Clinical examination findings. Affected cats often have traveled to tropical areas, but infestation in cats from the continental United States (southern
Florida, Illinois) has been reported.11-13 Infestation results from ingesting the second intermediate host (reptile or amphibian) in the fluke life cycle.11-13 Most infestations are caused by flukes of the family Opisthorchiidae (genus Opisthorchis and Metorchis), but infestations with Clonorchis sinensis, Platynosomum fastosum, and Platynosomum concinnum have also been reported in cats.3,11 While most cats are asymptomatic, clinical signs associated with heavy infestations include weight loss, anorexia, vomiting,
diarrhea, jaundice, hepatomegaly, and abdominal distention.11-13 Clinicopathologic data may include peripheral eosinophilia and evidence of cholestasis. Fluke eggs may be detected on fecal
examination through direct smears and routine fecal screening procedures.11-13
Lymphocytic portal hepatitis
Lymphocytic portal hepatitis is characterized by the infiltration of lymphocytes and plasma cells into portal areas that does
not extend into the hepatic parenchyma or involve the bile ducts.14 Lymphocytic portal hepatitis appears to be a common histopathologic lesion in older cats and is distinct from the previously
described forms of feline inflammatory hepatobiliary disease in that inflammation does not involve the biliary tree. In a
retrospective study, lymphocytic portal hepatitis was noted in 82% of cats more than 10 years old.14 Most of these cats were asymptomatic for liver disease and had mild and variable changes in serum liver enzyme activity.14
It has been speculated that lymphocytic portal hepatitis is an immune-mediated disease or represents a reactive pattern due
to subclinical disease in another organ system, but a nonspecific age-related change cannot be ruled out.2 The WSAVA Liver Disease Standardization Group has questioned the clinical importance of this disorder.4
Despite certain trends in clinical signs and clinicopathologic data, cats with various forms of inflammatory hepatobiliary
disease can only be distinguished based on histologic examination of a hepatic biopsy sample.1,15 Before performing a hepatic biopsy, conduct imaging studies, including abdominal radiography and ultrasonography.
Abdominal radiography may reveal hepatomegaly or a liver of normal size.15 In some cases, abnormalities of the biliary tree such as cholelithiasis or biliary tract mineralization may be observed.
In rare cases, abdominal effusion or a ground-glass appearance in the right cranial abdominal quadrant may be noted, consistent
with ascites and pancreatitis, respectively.
On abdominal ultrasonography, cats with inflammatory hepatobiliary disease have either diffuse changes in echogenicity (hypoechoic
most often) or no detectable alterations in the hepatic parenchyma.16 Cats with concurrent hepatic lipidosis may have a diffusely hyperechoic hepatic parenchyma. Biliary abnormalities are seen
in about 50% of all feline inflammatory hepatobiliary disease cases.16 These abnormalities include gallbladder or common bile duct distention, cholelithiasis, thickening of the walls of biliary
structures, and bile sludging.15,16 Common or intrahepatic bile duct distention may occur with extrahepatic bile duct obstruction and can be associated with
acute suppurative cholangitis or result secondary to stricture formation from chronic fibrotic biliary or pancreatic disease.2 Prominent portal vasculature was noted on ultrasonography in most feline inflammatory hepatobiliary disease cases.16 Ultrasonographic evaluation of the pancreas and intestines may reveal signs consistent with pancreatitis or inflammatory
A definitive diagnosis of feline inflammatory hepatobiliary disease requires histologic examination of a hepatic biopsy sample.
Hepatic biopsy will confirm an inflammatory cause and permits determination of disease stage (acute vs. chronic), which may
have prognostic value. Tissue can also be used for bacterial culture and antimicrobial sensitivity testing and special staining
techniques (e.g. copper, trichome). Ideally, bile should also be obtained by cholecystocentesis for cytologic examination and bacterial culture
and antimicrobial sensitivity testing. Cholecystocentesis may be performed by an experienced ultrasonographer via ultrasound
guidance or by direct visualization of the gallbladder in cases in which an exploratory laparotomy is elected. Preliminary
results suggest that bile may provide a better indication of primary or secondary infection in feline inflammatory hepatobiliary