HIV

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Disease

Features

Risk Factors for HIV infection

multiple sexual partners; anal sex; traumatic sex; any other STD

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HIV-1 Causative Agent

human immunodeficiency virus type-1; retrovirus (lentivirus subgroup that infect PMN phagocytes); responsible for AIDS in US and much of the world; enveloped; ssRNA

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HIV type-2

structurally similar to HIV-1, except genome is very different; prevalent in West Africa and India; progression to AIDS is slow

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HIV viral antigens

gp 120, gp 41, p17, p24

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gp 120

SU-surface; glycoprotein; partly responsible for attachment to host cells

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gp 41

TM-transmembrane; possible role of entry into host cells

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p17

MA-matrix ptn; helps maintain viral structure; transport viral genome to host cell nucleus and assembles new virions

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p24

CA-capsid antigen; neucleocapsid (NC); 3 important enzymes (Reverse transciptase (RT), Protease (PR), and Integrase (IN)) along with the 2 ssRNA genome from core of HIV virus

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gag

Group Antigen gene - translates matrix, capsid and nucleoprotein as a polyprotein which is cleaved by viral protease

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gag and pol

transcribed as a single unit; translation is often separated

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PR and RT

targets of major anti-HIV drugs

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RNA genome of HIV

consists of 9 genes flanked by long terminal repeats (LTRs)

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gag, pol, and env

genes common to all retroviruses; their protein products are present in virion; functions of genes are very complex and varies depending on cell the type infected

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HIV Pathogenesis

all cells resond differently; #1 cell type infected is CD4+ Tcells and APCs (both critycal for immune defense against viruses/fungi/some bacteria)

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CD4 Cell Function

1. critical for activating macrophages and cytotoxic T lymphocytes, 2. stimultes production of antibodies from B cells

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HIV - GI epithelium and brain cells

chronic diarrhea, lethargy and dementia

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HIV attachment to target cell via

host surface CD4 receptor; host must also have coreceptor to ensure viral entry

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HIV gp120 (SU)

binds host and exposes the binding sites for CD4 receptor and coreceptors

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Viral penetration into host is mediated by

fusion of grp41 with host cell plasma membrane

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HIV Variants: Macrophage tropic

interacts with CCR5 on MQ, DC, and CD4 Tcells; responsible for transmission between people

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HIV Variants: Lymphocyte tropic

interacts with CXCR4 on activated CD4 Tcells

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Macrophage and DC

first cells to be infected at site of viral entry

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Macrophage virus switch

to lymphocyte strain in 50% of cases, which starts to infect CD4 Tcells; result = rapid decline of CD4 Tcell count and progression to AIDS

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Replication of HIV in Host Thelper cells

releases virions from cell lysis

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Replication of HIV in host macrophages

release of virions occurs over longer period without killing cells

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HIV is genetically variable due to

high rate of errors during reverse transcription; result is different preferences for host cells, rates of replication, response to host cell immunity...

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Tcell activation is essential for production of infectious HIV virions with a complete genome

1. Tcell activation induces low level transcription of provirus; 2. RNA transcripts are spliced to allow synthesis of early ptns Tst and Rev; 3. Tst and Rev go to work; 4. late proteins gag, pol, and env are assembled with genomic RNA into virion buds

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Tat

(transactivator - positive regulator of transcription); amplifies transcription of viral RNA

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Rev

(regulator of viral expression - allows export of unspliced and partially spliced transcripts from nuleus); increases transport of singly spliced or unreplicated viral RNA to cytoplasm

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gag, pol, env

assembled with viral RNA into virions

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Production of HIV virion from provirus requires

activation of CD4 Tcells; leading to synthesis of transcription factor NFkB

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NFkB

binds to promoter region of provirus and directs host cell RNA-polymerase to transcribe viral RNA; encodes Tat and Rev ptns

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Tat binds to transcriptional activation region

(TAR, a sequence in LTR of viral mRNA) to prevent transcription from shutting off

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Rev ptn controls

supply of viral RNA to cytoplasm and extend of RNA splicing

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Early in infection, Rev

delivers RNA that encodes ptns needed for making virions

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Later in infection

viral genomes are supplied, which assembe with viral ptns to form complexes that bud through plasma membrane

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Mechanisms of Thelper cell destruction

1. lysis d/t HIV replic; 2. attack of HIV-specific cytotoxic T-cells; 3. NK cell-mediated killing; 4. Ab-dep cell-med cytotoxicity (gp120 on CD4+ SU); 5. autoimmune response; 6. fusion w/infected cells; 7. inc apoptosis; 8. accum of viral ptn in cytoplasm

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Polyclonal activation of B cells in HIV pts

overwhelms capacity to respond to specific antigens, resulting in unbalanced immune response that can give rise to malignancies or opportunistic infections

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Depletion of CD4 Tcells

1. initial drop below 500cells/uL 2. rise in CD4 cells 3. after a variable time, CD4 cells fall for the 2nd time below 500c/uL 4. when CD4 Tcell count <200cells/uL = FULL BLOWN AIDS; often progresses to death

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Acute Retroviral Syndrome (ARS)

50-70% of HIV-infected people; 6d-6wk incubation

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ARS symptoms

sore throat, fever, muscle/headaches, enlarged nodes; rash; disappears w/in a month with attempt to replenish first fall in CD4 count

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DDx for ARS

flue, infectious mononucleosis

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ARS asymptomatic period

months -years; virus can be isolated from blood, semen cervix;

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Long-term non-progresser cases

5% of HIV-infected/untreated pts show no second decrease in CD4 Tcells after 10yrs

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Levels of virion in blood: early vs late stage

<10/ml plasma vs 100-1000

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Malignant neoplasms and opportunistic infx

when CD4 count <300cell/uL: Kaposi's sarcoma, lymphomas (Bcell; non-hodgkin's; EBV Burkett's), cervical or anal carcinoma

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Definition of AIDS

HIV+ pts with CD4 Tcell count below 200cells/mL

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Long-term Non-progressors have mutant CCR5 gene

allows them to remain seropositive for HIV, but maintain a high level of CD4 cells; lack of CCR5 confers resistance to becoming infected with the macrophage-tropic variant

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CCR5

a receptor for chemokines CCL3 (MIP-1a), CCL4 (MIP-1b) and CCL5 (RANTES)

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Mutation of CCR5

induces a certain degree of immunodeficiency, but with HIV it proves to be an advantage

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Mutations of CCR5 and Resistance to HIV

mutations must be homozygous; found in 1% of Cauasian population

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Protozoal Opportunistic Infections in AIDS

toxoplasmosis, isosporal belli infection; cryptosporodiosis

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Fungal Opportunistic infections in AIDS

pneumocystosis, cryptococcosis, candidiasis, histoplasmosis (disseminated), mycobacterial, disseminated TB (extrapulmonary), mycobacterium avium-intracellulare complex

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Viral Opportunistic Infections in AIDS

persistant mucocutaneous herpes simplex, cytomegalovirus (retinitis, GI, or disseminated), Varicella zoster (persistent or disseminated), progressive multifocal leukoencephalopathy

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Dx of AIDS

Early stage - PCR detection of viral RNA/DNA in serum b/c ptns usually non-detectable for 1month; AFTER 1month: viral antibody or components via EIA(ELISA); confirmed by Western blot (envelope ptns gp160, 120, 41, gag, core ptns)

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Confirming HIV Dx by Western Blot

Positive Sample should exhibit antibodies to both envelope and GAG proteins, or to both envelope proteins (41 and 120/160 kD)

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HIV Prevention

No vaccine; education about sex and needle exchange; screening blood/organ donors; treating HIV+ moms and babies before and after delivery; avoiding contaminated fluids with delivery (effective c-section or vaginal)

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Immune response to HIV: Virions

high concentration first 4-8wks, then drops and may rise after 3 years

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Immune Responses to HIV: Antibodies

Antibodies to HIV envelope ptn and HIV core ptn stay elevated from about 8wks and begin to decline around 2-3 years

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Immune Response to HIV: HIV-specific cytotoxic Tcells

jump btw 4-8wks and stay pretty high for many years

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Initial Stages of Immune Response:

1. Th1 and Th2 responses; 2. production of neutralizing antibodies to envelop/core ptns; 3. generation of cytotoxic CD8 Tcells that kill virus-infected cells

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Immune response is evaded by mutant strains of HIV: neutralizing antibodies

those generated in initial phase eliminate original strains, but new mutants are selected to survive

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Immune response is evaded by mutant strains of HIV: Cytotoxic CD8 Tcells

those directed for original HIV strain kill it off, but surivor mutants w/epitope change produce variants

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Challenges of HIV mutants:

development of anti-HIV vaccine and effective anti-retroviral drugs

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Basic Mechanisms of HIV Immune Evasion

1. rapid multiplication (10^10/day); 2. high mutation rate/antigenic variation/immune response cannot keep up with epitopes; 3. elimination of CD4 Tcells by immune mechanisms; 5. Misdirected/exhausted Bcell response

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Streptococcus pneumoniae immune evasion

capsule; avoids phagocytosis

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G+ bacteria, some G- bacteria immune evasion

resist insertion of complement MAC; avoids complement-mediated lysis

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Mycobacterium tuberculosis immune evasion

blocks lysosome fusion with phagosome; avoids antibody and complement opsonization/macrophage killing

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Listeria monocytogenes immune evasion

escapes phagosome into cytoplasm; avoids macrophage killing and presentation on Class-II MHC

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Toxoplasma gondii immune evasion

escapes phagosome into own cytoplasmic vesicle; avoids macrophage killing, presentation on both Class-I and Class-II MHC

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Treponema pallidum immune evasion

covers membrane with host proteins; avoids immune system recognition

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Herpes virus immune evasion

persist in host cells w/o dividiong (latency); avoid immune system recognition

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Streptococcus pneumoniae, influenza and HIV immune evasion

antigenic variation; avoids memory response

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Herpes virus immune evasion

infects cells with little Class-I MHC expression (CNS); avoids presentation on Class-I MHC

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Staphylococcus aureus, Cytomegalovirus, Herpes simplex virus immune evasion

Expresses membrane Fc-binding protein; Avoids IgG opsonization

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Neisseria meningitidis, Neisseria gonorrhoeae, Haemophilus influenzae Immune evasion

Expresses IgA protease; Avoids IgA neutralization

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Herpes simplex virus immune evasion

Expresses membrane complement receptor; Blocks complement function

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Pseudomonas aeruginosa immune evasion

Secretes elastase that inactivates C3a and C5a; Blocks inflammation

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Vaccinia virus immune evasion

Expresses complement control protein on infected cell; Blocks complement-mediated lysis of infected cell

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Vaccinia virus immune evasion

Expresses soluble cytokine receptor; Blocks inflammation

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Epstein Barr virus (EBV) immune evasion

Inhibits host cell expression of LFA-3, ICAM-1; Blocks adhesion of CTL to infected cells

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Herpes simplex virus Cytomegalovirus immune evasion

Inhibits host cells Class I expression; Blocks CTL recognition

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Epstein Barr virus immune evasion

Expresses homolog of IL-10; Inhibits Th1 response, IFNg production, cellular immunity

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Herpes simplex virus immune evasion

Blocks TAP function; Blocks CTL recognition

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Staphylococcus aureus immune evasion

Secretes superantigens; Suppresses immune response

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Hepatitis B Virus, HIV immune evasion

Peptides act as antagonists; T cell activation is blocked

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Mycobacterium leprae immune evasion

Stimulates Th2 response; Suppresses Th1 response

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Measles virus immune evasion

Suppresses T and B cell immunity; Suppresses immune response to many pathogens

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When to initiate HIV treatment?

As soon as infx is detected (CD4 count <500 or plasma HIV viral RNA load >5000)

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Determinants against starting HIV treatment

drug toxicity, resistance development, quality of life, cost, patient compliance

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Death rate from HIV since 1998

declined d/t early Dx and Tx with HAART

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HAART (highly active antiretroviral therapy)

coctail of reverse transcriptase and protease inhibitors, once a day therapy; does NOT cure AIDS, rather it controls viremia and increases CD4 counts

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Nucleoside reverse transcriptase inhibitors (NRTI)

AZT, D4T, 3TC, ddl, ddC

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Non-nucleoside reverse transcriptase inhibitors

nevirapine, delavirdine, efavirenz

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HIV Protease Inhibitors

prevent packaging of viral proteins into virion; Saquinavir, ritonavir, indinavir, nelfinavir

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NTRI Mode of Action

similar to purine/pyrimidine viral nucleic acids --> incorporates into growing viral DNA chain during replication to block completion

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In addition to primary HIV treatment, prophylaxis against opportunistic infx is given

when CD4 count <200 - P. carinii; when CD4 count <75 - mycobacterial and fungal infx

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Resistance HIV Treatment

protease inhibitors - one mutation for resistance can occur w/in days; RTIs - 3 to 4 independent mutations over months

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Retroviral Transformation facilitates oncogenesis

continual replication w/o cell death; integration of a DNA copy of viral RNA into host genome

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3 mechanisms of retroviral transformation

1. oncogens - loss of normal growth control; 2, insertional mutagenesis (insertion of provirus into DNA next to proto-oncogene); 3. expression of trans gene that transcriptionally activates other cellular genes that allows cell proliferation

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Kaposi's Sarcoma

tumor arising from blood or lymph vessels (other forms in older men of eastern europe/africa/mediterranean; w/ AIDS associated herpesvirus-8 (HHV-8)

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Kaposi's Sarcoma and HHV-8

infection w/HIV-1 and HHV-8 greater risk of cancer; mostly latent; cells become lytic and lead to changes causing tumors -- 1. cells become spindly and proliferate; 2. extensive angiogenesis;

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Connection btw HIV-1, HHV-8 and Kaposi's

HIV-1 induced Tat causes endothelial proliferation and the co-infection with HHV-8 favors malignant transformation

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Lymphoma and AIDS

1st HIV case was isolated from a pt w/lymphadenopathy; proliferation d/t disregulated cytokine production compensating for lymphoic cell death in HIV and in response to viral gp41 antigen; B-cell lymphomas more common than T;

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Epstein-Barr virus (EBV), Lymphoma, AIDS

Probably EBV indirectly causes B-cell lymphoma in AIDS; especially in brain and Burkett's lymphoma is 1000x for frequent;

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EBV and HIV Mechanism of Action

latent EBV by HIV infection; EBV infects new Bcells with polyclonal proliferation and inc lifespan; malignant Bcells though to arise from this population of rapidly dividing cells

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HPV, Cervical and Anal carcinoma and AIDS

HPV-16/18 ONLY; sexual transmission infects cervical/anal epithelium; viral product blocks cell cycle regulators; HPV replication increases with decreased host cellular immunity; AIDS pts should be screened biannually

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Toxoplasmosis gondii - causative agent

obligate intracellular sporozoan; reproduces in GI of cats; oocytes passed in feces; morphology - oocyst, trophozoite, tissue cyst

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T. gondii in humans

brain, heart, skeletal muscle tissue cysts form from trophozoites and their protective membrane

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T. gondii epidemiology

worldwide, but >in tropics; 50% US pop seropositive

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T. gondii transmission

1. ingestion of oocysts (kids playing in litter box); 2. ingestion of tissue cyst in meat; 3. congenital 1/500 births; 4. transfusion/organ transplant

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Congenital toxoplasmosis - severe

abortion or stillbirth; live born w/CNS and visceral probs: micro/hydrocephaly, cerebral calcifications, convulsions, psychomotor retardation; hepatitis, pneumonia

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congenital toxoplasmosis - mild form

infected in 3rd trimester; healthy at birth w/later onset of epilepsy, MR, strabismus; very delayed Chorioretinitis - eye pain/loss of acuity from reactivation of latent infx in 20s

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Toxoplasmosis - Normal Hosts

asymptomatic localized lymphadenopathy (cervical); fever, sore throat, rash, hepatosplenomegaly (mimicks mono); ALSO occasionally, severe visceral meningoencephalitis, pneumonitis, myocarditis, hepatitis

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Toxoplasmosis - Immunocompromised hosts

reaction from latent infection; 50% of AIDS pts form Toxoplasmic encephalitis w/90% fatal

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Toxoplasmosis Diagnosis

detection of IgG via indirect hemagglutination or indirect fluorescence OR demonstration of trophozoites in lymph node w/Wright or Giemsa stain

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Toxoplasmosis Prevention

handwashing after handling uncooked meat; properly cook/freeze meat; avoid cat feces; prevent cats from hunting or eating raw meat

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Toxoplasmosis Treatment

pyrimentamine and sulfonamides (not against cyst form); pregnancy - spiramycin (cytostatic macrolide); CYST and TROPHOXOITE - atovaquone used in radical cure of toxoplasma encephalitis

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Cryptosporidium Gastroenteritis

obligate intracelular sporozoan parasite; C.paryum - spherical attach to epithelial microvilli, stains with Giemsa and HE; oocysts are acid fast

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Cryptosporidiosis Epidemiology

animal reservoir and person-person transmition; water contamination in cities; kids at most risk, followed by immunodeficient/AIDS pts

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Cryptosporidiosis Pathogenesis

entire GI tract, esp jejunum; villous atrophy, crypt enlragment and MNC in lamina propria

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Cryptosporidiosis Symptoms - Normal Pts

abdominal pain and profuse, watery diarrhea 5-10days, nausea, anorexia, vomiting, low fever, complete recovery w/o reinfx or relapse

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Cryptosporidiosis Symptoms - Immunocompromised Pts

(childhood malnutrition, AIDS, congenital hypogammaglobulinemia, cancer chemotherapy, transplant pts); indolent onset; severe diarrhea and other "normal" symptoms, but CHRONIC illness unless immune status is improved

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Cryptosporidiosis Dx

ID oocysts in stool via acid-fast or immunofluorescent Ab (ELISA)

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Cryptosporidiosis Prevention and Tx

stool precautions; rehydration, supportive Tx; if drug-induced immunosuppression stop Rx; NO Drugs available

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Mycobacterium avium-intracellulare complex

a group of acid-fast organisms that can be divided into serotypes; second to M. tuberculosis as cause of disease in US; resistant to antitubercular drugs; may require surgery

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M. avium-intracellular complex - manifestations

Most common systemic bacterial infx in AIDS pts; cavity pulmonary disease (superimposed on chronic lung disease), cervical lymphadenitis, osteomyelitis, renal and skin infection

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M. avium-intracellulare complex - symptoms, Dx, prognosis

progressive weight loss, intermittent fever, chills, night sweats, diarrhea; blood culture/DNA probes; grave

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Mycobacterium kansasii infection

3% of mycobacterial diseases in US (cities, IL, OK, TX); photochromogenic - yellow colonies

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M. kansasii - symptoms, Dx, Tx

TB-like symptoms (cavity pulmonary disease, cervical lympadenitis, skin infx; disseminated in AIDS pts); PPD+; Rx - INH, rifampin, ethambutol

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nef

negative regulation factor - augments viral replication in vivo and in vitro; downregulates CD4 and MCH Class-II

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Pneumocystis carinii pneumonia (Pneumocystosis)

d/t Pneumocystis carinii "fungus" that lacks ergosterol in cell wall and is not sensitive to traditional antifungal drugs; spread in infants/elderly/immunocompromised thru air (latent or new infx)

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Pneumocystosis symptoms

gradual onset, SOB/rapid, low-grade fever, 50% have non-productive cough, dusky skin/mucous membranes d/t poor oxygenation in advanced stages...DEATH from respiratory failure

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Pneumocystosis pathoghenesis

inhalation of P. carinii spores, attachement to alveolar walls, inflammatory response w/MNC and fluid accumulation in alveoli w/multiplying fungi; Later = thickened/scarred alveolar walls that prevent passage of O2

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X-ray findings in Pneumocystis pneumonia

Interstitial pneumonia in an AIDS pt has linear opacities w/hazy ground glass appearance

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Pneumocystosis diagnosis

NOT sputum b/c it's deeper than bronchi; BRONCHOALVEOLAR LAVAGE is least invasive (needle aspiration, biopsy, etc); cysts or trophozites by Wright, Giemsa, Papanicolaou stains; Confirm w/methanamine or antibody (PCR in future)

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Pneumocystosis Prevention and Treatment

2nd largest cause of death in AIDS pts; rates lowered w/use of Trimethoprim-sulphamethoxazole (TSX) when CD4<200 in addition to anti-HIV drug regimen

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Pneumocystosis Immunity

cell-mediated (macrophages and CD4 lymphocytes) play biggest protective role against P. carinii; Antibodies against surface glycoprotein and other antigens also play roles

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Cryptococcus neoformans

C. neoformans is yeast w/thick capsule (polysaccharide polymer - GXM) that does not stain w/indian ink; grows at 35-37* on blood, chocolate, sabouraud and potato dextrose agars in 1-2 days resembles bacterial colonies

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Cryptococcus neoformans epidemiology

soils contaminated with guano (bird droppings); sporadic, no occupational predisposition; CD4-compromised pts are susceptible (one of the top 4 killers in AIDS)

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Crytococcus neoformans Pathogenesis

yeast makes antiphagocytic capsule in respiratory tract (Virulence factor: interferes w/antigen presentation cell-mediated response and downreg of WBC migration); disseminates to CNS (meningoencephalitis); Melanin protects from oxid injury; rxn varies

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Cryptococcus neoformans symptoms

Most common presentation: Meningitis (slow, headache/dizzy; impaired cerebral fxn, fever, seizures, CN signs, dementia, LOC); rapidly worsens w/AIDS (5-15% of AIDS pts); Pneumonia is ASYMPTOMATIC

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Cryptococcus neoformans diagnosis

CSF: inc pressure, pleocytosis (>100 cells w/mostly lymphocytes; dec glucose); Isolate C. neoformans from centrifuged CSF sediments/stain w/indian ink; Detect GXM polysac antigen in CSF or serum (latex agglutination or enzyme immunoassay)

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Cryptococcus neoformans treatment

Amphoterecin B in combo w/Flucytosine or Fluconazole; 75% of pts respond to Tx, but relapse; chronic = repeated Tx; 50% of cured have residual damage

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Cyclomegalovirus disease agent

largest member of Herpesviridae family; enveloped dsDNA; infected cells double in size; usually a latent infx that reactivates later; may be a lytic infxn; Intranuclear inclusion bodies make a "owl's eye appearance

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Cytomegalovirus epidemiology

50% of pop is seropositive; transmitted by contact/sexual/transfusion/transplant/pregnancy; risk at day care; isolated from urine/saliva/semen/cervical secretions; infxn is lifelong (latent in leukocytes)

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Cytomegalovirus pathogenesis

infects: eye, CNS, liver tissue; can be latent or active; replication depends on infected cell type (monocytes:low vs. lymphocytes:latent); immunosuppression activates cycle; CMV inhibits MHC transfer to surface of infected cells to evade immune response

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Cytomegalovirus manifestations: Congenital cytomegalic inclusion disease

jaundice, hepatomegaly, anemia, chorioretinitis, low birth wt, microcephaly; remain asymptomatic for years w/5-25% hearing loss, MR, etc later

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Cytomegalovirus manifestations: Acute infections in immunocompetent hosts

asymptomatic, but teens/YAs can develop infectious mononucleosis-like symptoms (fever, fatigue, splenomegaly, lymphadenopathy)

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Cytomegalovirus manifestations: immunocompromised pts

Suffer from the severe form of the disease (pneumonia, chorioretinitis, gastroenteritis, neurologic disorders)

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Cytomegalovirus diagnosis

detection of CMV cytopathology, antigen or DNA in infected tissue; Isolateing virus from tissue or secretions; Demonstrating seroconversion (presence of specific IgM antibody)

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Cytomegalovirus prevention

(vaccine in clinical trials); screen blood/organ donors; safe sex; hyperimmune human anti-CMV globulin for CMV pneumonia in transplant recipients

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Cytomegalovirus treatment

Gancyclovir (inhibits DNA polymerase, bone marrow suppression); Foscarnet (inhibits DNA pol, nephrotoxic); Cidofovir (nucleotide agent, nephrotoxic) for retinitis; *Gancyclovir + immune globulin is effective in dec high mortality of CMV pneumonia*

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HIV compatible vaccines

MMR, pneumococcal polysaccharide, influenza, HAV, HBV

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HIV non-compatible vaccines

oral poliomyelitis, oral typhoid, BCG (TB vaccine), varicella-zoster, yellow fever

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