Infectious Canine Hepatitis in Dogs

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Infectious Canine Hepatitis in Dogs

Infectious canine hepatitis is an acute contagious disease caused by the canine adenovirus 1. This virus targets the spleen, kidneys, lungs, liver, the lining of blood vessels, and sometimes other organs. Symptoms can vary widely – from slight fever, thirst, or apathy to death.

OVERVIEW

  • Viral disease of dogs (Canidae) caused by CAV-1 is serologically homogeneous and antigenically distinct from respiratory CAV-2.
  • Infection—targets parenchymal organs (especially liver), eyes, and endothelium.
  • Oronasal exposure—viremia (4–8 days); virus shed in saliva and feces; initial dispersal to hepatic macrophages (hepatic Kupffer cells) and endothelium; replicates in Kupffer cells; damages adjacent hepatocytes producing massive viremia when released.
  • Adequate antibody response clears organs in 10–14 days; virus persists in renal tubules and maybe shed in urine for 6–9 months.
  • Chronic hepatitis—after infection in dogs with only partial neutralizing antibody response.
  • Cytotoxic ocular injury—anterior uveitis; leads to classic “hepatitis blue-eye”. Develops in ∼ 1% of dogs after MLV vaccine.
  • The virus can be shed for 6–9 mths in urine.

 

SIGNALMENT

  • No breed or sex predilections
  • Most common in dogs < 1 year of age

 

SIGNS

  • Depend on immunologic status of host and degree of initial cytotoxic injury.
  • Peracute—fever; CNS signs; vascular collapse; DIC; death within hours.
  • Acute—fever; anorexia; lethargy; vomiting; diarrhea; hepatomegaly; abdominal pain; abdominal effusion; vasculitis (petechia, bruising); DIC; lymphadenopathy; rarely, nonsuppurative encephalitis.
  • Uncomplicated—lethargy; anorexia; transient fever; tonsillitis; vomiting; diarrhea; lymphadenopathy; hepatomegaly; abdominal pain.
  • Late—20% of cases develop anterior uveitis and corneal edema 4–6 days post-infection; recover within 21 days; may progress to glaucoma and corneal ulceration. May be the only clinical feature of inapparent infection.

 

CAUSES & RISK FACTORS

CAV-1

  • Unvaccinated dogs susceptible
  • diagnosis DIAGNOSIS
  • DIFFERENTIAL DIAGNOSIS
  • Canine herpesvirus (neonatal)
  • Other infectious hepatopathies
  • Leptospirosis
  • Granulomatous hepatitis
  • Toxic hepatitis
  • Fulminant infectious disease—e.g., parvovirus, canine distemper

 

CBC/BIOCHEMISTRY/URINALYSIS

  • CBC—schistocytes; leukopenia during acute viremia, followed by leukocytosis with reactive lymphocytosis and nucleated RBCs.
  • Biochemistry—liver enzyme activity high initially, begin to decline within 14 days; low glucose and albumin reflect fulminant hepatic failure, vasculitis, and endotoxemia; low sodium and potassium levels reflect GI losses; hyperbilirubinemia if survive several days.
  • Urinalysis—proteinuria (glomerular injury); granular casts (renal tubule damage); bilirubinuria consistent with jaundice.

 

OTHER LABORATORY TESTS

  • Coagulation tests—reflect the severity of the liver injury and DIC.
  • Serology for antibodies to CAV-1—fourfold rise in IgM and IgG; recent vaccine-induced antibodies confuse interpretation.
  • Viral isolation—an anterior segment of eye, kidney, tonsil, and urine; difficult in parenchymal organs (especially liver) unless the first week of infection.

 

IMAGING

  • Abdominal radiography—normal or large liver; poor detail due to effusion.
  • Abdominal ultrasonography—may observe hepatomegaly, hypoechoic parenchyma (multifocal or diffuse pattern), and effusion.

 

DIAGNOSTIC PROCEDURES

  • Liver biopsy, cytologically evident intranuclear hepatocyte inclusions—aspirates
  • Viral culture
  • Acute and convalescent serology

 

PATHOLOGIC FINDINGS

  • Acute—edema and hemorrhage of lymph nodes; serosal visceral hemorrhages; liver large, dark-mottled; edematous gallbladder; fibrinous exudate on the liver, gallbladder, and other viscera; splenomegaly; renal infarcts; abdominal effusion. Perivascular necrosis in liver and other organs; widespread centrilobular to panlobular necrosis. The liver is discolored; abdominal effusion is also observed in canine herpes virus in neonates.
  • Chronic—small, fibrotic, or cirrhotic liver.

 

TREATMENT

  • Usually inpatient.
  • Fluid therapy—balanced polyionic fluids; avoid lactate if fulminant hepatic failure; carefully monitor fluids to avoid overhydration in the context of increased vascular permeability.
  • Judicious potassium (and other electrolyte) supplementation since electrolyte depletion may augment HE.
  • Avoid neuroglycopenia—supplement fluids with dextrose (2.5–5.0%) as necessary.
  • Blood component therapy for coagulopathy; blood component preferred to synthetic colloids for support of colloidal osmotic pressure; widespread vasculitis and DIC allow rapid systemic third space colloid dispersal.
  • Overt DIC—fresh blood products and low molecular weight heparin (e.g., enoxaparin 100 U/kg [1 mg/kg] q24h). See Coagulopathy of Liver Disease.
  • Nutritional support—frequent small meals as tolerated; optimize nitrogen intake; inappropriate protein restriction may impair tissue repair and regeneration; nitrogen restriction advised only if overt signs of HE.
  • If oral feeding is not tolerated, provide partial parenteral nutrition (maximum of 5 days) or, preferably, total parenteral nutrition.

 

PREVENTION/AVOIDANCE

MLV vaccination—at 6–8 weeks of age; two boosters 3–4 weeks apart until 16 weeks of age; booster at 1 year; highly effective vaccine; boosters may not be needed.

POSSIBLE COMPLICATIONS

  • Fulminant hepatic failure
  • Hepatic encephalopathy
  • Septicemia
  • Acute renal failure
  • DIC
  • Glaucoma
  • Chronic hepatitis

 

EXPECTED COURSE AND PROGNOSIS

  • Peracute—poor prognosis; death within hours.
  • Acute—variable: guarded to a good prognosis.
  • Poor antibody response (titer 1:16–1:50)—chronic hepatitis may develop.
  • Good antibody response (titer > 1:500 IgG)—complete recovery in 5–7 days possible.
  • Recovered patients—may develop chronic liver or renal disease.

 

MISCELLANEOUS

AGE-RELATED FACTORS

  • Maternal antibody—may protect some pups for first 8 weeks; depends on maternal antibody concentration and efficacy of passive transfer.
  • Vaccination of pups with high levels of passively acquired antibodies—successful at 14–16 weeks of age.

 

ABBREVIATIONS

CAV-1 = canine adenovirus-1

CRI = constant rate infusion

GSH = glutathione

HE = hepatic encephalopathy

Visit your veterinarian as early recognition, diagnosis, and treatment are essential.

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