Hepatitis can be caused by several viruses and other factors. Hepatitis A virus (HAV) causes an acute form of hepatitis that is often self-limiting. HAV is transmitted through the fecal-oral route and spreads through contaminated food or water. It has an incubation period of 4 weeks and causes liver inflammation. Hepatitis E virus (HEV) also causes an acute form of hepatitis through contaminated food or water. While self-limiting in most patients, HEV infection during pregnancy can lead to fulminant liver failure and death, especially in the third trimester. Prevention efforts focus on handwashing and water treatment to prevent transmission.

1. HEPATITIS

2. Cause of hepatitis
■ Hepatitis A
■ Hepatitis B
■ Hepatitis C
■ Hepatitis D
■ Hepatitis E
■ Herpes simplex
■ Cytomegalovirus
■ Epstein-Barr
■ Adenoviruses
■ Drugs
■ Toxins
■ Alcohol
■ Ischemia
■ Wilson'sdisease
■ Other

3. Hepatitis A
■ PROPERTIES:
■ member of the picornavirus family
■ cubic symmetry
■ containing a linear single-stranded RNA genome with a size of 7.5 kb
■ Only one serotype is known,There is no antigenic cross-reactivity with the other hepatitis viruses.
■ Stable to treatment with 20% ether, acid (pH1.0 for 2 hours), and heat (60°C for 1 hour), and
its infectivity can be preserved for at least 1 month after being dried and stored at 25°C or for years
at −20°C
■ Destroyed by autoclaving (121°C for 20 minutes), boiling in water for 5 minutes, dry heat
(180°C for 1 hour), ultraviolet irradiation (1 minute at 1.1 watts), treatment with formalin (1:4000 for
3 days at 37°C),chlorine (10–15 ppm for 30 minutes). Heating food to above 85°C for 1 minute
,sodium hypochlorite (1:100 dilution of chlorine bleach) are necessary to inactivate HAV.

6. Transmission

7. Pathology
■ Hepatitis is a general term meaning inflammation of the liver.
■ Incubation period 4 weeks
■ Liver damage and clinical syndrome result of immune response and not direct effect
of virus
■ Microscopically, there is spotty parenchymal cell degeneration, with necrosis of
hepatocytes, a diffuse lobular inflammatory reaction, and disruption of liver cell
cords.These parenchymal changes are accompanied by reticuloendothelial (Kupffer)
cell hyperplasia, periportal infiltration by mononuclear cells, and cell degeneration.
■ The damaged hepatic tissue is usually restored in 8–12 weeks.

8. Clinical Findings
■ In viral hepatitis, onset of jaundice is often preceded by gastrointestinal symptoms such as nausea,
vomiting, anorexia, and mild fever. Jaundice may appear within a few days of the prodromal period,
but anicteric hepatitis is more common.
■ The onset of disease tends to occur abruptly with HAV (within 24 hours)
■ The disease is more severe in adults than in children
■ Relapses of HAV infection can occur 1–4 months after initial symptoms have resolved.
■ Complete recovery

9. ■ Fatigue
■ Fever
■ Nausea
■ Appetite loss
■ Jaundice, a yellowing of the skin or the whites of the eyes owing
to hyperbilirubinemia
■ Bile is removed from the bloodstream and excreted in the urine, giving it a dark
amber color
■ Diarrhea
■ Light faeces
■ Abdominal discomfort
■ Extrahepatic manifestations:
■ Joint pains, red cell aplasia, pancreatitis

11. Lab diagnosis
■ Virus appears early in the disease and disappears within 2 weeks after the onset of
jaundice.
■ detected in the liver, stool, bile, and blood
■ Methods: 1-immunoassays 2-nucleic acid
■ detected in the stool from about 2 weeks before the onset of jaundice up to 2 weeks
after.
■ Anti-HAV appears in the immunoglobulin M (IgM) fraction during the acute phase,
peaking about 2 weeks after elevation of liver enzymes and usually declines to
nondetectable levels within 3–6 months.
■ Anti-HAV IgG appears soon after the onset of disease and persists for decades.

12. Virus–Host Interactions
■ Most cases of hepatitis type A presumably occur without jaundice during
childhood, and by late adulthood there is a widespread resistance to reinfection.
■ the incidence of infection may be declining as a result of
■ 1- improvements in sanitation
■ 2-rise in the standard of living
■ 3-expanded use of the vaccine in some countries

13. Epidemiology
■ HAV is widespread throughout the world.
■ Outbreaks of type A hepatitis are common in families and institutions, summer
camps, day care centers, neonatal intensive care units, and among military troops.
■ Stool specimens may be infectious for up to 2 weeks before to 2 weeks after onset of
jaundice.
■ In poor country children become immune by age 10 years.
■ The ratio of anicteric to icteric cases in adults is about one to three; in children, it
may be as high as 12 to one.
■ Fecal excretion of HAV antigen and RNA persists longer in the young than in adults.
■ Individuals with chronic liver disease are at increased risk for fulminant hepatitis if a
hepatitis A infection occurs.These groups should be vaccinated.

15. Prevention and Control
■ Formalin-inactivated HAV vaccines made from cell culture adapted virus were
licensed in the United States in 1995.The vaccines are safe, effective, and
recommended for use in Persons more than 1 year of age.Vaccination in tow dose
:1st dose at time 0 and 2nd dose 6-12 months
■ Routine vaccination of all children is now recommended also International
travelers, men who have sex with men, and drug users.
■ Control measures are directed toward the prevention of fecal contamination of
food, water, or other sources by the individual.
■ Reasonable hygiene—such as handwashing, the use of disposable plates, and the
use of 0.5% sodium hypochlorite as a disinfectant—is essential in preventing the
spread of HAV.
■ IG as passive immunization does not prevent infection but rather makes the
infection mild or subclinical and permits active immunity to develop.

16. HepatitisType E
■ HEV is transmitted enterically
■ occurs in epidemic form in developing countries, where water or food supplies are
sometimes fecally contaminated.
■ It was first documented in samples collected during the New Delhi outbreak of
1955
■ Similar illness to Hep A except high mortality to Pregnant women may have ahigh
(20%) mortality rate if develops associated with a clinical syndrome
called fulminant liver failure, especially those in the third trimester.
■ it is self-limiting infection
■ Resembles calicivirus
■ The viral genome has been cloned and is a positive-sense, single-stranded RNA 7.2
kb in size.
■ The virus is classified in the virus family Hepeviridae.

19. Epidemiology
■ Hepatitis E is endemic in Central Asia, while Central America and the
Middle East have reported outbreaks.
■ can develop an acute form of the disease that is lethal in 30% of
cases or more.
■ Most outbreaks associated with fecally contaminated drinking water
■ Minimal person-to-person transmission

20. Transmission

21. Clinical feature

22. Control