Washington Manual of Medical Therapeutics
Viral Hepatitis
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The hepatotropic viruses include hepatitis A (HAV), hepatitis B (HBV), hepatitis C (HCV), hepatitis D (HDV), and hepatitis E (HEV) (Tables 19-1 and 19-2). Nonhepatotropic viruses, which indirectly affect the liver, include Epstein–Barr virus, cytomegalovirus, herpes simplex virus, measles, Ebola, and others. The novel coronavirus SARS-CoV-2 is also a cause of viral hepatitis. The pathogenesis is thought to be a direct virus-induced cytopathic effect versus immune response damage from the cytokine release syndrome.1
| Organism | Hepatitis A | Hepatitis B | Hepatitis C | Hepatitis D | Hepatitis E |
| Incubation | 15–45 d | 30–180 d | 15–150 d | 30–150 d | 30–60 d |
| Transmission | Fecal–oral | Blood Sexual Perinatal | Blood Sexual (rare) Perinatal (rare) | Blood Sexual (rare) | Fecal–oral Organ transplantation |
| Risk groups | Residents of and travelers to endemic regions Children and caregivers in daycare centers | Injection drug users Multiple sexual partners Men who have sex with men Infants born to infected mothers Healthcare workers | Injection drug users Transfusion recipients | Any person with hepatitis B virus Injection drug users | Residents of and travelers to endemic regions Zoonosis: workers in pig farms |
| Fatality rate | 1.0% | 1.0% | <0.1% | 2%–10% | 1% |
| Carrier state | No | Yes | Yes | Yes | No |
| Chronic hepatitis | None | 2%–10% in adults; 90% in children <5 y | 70%–85% | Variable | Rare |
| Cirrhosis | No | Yes | Yes | Yes | No |
| Hepatitis | Acute | Chronic | Recovered/Latent | Vaccinated |
| HAV | IgM anti-HAV+ | NA | IgG anti-HAV+ | IgG anti-HAV+ |
| HCV | All tests possibly negative HCV NAT+ HCV RNA+ Anti-HCV Ab+ | Anti-HCV Ab+ HCV RNA+ | Anti-HCV Ab+ HCV RNA−b | NA |
| HDV | IgM anti-HDV+c HDV Ag+c | IgG anti-HDV+c | IgG anti-HDV+c | Vaccination against HBV |
| HEV | IgM anti-HEV | NA | IgG anti-HEV | NA |
Ab, antibody; HAV, hepatitis A virus; HCV, hepatitis C virus; HDV, hepatitis D virus; HEV, hepatitis E virus; NA, not applicable.
aFor hepatitis B virus serologies, see Table 19-3.
bNegative HCV RNA results should be interpreted with caution. Differences are found in thresholds for detection among assays and among laboratories.
cMarkers of HBV infection are also present because HDV cannot replicate in the absence of HBV.
Acute viral hepatitis is defined by an array of symptoms that may vary from mild, nonspecific symptoms to acute liver failure (ALF). This condition may resolve or progress to chronic hepatitis, in certain cases, or to liver failure as a consequence of diffuse necroinflammatory liver injury.
ALF is defined as the rapid development of severe liver injury with encephalopathy, jaundice, and coagulopathy in a patient without preexisting liver disease within <6 months from the onset of the acute illness.
Chronic viral hepatitis is defined as the presence of persistent (>6 months) virologic replication, as determined by serologic and molecular studies, with necroinflammatory and fibrotic injury. Symptoms and biochemical abnormalities may vary from none to moderate. Histopathologic classification of chronic viral hepatitis is based on etiology, grade, and stage. Grading and staging are measures of the severity of inflammation and fibrosis, respectively. Chronic viral hepatitis may lead to cirrhosis and HCC.
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The hepatotropic viruses include hepatitis A (HAV), hepatitis B (HBV), hepatitis C (HCV), hepatitis D (HDV), and hepatitis E (HEV) (Tables 19-1 and 19-2). Nonhepatotropic viruses, which indirectly affect the liver, include Epstein–Barr virus, cytomegalovirus, herpes simplex virus, measles, Ebola, and others. The novel coronavirus SARS-CoV-2 is also a cause of viral hepatitis. The pathogenesis is thought to be a direct virus-induced cytopathic effect versus immune response damage from the cytokine release syndrome.1
| Organism | Hepatitis A | Hepatitis B | Hepatitis C | Hepatitis D | Hepatitis E |
| Incubation | 15–45 d | 30–180 d | 15–150 d | 30–150 d | 30–60 d |
| Transmission | Fecal–oral | Blood Sexual Perinatal | Blood Sexual (rare) Perinatal (rare) | Blood Sexual (rare) | Fecal–oral Organ transplantation |
| Risk groups | Residents of and travelers to endemic regions Children and caregivers in daycare centers | Injection drug users Multiple sexual partners Men who have sex with men Infants born to infected mothers Healthcare workers | Injection drug users Transfusion recipients | Any person with hepatitis B virus Injection drug users | Residents of and travelers to endemic regions Zoonosis: workers in pig farms |
| Fatality rate | 1.0% | 1.0% | <0.1% | 2%–10% | 1% |
| Carrier state | No | Yes | Yes | Yes | No |
| Chronic hepatitis | None | 2%–10% in adults; 90% in children <5 y | 70%–85% | Variable | Rare |
| Cirrhosis | No | Yes | Yes | Yes | No |
| Hepatitis | Acute | Chronic | Recovered/Latent | Vaccinated |
| HAV | IgM anti-HAV+ | NA | IgG anti-HAV+ | IgG anti-HAV+ |
| HCV | All tests possibly negative HCV NAT+ HCV RNA+ Anti-HCV Ab+ | Anti-HCV Ab+ HCV RNA+ | Anti-HCV Ab+ HCV RNA−b | NA |
| HDV | IgM anti-HDV+c HDV Ag+c | IgG anti-HDV+c | IgG anti-HDV+c | Vaccination against HBV |
| HEV | IgM anti-HEV | NA | IgG anti-HEV | NA |
Ab, antibody; HAV, hepatitis A virus; HCV, hepatitis C virus; HDV, hepatitis D virus; HEV, hepatitis E virus; NA, not applicable.
aFor hepatitis B virus serologies, see Table 19-3.
bNegative HCV RNA results should be interpreted with caution. Differences are found in thresholds for detection among assays and among laboratories.
cMarkers of HBV infection are also present because HDV cannot replicate in the absence of HBV.
Acute viral hepatitis is defined by an array of symptoms that may vary from mild, nonspecific symptoms to acute liver failure (ALF). This condition may resolve or progress to chronic hepatitis, in certain cases, or to liver failure as a consequence of diffuse necroinflammatory liver injury.
ALF is defined as the rapid development of severe liver injury with encephalopathy, jaundice, and coagulopathy in a patient without preexisting liver disease within <6 months from the onset of the acute illness.
Chronic viral hepatitis is defined as the presence of persistent (>6 months) virologic replication, as determined by serologic and molecular studies, with necroinflammatory and fibrotic injury. Symptoms and biochemical abnormalities may vary from none to moderate. Histopathologic classification of chronic viral hepatitis is based on etiology, grade, and stage. Grading and staging are measures of the severity of inflammation and fibrosis, respectively. Chronic viral hepatitis may lead to cirrhosis and HCC.
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