Feline inflammatory hepatobiliary disease is the second most common cause of liver disease in cats, with hepatic lipidosis
being the most common. The disease is classified by hepatic histopathology1 ; terms used to describe it have included suppurative or acute cholangiohepatitis, chronic cholangiohepatitis, chronic lymphocytic cholangitis, progressive lymphocytic cholangitis, sclerosing cholangitis, lymphocytic-plasmacytic cholangitis/cholangiohepatitis, lymphocytic portal hepatitis, and biliary cirrhosis.2 A lack of consistency in terminology has made comparison of reported cases difficult and has hindered clarification of the
etiopathogenesis of feline inflammatory hepatobiliary disease subtypes. In this review, we first discuss the general classifications
of the disease and then describe how to diagnose and treat the various types.
A new classification scheme, proposed by the World Small Animal Veterinary Association (WSAVA) Liver Disease Standardization
Group, recognizes that feline inflammatory hepatobiliary disease largely centers on the biliary tree.3,4 They describe three distinct forms of feline inflammatory hepatobiliary disease: neutrophilic cholangitis (acute and chronic),
lymphocytic cholangitis, and chronic cholangitis caused by fluke infestation.3,4 Unfortunately, since there is not yet consensus within the veterinary community to use this scheme, for this review we use
two broad categories of clinically relevant feline inflammatory hepatobiliary disease: acute suppurative and chronic nonsuppurative
cholangitis. We also briefly discuss lymphocytic portal hepatitis.
Acute suppurative cholangitis
In suppurative cholangitis, hepatic histologic examination reveals neutrophils within the walls and lumina of intrahepatic
bile ducts and portal areas with accompanying bile duct epithelial degeneration and necrosis (Figure 1).4 Concurrent periportal parenchymal inflammation is common.4,5 In some instances, suppurative cholangitis occurs secondary to a primary nonsuppurative hepatobiliary disease. In these
cases, histologic examination may also reveal lymphocyte and plasma cell infiltration of portal areas with varying degrees
of bile duct proliferation and fibrosis.
1. Neutrophilic cholangitis. Neutrophils are present within the walls and lumina of the intrahepatic bile ducts and portal
areas. Bile duct epithelial degeneration is also present. Microvesicular fatty change can be noted within the hepatocytes
(hematoxylin-eosin stain; 400X).
Suppurative cholangitis is thought to be associated with infection.1,5,6 This may be a primary biliary tree infection or an infection secondary to septicemia, dissemination of a chronic infection
from another organ system, or treatment with systemic immunosuppressive therapy.1 Many cats with suppurative cholangitis demonstrate disturbances in biliary structure and function that predispose them to
ascending bacterial infections.1,5,6 These disturbances can be anatomic, functional, or both. Many of these predisposing conditions have a waxing and waning
course or result in subtle clinical signs (e.g. chronic pancreatitis, inflammatory bowel disease), so clinicians would not necessarily be able to determine whether the process
was active. These predisposing factors may result in damage to the biliary tree that then results in abnormalities in biliary
structure or function. Predisposing factors include inflammatory bowel disease, pancreatitis, abnormalities of gallbladder
structure and function, choledochitis, biliary parasites, previous biliary diversion surgery, and extrahepatic bile duct obstruction.1,5
The most commonly isolated organisms in cats with suppurative cholangitis are consistent with an enteric origin: Escherichia coli and alpha-hemolytic Streptococcus species, and Actinomyces, Enterobacter, Bacteroides, Klebsiella, and Clostridium species.2 Additional organisms associated with suppurative cholangitis include Toxoplasma species and possibly Bartonella species. In many reported cases, however, a bacterial cause is suspected, but culture results are negative.2 Reasons speculated for the failure to isolate bacteria include 1) lack of anaerobic culture submission, 2) difficulty in
growing anaerobic organisms in vitro, and 3) previous antibiotic treatment.1,2