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ACQUIRED IMMUNODEFICIENCY SYNDROME(AIDS).
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ACQUIRED IMMUNODEFICIENCY SYNDROME(AIDS) DEFINITION : AIDS IS A RETROVIRAL DISEASE CAUSED BY THE HUMAN IMMUNODEFICIENCY VIRUS(HIV),& IS CHARACTERIZED BY INFECTION & DEPLESION OF CD4 + VE LYMPHOCYTES & PROFOUND IMMUNOSUPPRESSION LEADING TO OPPORTUNISTIC INFECTIONS,SECONDARY NEOPLASMS & NEUROLOGICAL MANIFESTATIONS
ACQUIRED IMMUNODEFICIENCY SYNDROME(AIDS) • HISTORY • EPIDEMIOLOGY • ETIOLOGIC AGENT- RETROVIRUS- HUMAN IMMUNODIFICIENCY VIRUS(HIV)-A TYPE OF HTLV • HIV RESEMBLES HTLV –DIFFERS BY BEING CYTOLYTIC FOR T CELLS
HISTORY OF AIDS THE FIRST RECOGNISED CASES OF AIDS OCCURRED IN THE USA IN THE EARLY 1980S .A NUMBER OF GAY MEN IN NEW YORK AND CALIFORNIA SUDDENLY BEGAN TO DEVELOP RARE OPPORTUNISTIC INFECTIONS AND CANCERS THAT SEEMED STUBBORNLY RESISTANT TO ANY TREATMENT.
HISTORY OF AIDS AT THIS TIME, AIDS DID NOT YET HAVE A NAME, BUT IT QUICKLY BECAME OBVIOUS THAT ALL THE MEN WERE SUFFERING FROM A COMMON SYNDROME.
HISTORY OF AIDS HAITIANS ,HOMOSEXUALS, HAEMOPHILIACS AND HEROIN USERS TO MAKE THE 'FOUR-H CLUB' OF GROUPS AT HIGH RISK OF AIDS
THE HISTORY OF HIV/AIDS IN INDIA AT THE BEGINNING OF 1986, DESPITE OVER 20,000 REPORTED AIDS CASES WORLDWIDE, INDIA HAD NO REPORTED CASES OF HIV OR AIDS.ONE REPORT, PUBLISHED IN A MEDICAL JOURNAL IN JANUARY 1986
THE HISTORY OF HIV/AIDS IN INDIA LATER IN THE YEAR, INDIA’S FIRST CASES OF HIV WERE DIAGNOSED AMONG SEX WORKERS IN CHENNAI, TAMIL NADU CONTACT WITH FOREIGN VISITORS HAD PLAYED A ROLE
THE HISTORY OF HIV/AIDS IN INDIA IN 1987 A NATIONAL AIDS CONTROL PROGRAMME WAS LAUNCHED TO CO-ORDINATE NATIONAL RESPONSES. ITS ACTIVITIES COVERED SURVEILLANCE, BLOOD SCREENING, AND HEALTH EDUCATION.
THE HISTORY OF HIV/AIDS IN INDIA BY THE END OF 1987, OUT OF 52,907 WHO HAD BEEN TESTED, AROUND 135 PEOPLE WERE FOUND TO BE HIV POSITIVE AND 14 HAD AIDS.
THE HISTORY OF HIV/AIDS IN INDIA IN 1992 THE GOVERNMENT SET UP NACO (THE NATIONAL AIDS CONTROL ORGANISATION), TO OVERSEE THE FORMULATION OF POLICIES, PREVENTION WORK AND CONTROL PROGRAMMES RELATING TO HIV AND AIDS.
THE HISTORY OF HIV/AIDS IN INDIA IN THE SAME YEAR (1992), THE GOVERNMENT LAUNCHED A STRATEGIC PLAN, THE NATIONAL AIDS CONTROL PROGRAMME (NACP) FOR HIV PREVENTION.
THE HISTORY OF HIV/AIDS IN INDIA IN 1999, THE SECOND PHASE OF THE NATIONAL AIDS CONTROL PROGRAMME (NACP II) CAME INTO EFFECT WITH THE STATED AIM OF REDUCING THE SPREAD OF HIV THROUGH PROMOTING BEHAVIOUR CHANGE.
THE HISTORY OF HIV/AIDS IN INDIA DURING THIS TIME, THE PREVENTION OF MOTHER-TO-CHILD TRANSMISSION (PMTCT) PROGRAMME AND THE PROVISION OF FREE ANTIRETROVIRAL TREATMENT WERE IMPLEMENTED FOR THE FIRST TIME
ETIOLOGIC AGENT 2 SUBTYPES HIV I- EUROPE,AMERICA, CENTRAL AFRICA HIV II- WEST AFRICA,PARTS OF INDIA
ETIOLOGIC AGENT STRUCTURE OF VIRUS- SPHERICAL IN SHAPE,100-140 nm IN SIZE & IS COMPOSED OF 1. CORE PROTEINS- p24 AND p18 2. 2 STRANDS OF GENOMIC RNA
STRUCTURE OF HIV VIRUS 3.ENZYME REVERSE TRANSCRIPTASE 4.THE CORE IS COVERED BY DOUBLE LAYER OF LIPID MEMBRANE 5.THE LIPID MEMBRANE IS STUDDED WITH 2 VIRAL GLYCOPROTEINS gp120 AND gp 41
STRUCTURE OF HIV VIRUS 4IMPORTANT GENES WHICH CODE FOR RESPECTIVE COMPONENTS OF VIRION ARE 1. gag FOR CORE PROTEINS 2. pol FOR REVERSE TRANSCRIPTASE 3. env FOR ENVELOPE PROTEINS
STRUCTURE OF HIV VIRUS 4. tat GENE(TRANSACTIVATOR) FOR VIRAL FUNCTIONS SUCH AS AMPLIFICATION FOR VIRAL GENES, VIRAL BUDDING AND REPLICATION
FORMS OF HIV HIV I- MORE COMMON TYPE ASSOCIATED WITH AIDS IN US, EUROPE,CENTRAL AFRICA HIV 2- WEST AFRICA & PARTS OF INDIA BLOOD COLLECTED FOR TRANSFUSION IS ROUTINELY TESTED FOR BOTH TYPES
ROUTES OF TRANSMISSION 3 ROUTES 1 .SEXUAL CONTACT- 75% CASES 2 . PARENTERAL - BLOOD & IT’S COMPONENT TRANSFUSION,INTRAVENOUS DRUG USERS,SHARED NEEDLES,SYRINGES-THIS GROUP OCCUPIES THE PIVOTAL ROLE IN THE AIDS EPIDEMIC
ROUTES OF TRANSMISSION SCREENING FOR HIV,HEAT TREATMENT OF CLOTTING FACTOR CONCENTRATES HAS REDUCED THE RISK 3. PERINATAL – MOTHER TO CHILD-TRANSPLACENTAL,INTRAPARTUM, POSTPARTUM (BREAST MILK)
ROUTES OF TRANSMISSION HIV IS ISOLATED FROM A NUMBER OF BODY FLUIDS AND TISSUES SEMEN,CERVICAL SECRETIONS, VAGINAL SECRETIONS,BREAST MILK CSF,SYNOVIAL,PERITONEAL,PERICAR-DIAL, AMNIOTIC FLUID.
ROUTES OF TRANSMISSION CAN NOT BE TRANSMITTED BY CASUAL NONSEXUAL CONTACT LIKE SHAKING HANDS ,HUGGING,SHARING HOUSEHOLD FACILITIES
DISINFECTION OF COMTAMINATED MATERIAL CONTAMINATED WASTE PRODUCTS CAN BE STERILISED AND DISINFECTED BY MOST OF THE CHEMICAL GERMICIDES AT MUCH LOWERED CONCENTRATION.
ROUTES OF TRANSMISSION SODIUM HYPOCHLORITE(CHLORINE BLEACH), FORMALDEHYDE , HIV CAN BE INACTIVATED AT 56 DEGREE CENTIGRADE FOR 30 MINUTES
FIVE RISK GROUPS 1.HOMOSEXUAL & BISEXUAL MALES-CONSTITUTE THE LARGEST GROUP OF INFECTED INDIVIDUALS ACCOUNTING - 56 % OF INFECTED MEN 2. INTRAVENOUS DRUG ABUSERS WITH NO HISTORY OF HOMOSEXUALITY-COMPOSE THE NEXT LARGEST GROUP- 25% OF ALL PATIENTS
FIVE RISK GROUPS 3.RECIPIENTS OF BLOOD & BLOOD COMPONENTS (BUT NOT HAEMOPHILIACS)WHO RECEIVED TRANSFUSIONS OF HIV INFECTED WHOLE BLOOD OR COMPONENTS- 1% OF PATIENTS
FIVE RISK GROUPS 4. HAEMOPHILIACS- WHO RECIEVED LARGE AMOUNT OF FACTOR VIII OR IX 5. HETEROSEXUAL CONTACTS OF MEMBERS OF OTHER HIGH RISK GROUPS- 11% OF CASES
PATHOGENESIS THE SEQUECE OF EVENTS – 1. SELECTIVE TROPISM AND INTERNALISATION
PATHOGENESIS CD4 MOLECULE IS A HIGH AFFINITY RECEPTOR FOR HIV WHICH EXPLAINS THE SELECTIVE TROPISM OF THE VIRUS FOR CD4 +VE T CELLS,& IT’S ABILITY TO INFECT OTHER CD4 +VE CELLS
PATHOGENESIS 2. UNCOATING AND PROVIRAL DNA FORMATION – IN DIVIDING CELLS ENTER THE NUCLEUS- INTEGRATED IN HOST CELL GENOME.WITH ACTIVATION BY NEW INFECTION OR BY CYTOKINES, PROVIRAL DNA IS TRANSCRIBED TO FORM VIRAL PARTICLES .
SEQUENCE OF EVENTS IN INFECTION 3.VIRAL BUDDING, SYNCYTIA FORMATION-CELL FUSION BALLOONING AND DEATH.
SEQUENCE OF EVENTS IN INFECTION 4.CYTOPATHIC EFFECTS-QUANTITATIVE EFFECT ( T HELPER CELL DEATH BY CYTOPATHIC EFFECT AND BY CYTOTOXIC T CELLS) – LEADING TO REDUCED CD +VE T HELPER CELLS
PATHOGENESIS OF AIDS QUALITATIVE EFFECT-REDUCED ANTIGEN INDUCED T CELL PROLIFERATION,IMPAIRED TH1(MEMORY T HELPER CELLS )CYTOKINE PRODUCTION, SELECTIVE LOSS OF MEMORY T HELPER CELLS etc
PATHOGENESIS OF AIDS CD4+/CD8+=0.5(NORMAL-2) CD4 MOLECULE AND gp120 INTERACTION PROMOTES INFECTION WITH CMV, HEPATITIS,HERPES SIMPLEX etc.
PATHOGENESIS OF AIDS II .EFFECTS ON MACROPHAGES AND MONOCYTES ,DENDRITICCELLS(MUCOSAL DENDRITIC CELLS & FOLLICULAR DENDRITIC CELLS)& MICROGLIAL CELLS ARE ATTACKED BY THE VIRUS BUT RESISTANT TO CYTOPATHIC EFFECTS OF HIV. BUT REMAIN AS RESERVOIR OF INFECTION AND AS FACTORY OF VIRUS REPLICATION.
PATHOGENESIS OF AIDS III .HIV INFECTION OF NERVOUS SYSTEM-INFECTION IS CARRIED TO THE MICROGLIAL CELLS BY MONOCYTES MACROPHAGES AND ENDOTHELIAL CELLS. NEURONS ARE NOT INFECTED BUT AFFECTED BY gp120 AND RELEASE OF CYTOKINES BY MACROPHAGES
PATHOGENESIS OF AIDS INFECTION OF CENTRAL NERVOUS SYSTEM - NEUROLOGIC MANIFESTATIONS- A.ACUTE ASEPTIC MENINGITIS B.SUBACUTE ENCEPHALITIS C.VACUOLAR MYELOPATHY D.PERIPHERAL NEUROPATHY
PATHOGENESIS OF AIDS IV .B CELL DYSFUNCTION- Gp120 AND Gp41 OF HIV ENVELOPE AND EBV, CMV INFECTION PRODUCE
PATHOGENESIS OF AIDS DERANGEMENT OF B CELL FUNCTION - POLYCLONAL ACTIVATION LEADING TO HYPERGAMMAGLOBULINEMIA,FORMATION OF IMMUNE COMPLEXES. UNABLE TO MOUNT IMMUNE RESPONSE TO A NEW ANTIGEN.
SEQUENCE OF EVENTS IN PATHOGENESIS OF HIV INFECTIONCORECEPTORS CCR5(R5 STRAINS) ON MOSTLY MACROPHAGES & CXCR4(X4 STRAIN) ON T CELLS
PATHOGENESIS OF HIV INFECTION- FOLLICULAR DENDRITIC CELLS & MACROPHAGES ARE MAJOR SITES OF HIV INFECTION AND PERSISTENCEX4 & R5 STRAINS OF HIV VIRUS
DEFINITION OF AIDS DEFINITION OF AIDS. 2 MAJOR SIGNS AND ONE MINOR SIGNS FOR DIAGNOSIS OF AIDS MAJOR SIGNS- A.WEIGHT LOSS OF MORE THAN 10% OF BODY WEIGHT • B.CHRONIC DIARRHOEA OF MORE THAN ONE MONTH DURATION
DEFINITION OF AIDS C.PROLONGED FEVER- INTERMITTENT OR CONTINUOUS FOR MORE THAN ONE MONTH. MINOR SIGNS ARE- A.RECURRENT OROPHARYNGEAL CANDIDIASIS B. PERSISTANT GENERALISED LYMPHADENOPATHY
DEFINITION OF AIDS • C. PERSISTANT COUGH FOR MORE THAN ONE MONTH. • D. GENERALISED PRURITIC DERMATITIS. • E.RECURRENT HERPES ZOSTER • F.PROGRESSIVE DISSEMINATED HERPES SIMPLEX INFECTION
3 PHASES OF THE DISEASE ACUTE HIV SYNDROME (3 – 12 WEEKS) 1. HIGH LEVEL OF PLASMA VIRAEMIA DUE TO REPLICATION OF THE VIRUS 2.VIRUS SPECIFIC IMMUNE RESPONSE – SEROCONVERSION AFTER 3- 6 WEEKS,