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Pathology
Lecture 48 Infectious Hepatitis
1) Understand the primary nature of hepatotrophic viral hepatitis.
Varying degrees of parenchymal necrosis with no cellular reaction or minimal
lymphocytic response. Hepatocellular necrosis occurs through ballooning
degeneration, but may occur through apoptosis (shrunken eosinophilic hepatocytes
called Councilman or Acidophilic bodies). Viral infection may result in: 1) extensive
necrosis leading to death, 2) symptomatic disease with rapid recovery, 3)
symptomatic disease with delayed recovery, 4) symptomatic disease with chronic
damage and cirrhosis, or 5) persistence of disease with minimal effect (carriers).
2) Know the heptotrophic viruses. Review virology notes.
HAV, HBV, HCV, HDV, and HEV.
3) Recognize the short-term acute complications and long-term sequela of
hepatotrophic viruses.
HAV: 0.1% fatality, usually resolves, not chronic, no carrier state.
HBV: 2% acute necrosis and death, 10-33% chronic disease, 5-10% healthy carriers.
HCV: >50% chronic disease.
HDV: simultaneous infection with HBV 3-4% fulminant disease, superimposed on
chronic HBV = acute, fulminant, or chronic disease (80% of patients) with cirrhosis.
HEV: not associated with chronic liver disease or persistent viremia.
4) Know Hepatitis B viral disease well because of its global significance.
<1% die of acute disease, 5-10% healthy carriers,
4% with chronic disease (Chronic Persistent Hepatitis) will eventually recover
Cirrhosis is late to come, 60-65% sub-clinical disease,
10-15% with chronic disease will end up with Hepatocellular Carcinoma
5) Hepatitis C is relatively new but is a very important common disease with better
understanding of the virus now.
150,000-170,000 cases annually in the U.S.
Small single stranded RNA virus, Blood borne disease
1% of population are seropositive, 50-85% hemophiliacs and 8% people with
hemodialyis are seropositive
50% progress to chronic disease, Incubation period is 2-26 weeks
Clinical course in milder, Anti-HCV IgG does not provide immunity
6) Bacterial infections of the liver are usually secondary to systemic or GI infection.
In developing countries parasitic liver disease and abscesses are common (e.g.
amoebic liver abscess, ecchinococcal cysts, liver flukes, etc.), but is rarely seen in the
West (mostly immigrants). US incidence of liver abscess is from bacterial organisms,
which reach the liver through the portal vein, hepatic artery, or bile duct (ascending
cholangitis). A number of bacteria can infect the liver directly, including
Staphylococcus aureus in the setting of toxic shock syndrome, Salmonella typhi
setting of typhoid fever, and secondary or tertiary syphilis. The majority of hepatic
abscesses used to result from portal spread intra-abdominal infections (e.g.
appendicitis, diverticulitis, colitis), but now occurs primarily through the biliary tree
or the arterial supply in patients suffering from some form of immune deficiency.
7) Fungal and non-hepatotrophic viral infections are often seen in
immunocompromized patients. True that.