1. FECAL-BORNE HEPATITIS

2. ETIOLOGY Hepatitis A virus (HAV), Hepatovirus Picornavirus, enterovirus 72 27 nm 1 serotype only, although there are 4 genotypes Hepatitis E virus (HEV) Calicivirus-like virions 30 – 32 nm Both are ssRNA, naked icosahedral viruses

3. EPIDEMIOLOGY Natural hosts  Humans Distribution  HAV is worldwide.  High-prevalence areas: Africa, Asia, Central and South America.  Epidemics of HEV have been reported in India (1955 with 29000 cases).

4. Geographic Distribution of HAV Infection

5. Fecal-oral route The virus survive in the environment for over 3 months. Daycares are good places for HAV infections to spread. Transmission

6. HAV  Children 5-9 years  Young adults 25-35 years HEV  Young and middle-aged adults Prevalent  Crowded living conditions  Areas of low socioeconomic development >90% of the population in underdeveloped countries has experienced HAV infection, vs. to <50% of the population in developed countries. Incidence

7. PATHOGENESIS Portal:  After ingestion, the rigid capsid withstands the harsh conditions in the stomach and intestines. Viremia:  HAV replicates in the oropharynx and epithelial lining of the intestines, where it initiates a transient viremia and infects the liver. Replication:  HAV binds to and replicates within liver parenchymal cells. Virus shedding:  Virus is released into the bile and eventually the stools. Virus may be shed for 10 days before clinical symptoms appear.

8. Immunological role in pathology:  Antibody-antigen complexes and complement fixation contribute to inflammation and tissue damage. Self-limited disease: All HAV infections are acute, being self-limited by the induction of IgM and IgG, which confers long-lasting immunity. No chronic complications.

10. MANIFESTATIONS Incubation: 14 - 45 days. Children: 84 - 94% are asymptomatic Adults: 5 - 25% are asymptomatic; 66% have jaundice Initial symptoms: fever, malaise, fatigue, headache, anorexia, nausea, vomiting and pain in the right upper quadrant; and hepatosplenomegaly. Classic symptoms: Cholestasis: Dark urine, clay-colored stools followed in 1 - 5 days by clinical jaundice. The liver is enlarged and tender. Liver damage produces increased blood levels of:  Aspartate aminotransferase (AST=SGOT)  Alanine aminotransferase (ALT = SGPT)  Bilirubin

11. LABORATORY DIAGNOSIS Elevated liver enzymes High titer of anti-HAV IgM (only one serotype) in the serum during the acute phase of the illness using ELISA. 15% of people infected will have prolonged or relapsing symptoms over a 6 – 9 months period. HEV is serologically unrelated and detection of IgM antibodies is available.

12. THERAPY Supportive therapy and rest HAV: low mortality (0.1-0.2%) HEV: Mortality rate 10 times HAV (1-2%). Especially high mortality (20%) during pregnancy

13. PREVENTION Passive immunization using pooled human immune serum globulin (ISG). ISG is of no value once symptoms have appeared. Vaccination of children 2 years of age and older; adolescents and adults is required for people who live in intermediate or high-risk areas. Hepatitis A vaccine:  inactivated (killed) vaccines.  The vaccine should be administered by intramuscular injection into the deltoid muscle.