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454.e2  Hepatitis, Canine Infectious




            Hepatitis, Canine Infectious                                                           Client Education
                                                                                                         Sheet
  VetBooks.ir

            BASIC INFORMATION
                                              •  Signs  of  coagulopathy:  petechial  and
                                                ecchymotic hemorrhages, epistaxis, excessive   ○   Alanine aminotransferase and alkaline
                                                                                     phosphatase increase for 14 days after
           Definition                           bleeding from venipuncture sites     infection and then decline unless
           Viral  liver  disease  of dogs  caused  by canine   •  Central nervous system (CNS) signs con-  chronic hepatitis occurs.  With chronic
           adenovirus type 1 (CAdV-1) that can cause   sistent with hepatoencephalopathy or viral   hepatitis, signs of hepatic synthetic failure
           acute death or chronic hepatitis. Infectious   encephalitis (rare), including depression,   (hypoglycemia, hypoalbuminemia, hypo-
           canine hepatitis (ICH) is uncommon in   seizures, disorientation, coma    cholesterolemia, low blood urea nitrogen)
           well-vaccinated dog populations. CAdV-1 is                                may  be  present.  Hyperbilirubinemia  is
           antigenically and genetically related to CAdV-2,   Etiology and Pathophysiology  uncommon in the acute phase.
           which causes infectious tracheobronchitis.  •  CAdV-1 is transmitted by oronasal exposure   •  Urinalysis: proteinuria, bilirubinuria (NOTE:
                                                to secretions of infected animals, notably   mild bilirubinuria is normal in healthy dogs)
           Synonyms                             urine. It can also be transmitted by fomites,   •  Coagulation panel: changes are most often
           Canine infectious hepatitis (CIH), infectious   and ectoparasites can harbor CAdV-1.  seen during viremia and include thrombocy-
           canine hepatitis, Rubarth disease, blue eye  •  The virus initially localizes in the tonsils after   topenia, prolongation of prothrombin time,
                                                exposure. From the tonsils, it disseminates   activated partial thromboplastin time, and
           Epidemiology                         to regional lymph nodes and then through   thrombin time.
           SPECIES, AGE, SEX                    the thoracic duct to the systemic circulation.  •  Serum bile acids (postprandial): concentra-
           Dogs, coyotes, red foxes, wolves, and bears can   •  Virus is found in body tissues and secretions,   tions often high when hepatic encepha-
           be infected. Usually, the disease is seen in dogs   including urine, feces, and saliva, 4-8 days   lopathy is present; not useful in dogs with
           younger than 1 year of age, but unvaccinated   after infection.         hyperbilirubinemia
           dogs of any age can be affected.   •  The virus is found in many tissues, including
                                                the kidneys 10-14 days after infection, and   Advanced or Confirmatory Testing
           RISK FACTORS                         is secreted in urine for 6-9 months after   •  Cytologic (aspirates, impression smears) or
           Unvaccinated dogs                    infection.                         histologic examination of liver: characteristic
                                              •  Predisposition  for  hepatic  parenchymal   inclusion bodies (Cowdry type A); wide-
           CONTAGION AND ZOONOSIS               cells (causing acute hepatic injury/necrosis   spread centrilobular to panlobular necrosis
           •  Dog-to-dog transmission occurs directly or   characterized by necrohemorrhagic hepatitis)   •  Cerebrospinal fluid: usually normal
            indirectly (oronasal infection from secretions   and vascular endothelial cells (multiple organ   •  Bone marrow aspirate: decreased megakaryo-
            of infected animals such as saliva, urine, feces,   injury)            cytes during viremic stage
            respiratory secretions)           •  Cytotoxic effects of the virus cause initial   •  Serologic  testing  (complement  fixation,
           •  Not zoonotic                      cellular injury to the eye, liver, and kidney.  immunodiffusion, ELISA), virus isolation,
           •  The  virus  is  resistant  to  environmental   •  Subclinical infections are widespread, pre-  and immunofluorescent testing are available,
            inactivation and survives for days at room   dominantly in dogs with circulating antibody   but an accurate clinical diagnosis usually is
            temperature on soiled fomites; it can remain   at the time of infection.  possible without these tests. May not be able
            viable for months at temperatures below 39°F                           to distinguish CAdV-1 from CAdV-2.
            (4°C).                             DIAGNOSIS                         •  PCR  techniques  can  distinguish  CAdV-1
                                                                                   from CAdV-2 infection.
           ASSOCIATED DISORDERS               Diagnostic Overview                •  Virus can be cultured from any body tissue
           Chronic hepatitis may occur if the patient   The diagnosis is based on signalment (young,   5 days after infection; the kidney is the most
           survives the initial viremia.      unvaccinated dog) with clinical signs consistent   persistent site of infection.
                                              with acute hepatic injury/failure. Confirma-
           Clinical Presentation              tion requires ruling out other differentials and
           HISTORY, CHIEF COMPLAINT           serologic testing, virus isolation, or polymerase    TREATMENT
           •  Animals  usually  have  a  poor  vaccination   chain reaction (PCR) assay.  Treatment Overview
            history.                                                             Treatment is supportive and nonspecific.
           •  During acute viremia, animals can become   Differential Diagnosis  Uncomplicated cases may not show improve-
            moribund and die within a few hours.  •  Liver disease (p. 442)      ment in clinical signs for up to 5-7 days.
           •  After acute viremia, animals typically present   ○   Portosystemic shunts
            with vomiting, diarrhea, and/or abdominal   ○   Leptospirosis        Acute General Treatment
            pain.                               ○   Toxic hepatopathy            •  Fluid  therapy:  as  appropriate  to  replace
                                                ○   Copper hepatopathy             deficits and ongoing loss and provide for
           PHYSICAL EXAM FINDINGS               ○   Immune-mediated hepatopathy    maintenance needs. Address electrolyte
           •  Fever  (can  be  biphasic),  tonsillar  enlarge-  ○   Bacterial hepatopathy  disorders as necessary.
            ment, cervical lymphadenopathy, tachy-  ○   Cholelithiasis/cholangitis  •  Correct coagulation disturbances with fresh
            cardia, tachypnea, abdominal tenderness,   ○   Gallbladder rupture     frozen plasma (10-20 mL/kg as needed to
            hepatomegaly                      •  Pancreatitis                      normalize coagulation times) or fresh whole
           •  Icterus  is  uncommon  in  the  acute  phase.   •  Canine distemper  blood transfusion (20 mL/kg). Supplement
            Icterus and abdominal distention may be                                with  vitamin  K  0.625-1.25 mg/kg  PO  or
            seen in advanced cases that survive acute   Initial Database           SQ q 12h for up to 36 hours.
            viremia.                          •  CBC/serum biochemistry profile  •  N-Acetylcysteine: Dilute 10% sterile NAC
           •  Anterior  uveitis  and  corneal  edema  (blue   ○   Neutropenia and lymphopenia ini-  with sterile saline 1:4; administer 140 mg/kg
            eye) are hallmarks. They develop 7-21 days   tially, then rebound neutrophilia and   IV over 20 minutes, then 70 mg/kg IV q
            after infection.                      lymphocytosis                    6h. Micropore filter should be used.

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