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Group 3: Monthly Reported Diseases3.1 Viral Hepatitis ICD-10 B15: Acute Hepatitis AICD-10 B16: Acute Hepatitis BICD-10 B17: Other Acute Viral HepatitisICD-10 B18: Chronic Viral HepatitisICD-10 B19: Unspecified Viral Hepatitis3.1.1 Identification1) Hepatitis Types A and EClinical featuresThese share same clinical course; no evidence of chronic form. Infection occurs in childhood and young adults asymptomatically or with a mild illness- may be detectable only through laboratory tests of liver function. Onset of illness in adults is usually abrupt with fever, malaise, anorexia, nausea and abdominal discomfort, followed within a few days by jaundice. The disease varies in clinical severity from a mild illness lasting 1–2 weeks to a severely disabling disease lasting several months. Prolonged, relapsing hepatitis for up to 1 year occurs in 15% of cases. Convalescence is often prolonged. In general, severity increases with age, but complete recovery without sequelae or recurrences is the rule. Case-fatality for Hepatitis A is normally low, 0.1%–0.3%; it can reach 2.7% for adults over 50; persons with chronic liver disease have an elevated risk of death from fulminant hepatitis A. The case-fatality rate for HEV is similar to that of hepatitis A except in pregnant women, where it may reach 20% among those infected during the third trimester of pregnancy. Laboratory Diagnosis of types A and E:Acute Hepatitis A: demonstration of serum IgM anti-HAV detectable 5–10 days after exposure.. Acute hepatitis E: presence of IgM anti-HEV or exclusion of other causes of hepatitis, especially hepatitis A, by serological means. 2) Hepatitis Types B, and CClinical featuresUsually asymptomatic. In those with clinical illness, the onset is usually insidious, with anorexia, vague abdominal discomfort, nausea and vomiting, some- times arthralgia and rash, often progressing to jaundice. Fever may be absent or mild. Less than 10% of children and 30%–50% of adults with acute hepatitis B virus (HBV) infection show icteric disease.Severity ranges from unapparent cases detectable only by liver function tests to fulminating, fatal cases of acute hepatic necrosis. The case-fatality rate is about 1%; higher in those over 40. Fulminant HBV infection also occurs in pregnancy and among newborns of infected mothers. The risk of developing chronic infection varies inversely with age; occurs among about 90% of infants infected at birth, 20%–50% of children infected from 1 to 5 years, and 1%–10% of persons infected as older children and adults. Persons with chronic infection may or may not have a history of clinical hepatitis. About one-third have elevated aminotransferases; biopsy ?ndings range from normal to chronic active hepatitis, with or without cirrhosis. An estimated 15%–25% of persons with chronic HBV infection will die prematurely of either cirrhosis or hepatocellular carcinoma. Onset of acute hepatitis C is usually insidious, with anorexia, vague abdominal discomfort, nausea and vomiting; progression to jaundice less frequent than with hepatitis B. Asymptomatic in more than 90% of cases or mild, a high percentage (50%–80%) develop a chronic infection. Of chronically infected persons, about half will eventually develop cirrhosis or cancer of the liver.Type D: The delta agent is a defective virus. It occurs in 2 forms, either coinfection or superinfection with hepatitis B virus. It is prevented through the prevention of Hepatitis B.Laboratory Diagnosis of types B and C:Type B: serum HBsAg positive from several weeks before onset of symptoms to days, weeks or months after onset; it persists in chronic infections. The presence of HBsAg indicates that the person is potentially infectious. High titers of IgM anti-HBc occur during acute infection—IgM anti-HBc usually disappears within 6 months but can persist in some cases of chronic hepatitis; this test may reliably diagnose acute HBV infection.Anti HBcIgG replaces anti HBcIgM and continues forever.Type C: antibody to the hepatitis C virus (anti-HCV) - by the enzyme immunoassay (EIA) and the recombinant immunoblot assay. These tests do not distinguish between acute, chronic, or resolved infection. Acute or chronic HCV infection in a patient with a positive EIA test should be con?rmed by a sensitive HCV RNA assay. Quantitative determination of HCV levels provides information on the likelihood of response to treatment in patients undergoing antiviral therapy. Liver biopsy can provide direct histological assessment of liver injury due to HCV but cannot be used to diagnose HCV infection.Genotyping of HCV infection is important from epidemiological and treatment point of view.Case definitionAn acute illness that includes malaise, extreme fatigue, fever, nausea and sometimes vomiting and upper right quadrant abdominal tenderness, then dark urine followed by jaundice.Case classificationSuspected case: A case compatible with clinical description.Probable case: A Suspected Case + Positive Bile pigment in urine and elevated serum bilirubin and liver enzymes (ALT, SGPT and Serum Alkaline Phosphatase).Confirmed case: Probable/suspected case with positive specific serological tests. This is most commonly done by detecting Anti-HAV, HBsAg, Anti-HCV, and Anti-HEV. This can be done by different methods and the most famous one is ELISA method. In addition great increase of liver enzymes like alanine transaminase (ALT), serum alkaline phosphatase and SGOT etc.Chronic Hepatitis B cases: Any patient with positive HBsAg for more than 6 months and is considered as a case of chronic carrier state.Note: The patient should be tested for other markers (HBeAg, Anti- HBcIgM, and Anti- HBe) to determine the health status and infectivity level. Positivity for HBeAg indicates high infectivity while positivity for Anti- HBcIgM means acute infection.Positive Anti- HBe means less Infectivity. Chronic Hepatitis C: Any patient who is positive for HCV Abs should be referred to the specialist center for more evaluation because positivity for HCV Abs cannot differentiate infection from immunity and needs further investigations. PCR is very necessary to identify such cases. 3.1.2 Infectious agentHepatitis A virus (HAV): RNA virus, family Picornaviridae.Hepatitis B virus (HBV): a hepadnavirus, partially double-stranded DNA virus composed of nucleocapsid core (HBcAg), surrounded by an outer lipoprotein coat containing the surface antigen (HBsAg). 8 main genotypes (A-H). Hepatitis C virus (HCV): RNA virus, genus Hepacavirus, Flaviviridae family. At least 6 genotypes and approximately 100 subtypes. Hepatitis E virus (HEV): a spherical, nonenveloped, single-stranded RNA virus, family Hepeviridae.3.1.3 OccurrenceType A: Iraq is considered highly endemic as indicated by 96.4% prevalence of Anti HAV Abs. Type B: Iraq is considered with low endemic with HBsAg prevalence was 1.6% in 2006.Type C: In the Middle East, the prevalence of anti-HCV ranges from 1% to more than 12%. In Iraq, the prevalence of anti HCV Abs was found to be 0.4%.Type E: The prevalence of Anti HEV Abs in Iraq in 2006 was about 20%.. ................
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