Infections

Cards (745)

  • Acute viral hepatitis
    Lasts less than 6 months
  • Chronic viral hepatitis
    Lasts more than 6 months
  • Acute viral hepatitis typically presents with
    fatigue,
    malaise,
    nausea,
    vomiting,
    anorexia,
    low-grade fever,
    jaundice,
    dark urine,
    and RUQ tenderness
  • Chronic viral hepatitis can be asymptomatic or present with non-specific symptoms like malaise and fatigue
  • Histopathology of viral hepatitis
    • Hepatocyte injury and ballooning degeneration
    • Hepatocyte death and necrosis with replacement by scar tissue (bridging necrosis)
    • Pan-lobular mononuclear infiltration
  • Laboratory findings in viral hepatitis
    Increased serum AST and ALT, with ALT higher than AST
    Exception: In advanced fibrosis/cirrhosis, AST becomes higher than ALT
  • Hepatitis E virus (HEV)

    RNA virus, transmitted by fecal-oral route
    Acute, self-limiting disease, can cause fulminant hepatitis in pregnancy
    HEV antigen/RNA early, anti-HEV IgM during symptoms, anti-HEV IgG late
  • HBV transmission routes

    • Parenteral (blood, needlesticks, dialysis, transfusions)
    Sexual
    Perinatal
  • HBV serological markers
    HBsAg: Active infection
    Anti-HBs: Recovery or immunity
    HBeAg: Active viral replication, high infectivity
    Anti-HBe: Low infectivity
    Anti-HBc IgM: Recent infection
    Anti-HBc IgG: Past/chronic infection
  • Interferon alpha is used to treat chronic hepatitis B infection
  • Histopathology of chronic hepatitis B

    • Ground glass appearance of hepatocytes due to HBV proteins
  • Liver damage in chronic hepatitis B is mediated by cytotoxic T cells, not the virus itself
  • Extrahepatic manifestations of HBV
    • Hematologic (aplastic anemia)
    • Renal (membranous, MPGN)
    • Vascular (polyarteritis nodosa)
  • Hepatitis B vaccine is a subunit vaccine containing HBsAg
  • Hepatitis B infection phases
    1. Incubation period
    2. Appearance of HBsAg
    3. Appearance of HBeAg and viral DNA
    4. Appearance of IgM anti-HBc
    5. Disappearance of HBeAg
    6. Appearance of anti-HBe
    7. Disappearance of HBsAg
    8. Appearance of anti-HBs
  • Window period
    Period of infection without detectable HBsAg and anti-HBs
  • During acute hepatitis B, liver enzymes especially ALT are elevated
  • If HBsAg persists after 6 months, it indicates chronic hepatitis B infection
  • Serological markers in different hepatitis B infection stages
    • Acute infection: HBsAg, IgM anti-HBc
    • Window period: Anti-HBe, IgM anti-HBc
    • Chronic infectious: HBsAg, HBeAg, IgG anti-HBc
    • Chronic non-infectious: HBsAg, IgG anti-HBc
    • Recovery: Anti-HBs, Anti-HBe, IgG anti-HBc
  • Hepatitis D virus
    Single-stranded RNA virus that requires HBsAg to infect hepatocytes
  • HDV infection
    • Can occur as co-infection with HBV or super-infection in chronic HBV carrier
    • Associated with worse prognosis and increased risk of cirrhosis
  • Vaccination against hepatitis B also protects against hepatitis D
  • Hepatitis C virus (HCV)

    Enveloped, single-stranded RNA virus that lacks 3'-5' exonuclease activity, leading to high genetic variability
  • HCV has 6 or more genotypes and multiple sub-genotypes due to genetic mutations
  • HCV transmission
    • Mainly parenteral, also sexually and perinatally
    • Long incubation period of 2 weeks to 6 months
  • Acute HCV infection type

    Can be asymptomatic or mild hepatitis, but more commonly causes chronic infection
  • Extrahepatic manifestations of HCV
    • Hematologic (cryoglobulinemia, ITP, autoimmune hemolytic anemia, NHL)
    • Renal (MPGN, membranous GN)
    • Vascular (leukocytoclastic vasculitis)
    • Dermatologic (porphyria cutanea tarda, lichen planus)
    • Endocrine (diabetes, autoimmune hypothyroidism)
  • HCV screening
    Anti-HCV antibody test is the best screening test, HCV RNA is the gold standard
  • Chronic HCV infection
    Anti-HCV positive, HCV RNA positive, persistently elevated liver enzymes
  • Histopathology of HCV

    Lymphoid aggregates, focal macrovesicular steatosis
  • HCV treatment medications
    • NS5A inhibitors (ledipasvir, daclatasvir)
    • NS5B inhibitors (sofosbuvir, dasabuvir)
    • NS3/4A inhibitors (simeprevir, grazoprevir)
    • Ribavirin
  • HCV treatment
    • No monotherapy approved, combination therapy required
    • Interferon alpha can also be used
  • Viral hepatitis is inflammation of the liver parenchyma, most commonly caused by hepatitis viruses A, B, C, D, and E
  • Routes of transmission for hepatitis viruses
    • Fecal-oral: HAV, HEV
    • Parenteral, sexual, perinatal: HBV, HCV, HDV
  • Hepatitis A virus (HAV)
    RNA picornavirus with short incubation period, causes acute hepatitis with good prognosis
  • Hepatitis B virus (incubation T + common presentations)
    DNA hepadnavirus with long incubation period (1-6 months), can cause acute hepatitis, chronic hepatitis, cirrhosis, or fulminant hepatitis
  • Hepatitis C virus (HCV) {Taxonomy + Incubation}

    RNA flavivirus with long incubation period, commonly causes chronic hepatitis that can progress to cirrhosis or HCC
  • Hepatitis D virus
    RNA delta virus that requires HBsAg to infect, can cause co-infection or super-infection in chronic HBV, associated with worse prognosis
  • Hepatitis E virus {Class + Incubation T + complications (2)}

    RNA hepeviridae with short incubation period, causes self-limiting acute hepatitis, but can cause fulminant hepatitis in pregnant women
  • Measles (Who is affected?)

    One of the most contagious infectious diseases and remains a leading cause of death particularly among young children especially in areas with low rates of vaccination