FECAL-BORNE HEPATITIS

ETIOLOGY

Hepatitis A virus (HAV), Hepatovirus

Picornavirus, enterovirus 72

27 nm1 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 29000 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 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

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: 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

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 restHAV: low mortality (0.1-0.2%) 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.inactivated (killed) vaccines. The vaccine should be administered by intramuscular

injection into the deltoid muscle.