Chapter 18 –Liver: Infectious Disorders Flashcards
Inflammatory disorders of the liver dominate the clinical practice of hepatology.
Why?
This is partly
because virtually any insult to the liver can kill hepatocytes and recruit inflammatory cells, but
also because inflammatory diseases are frequently long-term chronic conditions
Among
inflammatory disordersof the liver, what is by far most frequent?
viral infection
Systemic viral infections can involve the liver as in
- (1) infectious mononucleosis (Epstein-Barr virus), which may cause a mild hepatitis during the acute phase;
- (2) cytomegalovirus infection, particularly in the newborn or immunosuppressed patient; and
- (3) yellow fever (yellow fever virus), which has been a major and serious cause of hepatitis in tropical countries.
Infrequently, in children and immunosuppressed patients, the liver is affected in the course of what?
- rubella,
- adenovirus,
- herpesvirus, or
- enterovirus infections
What is hepatitis?
However, unless otherwise specified, the
term viral hepatitis is applied for hepatic infections caused by a group of viruses known as
hepatotropic virus(hepatitis viruses A, B, C, D, and E) that have a particular affinity for the liver
( Table 18-4 ).
We first present the main features of each hepatotropic virus, followed by a
discussion of the clinicopathologic characteristics of acute and chronic viral hepatitis.
TABLE 18-4 – The Hepatitis Viruses
Virus
- Hepatitis A
- Hepatitis B
- Hepatitis C
- Hepatitis D
- Hepatitis E
TABLE 18-4 – The Hepatitis Viruses
Type of
virus
- Hepatitis A:ssRNA
- Hepatitis B:partially dsDNA
- Hepatitis C: ssRNA
- Hepatitis D: Circular defective ssRNA
- Hepatitis E: ssRNA
TABLE 18-4 – The Hepatitis Viruses
Viral family
- Hepatitis A:Hepatovirus; related to picornavirus
- Hepatitis B:Hepadnavirus
- Hepatitis C: Flaviridae
- Hepatitis D: Subviral particle in Deltaviridae family
- Hepatitis E: Calicivirus
TABLE 18-4 – The Hepatitis Viruses
Route of
transmission
- Hepatitis A:Fecal-oral (contaminated food or water)
- Hepatitis B:Parenteral, sexual contract, perinatal
- Hepatitis C:Parenteral; intranasal cocaine use is a risk factor
- Hepatitis D: Parenteral
- Hepatitis E: Fecal-oral
TABLE 18-4 – The Hepatitis Viruses
Mean
incubation
period
- Hepatitis A:2–4 weeks
- Hepatitis B:1–4 months
- Hepatitis C:7–8 weeks
- Hepatitis D: Same as HBV
- Hepatitis E: 4–5 weeks
TABLE 18-4 – The Hepatitis Viruses
Frequency of chronic liver disease
- Hepatitis A:Never
- Hepatitis B:10%
- Hepatitis C:∼80%
- Hepatitis D: 5% (coinfection); ≤70% for superinfection
- Hepatitis E: Never
TABLE 18-4 – The Hepatitis Viruses
Diagnosis
- Hepatitis A:Detection of serum IgM antibodies
- Hepatitis B:Detection of HBsAg or antibody to HBcAg
- Hepatitis C:PCR for HCV RNA; 3rdgeneration ELISA for antibody detection
- Hepatitis D: Detection of IgM and IgG antibodies; HDV RNA serum; HDAg in liver
- Hepatitis E: PCR for HEV RNA; detection of serum IgM and IgG antibodies
What is Hepatitis A?
Hepatitis A virus (HAV), the scourge of military campaigns since antiquity, is a benign, selflimited
disease with an incubation period of 3 to 6 weeks.
What is the clinical course of HAV?
HAV does not cause chronic hepatitis
or a carrier state and only rarely causes fulminant hepatitis, so the fatality rate associated with
HAV is about 0.1%.
What is the epidemiology of HAV?
HAV occurs throughout the world and is endemic in countries with substandard hygiene and sanitation, where populations may have detectable antibodies to HAV by the age of 10 years.
What are the clinical symptoms of
Clinical disease tends to be mild or asymptomatic, and is rare after childhood.
In developed countries, the prevalence of seropositivity (indicative of previous exposure) increases gradually with age, reaching 50% by age 50 years in the United States.
In this population acute HAV tends to be a sporadic febrile illness. Affected individuals have
nonspecific symptoms such as fatigue and loss of appetite, and often develop jaundice.
Overall, HAV accounts for about 25% of clinically evident acute hepatitis worldwide and an estimated
30,000 to 50,000 new cases per year in the United States.
What is the biology of HAV?
- discovered in 1973, is a
- small,
- nonenveloped,
- positive-strand RNA picornavirus that occupies its own genus, Hepatovirus.
- icosahedral capsid
- 27 nm in diameter and can be cultured in vitro.
- The receptor for HAV is HAVcr-1, a 451–amino acid class I integralmembrane mucin-like glycoprotein of unknown normal function. [21]
WHat is the MOT of HAV?
HAV is spread by ingestion of contaminated water and foods and is shed in the stool for 2 to 3 weeks before and 1 week after the onset of jaundice.
Thus, close personal contact with an infected individual or fecal-oral contamination during this period accounts for most cases and explains the outbreaks in institutional settings such as schools and nurseries, and the water-borne epidemics in places
where people live in overcrowded, unsanitary conditions.
HAV can also be detected in serum
and saliva.
Because HAV viremia is transient, blood-borne transmission of HAV occurs only rarely; therefore, donated blood is not specifically screened for this virus.
FIGURE 18-8 The sequence of serologic markers in acute hepatitis A infection. HAV,
hepatitis A virus.
FIGURE 18-9 Potential outcomes of hepatitis B infection in adults, with their approximate
frequencies in the United States.
- *Recovery from acute hepatitis refers to complete recovery as well as latent infections with maintenance of T cell response.
- **Recovery from chronic hepatitis is indicated by negative test for HBsAg.
- ***Healthy carrier state is indicated by positive HBsAg >6 months;
- HBeAg negative; serum HBV DNA <10 5 copies/mL; persistently normal AST and ALT levels; absence of significant inflammation and necrosis on liver biopsy.
