Acute viral hepatitis is a systemic infection predominantly affecting the liver. Clinically characterized by malaise, nausea, vomiting, diarrhea, and low-grade fever followed by dark urine, jaundice, and tender hepatomegaly; may be subclinical and detected on basis of elevated aspartate and alanine aminotransferase (AST and ALT) levels. Hepatitis B may be associated with immune-complex phenomena, including arthritis, serum sickness-like illness, glomerulonephritis, and a polyarteritis nodosa–like vasculitis. Hepatitis-like illnesses may be caused not only by hepatotropic viruses (A, B, C, D, E) but also by other viruses (Epstein-Barr, CMV, coxsackievirus, etc.), alcohol, drugs, hypotension and ischemia, and biliary tract disease (Table 163-1).
TABLE 163-1THE HEPATITIS VIRUSES |Favorite Table|Download (.pdf) TABLE 163-1THE HEPATITIS VIRUSES
| ||HAV ||HBV ||HCV ||HDV ||HEV |
|Viral Properties || || || || || |
|Size, nm ||27 ||42 ||~55 ||~36 ||~32 |
|Nucleic acid ||RNA ||DNA ||RNA ||RNA ||RNA |
|Genome length, kb ||7.5 ||3.2 ||9.4 ||1.7 ||7.5 |
|Classification ||Picornavirus ||Hepadnavirus ||Flavivirus-like ||— ||Calicivirus-like or alpha-virus-like |
|Incubation, days ||15–45 ||30–180 ||15–160 ||21–140 ||14–63 |
|Transmission || || || || || |
|Fecal-oral ||+++ ||— ||— ||— ||+++ |
|Percutaneous ||Rare ||+++ ||+++ ||+++ ||— |
|Sexual ||? ||++ ||Uncommon ||++ ||— |
|Perinatal ||— ||+++ ||Uncommon ||+ ||— |
|Clinical Features || || || || || |
|Severity ||Usually mild ||Moderate ||Mild ||May be severe ||Usually mild |
|Chronic infection ||No ||1–10%; up to 90% in neonates ||80–90% ||Common ||No |
|Carrier state ||No ||Yes ||Yes ||Yes ||No |
|Fulminant hepatitis ||0.1% ||1% ||Rare ||Up to 20% in superinfection ||10–20% in pregnant women |
|Hepatocellular carcinoma ||No ||Yes ||Yes ||? ||No |
|Prophylaxis ||Ig; vaccine ||HBIg; vaccine ||None ||None (HBV vaccine for susceptibles) ||None |
27-nm picornavirus (hepatovirus) with single-stranded RNA genome.
Scheme of typical clinical and laboratory features of HAV.
Recovery within 6–12 months, usually with no clinical sequelae; a small proportion will have one or two apparent clinical and serologic relapses; in some cases, pronounced cholestasis suggesting biliary obstruction may occur; rare fatalities (fulminant hepatitis), no chronic carrier state.
IgM anti-HAV in acute or early convalescent serum sample.
Fecal-oral transmission; endemic in underdeveloped countries; food-borne and waterborne epidemics; outbreaks in day-care centers, residential institutions.
After exposure: immune globulin 0.02 mL/kg IM within 2 weeks to household and institutional contacts (not casual contacts at work). Before exposure: inactivated HAV vaccine 1 mL IM (unit dose depends on formulation); half dose to children; repeat at 6–12 months; target travelers, military ...