Acquired immunodeficiency syndrome presented by deepti awasthi
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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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ACQUIRED IMMUNODEFICIENCY SYNDROMEpresented by :DeeptiAwasthi


CONTENTS

  • Introduction

  • History

  • Epidemiology

  • HIV Virus

  • Routes of transmission

  • Pathogenesis

  • Clinical signs and manifestations

  • Oral manifestations

  • Lab diagnosis

  • Prophylaxis

  • Treatment

  • Universal precautions

  • References


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.


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


Status of HIV epidemic in India

Maharashtra

Manipur Andhra Pradesh Nagaland Tamil Nadu Karnataka

High Prevalent states


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


  • 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


HIV virus

  • Lentivirus subgroup, family retroviridae.

  • 2 forms :

    HIV-1 : US & central africa

    HIV-2 : west africa & india


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


ROUTES OF TRANSMISSION

  • 1. SEXUAL CONTACT

    - 75% of all cases

    - male to male & male to female is more potent route than female to male.


  • 2. PARENTERAL

    - 25%

    1) I.V. Drug abusers

    2) hemophiliacs

    3) blood recipients


  • 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.


  • 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


  • 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%


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


  • 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


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


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


3) PERSISTENT GENERALIZED

LYMPHADENOPATHY

4) AIDS RELATED COMPLEX (ARC)

  • Includes various constitutional symptom :

  • unexplained fever > 1mth

  • weight loss > 10%

  • chronic diarrhoea > 1mth

  • Oppurtunistic infections


  • 5) AIDS

  • End stage disease

  • Irreversible breakdown of immune defence mechanism

  • Progressive oppurtunistic infection & malignancies.


OPPURTUNISTIC INFECTIONS & MALIGNANCIES

  • MALIGNANCIES:

  • Kaposi sarcoma

  • Lymphoma

  • BCC

  • Melanoma


  • VIRAL

    CMV HERPES SIMPLEX


  • BACTERIAL

  • TB

  • Salmonellosis

  • Campylobacter inf

  • Nocardia & actinomycetes

  • Legionellosis


  • PARASITIC

  • PNEUMOCYSTITIS

    CARINII PNEUMONIA

  • TOXOPLASMOSIS


  • MYCOTIC

  • Candidiasis

  • Cryptococcosis

  • Aspergillosis

  • Histoplasmosis


ORAL LESIONS in child

PAROTID SWELLINGS ORAL CANDIDIASIS


HAIRY LEUKOPLAKIA HERPETIC LESIONS

DELAYED TOOTH ERUPTION


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


  • 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.


Testing Options for HIV


LAB DIAGNOSIS OF AIDS

  • A. IMMUNOLOGICALTESTS

  • Leucopenia

  • Lymphopenia

  • Thrombocytopenia

  • CD4+T cell < 200 / mm3

  • T4 : T8 is reversed.

  • Lymph node biopsy


  • 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


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


  • 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.


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


Treatment Options


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


  • NRTI

  • Zidovudine , stavudine , lamivudineDidanosine , abacavir.

  • NNRTI

  • Nevirapine, delavirdine

  • PI

  • Saquinavir , ritonavir , indinavir

  • FI

  • Enfuvirtide

  • Integrase I

  • Raltegravir

  • CCR5 antagonist

  • Maraviroc


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 %.


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


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


  • Biohazard to Dental workers :

  • Larger quantity of blood loss

  • Repeated blood to blood contact

  • Longer

  • Length of surgical procedure

  • Needle prick injuries


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


  • In suction bottle – 2% glutaraldehyde 30 ml

    2% NaOCl 60 ml

  • Needles discarded immediately

  • Bag containing waste – incineration

  • Instruments – reautoclaved twice by double

    sterilization


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


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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