthly cost of
treatment as $2,100, with a lifetime cost of treatment
of $618,900.

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