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ACQUIRED IMMUNODEFICIENCY SYNDROME presented by : Deepti Awasthi

ACQUIRED IMMUNODEFICIENCY SYNDROME presented by : Deepti Awasthi. CONTENTS. Introduction History Epidemiology HIV Virus Routes of transmission Pathogenesis. Clinical signs and manifestations Oral manifestations Lab diagnosis Prophylaxis Treatment Universal precautions References.

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ACQUIRED IMMUNODEFICIENCY SYNDROME presented by : Deepti Awasthi

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  1. ACQUIRED IMMUNODEFICIENCY SYNDROMEpresented by :DeeptiAwasthi

  2. CONTENTS • Introduction • History • Epidemiology • HIV Virus • Routes of transmission • Pathogenesis • Clinical signs and manifestations • Oral manifestations • Lab diagnosis • Prophylaxis • Treatment • Universal precautions • References

  3. INTRODUCTION • Since, the initial recognition of AIDS in the US in 1981,tremendous advances have taken place in the understanding of this dreaded disease in the last decade as regards its epidemiology, etiology, immunology, pathogenesis, clinical features & morphologic changes in various tissue and organs of the body. • . • 1st DEC - world AIDS day by the WHO.

  4. EPIDEMIOLOGY • Acc. To WHO, in nov 2003 40 million - infected worldwide 5 million – newly infected 3 million – died 2.2 million children - <15 yr • In india, 2nd largest after south africa In 2003, 5 million infected

  5. Status of HIV epidemic in India Maharashtra Manipur Andhra Pradesh Nagaland Tamil Nadu Karnataka High Prevalent states

  6. HISTORY • In monkeys – for over 100,000 years • In 1956 – in central africa : “ gay fever ” • In 1981 – first indication came from new york & los angeles • In 1983 – Luc Montagnier & colleagues from pasteur institute ,paris , isolated a retrovirus – LAV • In 1984 – Robert gallo & colleagues , USA : HTLV- III

  7. In 1985, serological tests available for anti-HIV antibodies. • In 1986, international committee decided on the generic name - HIV • In india – 1st case reported in chennai

  8. HIV virus • Lentivirus subgroup, family retroviridae. • 2 forms : HIV-1 : US & central africa HIV-2 : west africa & india

  9. The genome – 3 str. Genes : gag, pol, env.

  10. ROUTES OF TRANSMISSION • 1. SEXUAL CONTACT - 75% of all cases - male to male & male to female is more potent route than female to male.

  11. 2. PARENTERAL - 25% 1) I.V. Drug abusers 2) hemophiliacs 3) blood recipients

  12. 3. PERINATAL • Vertical transmission • Several risk factors: - pre term delivery - low maternal antenatal CD4 count - illicit drugs during pregnancy. - elective cesarean delivery – by 87% + ZVT in the mother & infant.

  13. Besides blood ,HIV has been isolated from no. of body fluids & tissues : semen, vaginal secretions , cervical secretions, breast milk, CSF, synovial, pleural, peritoneal, pericardial & amniotic fluid. • Salivary protein – secretoryleucocyte PI anti –HIV activity

  14. STERILIZATION & DISINFECTION • HEAT : Virus is very fragile & can be eliminated easily by hot water at 56% for 30 mins. • CHEMICALS : NaOCl – 0.1% Ethanol – 70% Formaldehyde – 5% Glutaraldehyde – 2% H2O2 – 0.3%

  15. PATHOGENESIS Interaction of gp120 of HIV to CD4+T cell internalisation of virion uncoating of virion reverse transcriptase proviral DNA unintegrated, integrated Activated CD4+T cell inactivated CD4+T cell budding,syncytia LATENT PHASE CYTOPATHIC PHASE Quantitative depletion qualitative failure to respond

  16. HIV infection of nervous system : • Out of non-lymphoid organ involvement, HIV inf of nervous system is the most serious. • Some presenting features include : acute aseptic meningitis subacute encephalitis vacuolar myelopathy peripheral neuropathy

  17. STAGES 1) ACUTE HIV INFECTION • 3-6 wks – 50% persons experience low grade fever, malaise, headache, lymphadenopathy. Resolves within wks • Tests for HIV antibodies are –ve at onset & becomes +ve during its course- “SEROCONVERSION ILLNESS” . • P 24 antigen

  18. 2) ASYMPTOMATIC OR LATENT INFECTION • All persons pass through this phase which may last upto several years. • +ve HIV antibody tests • This period of clinical latency , does not mean microbiological latency as virus replication goes on throughout. • The CD4+T cell count decreases < 200 = clinical AIDS sets in

  19. 3) PERSISTENT GENERALIZED LYMPHADENOPATHY 4) AIDS RELATED COMPLEX (ARC) • Includes various constitutional symptom : • unexplained fever > 1mth • weight loss > 10% • chronic diarrhoea > 1mth • Oppurtunistic infections

  20. 5) AIDS • End stage disease • Irreversible breakdown of immune defence mechanism • Progressive oppurtunistic infection & malignancies.

  21. OPPURTUNISTIC INFECTIONS & MALIGNANCIES • MALIGNANCIES: • Kaposi sarcoma • Lymphoma • BCC • Melanoma

  22. VIRAL CMV HERPES SIMPLEX

  23. BACTERIAL • TB • Salmonellosis • Campylobacter inf • Nocardia & actinomycetes • Legionellosis

  24. PARASITIC • PNEUMOCYSTITIS CARINII PNEUMONIA • TOXOPLASMOSIS

  25. MYCOTIC • Candidiasis • Cryptococcosis • Aspergillosis • Histoplasmosis

  26. ORAL LESIONS in child PAROTID SWELLINGS ORAL CANDIDIASIS

  27. HAIRY LEUKOPLAKIA HERPETIC LESIONS DELAYED TOOTH ERUPTION

  28. ADVANCED HIV/AIDS DISEASE DEFINITIONS FOR SURVEILLANCE FOR ADULTS Any clinical stage 3 or stage 4 disease or, where CD4 is available, any clinical stage and CD4 <350/mm3

  29. Diff. b/w adult & pediatric AIDS: • Children develop humoralimmunodef. early, leading to recurrent bacterial inf. • Failure to thrive, chronic diarrhoea ,lymphadenopathy, TB – common manifestation. • Lymphocytic interstitial pneumonia- seen mostly in children.

  30. Testing Options for HIV

  31. LAB DIAGNOSIS OF AIDS • A. IMMUNOLOGICALTESTS • Leucopenia • Lymphopenia • Thrombocytopenia • CD4+T cell < 200 / mm3 • T4 : T8 is reversed. • Lymph node biopsy

  32. B. SPECIFIC TESTS : • Antigen detection • The major core antigen , P24, earliest virus marker to appear in blood. • IgM antibodies appear in 4-6 wks, followed by IgG antibodies. 2. Virus isolation & culture • From peripheral lymphocytes • Viral replication can be detected by- reverse transcriptase activity

  33. 3. POLYMERASE CHAIN REACTION • Most sensitive & specific test • Gold standard for diagnosis in all stages • 2 forms : DNA & RNA 4. ANTIBODY DETECTION • Simplest & most widely employed technique. • 2-8 wks to months for antibodies to appear • Highly infectious • Seronegative infective – “window period” • 2 types : screening & confirmatory tests

  34. Screening tests – high sensitivity not highly specific false + ve results The most widely used screening test is ELISA. • Confirmatory tests – WESTERN BLOT. In this HIV proteins are seperated acc. to their electrophoretic mobility by poly- acramide gel electrophoresis are blotted onto strips of nitrocellulose paper.

  35. PROPHYLAXIS • The prevention aims at – Health education Identification of sources Elimination of high risk activities • No specific vaccine is available. • Several possible strategies have been explored for vaccine production. These include immunisation with – • Modified whole virus • Subunits c)Target cell protection by anti-CD4 antibody

  36. Treatment Options

  37. TREATMENT • Treatment & prophylaxis of infections & tumours 2. General management 3. Immunorestorative measures- Administration of IL-2, thymic factors ,leucocyte transfusion & bone marrow transplantation. 4. Specific anti – HIV agents

  38. NRTI • Zidovudine , stavudine , lamivudineDidanosine , abacavir. • NNRTI • Nevirapine, delavirdine • PI • Saquinavir , ritonavir , indinavir • FI • Enfuvirtide • Integrase I • Raltegravir • CCR5 antagonist • Maraviroc

  39. PREVENTION • Safer sex methods • Screening of blood donors • Disposable syringes, needles etc • Infected women – advised against pregnancy • For interruption of perinatal transmission ZVT 200 mg TID to the women & continued during delivery decreases rate to < 8 %.

  40. IRIS • When a pt. starts ART, his immune deficiencies improve. This sometimes results in uncontrolled inflammatory responses. Hence, pt. may show worsening of clinical features or lab parameters inspite of improving CD4 counts & decrease viral load. • TREATMENT - Symptomatic - NSAIDS - severe: prednisolone - life threatening: stop ART

  41. PEP • ART should be started within the first few hours & no later than 72 hrs . • HIV testing should be done initially & following 3 & 6 months. • EXPOSURE Less severe - 2 drug PEP more severe - 3 drug PEP

  42. Biohazard to Dental workers : • Larger quantity of blood loss • Repeated blood to blood contact • Longer • Length of surgical procedure • Needle prick injuries

  43. UNIVERSAL PRECAUTIONS • Alert all the time. • Single chair room • Gloves – examination • Dental units covered with water proof sheets. • Impervious surgical gown, cap & mask. • For procedure – double gloves • Airotor use – avoided

  44. In suction bottle – 2% glutaraldehyde 30 ml 2% NaOCl 60 ml • Needles discarded immediately • Bag containing waste – incineration • Instruments – reautoclaved twice by double sterilization

  45. Spillage of blood & body fluids , area saturated with 1% NaOCl for 30 mins. Then mopped with an old linen towel.

  46. References : • Ananthanarayan and paniker’s textbook of microbiology ; 8th ed. • Kliegman, behrman, jenson,stanton. Nelson textbook of pediatrics ; vol.1 • Harsh mohan . Essential pathology ; 3rded • Mehta PJ. Practical medicine ;19thed • Chandra S, chandra S. Textbook of pedodontics. 2002 • Davidson S. principles & practice of medicine;19th ed. • www.google.com

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