1. Hepatitis:
Hepatitis is the inflammation of liver caused by immune response against : liver parenchyma induced by viral infections, or some intracellular pathogens that survive in Kupffer cells causing granulomatous infections (Typhoid fever, brucellosis, Q fever, T.B).
Liver abscesses:
1-Portal Vein Bacteremia.
2-Hepatic Artery Systemic Bacteremia.
3-Ascending Cholangitis.

2. Viral causative agents for hepatitis are:
1- Professional-hepatitis viruses:
Hepatitis A,B,C,D, and E; strong tropism to hepatocyte.
2-Non-Professional viruses that cause extra-hepatic
diseases:
Yellow fever viruses, E.B virus secondary to I.M,
CMV, adenovirus, Herpes simplex, and VZV.

3. Hepatitis Viruses: Hepatitis A, B, C, D, and E:
Type
Hepatitis A B C D E
Mode of
Transmission
Fecal-Oral
Bloodborne
Sexual
Vertical
Bloodborn
Classification
& genetic
material
Picornaviridae.
Linear SS-RNA
Hepadnaviridae.
Circular DS-
DNA-R.T enz
Flaviviridae
Linear SS-
RNA
Deltaviridae.
Circular SS
Caliciviridae
Incubation &
Chronic infection
15-40 days
NO.
days
YES(5%)
days
YES (80%)
YES
21-42 days
Clinical outcomes
of Chronic Inf NO
Cirrhosis or
Hepatocellul-ar Carcinoma
Co-infection

4. Hepatitis B virus: Pathogenesis:
-Infection of hepatocytes.
-T-cell mediated cytotoxicity: interaction between
hepatocyte-MHC class I-HBcAg or HBeAg fragments and
CD8+-TCR.
-Kupffer cell response; release of cytokines and
inflammatory mediators; chemotaxis.
-Enhanced natural killer cell activity; cytotoxicity.
-Interferon-α production; Up-regulates MHC-I expression
and inhibits viral replication cycle.
-HBsAg/Anti-HBsAg Antibodies complexes activate
complement system damage.

5. Clinical presentation of Hepatitis B infection:
-Incubation period.
-Acute infection period:
A-Pre-Icteric phase: (days to week):
mild fever, anorexia, myalgia, and nausea.
B-Icteric acute phase: (one to two months):
Jaundice (yellowish coloration of mucous membrane,
conjunctivae, and skin), enlarged and tender liver.
C-Fulminant hepatitis: (In 1-2% of patients):
Much more extensive necrosis of liver during icteric phase;
elevated fever, abdominal pain, renal dysfunction,
Lethal in 8% of cases.

6. Acute Hepatitis B infection
Virulent strain of hepatitis, Co-infection (HDV), Uncontrolled immunity and cytokines
Limited cell-mediated and humoral immunity
Effective cell-mediated and humoral immunity
Chronic stage; Asymptomatic carrier
Chronic active hepatitis
Minimal chronic hepatitis (persistent)
Resolution
Fulminant Hepatitis
Liver Cirrhosis
Hepatocellular Carcinoma

7. Diagnosis of Hepatitis B infection:
-In incubation period and pre-icteric phase:
The first indicator is HBsAg and HBeAg (envelope).
-In acute icteric phase:
Elevated Bilirubin(T,D), Liver enzymes (Transaminases),
Bilirubinuria , elevated Anti-HBc Antibodies in serum.
-In Convalescence phase:
Anti-HBs Antibodies starts elevation in serum(positive).
-In Chronic period:
HBs Ag: positive
Anti-HBc Antibodies: positive
Anti-HBs Antibodies: negative.

8. Diagnosis of Hepatitis B infection:Ni

9. Treatment and Prevention:
-Reduction or elimination of HBV replication indicators
could be performed by Interferon-alpha therapy.
-Antiviral-nucleoside analogs that given orally have
similar effect on viral replication (Lamivudine or adefovir:
inhibition of viral reverse transcriptase).
Prevention:
1-Active vaccine: HBsAg (children vaccination or others).
2-Passive vaccine: Serum Anti-HBsAg (exposed persons;
needlestick , infants born to seropositive mother, sexual)

10. Hepatitis C virus infection:
HCV accounted for ninety percent of cases of non-A, non-B hepatitis.
Transmission:
1-It was initially identified as a major cause of post-
transfusion hepatitis Intravenous drug users
3-Patients on hemodialysis Sexual route, and vertical.
Pathogenesis:
-Replication of virus in hepatocytes, lymphocytes, and
macrophages.
-Destruction of cells by viral replication cycle and immunity.

11. Clinical outcomes of acute hepatitis C infection:
Subclinical infection in 75% of cases
Acute hepatitis C (25% of cases)
Resolution of disease (months)
Chronic hepatitis C (10-15 years)
Mixed Cryoglobulinemia
Cirrhosis (20%)
Hepatocellular Carcinoma
Liver failure

12. Treatment and Prevention:
Diagnosis of HCV:
-Detection of Anti-HCV-Recombinant viral protein
antibodies in patient serum by ELISA.
-Detection of viral nucleic acid in serum by RT-PCR
technique.
Treatment and Prevention:
-Combination therapy of interferon-α and ribavirin provides
a significantly improved response ( 30-50% for genotype 1
and 70-75% for viral genotype 2 and 3).
-No available vaccine. N

13. Hepatitis A infection:
-HAV is responsible for most cases of infectious hepatitis.
-Non-enveloped SS-RNA Virus.
-Transmission: Fecal-Oral route or contaminated water.
-Pathogenesis:
-Absorbed into bloodstream by intestine; portal system of
liver.
-Replication in hepatocytes; destruction, exported into
bile ducts; excreted into stool ( a high titer=1011 viron/ml)
-Released in bloodstream (to a lesser extent); transient
viremia.
-Acute hepatitis; inactivated vaccine (cell-cultured).
Post-exposure prophylaxis (Anti-HAV-Abs).

14. Other causative agents for liver infection:
Bacterial infections: Liver abscesses formation.
1-Portal-vein bacteremia.
2-Hepatic artery bacteremia.
3-Ascending cholangitis; E.coli is the most frequent agent
40% Facultative anaerobic and obligate anaerobic
ascends from the duodenum.
Several Parasitic infections:
1-Leishmaniasis: Leishmania donovani ;
Visceral leishmaniasis (Kala-azar); jaundice, A/G ratio.
In liver: intracellular Amastigote stage.

15. 2-Extra-intestinal Amebiasis: Entamoeba histolytica
Causes hepatic cyst due to transfer of trophozoite via
portal system.
3-Schistosomiasis: Schistosoma mansoni;
Schistosomula migrates to venous system of liver then to
venous plexuses of large intestine.
In liver: Egg-Granulomas in portal area.
Pipe stem fibrosis of portal tracts.
4-Malaria life cycle: Plasmodium causes liver Schizonts. N