Viral Hepatitis - All types

Hepatitis is inflammation of the liver; when severe and/or long-term, damage can lead to cirrhosis and liver failure. Some Hepatitis viruses are also associated with liver cancer. Some individuals are asymptomatic. Common symptoms of active infection include: fatigue, jaundice, nausea, and abdominal pain. Hepatitis A Aka, "Infectious hepatitis." Positive-sense RNA Picornavirus, with a naked, icosahedral capsid Transmitted via the fecal-oral route. Outbreaks have been associated with consumption of contaminated shellfish. Rapid Onset. Infection is common; usually benign, especially in children. Adults are more likely to experience acute iteric hepatitis (iteric means they show signs of jaundice). Fulminant hepatitis, which involves the nervous system, is rare. Histopathology: Monocyte infiltration, Councilman Bodies (eosinophilic, shrunken cells), Ballooning degenerating cells. Serological Values: Acute, active infection = anti-HAV IgM Previous infection = anti-HAV IgG Vaccines can prevent Hepatitis A infection. Infection is usually self-limiting, so supportive care is sufficient. Patients who recover benefit from life-long immunity due to IgG antibodies. Hepatitis B Aka, "Serum hepatitis." DNA Hepadnavirus, with an enveloped, icosahedral capsid. Antigens: Surface antigen = HBsAg (outnumbers HBV virions in serum) Envelope antigen = HBeAg Core antigens = HBcAg, HBeAg Carried in the blood, tissue, and semen; transmitted via intravenous drug use, during birth, and is a sexually-transmitted infection. Chronic carriers facilitate viral spread. Clinical course: Varies depending on the host's ability to clear the virus. Acute infection with resolution. Adults are more often symptomatic, and have "serum sickness-like" problems due to the development of Hypersensitivity Type III reactions. For example, patients can experience rash, vasculitis, joint pain, and renal damage due to immune complex formation. Chronic infection with liver destruction. Complications include cirrhosis, liver failure, and hepatocellular cancer. Hepatocellular cancer (HHC) is a significant cause of cancer-related mortality. Neonates: Establishment of chronic infection and long-term complications are more likely in neonates. Extrahepatic problems (uncommon) – Glomerulonephritis – Polyarthritis – Polyarteritis nodosa – Guillain-Barre Histopathology: Chronic infection = "Ground glass" hepatocytes. Serological values: – HBV infection = HBsAg – Acute = IgM & HBeAg – Chronic = IgG. Higher infectivity HbeAg; Lower infectivity Anti-HBeAg – Replication/Infectious = HBeAg – Recovery = Anti-HBs; IgG – Immunized = Anti-HBs Vaccine available Post-exposure prophylaxis = Hepatitis B immune globulin. Chronic infection treatment = antivirals, including entecavir, tenofovir, and others. Hepatits C Aka, "Non-A, Non-B Hepatitis" Positive-sense RNA Flavivirus with an enveloped icosahedral capsid. Carried in the blood, tissue, and semen: transmission to the blood via contaminated needles is currently the most significant form of transmission. Infected individuals can enter a carrier state. Clinical Course: – Acute hepatitis with resolution. – Rapid onset of cirrhosis – Chronic infection is the most common outcome. Chronic infection is usually asymptomatic, at first; over time, it can progress to cirrhosis, liver failure, or hepatocellular cancer. Extrahepatic manifestations – Mixed cryoglobulinemia vasculitis (Cryovas) – B-cell non-Hodgkin's lymphoma – Membrano-proliferative glomeruloneprhitis – Diabetes mellitus (increased risk) – Atherosclerosis (increased risk) – Thyroid disease (increased risk) Histopathology Cholestasis, necroinflammation, lymphocyte aggregation, and fibrosis. No vaccine is yet available to prevent hepatitis C. Avoidance of unprotected sex and contaminated needles is recommended. Treatment = Antivirals, including glecaprevir, paritaprevir. Hepatitis D Aka, "Delta agent" Negative-sense RNA Deltavirus with an enveloped icosahedral capsid. "Defective" virus: Relies on components of its helper virus, Hepatitis B, for replication in the host. Derives its envelope from HBsAg Increases severity of Hepatitis B infection. Transmitted in blood, tissue, and semen. Patients can enter a carrier state. Clinical course: Depends on its timing in relation to Hepatitis B infection: HBV co-infection occurs when the two viruses are contracted at the same time. HBV superinfection occurs when Hepatitis D is contracted after Hepatitis B has already established infection. In both cases, Hepatitis D exacerbates the symptoms of Hepatitis B infection. Symptoms can be mild to severe, and can include fulminant hepatitis. Fulminant hepatitis is characterized by encephalopathy and hepatic necrosis, and is often fatal. Superinfection is more often associated with severe outcomes. Hepatitis B co-infection has a slow onset. This is because Hepatitis D cannot replicate until its helper virus has established infection and made its components available for use. Hepatitis B superinfection onset occurs rapidly because the necessary components of Hepatitis B are readily available to Hepatitis D. Serological Values HDV RNA Vaccination against Hepatitis B robs Hepatitis D of its helper virus. Infected patients may be given interferon treatments. Hepatitis E Aka, "Non-A, Non-B Enteric/Epidemic" hepatitis. Positive-sense RNA Hepevirus with a quasi-enveloped icosahedral capsid. In feces and bile, the virion is naked; in blood, it is enveloped in a cellular membrane. Transmitted via the fecal-oral route. Epidemics are associated with contaminated water supply. Acute hepatitis with resolution. Mortality is high among pregnant people, especially during the third trimester, when fulminant hepatitis is most likely to develop. Many authors state that HEV only causes acute hepatitis; however, some evidence suggests that Genotype 3 causes chronic hepatitis in immunosuppressed individuals. No vaccine Prevention includes thorough sanitation, particularly of water supplies. Treatment = supportive care.