FECAL-BORNE HEPATITIS

ETIOLOGY Hepatitis A virus (HAV), Hepatovirus Picornavirus, enterovirus 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

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 cases).

Geographic Distribution of HAV Infection

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

HAV  Children 5-9 years  Young adults 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

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.

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.

MANIFESTATIONS Incubation: days. Children: % are asymptomatic Adults: % 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 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

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.

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

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.