HIV Infection/AIDS

and ENT Manifestations

Prepared By: Dr Fayaz Rajabzada

 ACQUIRED IMMUNODEFICIENCY
SYNDROME) AIDS)
 Acquired immunodeficiency syndrome is caused by
retroviruses.
 Those infecting the human beings are of two types:
 (i) HIV type I—which is the most common and very pathogenic
 (ii) HIV type II—which is less common and less pathogenic.
 Once virus enters the body, it attacks T-lymphocytes and other cells which
have CD4 surface marker.
 CD4 T-lymphocytes are normally associated with helper-inducer function of
the immune system. With the fall in CD4 lymphocytes below 500 cells/mm3,
(normal 600–1500 cells/mm3), the immune system starts breaking down
with the appearance of opportunistic infections and unusual malignancies,
when it is called AIDS. When CD4-cell count falls below 200 cells/mm3,
death occurs within 2–3 years.
 MODES OF TRANSMISSION
1. Sexual contact—homosexual or heterosexual.
2. Use of nonsterile needles, syringes or other
skin-piercing instruments.
3. Blood and blood products.
4. Infected mother to infant—During pregnancy,
during birth, and via breast milk.
 High-risk Groups
(i) Heterosexually Promiscuous Individuals
(ii) Homosexuals
(iii)Prostitutes And Truck Drivers
(iv)IV Drug Users
(v) Recipients Of Blood And Blood Products
(Haemophilics, Thalassaemia Patients And
Those Undergoing Dialysis).
(vi)Children Born To Hiv Infected Mothers.
Major hazard to healthcare workers is from
blood and body fluids like amniotic, pleural,
peritoneal or pericardial fluid.
Risk of acquiring infection from the specimens
of urine, stool, saliva, sputum, tears, sweat and
vomitus is negligible unless they are visibly
bloody.
 STRUCTURE OF HIV-I VIRION
1. Lipid membrane has two layers.
2. Envelope glycoproteins
(a) Glycoprotein 120 (helps virus to bind to host cell).
(b) Glycoprotein 41 (helps in fusion of viral and cellular membranes).
3. Viral core proteins
(a) Matrix protein p17
(b) Capsid protein p24
(c) Nucleocapsid protein p6, p7
(d) Single-stranded RNA: Two copies
(e) Viral enzymes
(i) Reverse transcriptase
(ii) Integrase
(iii) Protease
 LIFE CYCLE OF HIV
1. Virus enters the body of an individual through various
modes of transmission. It binds to CD 4+ receptors situated on the surface of
helper T-cells and macrophages. Such receptors are also present on monocytes,
macrophages and CNS dendritic cells.
2. Fusion of virus to cell membrane allows the viral core to be injected into the
host cell.
3. Reverse transcriptase, an enzyme present in viral core, changes viral RNA to
DNA and the latter migrates to host genome.
4. Viral integrase helps viral DNA to integrate into host’s genome and the latter is
then called a provirus.
5. Provirus directs synthesis of new HIV particles.
6. During RNA transcription, there is also formation of
protein precursors or polyproteins which are cleaved by proteases to form
functional viral proteins. The latter increase the infectivity of the new virus
particles.
 COURSE OF DISEASE
1. Initial viraemia. Primary infection with HIV,
first causes viraemia which produces mild
clinical disease like fever, headache, body aches
and pains, macular skin rash and lymph nodes
enlargement. This picture resembles infections
like mononucleosis and subsides in 1–2 weeks.
The virus is then taken up by lymphoid organs
like lymph nodes, tonsils, adenoids and spleen.
Initial plasma viraemia lasts for a few weeks.
 COURSE OF DISEASE
2. Latent period. This is the asymptomatic period and may
last for a variable period, on an average 10 years. In up to 5–
10% of cases latent period may be 15 years or more.
They are called long-term survivors or long-term
nonprogressors.
In some cases, about 10%, latent period is short, nearly 3
years. They are called rapid progressors. During this period
no virus is detectable in plasma though it is replicating in the
lymphoid tissue and the CD4 T-helper cell number and
function is deteriorating. Antibody test becomes positive in
2–4 months of infection.
 COURSE OF DISEASE
3. Advanced disease. It starts after several
years. The CD4 T-cell count falls below 200
cells/mm3 and patient becomes susceptible to
opportunistic infections. There are clinical signs
and symptoms of AIDS and death may occur
within 2 years.
ENT MANIFESTATIONS OF HIV INFECTION

Three types of lesions are seen:

1. Opportunistic infections
2. Unusual malignancies
3. Neurological disorders
Opportunistic infections
All types of infection can occur―viral, bacterial,
protozoal or mycobacterial. They can involve any
area of ear, nose and throat, head and neck, and
central nervous system.
Unusual malignancies
• Kaposi sarcoma (KS) and lymphomas are common.
KS can involve skin, mucous membranes or viscera.
KS may be seen in the skin of face (nose, ear or
external ear canal), neck or extremities.
• It can also occur in oral, nasal, nasopharyngeal,
oropharyngeal or laryngeal mucosa. KS causes
obstructive symptoms.
• Non-Hodgkin lymphoma can involve nodal and
extranodal sites. Hodgkin lymphoma is less
common.
Neurological disorders
They can be due to primary HIV infection or
opportunistic organisms. Primary HIV infection
of CNS can cause encephalopathy (AIDS
dementia complex), myelopathy, peripheral
neuropathy and cranial nerve involvement,
most often VIIth but occasionally Vth and VIIIth.
1. Ear:
Viral, bacterial or fungal infections which can
involve external, middle or internal ear are:
• Kaposi sarcoma
• Seborrhoeic dermatitis of external canal
• Malignant otitis externa
• Serous otitis media
• Acute otitis media
• Pseudomonas and candida infection of the
external and middle ear
• Mycobacterial infections
• Sensorineural hearing loss—due to viral
infection of auditory nerve or cochlea and
demyelination of CNS
• Herpes zoster
2. Nose and paranasal sinuses
• Herpetic lesions of nose
• Recurrent sinusitis
• Chronic sinus infection
• Fungal sinusitis
• Kaposi sarcoma
• Lymphomas–B cell type
• Burkitt lymphoma
3. Oral cavity and oropharynx
• Candidal infection of oral cavity can be thrush-like,
atrophic or hypertrophic forms of candidiasis. Candida infection also
involves oropharynx, hypopharynx or oesophagus. They cause difficulty and
painful swallowing.
• Herpetic lesions of palate, buccal mucosa, lips or gums.
Such lesion may form large ulcers
• Giant aphthous ulcers
• Adenotonsillar hypertrophy.
• Generalized lymphadenopathy
• Kaposi sarcoma of palate
• Non-Hodgkin lymphoma of tonsil or tongue
• Hairy leukoplakia
• Gingivitis
4. Larynx
• Laryngitis—fungal, viral (herpes simplex,
cytomegalovirus) or tubercular
• Kaposi sarcoma
• Non-Hodgkin lymphoma
5. Salivary Glands
• Parotitis
• Xerostomia (Dry mouth)
• Diffuse Parotid Enlargement
• Lymphoepithelial Cysts Of
Parotid. They Arise From
Parotid Nodes, Often On Both
Sides.
• Kaposi Sarcoma
• Non-hodgkin Lymphoma
6. Neck
• Lymphadenopathy. It could be only a follicular
hyperplasia or due to a disease such as
tuberculosis, histoplasmosis, toxoplasmosis or
non-Hodgkin or Hodgkin lymphoma.
 KAPOSI SARCOMA
• It is a multicentric neoplasm which may involve any part of the
skin, mucosa or the viscera.
• There is excessive proliferation of spindle cells of vascular
origin. It is noninvasive and respects the fascial planes.
• In the oral cavity, Kaposi sarcoma is mostly seen in the palate,
but may occur on the tongue or gingiva or on the posterior
wall of the pharynx.
• It appears purplish in colour and may need to be
differentiated from angioma or pyogenic granuloma.
• It can occur at any stage of HIV infection, even in those with
normal CD4 counts.
• Size of the tumour may vary from a few mm to several
centimetres.
• Diagnosis is based on biopsy which may show
proliferation of spindle cells, endothelial cells, extravasation of
red blood cells and haemosiderin-laden macrophages.
• Treatment includes localized radiation, intralesional
vinblastine or cryotherapy. Systemic chemotherapy may be
given in those with multiple lesions.
 NON-HODGKIN LYMPHOMA
• HIV patients have high incidence of lymphomas.
• B-cell lymphomas are more common (90%) and many
are due to Epstein–Barr virus.
• Risk of lymphomas increases as disease progresses
generally in patient with CD4+ count less than
200/mm3.
• CNS lymphomas occur in late stages of the disease
while systemic ones can occur early.
• Both nodal and extranodal sites can be involved; the
latter include nose and paranasal sinuses, tonsils,
nasopharynx, tongue, orbit and larynx.
• They also involve gastrointestinal tract, lung and
bone marrow.
• Cervical lymphadenopathy can occur.
• Hodgkin lymphoma is less common.
 HAIRY LEUKOPLAKIA
• It is a white, vertically corrugated lesions on the
anterior part of the lateral border of tongue.
• Caused by epstein–barr virus.
• It develops early and gives clue to hiv infection.
• Aids develops in 50% of such patients in 16
months or 80% in 30 months.
• Differential diagnosis includes leukoplakia,
carcinoma in situ, hypertrophic candidiasis or
lichen planus.
• Biopsy should be done to confirm.
 DIAGNOSTIC TESTS
• Diagnostic tests are based on identification of
antibodies or viral antigens.
• Antibodies are formed within 3 months (2
weeks–12 weeks) of infection.
1. ELISA test (enzyme-linked immunosorbent
assay). It is a very sensitive test (sensitivity
more than 95.5%).
2. Western blot. It is a confirmatory test and
specific for HIV antibodies.
DIAGNOSTIC TESTS...

3. CD4 count. Normal count is 600–1500/mm3. Disease has

been classified according to CD4 counts such as
(i) less than 500 cells/mm3;
(ii) 200–499 cells/mm3
(iii) less than 200 cells/mm3; AIDS-defining illnesses appear
when CD4 count fall below 200/mm3.
4. p24 antigen assay. It detects p24 core protein of HIV.
The test is positive even prior to seroconversion. High levels
of p24 antigen are present before development of
antibodies and are useful in those suspected of acute HIV
syndrome.
5. PCR tests. They determine HIV-RNA. Two
important tests are reverse transcriptase PCR
and branched DNA assay. They determine
number of copies of RNA per millilitre of plasma
and indicate viral load.
 UNIVERSAL PRECAUTIONS
• Wash hands before and after patient or specimen contact.
• Handle the blood of all patients as potentially infectious.
• Wear gloves for potential contact with blood and body fluids. All sharps like blades, needles,
etc. to be put in impermeable container and destroyed.
• During operation, knife to be passed to the surgeon in a tray.
• Place used syringes immediately in a nearby impermeable container; DO NOT recap, bend or
manipulate needle in anyway!
• Use double gloves where they are likely to be pierced as in fracture surgery. Quality of gloves
is important as many of them may have holes. Impermeable gloves are also available.
• Wear protective eyewear and mask if splatter with blood or body fluids is anticipated (e.g.
bronchoscopy, oral surgery).
• Wear gowns when splash with blood or body fluids is anticipated.
• Handle all linen soiled with blood and/or body secretions as potentially infectious.
• Refrain from patient care if you suffer from exudative or weeping skin lesion or dermatitis.
• Process all laboratory specimens as potentially infectious.
• Wear mask to protect against TB
 ANTIRETROVIRAL DRUGS
• There are four major classes of antiretroviral drugs:
1. Nucleoside reverse transcriptase inhibitors (prevent
conversion of RNA to DNA.).
• Zidovudine (AZT)
• Didanosine (ddI)
• Zalcitabine (ddC)
• Stavudine (d4T)
• Lamivudine (3TC)
2. Non-nucleoside reverse transcriptase
inhibitors (prevent conversion of RNA to DNA).
They bind to reverse transcriptase.
• Delavirdine
• Nevirapine
• Efavirenz
• Tenofovir (nucleotide analogue)
3. Protease inhibitors (prevent cleavage of viral
proteins
into their functional forms by binding to viral
protease enzyme.
• Saquinavir
• Ritonavir
• Indinavir
4. Fusion inhibitors (interfere with entry of virus
into target cells). They bind to HIV–gp 41
• Enfuvirtide
NOTE:
Antiretroviral drugs can prevent progression of HIV to
AIDS.
Drug resistance can occur.
Second line drugs are more expensive.
Toxicity of drugs should be kept in mind.
Drug interactions are common and should be avoided.
Combination drug therapy is more effective and
prevents drug resistance; it is the standard of
treatment today to combine two or more drugs.