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Hepatitis A Silas Helao Pediatrics. Virology Family: Piconaviridae Genus: Hepatovirus (was classified as Enterovirus, reclassified into Hepatovirus)

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Presentation on theme: "Hepatitis A Silas Helao Pediatrics. Virology Family: Piconaviridae Genus: Hepatovirus (was classified as Enterovirus, reclassified into Hepatovirus)"— Presentation transcript:

1 Hepatitis A Silas Helao Pediatrics

2 Virology Family: Piconaviridae Genus: Hepatovirus (was classified as Enterovirus, 19991 reclassified into Hepatovirus) Serotype: One human Genotype: 4 Nucleic Acid: Linear, ss-RNA Genome size:7.5 kb Open reading frame: single, 6.7kb Size:27-28nm icosahedral particle Envelope: NONE Replication: hepatocytes cytoplasm Capsomeric structural proteins:4, VP1-4 None structural protein: 7

3 Viral Hepatitis A Acute viral Hepatitis A is a cyclical infectious disease caused by a RNA virus and is featured by short term symptoms of intoxication, transient disturbances in the liver functions, and in most cases, a benign course. It is the most common viral Hepatitis which affects children without symptoms. Often with jaundice (when >50% liver affected). Regeneration of liver process in kids is active, hence symptoms sometimes are not seen.

4 Virology continues… HAV is small, non envelope with cubic symmetry. It is chemically and resistant to acid. It was classified in genus Enterovirus, and in 1999 was sub classified into its own genus Hepatovirus. Infection titre of HAV in feces is as 1 000 000 000 infectious dose/g

5 Etiology Hepatitis A genus Hepatovirus family Piconaviridae, is the causative agent of Hepatitis A. Causative agent is featured by one antigenic type, and contain the main Ar. It is stable in the environment and very tolerant to low temperature at 21 degrees Celsius for weeks, and completely inactivated at 85 degrees Celsius. The virus is resistant to chlorine, hence preserved in treated drinking water (chlorinated water).

6 Epidemiology Most common infectious diseases of childhood. Most affected are children 5-14 years. Mostly common in countries with low economic development, where by approximately 90% of children tend to test positive to HAV. Sources of infection- sick man Transmission-fecal-oral transmission, through contaminated water, food, dirty hands, various objects etc. Parental transmission is possible, but rare. Blood transfusion of someone in incubation period cause infection. Local outbreaks are likely to occur in institutions such as military personnel. Oral-anal practice or digital-rectal intercourse increase the risk of transmission (especially in homosexual individuals-adults). HAV is highly endemic in Africa, Central & SEA, and Latin America.

7 Pathogenesis

8 Clinical picture Manifested by five cyclical periods, namely: 1.Incubation period (10-45 days, usually 15-30 days) 2.Prodromal (pre-jaundice) or pre-icteric 3.Height (jaundice) or icteric 4.Post icteric 5.Convalescence period

9 Clinical picture Pre icteric Lasts 3-10 days Develops accurately in children with 38-39⁰ C body temperature Intoxication symptoms: malaise, weakness, sleep disturbance, irritability, headache, loss of appetite, nausea & vomiting. Catarrhal phenomenon may appears Dullness pain in RUQ with feel of heaviness Mild change of feces and urine at the end of this period Lab studies All liver enzymes are increased Thymol & content (Z-Lipoproteins feature of dysproteinemia du to gamma-globulin increment, with conjugated bilirubin concentration increment) Bile pigments appear in urine at the end of the of the period. Presence of dominant IgM and IgG

10 Clinical picture continues… Height (Icteric) period Jaundice of scleral, facial skin, body, hard and soft palate plus extremities, spreading for 1-2 days. Can be mild, moderate or intense. Maximum of liver edge is compressed rounded, painful on palpation. In some children, spleen increase in size. Dark urine and discolored feces. ALT and AST increased. Total bilirubin in blood correlates to severity of the disease: mild 57.7+25.9mmol/L, Moderate 111.3+47.4mmol/L Hyperbilirubinemia due to increased concentrations of conjugated bilirubin. CBC= reveals sometimes Leukopenia, neutropenia, monocystosis, lymphocytosis and normal ESR. By the 7 th and 10 th day of onset of jaundice starts to decrease, with disappearance of intoxication, improved appetite, and polyuria. Bile pigments decreases and stool still colored.

11 Clinical picture continues… Post icteric period Slow decrease of liver size. Children feel quite healthy Liver function tests are slightly modified Convalescence period Lasts 2-3 months or even up to 1 year. Disappearance of all clinical and lab manifestations of the disease. Anti IgG>IgM

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13 HAV Classification 1.Type 2.Severity 3.Flow

14 By type Atypical: it includes all cases, accompanied by the appearance of jaundice. Can be mild, moderate, severe and fulminant forms. Atypical: anicteric, erased, cholesteric Form and subclinical always regard as lungs.  Anicteric Hepatitis, featured by the complete absence of yellowness skin and sclera throughout the disease.  Warm Form Hepatitis, major symptoms such like yellow skin and sclera and disappearing after a few days.  Subclinical Form, complete absence of clinical manifestations. Diagnosis made only biochemical blood examination of kid. Featured by obstructive jaundice. It is due to intrahepatic biliary ducts.

15 Criteria for Severity of Hepatitis SeverityCriteria gravity LightweightSymptoms of intoxication AnictericBilirubin concentration in blood to 85mmol/ prothrombin index 80% MiddleIntoxication symptoms Bilirubin concentration in blood up to 150mmol/L prothrombin index of 60-70% WeightliftingSymptoms of intoxication Bilirubin in the blood up to 150mmol/L prothrombin index of 40-60% MalignantComma I OR II coma FulminantHaemorrhagic syndrome decrease the size of the liver Bilirubin-protein and bilirubin –enzymatic dissociation

16 Complications Prolonged jaundice lead to pruritus Thrombocytopenia Aplastic anemia

17 Diagnosis Serological Diagnosis Liver function test: ALT/AST levels (non specific for HAV) Biochemical test: HBV, HCV, HDV AP-mild but related to cholestasis Anti IgM and IgG

18 Prevention 1.Passive immunization Human immunoglobulin given to a person come in contact with HAV ASA Dose dependent 2. Vaccine (live-attenuated and inactivated) Inactivated is more widely used. Active in 15 th day after vaccination 3. Health food, choleric agents, mineral water, multivitamins (B, B2, B6)


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