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ENT MANIFESTATIONS
OF
HIV INFECTION
Introduction to HIV
 AIDS (acquired immunodeficiency syndrome) is a syndrome caused by a virus
called HIV (human immunodeficiency virus).
 The HIV Virus infecting humans is of two types HIV 1 and HIV 2.
 HIV 1 is the most common and very pathogenic where is HIV type 2 is less
common and less pathogenic.
 Once the virus enters the body it attacks T Lymphocytes and other cells which
have CD4 surface marker.
 When the CD4 cell count falls below 500 cells/mm3, (normally 600- 1500
cells/mm3), the immune system starts breaking down with the appearance of
opportunistic infections and unusual malignancies, then it is called as AIDS.
Modes of transmission
HIV infection is transmitted through:
 Sexual contact – homosexual and heterosexuals
 Use of nonsterile needles, syringes
 Blood and blood products
 Infected mother to infants – during pregnancy, during birth and via breast
milk.
High risk groups : multiple sexual partners,
homosexuals,
prostitutes and truck drivers,
I.V. drug users,
recipients of blood and blood products,
children born to HIV infected mothers.
Major hazard to health workers is from blood and body fluids like
amniotic, pleural, peritoneal or pericardial fluid.
Structure of HIV virus
Course of disease
After exposure, the disease runs through the following stages:
 Initial viraemia.
Primary infection with HIV, first causes viraemia which produces mild
clinical disease like fever, headache, body ache and pain, macular
skin rashes and lymph node enlargement.
The virus is then taken up by lymphoid organs like lymph nodes,
tonsils, adenoids and spleen. Initial plasma viraemia last for a few weeks
and then no virus can be detected in the plasma.
 Latent period.
This is asymptomatic phase and may last for variable period, on an
average for 10 years.
During this period no virus is detectable in plasma though it is replicating
replicating in the lymphoid tissue and the CD 4 T-helper cell number and
function is deteriorating.
 Advanced disease.
It starts after several years. the patient becomes susceptible to
opportunistic infections as the CD4 T Cell count falls below 200 cells/mm3.
There are clinical signs and symptoms of AIDS and that may occur within 2
years.
Types of
HIV
manifestation
HIV infection caused loss of helper T-cell population,which is important in cell
mediated immunity. As the T-cell count gradually diminishes , morbidity and
mortality due to HIV increases.
Three types of lesion seen are:
 Opportunistic infections.
All types of infection can occur : viral, bacterial, protozoal,
mycobacterial, or
fungal.
They can involve any area of ear, nose, throat, head and neck and central nervous system.
 Unusual malignancies.
Kaposi sarcoma and lymphomas are common.
Kaposi sarcoma (KS) can involve skin, mucous membranes or viscera. It may be seen in the skin of
the face, neck, or extremities.
It can also occur in oral, nasal, nasopharyngeal, oropharyngeal, or laryngeal mucosa.
Non Hodgkin lymphoma can involve nodal and extranodal sites.
 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.
HIV MANIFESTATIONS
IN DIFFERENT AREAS IN ENT
AND
HEAD & NECK
1. Ear
 Kaposi sarcoma
 Sebbhoeric dermatitis of external canal
 Malignant otitis externa
 Serous otitis media
 Acute otitis media
 Pseudomonas and Candida infection of external and middle ear
 Mycobacterial infections
 Sensorineural hearing loss
 Ramsay Hunt Syndrome
 Facial paralysis
Sebbhoeric dermatitis of external canal
 As HIV disease progresses, up to 83% of patients develop extensive
seborrheic dermatitis, often involving the face, scalp, and, less
commonly, the periauricular region.
 Patients with seborrheic dermatitis of the external ear may present
with recurrent superinfections of the involved skin, in some cases
including the external ear.
 Treatment is the use of a topical steroid (cortisone).
 Recurrences are common.
Serous Otitis Media
 The most common otologic problems reported in HIV-infected patients are
serous otitis media.
 These conditions frequently affect pediatric patients with HIV disease because
eustachian tube dysfunction typical of this age group combined with depressed
cell-mediated immunity markedly increases their susceptibility to middle ear
infection.
 Suspicion of HIV infection is created when there is presence of large lymphoid
proliferated adenoids and a positive history of presence of risk factors of HIV.
 Adenoidectomy (resection of the adenoid) is the treatment of choice which
relieves obstructions in the eustachian tube.
Malignant Otitis Externa
 In patients with HIV infection, malignant (necrotising) external otitis may also be
seen.
 AIDS patients who develop malignant external otitis tend to be younger than the
typical elderly patient with this invasive ear infection .
 Aspergillus fumigatus as well as Pseudomonas aeruginosa have been isolated in
HIV-infected patients.
 Diagnosis for HIV should be considered in any patient who presents with painful
otorrhea and is unresponsive to treatment regimens for simple external otitis.
Sensory Neural Hearing Loss
 Hearing loss may be common among HIV-infected people, most of them having
sensorineural hearing loss.
 In these patients, the hearing loss steadily worsenes with increasing frequencies,
and becomes moderate at high frequencies.
 But speech discrimination is usually normal for them.
 The cause of SNHL may be a primary infection by HIV of either the central
nervous system or peripheral auditory nerve.
2. Nose and Paranasal sinuses
 Herpetic lesion of nose
 Recurrent sinusitis
 Chronic sinus infection
 Fungal sinusitis
 Kaposi sarcoma
 Lymphoma B-cell type
 Burkitt lymphoma
Herpetic lesion of nose
 Patients with immunodeficiency due to HIV infection may suffer from giant herpetic ulcers
caused by either herpes simplex virus or herpes zoster virus.
 The lesions commonly originate in the nasal vestibule and may extend to involve the
nasolabial region.
 Ulcers are usually caused by the reactivation of chronic herpes infection of the geniculate
ganglion.
 The lesion can be diagnosed by history and clinical appearance, and the diagnosis can be
confirmed by culture or Tzanck smear.
Chronic Sinusitis
 It s common in HIV-infected patients, with a prevalence of between 20 and 68%.
 The reason these patients are so prone to infection is not entirely clear, but
changes in the mucociliary clearance, a primary local defense mechanism for
the sinuses, has been reported.
 Causative organisms include atypical opportunistic organisms, such as Alternaria
alternata, Aspergillus sp., Cryptococcus neoformans and Candida albicans
 The most commonly involved sinus is ethmoidal, followed by maxillary.
 It is an important differential diagnosis of unexplained fever or headache,
especially in individuals with low CD4 cell counts.
 The severity of sinusitis in HIV-positive patients correlates directly with the level
of CD4 count
 The diagnosis is confirmed with Plain Sinus Radiograph.
CT SCAN showing left sided
maxillary and ethmoidal
sinusitis
3. ORAL CAVITY & OROPHARYNX
 Candial infection of oral cavity
 Herpetic lesion of palate, buccal mucosa, lips or gums
 Giant aphthous ulcer
 Adenotonsillar hypertrophy
 Generalized lymphadenopathy
 Kaposi sarcoma of palate
 Non – Hodgkin lymphoma of tonsil or tongue
 Hairy leukoplakia
 Gingivitis
Oral Candidiasis
 It’s also known as oral thrush.
 This infection typically presents as tender, white, pseudomembranous or
plaque-like lesions with underlying erosive erythematous mucosal
surfaces.
 The diagnosis is confirmed by clinical examination, microscopic
examination and further by fungal culture report.
 Treatment is either by topical or systemic therapy :
Topical therapy – Nystatin
Systemic therapy – Ketoconazole Or Fluconazole
Giant Apthous Ulcers
 One of the most painful and troublesome conditions of the oral cavity is
recurrent aphthous ulcerations.
 Normally patients minor (< 6 mm in diameter) aphthous lesions.
 HIV-infected patients frequently present with giant (several centimeters
in diameter) aphthous ulcerations.
 These lesions are usually the result of smaller lesions coalescing into
large ulcers that can present anywhere in the oral cavity or pharynx.
 Symptoms like severe odynophagia associated with giant aphthous
stomatitis can produce anorexia and dehydration, and thus leads to
weight loss.
 Secondary infection further adds to the severe pain and constitutional
symptoms accompanying this condition.
4. Larynx
 Laryngitis
 Kaposi sarcoma
 Non-profit Hodgkin lymphoma
5. Salivary gland
 Parotitis
 Xerostomia
 Diffuse parotid enlargement
 Lymphoepithelial cysts of parotid
 Kaposi sarcoma
KAPOSI SARCOMA
Kaposi sarcoma is a rare tumor that has numerous types, the most common of
which is associated with advanced HIV.
All forms of Kaposi sarcoma (KS) are caused by a type of herpesvirus, Kaposi
sarcoma herpesvirus (KSHV).
 It is a multicentric vascular tumor , meaning that it involves blood vessels and
affects soft tissue in multiple areas of the body i.e, skin, mucosa, or the
viscera.
 It originates in the endothelial cells that line blood vessels and lymphatic
vessels
 It is non invasive type tumor and respects the fascial planes.
There are four main types of Kaposi sarcoma:
 Classic KS: This occurs mainly in older adults of Mediterranean, Eastern
European, and Middle Eastern descent. It is more common in males than females.
 Epidemic KS: This is the most common form of KS.
 Endemic KS: Also known as African Kaposi sarcoma, this form is relatively
common in equatorial Africa and can affect children and adults independently of
HIV transmission.
 Iatrogenic KS: This is also known as immunosuppressive treatment-related
Kaposi sarcoma, immunosuppressive Kaposi sarcoma, or transplant-related
Kaposi sarcoma.
 In the oral cavity, the Kaposi sarcoma is commonly seen in in the palate, but may
also be seen on the tongue, or gingiva, or the posterior wall of pharynx.
 It appears purple in colour and has to be differentiated from angiomaor pyogenic
granuloma.
 It acn occur in any stage of HIV infection.
 Size of the tumor varies from few millimetres to several centimetres.
Diagnosis:
 Biopsy.
Suspected lesion is subjected to punch biopsy examination.
The biopsy shows proliferation of spindle cells, endothelial cells,
extravasation of red blood cells and hemosiderin laden macrophages.
If internal tumors are suspected or are considered likely, such as in
patients with HIV infections or AIDS or other immunosuppression, tests
may include:
 CT or X-ray scans of the chest and abdomen
 bronchoscopy
 Gastrointestinal endoscopy
Treatment:
 Localized radiation
 Intralesdional vinblastine
 Cryotherapy
 Systemic chemotherapy given in patients with multiple lesions.
Non – Hodgkin lymphoma
 HIV Patients have high incidence of lymphomas.
 B-Cell Lymphoma is most common and occurs due to Epstein
Barr virus.
 The risk of lymphomas increases with progression of disease,
commonly in patients with CD4 cell count <200/mm3
 CNS Lymphomas are seen in late stages of the disease while
other systemic Lymphomas occurs early.
 Symptoms seen are fever, night sweats, and significant weight
loss
 Both nodal and extranodal sites are involved. The extranodal
sites are nose, Paranasal sinuses, tonsils, nasopharynx, tongue,
orbit, and larynx.
 GI Tract , lungs, and bone marrow may also get involved.
 Hodgkins lymphoma is less common.
Diagnosis :
 FNAB. (Fine Needle Aspiration Biopsy)
. This test helps in the diagnosis of the lymphoma.
 Open Biopsy
It helps in evaluation of cell architecture and
immunohistochemical analysis
Hairy Leukoplakia
 It’s a white, vertically corrugated lesions on the anterior part of the lateral
border of the tongue.
 It’s is caused by Epstein Barr virus
 It’s an early manifestation, thus gives clues to HIV infection.
 AIDS develops in 50% of the patients in 16 months or 80% in 30 months.
 Diagnosis is Confirmed by biopsy.
 Treatment is done with high dose acyclovir (antiviral drugs).
 But recurs once this therapy is stopped, or as the underlying
immunocompromise worsens
Diagnostic Tests
These are based on the identification of antibodies or viral antigens.
Antibodies are formed within 3 months of infection.
 ELISA TEST: It is a very sensitive test with its sensitivity more than 95.5%.
 WESTERN BLOT: It’s a confirmatory test and specific for HIV antibodies.
 CD4 COUNT: Decreasing count indicates immune compromise and the corresponding
risk for development of opportunistic infections and malignancies.
AIDS defining illness appears when CD4 count decreases <200cells/mm3
 p24 Antigen Assay: it’s detects p24 core protein of HIV. The test is positive even prior to
seroconversion. High levels before development of antibodies useful for suspected
acute HIV syndrome.
 PCR Test : It detects HIV – RNA. The two important tests are reverse transcriptase PCR
and branched DNA assay. It determines number of copies of RNA per millimetres of
plasma. It indicates viral load.
HIV infection and health workers
Doctors, particularly the surgeons nurses and laboratory staff handling the
blood and blood stained body Fluids and other secretions Mein contract the
disease as occupational hazard.
The risk is due to:
 Needle stick injury. Hollow needle is more dangerous than solid needle.
 Cuts with contaminated knife or other sharp instruments
 Exposure of open wound to infected blood or body fluid of the patient
 Large mucous membrane exposure.
 Exposure of skin to infected blood and body fluids.
ALL THESE CAN BE PREVENTED BY STRICT FOLLOW OF
UNIVERSAL PRECAUTIONS
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 operations knife to be passed to surgeon in a tray.
 Place used syringes immediately in a nearby impermeable
container.
 Use double gloves where there are likely to be pierced as in
fracture surgery.
 Wear protective eyewear and mask if if splatter with blood is
anticipated.
 Wear gowns when splash with blood or body fluid is anticipated.
 Handle all linen soiled with blood or body secretions as potentially infectious.
 Refrain from patient care if you suffer from exudative or weeping skin lesion or
dermatitis.
 Process all laboratory specimen as potentially infectious
 Wear mask to protect against TB and other respiratory organisms.
ENT HIV manifestation

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ENT HIV manifestation

  • 2. Introduction to HIV  AIDS (acquired immunodeficiency syndrome) is a syndrome caused by a virus called HIV (human immunodeficiency virus).  The HIV Virus infecting humans is of two types HIV 1 and HIV 2.  HIV 1 is the most common and very pathogenic where is HIV type 2 is less common and less pathogenic.  Once the virus enters the body it attacks T Lymphocytes and other cells which have CD4 surface marker.  When the CD4 cell count falls below 500 cells/mm3, (normally 600- 1500 cells/mm3), the immune system starts breaking down with the appearance of opportunistic infections and unusual malignancies, then it is called as AIDS.
  • 3. Modes of transmission HIV infection is transmitted through:  Sexual contact – homosexual and heterosexuals  Use of nonsterile needles, syringes  Blood and blood products  Infected mother to infants – during pregnancy, during birth and via breast milk. High risk groups : multiple sexual partners, homosexuals, prostitutes and truck drivers, I.V. drug users, recipients of blood and blood products, children born to HIV infected mothers. Major hazard to health workers is from blood and body fluids like amniotic, pleural, peritoneal or pericardial fluid.
  • 5. Course of disease After exposure, the disease runs through the following stages:  Initial viraemia. Primary infection with HIV, first causes viraemia which produces mild clinical disease like fever, headache, body ache and pain, macular skin rashes and lymph node enlargement. The virus is then taken up by lymphoid organs like lymph nodes, tonsils, adenoids and spleen. Initial plasma viraemia last for a few weeks and then no virus can be detected in the plasma.  Latent period. This is asymptomatic phase and may last for variable period, on an average for 10 years.
  • 6. During this period no virus is detectable in plasma though it is replicating replicating in the lymphoid tissue and the CD 4 T-helper cell number and function is deteriorating.  Advanced disease. It starts after several years. the patient becomes susceptible to opportunistic infections as the CD4 T Cell count falls below 200 cells/mm3. There are clinical signs and symptoms of AIDS and that may occur within 2 years.
  • 8. HIV infection caused loss of helper T-cell population,which is important in cell mediated immunity. As the T-cell count gradually diminishes , morbidity and mortality due to HIV increases. Three types of lesion seen are:  Opportunistic infections. All types of infection can occur : viral, bacterial, protozoal, mycobacterial, or fungal. They can involve any area of ear, nose, throat, head and neck and central nervous system.  Unusual malignancies. Kaposi sarcoma and lymphomas are common. Kaposi sarcoma (KS) can involve skin, mucous membranes or viscera. It may be seen in the skin of the face, neck, or extremities. It can also occur in oral, nasal, nasopharyngeal, oropharyngeal, or laryngeal mucosa.
  • 9. Non Hodgkin lymphoma can involve nodal and extranodal sites.  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.
  • 10. HIV MANIFESTATIONS IN DIFFERENT AREAS IN ENT AND HEAD & NECK
  • 11. 1. Ear  Kaposi sarcoma  Sebbhoeric dermatitis of external canal  Malignant otitis externa  Serous otitis media  Acute otitis media  Pseudomonas and Candida infection of external and middle ear  Mycobacterial infections  Sensorineural hearing loss  Ramsay Hunt Syndrome  Facial paralysis
  • 12. Sebbhoeric dermatitis of external canal  As HIV disease progresses, up to 83% of patients develop extensive seborrheic dermatitis, often involving the face, scalp, and, less commonly, the periauricular region.  Patients with seborrheic dermatitis of the external ear may present with recurrent superinfections of the involved skin, in some cases including the external ear.  Treatment is the use of a topical steroid (cortisone).  Recurrences are common.
  • 13.
  • 14. Serous Otitis Media  The most common otologic problems reported in HIV-infected patients are serous otitis media.  These conditions frequently affect pediatric patients with HIV disease because eustachian tube dysfunction typical of this age group combined with depressed cell-mediated immunity markedly increases their susceptibility to middle ear infection.  Suspicion of HIV infection is created when there is presence of large lymphoid proliferated adenoids and a positive history of presence of risk factors of HIV.  Adenoidectomy (resection of the adenoid) is the treatment of choice which relieves obstructions in the eustachian tube.
  • 15.
  • 16. Malignant Otitis Externa  In patients with HIV infection, malignant (necrotising) external otitis may also be seen.  AIDS patients who develop malignant external otitis tend to be younger than the typical elderly patient with this invasive ear infection .  Aspergillus fumigatus as well as Pseudomonas aeruginosa have been isolated in HIV-infected patients.  Diagnosis for HIV should be considered in any patient who presents with painful otorrhea and is unresponsive to treatment regimens for simple external otitis.
  • 17.
  • 18. Sensory Neural Hearing Loss  Hearing loss may be common among HIV-infected people, most of them having sensorineural hearing loss.  In these patients, the hearing loss steadily worsenes with increasing frequencies, and becomes moderate at high frequencies.  But speech discrimination is usually normal for them.  The cause of SNHL may be a primary infection by HIV of either the central nervous system or peripheral auditory nerve.
  • 19. 2. Nose and Paranasal sinuses  Herpetic lesion of nose  Recurrent sinusitis  Chronic sinus infection  Fungal sinusitis  Kaposi sarcoma  Lymphoma B-cell type  Burkitt lymphoma
  • 20. Herpetic lesion of nose  Patients with immunodeficiency due to HIV infection may suffer from giant herpetic ulcers caused by either herpes simplex virus or herpes zoster virus.  The lesions commonly originate in the nasal vestibule and may extend to involve the nasolabial region.  Ulcers are usually caused by the reactivation of chronic herpes infection of the geniculate ganglion.  The lesion can be diagnosed by history and clinical appearance, and the diagnosis can be confirmed by culture or Tzanck smear.
  • 21.
  • 22. Chronic Sinusitis  It s common in HIV-infected patients, with a prevalence of between 20 and 68%.  The reason these patients are so prone to infection is not entirely clear, but changes in the mucociliary clearance, a primary local defense mechanism for the sinuses, has been reported.  Causative organisms include atypical opportunistic organisms, such as Alternaria alternata, Aspergillus sp., Cryptococcus neoformans and Candida albicans  The most commonly involved sinus is ethmoidal, followed by maxillary.  It is an important differential diagnosis of unexplained fever or headache, especially in individuals with low CD4 cell counts.  The severity of sinusitis in HIV-positive patients correlates directly with the level of CD4 count  The diagnosis is confirmed with Plain Sinus Radiograph.
  • 23. CT SCAN showing left sided maxillary and ethmoidal sinusitis
  • 24. 3. ORAL CAVITY & OROPHARYNX  Candial infection of oral cavity  Herpetic lesion of palate, buccal mucosa, lips or gums  Giant aphthous ulcer  Adenotonsillar hypertrophy  Generalized lymphadenopathy  Kaposi sarcoma of palate  Non – Hodgkin lymphoma of tonsil or tongue  Hairy leukoplakia  Gingivitis
  • 25. Oral Candidiasis  It’s also known as oral thrush.  This infection typically presents as tender, white, pseudomembranous or plaque-like lesions with underlying erosive erythematous mucosal surfaces.  The diagnosis is confirmed by clinical examination, microscopic examination and further by fungal culture report.  Treatment is either by topical or systemic therapy : Topical therapy – Nystatin Systemic therapy – Ketoconazole Or Fluconazole
  • 26.
  • 27. Giant Apthous Ulcers  One of the most painful and troublesome conditions of the oral cavity is recurrent aphthous ulcerations.  Normally patients minor (< 6 mm in diameter) aphthous lesions.  HIV-infected patients frequently present with giant (several centimeters in diameter) aphthous ulcerations.  These lesions are usually the result of smaller lesions coalescing into large ulcers that can present anywhere in the oral cavity or pharynx.  Symptoms like severe odynophagia associated with giant aphthous stomatitis can produce anorexia and dehydration, and thus leads to weight loss.  Secondary infection further adds to the severe pain and constitutional symptoms accompanying this condition.
  • 28.
  • 29. 4. Larynx  Laryngitis  Kaposi sarcoma  Non-profit Hodgkin lymphoma 5. Salivary gland  Parotitis  Xerostomia  Diffuse parotid enlargement  Lymphoepithelial cysts of parotid  Kaposi sarcoma
  • 30.
  • 31. KAPOSI SARCOMA Kaposi sarcoma is a rare tumor that has numerous types, the most common of which is associated with advanced HIV. All forms of Kaposi sarcoma (KS) are caused by a type of herpesvirus, Kaposi sarcoma herpesvirus (KSHV).  It is a multicentric vascular tumor , meaning that it involves blood vessels and affects soft tissue in multiple areas of the body i.e, skin, mucosa, or the viscera.  It originates in the endothelial cells that line blood vessels and lymphatic vessels  It is non invasive type tumor and respects the fascial planes.
  • 32. There are four main types of Kaposi sarcoma:  Classic KS: This occurs mainly in older adults of Mediterranean, Eastern European, and Middle Eastern descent. It is more common in males than females.  Epidemic KS: This is the most common form of KS.  Endemic KS: Also known as African Kaposi sarcoma, this form is relatively common in equatorial Africa and can affect children and adults independently of HIV transmission.  Iatrogenic KS: This is also known as immunosuppressive treatment-related Kaposi sarcoma, immunosuppressive Kaposi sarcoma, or transplant-related Kaposi sarcoma.
  • 33.
  • 34.  In the oral cavity, the Kaposi sarcoma is commonly seen in in the palate, but may also be seen on the tongue, or gingiva, or the posterior wall of pharynx.  It appears purple in colour and has to be differentiated from angiomaor pyogenic granuloma.  It acn occur in any stage of HIV infection.  Size of the tumor varies from few millimetres to several centimetres. Diagnosis:  Biopsy. Suspected lesion is subjected to punch biopsy examination. The biopsy shows proliferation of spindle cells, endothelial cells, extravasation of red blood cells and hemosiderin laden macrophages.
  • 35. If internal tumors are suspected or are considered likely, such as in patients with HIV infections or AIDS or other immunosuppression, tests may include:  CT or X-ray scans of the chest and abdomen  bronchoscopy  Gastrointestinal endoscopy Treatment:  Localized radiation  Intralesdional vinblastine  Cryotherapy  Systemic chemotherapy given in patients with multiple lesions.
  • 36. Non – Hodgkin lymphoma  HIV Patients have high incidence of lymphomas.  B-Cell Lymphoma is most common and occurs due to Epstein Barr virus.  The risk of lymphomas increases with progression of disease, commonly in patients with CD4 cell count <200/mm3  CNS Lymphomas are seen in late stages of the disease while other systemic Lymphomas occurs early.  Symptoms seen are fever, night sweats, and significant weight loss  Both nodal and extranodal sites are involved. The extranodal sites are nose, Paranasal sinuses, tonsils, nasopharynx, tongue, orbit, and larynx.  GI Tract , lungs, and bone marrow may also get involved.  Hodgkins lymphoma is less common.
  • 37.
  • 38. Diagnosis :  FNAB. (Fine Needle Aspiration Biopsy) . This test helps in the diagnosis of the lymphoma.  Open Biopsy It helps in evaluation of cell architecture and immunohistochemical analysis
  • 39.
  • 40. Hairy Leukoplakia  It’s a white, vertically corrugated lesions on the anterior part of the lateral border of the tongue.  It’s is caused by Epstein Barr virus  It’s an early manifestation, thus gives clues to HIV infection.  AIDS develops in 50% of the patients in 16 months or 80% in 30 months.  Diagnosis is Confirmed by biopsy.  Treatment is done with high dose acyclovir (antiviral drugs).  But recurs once this therapy is stopped, or as the underlying immunocompromise worsens
  • 41. Diagnostic Tests These are based on the identification of antibodies or viral antigens. Antibodies are formed within 3 months of infection.  ELISA TEST: It is a very sensitive test with its sensitivity more than 95.5%.  WESTERN BLOT: It’s a confirmatory test and specific for HIV antibodies.  CD4 COUNT: Decreasing count indicates immune compromise and the corresponding risk for development of opportunistic infections and malignancies. AIDS defining illness appears when CD4 count decreases <200cells/mm3  p24 Antigen Assay: it’s detects p24 core protein of HIV. The test is positive even prior to seroconversion. High levels before development of antibodies useful for suspected acute HIV syndrome.  PCR Test : It detects HIV – RNA. The two important tests are reverse transcriptase PCR and branched DNA assay. It determines number of copies of RNA per millimetres of plasma. It indicates viral load.
  • 42. HIV infection and health workers Doctors, particularly the surgeons nurses and laboratory staff handling the blood and blood stained body Fluids and other secretions Mein contract the disease as occupational hazard. The risk is due to:  Needle stick injury. Hollow needle is more dangerous than solid needle.  Cuts with contaminated knife or other sharp instruments  Exposure of open wound to infected blood or body fluid of the patient  Large mucous membrane exposure.  Exposure of skin to infected blood and body fluids. ALL THESE CAN BE PREVENTED BY STRICT FOLLOW OF UNIVERSAL PRECAUTIONS
  • 43. 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 operations knife to be passed to surgeon in a tray.  Place used syringes immediately in a nearby impermeable container.  Use double gloves where there are likely to be pierced as in fracture surgery.  Wear protective eyewear and mask if if splatter with blood is anticipated.
  • 44.  Wear gowns when splash with blood or body fluid is anticipated.  Handle all linen soiled with blood or body secretions as potentially infectious.  Refrain from patient care if you suffer from exudative or weeping skin lesion or dermatitis.  Process all laboratory specimen as potentially infectious  Wear mask to protect against TB and other respiratory organisms.