Serologic Diagnosis.

Specific antibody against HAV of the immunoglobulin (Ig) M type appears in blood at the onset of symptoms, constituting a reliable marker of acute infection ( Fig. 18-8 ). Fecal shedding

of the virus ends as the IgM titer rises. The IgM response usually begins to decline in a few months and is followed by the appearance of IgG anti-HAV. The latter persists for years,

perhaps for life, providing protective immunity against reinfection by all strains of HAV. Hence, the HAV vaccine is effective.

Hepatitis B Virus

Hepatitis B virus (HBV) can produce (1) acute hepatitis with resolution, (2) chronic hepatitis, which may evolve to cirrhosis, (3) fulminant hepatitis with massive liver necrosis, and (4) the

backdrop for hepatitis D virus infection. Patients with chronic hepatitis represent carriers of actively replicating virus and hence are a source of infection to other individuals.[17] HBV also

plays an important role in the development of hepatocellular carcinoma. The approximate frequencies of clinical outcomes of HBV infection are depicted in Figure 18-9 .

Liver disease due to HBV is an enormous problem globally, with an estimated worldwide carrier rate of 350 million. It is estimated that HBV has infected over 2 billion of the individuals

alive today at some point in their lives. Seventy-five percent of all chronic carriers live in Asia and the Western Pacific rim. The global prevalence of chronic hepatitis B infection varies

widely, from high (>8%) in Africa, Asia, and the Western Pacific to intermediate (2% to 7%) in Southern and Eastern Europe to low (<2%) in Western Europe, North America, and

Australia. In the United States alone, there are

Figure 18-8Sequence of serologic markers in acute hepatitis A viral hepatitis.

Figure 18-9Schematic of the potential outcomes of hepatitis B infection in adults, with their approximate frequencies in the United States.

Figure 18-10Diagrammatic representation of genomic structure and transcribed components of the hepatitis B virion. The innermost circles represent the DNA (+) strand and the DNA (-)

strand of the virion. The thick bars labeled "P," "X," "pre-C," "C," "pre-S1," "pre-S2," and "S" denote the peptides derived from the virion. The outermost lines denote the mRNA

transcripts of the virion. (After Kidd-Ljunggren K, Myakawa Y, Kidd AH: J Gen Virol 83:1267–1280, 2002.)

Figure 18-11Sequence of serologic markers for hepatitis B viral hepatitis demonstrating (A) acute infection with resolution and (B) progression to chronic infection.

Figure 18-12Schematic of the potential outcomes of hepatitis C infection in adults, with their approximate frequencies in the United States.

Figure 18-13Diagrammatic representation of the genomic structure and transcribed components of the hepatitis C virion. The hepatitis C virion is transcribed in one single transcript, as

depicted in the top line; 340 nucleotides at the 5' end and 128 nucleotides at the 3' end are not translated into protein. The protein products cleaved from the single translated peptide are

shown in the bottom bar.

Figure 18-14Sequence of serologic markers for hepatitis C viral hepatitis demonstrating (A) acute infection with resolution and (B) progression to chronic relapsing infection.

Figure 18-15Differing clinical consequences of two patterns of combined hepatitis D virus and hepatitis B virus infection.

Figure 18-16Sequence of serologic markers for hepatitis D viral hepatitis depicting (A) coinfection with hepatitis B virus (HBV) and (B) superinfection of an HBV carrier.

TABLE 18-7-- Key Morphologic Features of Viral Hepatitis

Acute Hepatitis

Enlarged, reddened liver; greenish if cholestatic

Parenchymal changes:

••Hepatocyte injury: swelling (ballooning degeneration)

••••Cholestasis: canalicular bile plugs

••••HCV: mild focal fatty change of hepatocytes

••Hepatocyte necrosis: isolated cells or clusters

••••Cytolysis (rupture) or apoptosis (shrinkage)

••••If severe: bridging necrosis (portal-portal, central-central, portal-central)

••••Lobular disarray: loss of normal architecture

••Regenerative changes: hepatocyte proliferation

••Sinusoidal cell reactive changes:

••••Accumulation of phagocytosed cellular debris in Kupffer cells

••••Influx of mononuclear cells into sinusoids

••Portal tracts:

••••Inflammation: predominantly mononuclear

••••Inflammatory spillover into adjacent parenchyma, with hepatocyte necrosis

Chronic Hepatitis

Changes shared with acute hepatitis:

••Hepatocyte injury, necrosis, and regeneration

••Sinusoidal cell reactive changes

Portal tracts:

••Inflammation:

••••Confined to portal tracts, or

••••Spillover into adjacent parenchyma, with necrosis of hepatocytes ("interface hepatitis"), or

••••Bridging inflammation and necrosis

••Fibrosis:

••••Portal deposition, or

••••Portal and periportal deposition, or

••••Formation of bridging fibrous septa

HBV: "ground-glass" hepatocytes, "sanded" nuclei

HCV: bile duct epithelial cell proliferation, lymphoid aggregate formation

Date: 2016-04-22; view: 615