Infectious Exam 3 Test Questions – Flashcards
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| Human Immunodeficiency Virus -etiology |
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| retrovirus with diploid RNA genome important components of infectious viral particles: -ssRNA -core has viral p24 Gag protein RNA dependent DNA polymerase - we dont have it, so good selective toxicity -integrase p11 -protease p32 -surface glycoprotein gp120 -surface glycoprotein gp41 -two strains HIV 1 and 2 -multiple subtypes of HIV1 exist |
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| Human Immunodeficiency Virus -epidemiology |
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| sole reservoir is humans -transmission in USA: sexual contact; largest incidence is men with men -most reported cases are heterosexuals -concurrent STDS increase risk; men passing to women more likely then women passing to men transmitted parenterally: transfusion of blood IV drug abusers transmitted mother to child: high risk occurs in utero, during birth, or breast feeding others: casual contact not a risk factor organ transplant occupational exposure (needles) |
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| Human Immunodeficiency Virus -pathogenesis |
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| A. incubation period 2-4 weeks B. infection begins with gp120 binding to CD4 cells on T cells and macrophages and chemokine receptors (CXCR4 and CCR5). the binding causes conformational change in gp41 which mediates viral membrane fusion with host cell. viral strains vary in affinity for primary and co-receptors -gp120 binds CD4 -CD4 is marker for T helper; also found on monocytes, macrophages, dendritic cells -WITHOUT CO-RECEPTOR infection will not proceed! -during primary infection as well as asymptomatic stages of infection, predominant HIV strain uses CCR5 co-receptor -CCR5 is found on memory CD4, activated CD4, macrophages, dendritic cells, monocytes -as infeciton proceeds, viral phenotype switches to produce HIV subtypes that utilize CXCR4 co receptor (these strains are called X4 or t-trophic HIV) -CXCR4 co receptor is found on naive CD4 or macrophages |
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| Human Immunodeficiency Virus -pathogenesis -2 specific subtypes of HIV |
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| based on cell tropism and syncytium forming ability 1. primary macrophage-tropic (M-tropic R5 strains) -infects macrophages/primary T lymphocytes -non-syncytia forming strains -predominant HIV strain in primary infection as well as asymptomatic stages that follow -excellent prognositc indicator of lack of progression to AIDS 2. T lymphocyte-tropic (T-tropic X4 strains) -infects in PB T lymphocytes and T cell lines -syncytia forming strains -T cells do not survive productive HIV infection as macrophages do -conversion to T tropic strains results in steep decline in CD4 cells and development of AIDS |
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| Human Immunodeficiency Virus -pathogenesis continued |
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| C. inside cell, ssRNA is converted/transcribed to ssDNA by virus-specified reverse transcriptase and ribonuclease H, then ds DNA -many mutations occur, hard to treat D. viral double stranded DNA is integrated into host DNA via integrase p11. latent stage is permanently established -once infected, person is infected for life, HIV treatment MUST BE LIFE LONG -until CD4 cell bearing latent HIV genome is activated, there is no expression of HIV components; no virions are produced --you can suppress active replication, but cannot cure infection E. activation of HIV and production of virions occurs while double stranded DNA viral genome remains integrated in host genome -need viral protease p32 to cleave proteins; VIRAL PROTEASE IS TARGET FOR ANTIVIRAL DRUGS F. HIV causes destruction of CD4 cells via 2 mechanisms: primary effect is depletion of CD4 t cells -direct infectious cytopathic effect -indirectly by immunopathogenesis - autoimmune reactions destroy immune system; apoptic cell death G. acute phase of infection - HIV replicates in T cells of GIT (one half of T cells in human body); most cells gone by third week of infection but depletion is not reflected in peripheral blood CD4 count -gut is leaky so microbial translocation occurs, which activates immune system; ONE OF THE STRONGEST predictors for progression from HIV infection to AIDs and may be the main cause of CD4 cell depletion --for 7 years CD8 fight CD4 and HIV then T cells die! H. after resolving acute HIV, enter clinical latency (no S&S, low viral count in blood, but seropositive); then get diagnosed with AIDS. during latent period, virus replicates in CD4 lymphocytes in lymph nodes throughout body; eventually virus overwhelms immune system --AIDS |
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| Human Immunodeficiency Virus -manifestations of acute HIV |
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| fever lymphdenopathy pharyngitis rash - erythematous maculopapular on face, truck, palms, and soles; mucocutaneous ulceration in mouth myalgias or arthralgia diarrhea n/v headache hepatosplenomegaly thrush neurological symptoms |
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| Human Immunodeficiency Virus -AIDS manifestations |
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| patients CD4 cell count decreases to less than 200 manifestations due to low CD4 count -oral esophageal candidiasis -pneumocystis pneumonia -cytomegalovirus illness -mycobacterium avium complex -cryptococcosis -toxoplasmosis -selected tumors -wasting -neurological complication |
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| Human Immunodeficiency Virus -neurologic dimensions of HIV infection |
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| HIV associated dementia - HAD aka HIV1-associated cognitive/motor complex aka AIDS dementia complex -frequent complication of infection with HIV and is defined as slowly progressive demyelinating disease with neuronal loss of CNS 1. incidence of CNS disease - preHAART; common -even with HAART, cognitive impairment occurs in many people with AIDS and frank dementia occurs in 15% with an annual incidence after onset of AIDS of 5% -risk factor for progression despite HAART is history of IV drug abuse -plasma and CSF viral load suppression is a good prognostic indicator |
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| Human Immunodeficiency Virus -pathology of dementia complex |
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| -HIV directly infects CNS and PNS early in patient's infection -HIV infection/replication only occurs in monocytes, macrophages, microglia in the CNS -HIV does not infect neurons or oligodendrocytes -diffuse or focal myelin pallor of white matter = demyelination -neuronal loss |
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| Human Immunodeficiency Virus -characteristics of HAD |
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| infected macrophages (multinucleated giant cells) astrocytosis microglial nodules neuronal loss |
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| Human Immunodeficiency Virus -manifestations of neurological disease due to HIV |
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| acute and chronic peripheral neuropathies aseptic meningitis acute encephalitis HIV1 associated cognitive/motor complex painful sensore neuropathy or ASYMPTOMATIC NEUROCOGNITIVE impairment - demonstrated by cognitive testing but are asymptomatic in daily life |
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| Human Immunodeficiency Virus -HIV-associated mild Neurocognitive Disorder (MND) |
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| patient has impairments causing mild disturbance of activities of daily living ANI and MND are common in era of ART/HAART -patient has mild difficulties in concentration, attention, and memory may be present -neurologic examination is remarkable -lose concentration, every day activities take longer |
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| Human Immunodeficiency Virus -HAD |
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| diffuse or focal encephalitis; rare due to ART/HAART if HIV not stopped then: early changes: MND -cognitive changes -motor problems -behavioral - apathy Late changes: HAD -progression is abrupt - 3-6m until death -mutism -incontinence and generalized spasticity -death theoretically a person could die of HAD and never be diagnosed with AIDs |
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| Human Immunodeficiency Virus -entire sequence |
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| without treatment, it is 10 yrs from seroconversion to death due to opportunistic infection and certain tumors (most common) or neurologic complications (less common) -survival after 1st appearance of AIDS defininig illness, without treatment is 1 yr ANTIVIRALS AND AB ARE NOT ENOUGH TO CONTROL IT NEEEDDD IMMUNE SYSTEM!!!!! |
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| Human Immunodeficiency Virus -Diagnosis |
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| HIV serology - ELISA assay; Western blot Test for p24 antigen in blood (when donating) detect viral genome - PCR for plasma HIV RNA to determine viral load for treatment or PCF for HIV DNA in wbc --DONT LOOK FOR AB |
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| Human Immunodeficiency Virus -clinical staging |
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| HIV latencyAIDS M tropic T tropic |
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| Human Immunodeficiency Virus -treatment -reverse transcriptin/latency inhibitor |
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| antiviral /antiHIV drugs - HAART - highly active antiretroviral therapy two types of drugs target reverse transcriptase and suppress HIV replication from being latently infected; decreased new virus production 1. Nucleoside analogue reverse transcriptase inhibitors (NRTI/RTIs) ie AZT -CAUSE CHAIN TERMINATION competitive inhibitors 2. Non-nucleoside reverse transcriptase inhibitors (NNRTIs) ie nevirapine, loviridine -INHIBIT REVERSE TRANSCRIPTASE ENZYME ITSELF, but DO NOT cause chain termination non competitive inhibitors |
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| Human Immunodeficiency Virus -treatment -protease inhibitors |
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| saquinavir, indinavir, amprenavir prevents viral protease from releasing the individual proteins from molecule so new virions cannot become infectious --maturation/protein cleavage inhibitors inhibit viral maturation! |
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| Human Immunodeficiency Virus -treatment -Fuzeon |
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| T-20; enfuvirtide inhibits viral fusion into host cell -fusion inhibitor |
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| Human Immunodeficiency Virus -treatment -selzentry |
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| maraviroc -inhibitor of HIV1 co-receptor CCR5 -attachment/binding inhibitor |
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| Human Immunodeficiency Virus -treatment -raltegravir |
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| also sold as isentress inhibitor of HIV1 integrase -integrase inhibitor |
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| Human Immunodeficiency Virus -treatment -monotherapy |
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| NOT EFFICACIOUS LONG TERM due to high mutation rate of virus one drug is never enough! |
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| Human Immunodeficiency Virus -treatment -HAART |
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| 2RTI plus either NNRTI or protease inhibitor -does not stop all new infections; not 100% effective -not a cure! intact virus and integrated, latent viral genome are unaffected -even if no viral RNA level in blood, patient still infectious via sexual contact -drug resistant HIV occurs even with HAART and is major problem in patients due to high mutation rate SERIOUS PROBLEM! -key questions: when should it start, what regimen should be used, when should therapy change, what should it change to treat ppl will less than 200 CD4 treat ppl with symptoms treat people with CD4 between 200 and 350 -intermittent therapy depending on CD4 counts is not a good option; should be CONTINUOUS bc drug resistance always a problem, latent cells still remain DELAY TREATMENT BECAUSE SO MANY PROBLEMS; easy to reach toxicity use of HAART restricted to: HIV associated cognitive motor complex cryptococal meningitis CNS toxoplasmosis primary CNS lymphoma MANY ADVERSE EFFECTS OF HAART |
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| Human Immunodeficiency Virus -prevention |
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| education clean needles barrier techniques |
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| Epstein Barr Virus synonyms / etiology |
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| heterophile-positive infectious mononucleosis (glandular fever) aka kissing disease EBV is part of herpesvirus group; HHV4 |
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| Epstein Barr Virus -epidemiology |
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| saliva worldwide; lifelong subclinical in early childhood poor sanitation like polio, infectious mononucleosis (mono) is diagnosis of industrialized countries when young adults are exposed to EBV, many of them manifest with IM |
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| Epstein Barr Virus -pathogenesis |
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| virus produced in epithelial cells of oropharynx with release of virus in saliva for weeks to months -infection of B lymphocytes occurs early in infection; virus remains latent in these cells lifelong -latently infected B lymphocytes proliferate/undergo hyperplasia -EBV is type 1 t-ind antigen polyclonal B cell response results in hypergammaglobulinemia -B lymphocytes spread to blood where they are destroyed by EBV cells |
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| Epstein Barr Virus -manifestations |
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| long incubation; 2-3 wks prodrome 3-5 days; flu like symptoms; fever headache, general malaise, lethargy presentation: lymphadenopathy (back of neck, armpits) pharyngitis fever up to 3 wk splenomegaly hepatomegaly fatigue disease may linger for up to 1 yr |
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| Epstein Barr Virus -EBV assoicated disease |
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| 1. chronic active EBV aka chronic mononucleosis -rare 2. lymphomas: nasopharyngeal carcinoma burkitts lymphoma non-hodgkin's lymphoma hodgkin's disease 3. hairy oral leukoplakia - lesions on tongue; treat with acyclovir 4. other: MS; predicted by rising igG titer against EBNA and VCA -can occur within 4-5 yrs |
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| Epstein Barr Virus -diagnosis |
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| -present with manifestations -atypical lymphocytosis (downey cells) -positive heterophile AB test -EBV specific antibodies (igM or IgG; not protective |
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| Epstein Barr Virus -differential diagnosis |
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| CMV!!!!! (heterophile negative IM; if its this, then no treatment; no acyclovir or ampicillin -viral hepatitis -acute toxoplasmosis -rubella -HIV primary infection -strep throat -viral pharyngitis |
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| Epstein Barr Virus -treatment |
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| largely supportive, patient will recover without specific therapy |
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| Cytomegalovirus (CMV) -etiology |
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| CMV is herpesvirus group; called HHV5 |
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| Cytomegalovirus (CMV) -epidemiology |
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| MOST are asymptomatic infections leading cause by far of infection and morbidity in neonate one of most frequent disseminated opportunisitc infection seen with AIDS primary and recurrent infection -with recurrent, it is either reinfection or reactivation of infection |
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| Cytomegalovirus (CMV) -transmission |
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| close contact with urine, salive, secretions -blood transfusions -vertical transmission due to mom with primary or recurrent infection -in utero, during birth, breast feeding -primary infection in mom is big concern bc immune pregnant woman results in asymptomatic congenital infection in infant --MOST COMMON CAUSE OF CONGENITAL INFECTION organ transplant recipient -most develop due to immunosuppression sources: environmental, transplanted organs (both are primary infection) transplant pateitn (reactivation infection |
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| Cytomegalovirus (CMV) -pathogenesis |
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| CMV infects: many cell types site of latency is not identified - dont knw where it is reactivated immunosuppression reactivates latent CMV both humoral and cellular immune responses are important in CMV infections |
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| Cytomegalovirus (CMV) -clinical features |
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| in neonates with fulminant congenital cytomegalic inclusion disease CID: infection of liver, lungs, eye-retina, brain if asymptomatic at birth then develop into progressive, late onset, bilateral sensorineural hearing loss -vision loss, neurological deficits, behavioral changes CMV symptomatic infection acquired in infancy: first 3m, lymphadenitis, pneumonitis, hepatosplenomegaly, rash CMV induced mononucleosis -in young adults symptomatically indistinguishable from EBV infectious mono complication: hepatitis, meningoencephalitis, mycorditis, guillian barre |
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| Cytomegalovirus (CMV) -diseases associated with infection |
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| pneumonia retinitis- causes blindness in AIDS pt encephalitis gastroenteritis |
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| Cytomegalovirus (CMV) -laboratory diagnosis |
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| suspect CMN mono in any case of infectious mono where heterophile agglutin test is negative and patient has fever of unknown origin observe "owls eye' appearance in tissues or urine (congenital) atypical lymphocytosis (downey cells) like EBV-IM use TORCH for igM in chord blood |
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| Cytomegalovirus (CMV) -treatment |
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| for IM: largely supportive, patients recover without specific therapy for reactivation: ganciclovir, foscarnet, cidofovir (acycylovir resistant) antisense product formivirsen for treatment of CMV retinitis that dont respond to above. inject into eyeball. |
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| Cytomegalovirus (CMV) -prevention |
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| vaccine or passive immune prophylaxis |
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| Cytomegalovirus (CMV) -vaccine |
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| orphan drug status prevents CMV viremia, CMV disease, associated complications |
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| Cytomegalovirus (CMV) -passive immunity |
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| use CMVIG if kidney transplant patient receives seropositive kidney |
