Viral Hepatitis

Overview

• Hepatitis A (HAV) - RNA picornavirus; non-enveloped
• Hepatitis B (HBV) - DNA virus (replicates like retrovirus)
• Hepatitis C (HCV) - RNA virus in Flaviviridae family
• Hepatitis D (HDV) - Requires HBV co-infection
• Hepatitis E (HEV) - RNA virus

Hepatitis A

• Incubation: 3-4 weeks (range 15-45 days, typically 30 days)
• Replication limited to liver; virus present in bile, stool, and blood during late incubation and pre-icteric phase
• Fecal shedding peaks before jaundice onset and diminishes rapidly once jaundice appears
• Maximum infectivity occurs before symptom onset
• Inactivated by boiling (1 min), formaldehyde, chlorine, or UV irradiation (Harrison's, p. 1188-1194)

• Self-limited; does not progress to chronic hepatitis
• Most symptomatic cases present 2-6 weeks post-exposure
• In children, often asymptomatic
• Patients remain contagious until 1 week after jaundice appears (ROSEN's, p. 2771)

• Inactivated HAV vaccine available since 1995; highly effective (>95% seroconversion with three-dose series)
• Routine vaccination recommended for all children and high-risk groups
• Passive immunization (immune globulin) effective within 1-2 weeks of exposure; can be given to pre-exposure prophylaxis in immunocompromised patients, those <6 months old, with chronic liver disease, or vaccine allergy (ROSEN's, p. 2773; Jawetz Microbiology, p. 2563-2575)

Hepatitis B

• HBsAg (hepatitis B surface antigen) - Earliest marker of infection; persists in chronic infection
• Anti-HBc (hepatitis B core antibody) - Appears shortly after HBsAg; remains for life
• IgM anti-HBc - Indicates acute infection; typically peaks at clinical presentation and disappears within 6 months
• HBeAg (hepatitis B e antigen) - Correlates with high infectivity and viral replication
• Anti-HBe - Appears with viral clearance or during chronic infection with lower replication
• Anti-HBs (hepatitis B surface antibody) - Appears after HBsAg clearance; indicates immunity

• 95-99% of immunocompetent adults who acquire HBV recover spontaneously without chronic infection
• ~5-10% develop chronic HBV infection
• Risk of chronicity is age-dependent: up to 90% of infected infants develop chronic infection
• Chronic HBV can progress to cirrhosis and hepatocellular carcinoma (Harrison's, p. 1203)

• Recombinant DNA vaccine (HBsAg produced in yeast or mammalian cells) available since 1982
• Universal infant vaccination recommended; >95% efficacy with three-dose series to deltoid
• Catch-up vaccination for adolescents and high-risk adults
• HBIG (hepatitis B immune globulin), 0.06 mL/kg IM, recommended for non-vaccinated exposures; reduces infection risk by 75%
• Immunosuppressed groups (hemodialysis patients, HIV+, cancer patients) respond less well to vaccination (Jawetz, p. 2580-2588)

Hepatitis C

• Incubation ~50 days
• Acute phase lasts up to 12 weeks, rarely causing acute hepatic failure
• ~90% progress to chronic infection
• Over 20-30 years: 10-20% develop cirrhosis or hepatocellular carcinoma
• ~57% have no identified source of infection
• Risk of transfusion-acquired HCV now <1 in 2 million units (improved screening since 1992) (ROSEN's, p. 2668-2672; Harrison's, p. 1691)

• No vaccine available
• Occupational exposure: risk of seroconversion after percutaneous needle stick ~1.8%
• No effective postexposure prophylaxis; insufficient evidence for DAA prophylaxis
• Prevention relies on universal precautions (gloves, masks, eye protection, gowns) (ROSEN's, p. 2779)

Hepatitis D (Delta)

• Co-infection: may result in more severe acute hepatitis
• Superinfection: typically causes chronic HDV with accelerated progression to cirrhosis
• HDV replication tends to suppress HBV replication, resulting in lower HBV viral loads

• IgM anti-HDV predominates during acute infection
• 30-40 days may elapse after symptom onset before anti-HDV detection
• Chronic infection: high-titer anti-HDV (IgM and IgG); HDV RNA detectable in serum and liver (Harrison's, p. 1300-1301)

Hepatitis E

• Usually self-limited in immunocompetent hosts
• Severe or fulminant disease in pregnant women (30% mortality in third trimester)
• Chronic infection in immunocompromised patients (organ transplant recipients, HIV+ patients)
• No vaccine available in most countries; limited oral vaccine use in some regions

Clinical Features of Acute Viral Hepatitis

• Prodromic phase: malaise, anorexia, arthralgias, nausea, right upper quadrant discomfort
• Icteric phase: jaundice, dark urine (bilirubinuria), pale stools, pruritus
• Convalescent phase: gradual resolution over weeks to months
• Children often asymptomatic or mildly symptomatic

• Markedly elevated transaminases (ALT >AST in viral hepatitis; opposite in alcoholic hepatitis)
• Mild-to-moderate hyperbilirubinemia
• Alkaline phosphatase usually mildly elevated
• Coagulopathy and prolonged PT/INR in severe cases
• Hepatitis A: anti-HAV IgM diagnostic during acute phase
• Hepatitis B: HBsAg, IgM anti-HBc, elevated HBV DNA
• Hepatitis C: HCV RNA detectable by PCR; anti-HCV develops later (ROSEN's, p. 2483)

• Fulminant hepatic failure (highest risk with HAV in elderly, HBV superinfection with HDV)
• Hepatic encephalopathy
• Acute kidney injury (hepatorenal syndrome)
• Upper GI bleeding from esophageal varices
• Hypoglycemia, electrolyte imbalances
• Severe vomiting with esophageal tears (ROSEN's, p. 2769)

Management

• Most cases self-limited; specific antiviral therapy not required for mild-moderate disease
• Hospitalization for clinically severe illness or evidence of hepatic failure
• High-calorie diet (major intake in morning to minimize nausea)
• IV hydration for persistent vomiting
• Avoid hepatotoxic drugs and those metabolized by liver; dose-adjust or discontinue if significant dysfunction develops
• Cholestyramine for severe pruritus
• No role for corticosteroids (may increase chronicity risk)
• For fulminant hepatic failure: nucleoside analogues (HBV) considered; urgent referral to transplant center

• Standard and contact precautions
• Handwashing, separate eating utensils
• 0.5% sodium hypochlorite (1:10 bleach dilution) for disinfection
• Patients with HAV contagious until 1 week post-jaundice onset

Key Prevention Points

1. HAV & HBV: Effective vaccines exist; recommended for routine immunization
2. HCV: No vaccine; relies on harm reduction (sterile equipment), occupational precautions, and early treatment
3. HDV: Prevented by HBV vaccination (HDV cannot exist without HBV)
4. HEV: Sanitation, food/water safety; vaccine available in limited markets

• Harrison's Principles of Internal Medicine, 22E (2025) - Acute & Chronic Viral Hepatitis chapters
• ROSEN's Emergency Medicine: Concepts & Clinical Practice, p. 2463-2779
• Jawetz, Melnick & Adelberg's Medical Microbiology, 28E, p. 2561-2604