2. HIV
Retrovirus – Viral RNA into DNA
Two types – Type 1 and type 2
Type 1 - more common and more pathogenic
Type 2 – less common and less pathogenic
Once entering the host, this attacks the T-lymphocytes and other CD4
surface markers.
With the fall of the CD4 lymphocytes(<500/cu. mm) , the
immunodeficiency is seen and many other opportunistic and malignancy
can appear.
When the CD4 cell counts appear less than 200, death may appear in
about 2-3 years.
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3. Epidemiology
• First case came into medical attention as early as 1980’s.
• These cases were detected by retrospective analysis to have occurred
in 1978 in USA and in late 1970’s in Equatorial Africa.
• The first case was registered in 1986 in India.
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5. Current scenario
• Its magnitude has increased to over 100 folds since AIDS was first
discovered.
• India has over 5.2 million people who are HIV infected with only
south Africa ahead in terms.
• 72000 new cases were reported in the year 2005.
• Globally about 39.4 million people are infected
• About 8 to 10% are from south-east Asia region.
• The prevalence of HIV is about 0.91%.
• There are focal epidemics in states like Tamil Nadu, Maharastra,
Gujrat and Andhra pradesh (NACO).
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7. Risk Groups
i. Homosexuals.
ii. Heterosexually promiscuous individuals.
iii. Prostitutes and truck drivers.
iv. I. V. drug users.
v. Recipients of blood and its products (haemophilia, thalassemia,
dialysis).
vi. Children born to HIV mothers.
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8. Hazard to health workers is from blood and the body fluids such as
• Amniotic
• Pleura
• Peritoneal
• Pericardial
Risk of acquiring infections from specimen of Urine, sputum, stool
saliva, tears, sweat and vomitus is negligible.
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11. • Latent period:
• Asymptomatic up to 10 years.
• No virus is detected in plasma
• Virus replicates in lymphoid tissues such as LYMPH
NODES, TONSILS and ADENOIDS.
• Infection can be detected by CD4 number and their
detonating function.
• Antibody test becomes positive in 2-4 months of
infection.
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12. • Advanced disease: After several years.
• CD4<200 cells/cu. mm
• Patient’s immunity is compromised and is more susceptible
for opportunistic infections.
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13. ENT MANIFESTATIONS OF AIDS
• Due to opportunistic infections of viruses, bacteria, fungi and
protozoa (or) due to activation of neoplastic processes.
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15. External Ear:
• Otitis externa
• Malignant otitis externa caused predominantly by Pseudomonas or by Aspergillus
fumigatus.
• Treatment is by antibiotics for pseudomonas or IV amphotericin B followed by oral
itraconazole for aspergillus.
• Kaposi’s sarcoma of ear
• Most common
• 300 times more common in people with AIDS
• Kaposi’s sarcoma of auricle is more common
(others such as ext. auditory canal, middle ear)
• Clinically it appears as RED PURPLE plaques or Nodules.
• Treatment
• Medical: Bleomycin, vincristine, liposomal doxorubicin
• Surgical: local cutaneous lesions - surgical extirpation.
• ZIDOVUDINE should be included in treatment to reduce the extent of
immunosuppression and improve the prognosis.
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16. Middle Ear
• Serous Otitis Media
• Seen in both adults and paediatric cases up to 80% of population
• Due to poor Eustachian tube functions
• Secondary to viral infection, adenoid hypertrophy from HIV (or) due to viral
induced allergy or nasopharyngeal tumors
• Treatment: Adnoidectomy to rule out B cell tumors and Kaposi’s sarcoma. An
early myringotomy or grommet insertion is recommended.
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17. • Acute Otitis Media
• Seen in both adults and paediatric patients
• Recurrent otitis media and chronic sinusitis are seen in paediatric cases.
• Common pathogens include Str. Pneumoniae, H. influenza and Moraxella
catarrhalis.
• Treatment:
• Medical: Ampicillin or amoxicillin, failure may be due to beta lactamase in such
cases, clavulinic acid may be needed.
• Surgical: tympanocentesis may be required if patient is not responding to
antibiotics and also in toxic patients.
• Myringotomy and drainage or with grommet insertion is necessary to treat
recurrent Otitis Media
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18. • Mastoiditis
• Caused by Str. Pneumoniae, aspergillus (rare), Mycobacterium tuberculosis
• Chronic Otitis Media
• Often by pneumocystis carinii.
• Seen even in asymptomatic patients
• Pateint presents with otalgia, otorrhoea, hearing loss.
• Aural polyp is seen frequently in External auditory canal or middle ear.
• Audiogram demonstrates conductive or mixed hearing loss.
• The infection is spread through
a) Eustachian tube from nasopharynx.
b) Haematogenous
c) External auditory canal
• Treatment: trimethoprim-sulfamethoxazole for 3 weeks
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19. Inner Ear
• SNHL
• Frequent
• 21 – 49%
• Commonest by HIV itself
• Exact site is uncertain but maybe cochlear or central lesion.
• CMV is the most common secondary infection.
• Toxoplasma causes abscess
“NEUROSYPHILIS, TB, MENINGITIS, side effects of HIV DRUG REGIMEN,
RADIOTHERAPY can cause SNHL”
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20. • Cryptococcus Meningitis:
• 30% patients
• sub acute hearing loss
• infiltration of cochlear and vestibular nerves and scarpa’s ganglion with Cryptococcus
and macrophages resulting in necrosis of nerve.
• Diagnosis by India ink preparation. Should be tested for all HIV patients with H/O new
onset headache.
• Treatment: Amphotericin B and 5-fluorocytosine.
• Syphilis
• Otosyphilis and Neurosyphilis may accelerate the primary syphilis or reactivate the
latent syphilis.
• Manifestations are shortened from 15-30 years to 2-3 years.
• Diagnosis by history, unilateral or bilateral SNHL, VDRL, fluorescent treponemal antibody
absorption test which remains positive throughout life.
• Treatment 24MU of penicillin IV for 3weeks. 20
21. • Facial nerve paralysis
• 30% get affected.
• Due to direct HIV infections of CNS, opportunistic infections , primary or secondary
tumours or auto immunity.
• Most common CNS pathology associated is toxoplasmosis.
• Bell’s palsy is most common diagnosis for 7th nerve with HIV infection.
• HERPES ZOSTER is 7 times more common in HIV patients
• They present with pain, herpetic vesicles of external auditory canal and concha along
the distribution of 7th nerve and peripheral facial palsy.
• Treatment: High dose acyclovir. Role of steroids is controversial.
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23. • Cutaneous Lesions:
• Kaposi’s, sarcoma: Pigmented irregular lesions (macular or nodular, black to dark
brown or red) on mucous membrane or skin of nose.
• Herpes zoster: region of distribution of 5th cranial nerve. Due to reactivation of
Varicella zoster in trigeminal ganglion. Characteristic vesicles seen along sensory
distribution. Giant ulcer of nose and face extending to surrounding facial skin.
• Seborrhic dermatitis: seborrhea like rash involving nasolabial folds –red eruptions with
greasy scales. Can involve eyebrows, nasal and malar regions, post auricular regions,
forehead and back. Treated by topical steroids and ketoconazole
• Nasal obstruction: adenoid hypertrophy, allergic rhinitis, polyposis, chronic
sinusitis, neoplasms of nose or PNS.
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24. • Sinusitis:
• 20-68%
• Cases from acute to chronic with mucosal changes maybe seen.
• Organisms involved are H. influenza, Staph. aureus, Pseudomonas aeruginosa cause
chronic sinusitis.
• Fungal sinusitis by Pseudoallescheria boydii, Alterneria alternate, Aspergillus,
Cryptococcus and Candida.
• Others include Legionella pneumoniae, Acanthamoeba castellani and CMV.
• C/F
• Thick mucopurulent discharge with features of pneumonia and bronchospasm
• Nasal congestion
• Periorbital pain or pain over canine
• Other constitutional symptoms such as fever, headache.
• Diagnosis by CT to know the extent
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25. • Treatment:
• Amoxiclav or cephalosporins – minimum period of 3 weeks
• In case of resistance, hospital admission is to be done and treated with IV
antibiotics or surgical drainage is done.
• Mucolytics and decongestants for symptomatic relief and facilitate drainage.
• If medical therapy fail, repeated antral irrigation is helpful. Endoscopic sinus is often
recommended to enhance drainage. Culture and sensitivity is a must to rule out
opportunistic infections.
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26. Neoplasms
• Kaposi’s sarcoma
• Excessive proliferation of spindle cells of vascular origin
• Non invasive
• Mostly seen on palate, tongue or post. Pharyngeal wall
• Purpulish should be differentiated from angioma or pyogenic granuloma
• Can occur even when the CD4 counts are normal
• Diagnosis by Biopsy which may show
• Proliferation of spindle cells
• Endothelial cells
• Extravasation of RBC
• Hemosiderin laden macrophages
• Treatment includes radiation, intralesionoal vinblastine or cryotherapy.
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28. • NHL
• 10-30%
• Nose, PNS, nasopharynx and oral cavity are commonly involved
• Tends to be more aggressive when the CD4 cells count drops less than 200
• Both nodal and extra nodal symptoms may occur
• CNS lymphoma are more common with patients of HIV
• C/F – Bleeding, nasal obstruction, rhinorrhoea, mass effect on face, orbit or
surrounding structures
• Diagnosis by Needle aspiration, tissue biopsy, Lumbar puncture if CNS and
bone marrow are involved
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29. Airway manifestations
• Upper airway
• Viral tracheitis
• Fungal infections are rare
• Neoplasms such as KS – stridor is an important symptom, fibroptic
bronchoscopy is important for diagnosis.
• Lower airway
• Pneumocystii carnii pneumonia is very common (65%)
• C/F – chest or sternal discomfort, cough, dyspnea on exertion and fever
• X-ray shows diffuse bilateral alveolar or interstitial infiltrates
• Diagnosis by hypertonic NaCl nebulization, staining with toluidine blue,
bronchoalveolar lavage can be done.
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31. • Oral candidiasis (30-90%)
• Most common intraoral fungal infection
• Oral candidiasis is an early sign of immunosuppression
• Three forms
• Pseudomembranous – creamy plague which wipes off easily leaving a bleeding surface
• Atrophic – red patches, tender.
• Hyperplastic – thick heaped white plaques resembling leukoplakia cannot be wiped off
• Angular chelitis is another form with features such as fissuring, cracking, erythema,
ulcerations at corner of mouth
• Diagnosis by KOH preparation – mycelia, hyphae, spores; biopsy with PAS and culture
on SDA
• Treatment: Topical and systemic antifungals ( Ketaconazole, fluconazole,
Amphotericin B in severe cases)
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33. • Hairy leukoplasia
• White, hairy, slightly raised lesions of the lateral border of tongue, bilateral and does
not improve on therapy for oral candidiasis
• Good indicator that that patient may progress to full blown immunodeficiency
• Seen in floor of mouth, pharynx, buccal mucosa
• Biopsy demonstrates ballooning in epithelium, hyperkeratosis, parakeratosis, acanthosis
• Probably caused by EBV
• Treatment by acyclovir, sulfa drugs
• Herpes simplex
• 9%
• Affects the palate, lips, perioral and gingival area.
• Responds to acyclovir
• CMV, herpes zoster, HPV also cause oral lesion
• Ginivitis and Periodontal disease
• Acute necrotising ulcerative gingivitis by gram negative bacteria, anaerobic or candida
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34. ORAL NEOPLASMS
• Kaposi’s Sarcoma – any mucosal surface, hard palate are common
• Lymphoma - tonsils
• Squamous cell carcinoma - tongue
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35. IDIOPATHIC ORAL LESIONS
• Aphthous ulcers
• 20%
• <6mm minor, >6mm major
• Well circumscribed erythematous border
• Large lesion should be biopsied to rule out Carcinoma
• Treated by steroids topically
• Xerostomia
• Fairly frequent, unknown cause
• Frequent oral salines, sugarless gum, salivary substitutes can be used for treatment
• Vocal cord edema
• Previous radiation therapy or obstruction from KS
• Recurrent laryngeal nerve paralysis due to CMV
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36. OTHER MASSES
• HIV Lymphadenopathy
• 2 or more sites for more than 3 months
• LN are soft, symmetric 1-5cm
• Sites – post. Triangle, Waldeyers ring, submental and sub clavicular.
• ROUTINE BIOPSY “NOT HELPFUL”
• Parotid cyst and parotitis
• Cyst is unique to HIV
• Minimally tender, progressive, bilateral and generalised cervical lymphadenopathy
• CT and MRI help in diagnosis
• Surgery limited due to diagnostic difficulties and deforming lesions
• Tetracyline is proved to be successful.
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38. Occupational risks
• More risk is from cutaneous puncture than from contact with skin or
mucous membrane.
• People such as surgeons, nurses, laboratory staff handling blood and
its products are at more risk.
• On such incidents of injury, ELISA test is performed to establish
negative baseline.
• Zidovudine therapy for 6weeks can be offered after exposure.
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39. Diagnosis of HIV
• ELISA: sensitivity of 99.9%
• Western blot
• Blood tests: anaemia, leukopenia (lymphopenia & thrombocytopenia)
• CD4 cell counts
• P-24 antigen: core protein of AIDS. This is positive prior to seroconversion.
• PCR: Quantitative test measuring virus load and relates the progression of
disease
• ß2-macroglobulin levels – indicates macrophage-monocyte level. It rises at
seroconversion and rises with the progression of disease.
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40. Universal precautions
• Wash hands before and after patient contact
• Handle blood as potentially infections
• Wear gloves for potential contact with blood and its products
• Place used syringes in an impermeable container. DO NOT RECAP OR
MANIPULATE
• Wear protective eyewear or mask during procedures such as bronchoscopy or
oral surgery
• Wear gowns when blood splash is anticipated
• Process all lab specimens as potentially infectious
• Do not hold needle or tissue in your fingers while suturing
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Worldwide, the predominant virus is HIV-1, and generally when people refer to HIV without specifying the type of virus they will be referring toHIV-1. The relatively uncommon HIV-2 type is concentrated in West Africa and is rarely found elsewhere.
Process all lab specimens as potentially infectious
Do not hold needle or tissue in your fingers while suturing
