Enterically transmitted hepatitis :
Enterically transmitted hepatitis Caused by:-
Hepatitis A virus
Hepatitis E virus
Self- limiting viral infections
Vary from subclinical to acute
Both viruses spread via fecal contaminated food and water
Spread controlled by improvement of the sanitary system and personal hygiene
Hepatitis A virusDiscovery &General properties :
Hepatitis A virusDiscovery &General properties 1973
Enteric ally transmitted hepatitis
Infectious hepatitis
27-28 nm
SSRNA ,
Icosahedral
Non-enveloped
Slide 4:
Stable @pH 3x3hrs@RT
Stable@56ºCx30 min
Stable for several wks @RT
Completely inactive@70 ºCx4min
Instant inactive@85ºC
Reliable inactivation (121ºCx30min)
Inactive: hypochlorite 1.5-2.5mg/l for 15 min
Inactive: 2% gluteraldehyde
Inactive: 3% formalin
Resistant to organic solvent: diethyl ether, tri-chloro- & tri-floroethane
Clinical course/pathogenesis :
Clinical course/pathogenesis Following ingestion, HAV enters the bloodstream through the epithelium of the oropharynx or intestine. The blood carries the virus to its target, the liver, and multiplies within hepatocytes and Kupffer cells (i.e., liver macrophages).
There is no apparent virus-mediated cytotoxicity, and liver pathology is likely immune-mediated. Virions are secreted into the bile and released in stool. HAV is excreted in large quantities approximately 11 days prior to appearance of symptoms or anti-HAV IgM antibodies in the blood. The incubation period is 15-50 days, and mortality is less than 0.5%.
Clinical course/pathogenesis :
Clinical course/pathogenesis Incubation period: 2-6wk
Viral excretion may precede jaundice symptoms
Cease near time of Jaundice onset
Jaundice onset about time of IgG & IgM
IgM decline over 3-6 months
IgG life long
Slide 8:
Prodromal: Anorexia- Nausea-Vomiting – Jaundice
Specific: Dark urine, Clay-coloured stool
Discoloration of :Skin, Sclera, Mucous membrane
Resolution: return of colour to stool