Infectious Exam 3 Flashcard
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| INFECTIONS OF CIRCULATORY AND LYMPHORETICULAR SYSTEM |
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| VIRAL hepatitis |
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| Hepatitis -intro |
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| General term for inflammation of liver - can be caused by variety of agents extent of liver damage ranges from mild to fulminant TO DETERMINE ETIOLOGY AND TREATMENT, BLOOD TESTS MUST BE DONE BEFORE ANY TREATMENT IS INITIATED -when diagnosed with viral hep, dont treat! first figure out cause |
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| Viral Hepatitis -intro |
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| liver is primary target things like CMV, EBV or VZV target liver secondarily |
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| Viral Hepatitis -general remarks |
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| types: A- infectious; fecal oral; water borne B - serum (saliva, semen) C - transfusion associated D - delta E- epidemic; fecal oral; water borne |
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| Viral Hepatitis -consequences |
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| subclinical and anicteric (no jaundice) hepatitis A-E -only detected through blood typical, acute, icteric hep - jaundice; yellow skin; A-E chronic hep - cirrhosis; liver cancer ONLY B, C, AND D fulminant hep: massive necrosis resulting in coma and death A-E |
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| Viral Hepatitis -course and symptoms |
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| 1. incubation period is variable and prolonged; wks-months 2. prodrome - fever, fatigue, GI symptoms n/v 3. icteric phase: prodrome continues, dark urine, clay stool, jaundice hepatomegaly, increased AST and ALT and iron increased prothrombin time serum albumin is low 4. convalescent phase: disappearance of jaundice and major symptoms; but fatigue and malaise may persist |
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| Viral Hepatitis -treatment |
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| A: HISG (serum globulin B + D: HBIG chronic HBV: PEG interferon and anti HIV drug - lamivudine, adefovir, entcavir C: peg-interfereon alpha and ribavirin |
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| Viral Hepatitis -vaccine |
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| for A and B intramuscular for adults into thigh for infants person immune to B is also immune to D. vaccinate b means you are safe from D too |
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| Hepatitis B Virus -Serum Hepatitis -etiology |
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| surface antigen is HBsAg: can be detected in clinic; HBsAg indicates infection -neutralizing immunity: production of anti HBsAg Ab results in complete recover from HBV with clearance of HBsAg from blood and immunity from future infection -all you need is surface Ag to be immune to HBV -being immune means you have Ab to surface Ag; called antiHBsAg Ab core antigen: HBcAg cannot be detected in clinic non-neutralizing immunity - Ab are produced but result in non-neutralizing immunity soluble Ag of the core: HBeAg -can be detected in clinic; free HBeAg in blood means active virus replication some HIV drugs are useful because viral polymerase possesses reverse transcriptase activity eight genotypes A and C predominate in US |
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| Hepatitis B Virus -Serum Hepatitis -transmission and reservoir |
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| transmission by serum, saliva, semen -sexual contact -parenteral -perinatal humans are sole host and reservoir |
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| Hepatitis B Virus -Serum Hepatitis -chronic disease |
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| infants and kids will develop chronic some will die from cirrhosis or primary hepatocellular carcinoma 2 forms of chronic: HBeAG positive and negative |
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| Hepatitis B Virus -Serum Hepatitis -pathogenesis |
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| infects liver cells not a lytic virus! does not kill liver cells CD4 and CD8 kill infected cells to control infection anti-HBsAG Ab (aka anti-HBs) neutralizes extracellular virus; serves as serological markerfor immunity |
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| Hepatitis B Virus -Serum Hepatitis -diagnosis acute HBV |
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| serological markers vary markers show if acute or chronic ACUTE HBV infection -HBsAG detected 1-2 wk before onset of symptoms, as last as 12 wk after exposure -igM anti-HBcAg detected -HBeAg detected in acute infection -anti HBsAg Ab detected after vaccination INDICATES IMMUNITY -igG anti-HBc persists indefinitely as marker of past infection |
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| Hepatitis B Virus -Serum Hepatitis -diagnosis chronic HBV |
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| -persistence of HBsAg for more than 6 months |
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| Hepatitis B Virus -Serum Hepatitis -treatment |
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| chronic HBV: peg interferon alpha2a or antiviral drugs: lamivudine, adefovir dipivoxil, entecavir |
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| Hepatitis B Virus -Serum Hepatitis -prevention |
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| HBIG passive immunity high level sof HBs Ab; given soon after exposure reduces acquisition of symptomatic disease -when baby born to HBV mom, wash it, give Ab and vaccine in two thighs and it will prevent baby from gettin sick active immunization is recommended for all children -only HBsAg; recombinant surface Ag made in yeast -deltoid muscle for adults -injection into gluts is for decreased immunogenicity |
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| Hepatitis D Virus HDV -etiology |
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| RNA virus smallest genome of all viruses encodes for two proteins needs HBV to replicate - IF YOU DONT HAVE HBV INFECTION YOU CANNOT GET D can cause either a disease associated with co-infection or superinfection with HBV and causes great morbidity by increasing severity and accelerating pace of chronic HBV infection |
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| Hepatitis D Virus HDV -epidemiology |
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| similar to HBV transmission and reservoir: similar to HBV; mostly passed through blood -percutaneous exposures are most efficient mode of transmission -sexual transmission less efficient than for HBV -perinatal HDV transmission is rare |
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| Hepatitis D Virus HDV -manifestations |
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| co-infection with HBV clinically same as HBV. D accelerates B; having both means severe disease B+D is really bad. superinfection in chronic HBV infection - first HBV then HDV; patients suffer relapse of jaundice; higher chance of developing chronic cirrhosis |
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| Hepatitis D Virus HDV -diagnosis |
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| presence of igG ab to delta antigen in serum igG anti-HDV persists for years |
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| Hepatitis D Virus HDV -treatment/prevention |
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| treatment: no products prevent HDV superinfection of pt with HBV infection prevention: prevent HBV-HDV coinfection by either HBV pre-or postexposure prophylaxis |
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| Hepatitis C - HCV; transfusion Associated Hep -etiology |
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| HCV is enveloped RNA virus -6 genotypes and 100 subtypes -viral RNA polymerase has no proofreading ability; leads to rapid accumulation of mutations; virus escapes immune surveillance; leads to chronic infection |
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| Hepatitis C - HCV; transfusion Associated Hep -epidemiology |
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| worldwide causes 10k deaths; single most common reason for liver transplants -accounts for most cases of chronic hep; many cases of end-stage liver disease in US cause of most parenterally transmitted non-A non-B hep all ages affected; mostly 20-39 yrs risk factors: exposure to blood - transfusion; shared needles -sexual and vertical transmission is low -happens in tattoos or piercings chronic: occurs in many asymptomatic infection and nearly all acute symptomatic HCV chronically infected pt is at risk for developing cirrhosis or carcinoma -HBV only was chronic in kids |
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| Hepatitis C - HCV; transfusion Associated Hep -clinical features |
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| either asymptomatic 70% or acute symptomatic HCV - mild illness; malaise; abdominal pain -about 1/3 will resolve infection without seroconvertin |
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| Hepatitis C - HCV; transfusion Associated Hep -diagnosis |
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| detect anti HCV ab 5-12 we after onset of hep cannot distinguish acute from chronic infection |
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| Hepatitis C - HCV; transfusion Associated Hep -therapy |
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| combination therapy: peg interferon-a and ribavirin but: only 1/3 chronic pt are cured very expensive difficult-flu like symptoms for 48 wks cure is "persistent loss of HCV RNA" during follow ups criteria for treatment: persistent elevation of aminotransferases quantitative HCV RNA severe histologic changes on liver biopsy response to therapy is related to person's hep C genotype -2 and 3 respond more than 1 |
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| Hepatitis C - HCV; transfusion Associated Hep -prevention |
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| screen blood, organ, tissue donors modify high risk behavior implement and adhere to strict universal precautions |
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| Hepatitis A virus -infectious Hepatitis -epidemiology |
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| sporadic outbreaks; under reported pop at risk: day care center; closed population where no sanitation and hygiene; foods like oysters, some fruits transmission: fecal oral; food and water are major vehicles person to person can occur |
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| Hepatitis A virus -infectious hepatitis -clinical features |
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| igM anti HAV is present 5-10 days before onset of symptoms and lasts up to 6 months igG anti-HAV appears early, stays for life --lifelong immunity disease is mild and prolonged but self limited; does not become chronic recover within 3 weeks; some may relapse up to 6 months most infants do not manifest with jaundice elderly are likely to have fulminant hep all A-E fulminant pt will die in few weeks b/c rapid deterioration of liver |
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| Hepatitis A virus -infectious hepatitis -diagnosis |
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| detect igM and total anti HAV in serum anti HAV igM - recover from acute disease anti HAV-IgG - past disease or vaccination; in person with current hepatitis, HAV is not the etiologic agent of current symptoms |
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| Hepatitis A virus -infectious hepatitis -treatment and vaccination |
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| passive: normal human immune globulin not HAIG given within 2 wk post exposure prevents disease but does NOT prevent infection or transmissibility; protection lasts 3 months active: KILLED vaccine havriX = vaqta = hep A only twin rix = A and B |
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| Hepatitis E Virus -epidemiology |
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| enterically transmitted NonA-nonB hep -large outbreaks -fecal oral transmission; water most common vehicle -zoonosis with swine as reservoir -farmers, butchers, water contaminated from farms -HIGH MORTALITY in pregnant!!!! 25% |
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| Hepatitis E Virus -clinical feature |
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| acute HEV same as HAV does not become chronic |
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| HEV -prevention |
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| clean water supplies |
