Clinical examination findings
Clinically, cats with suppurative cholangitis tend to be young (median age 3.3 years).1,2,5,6 A predisposition in male cats has been noted. An acute presentation with a short duration of clinical signs (< 5 days) is
common.1,2,5,6 History may include anorexia, lethargy, vomiting, and diarrhea. Physical examination findings may include jaundice, abdominal
pain, fever, dehydration, lethargy, and, less commonly, hepatomegaly and hypothermia.1,2,5,6
The results of a complete blood count reveal a left shift with toxic neutrophils, with or without a leukocytosis, in about
30% of cases.1,2 Moderate increases in serum alanine transaminase (ALT), aspartate transaminase (AST), and gamma-glutamyltransferase (GGT)
activities are frequently noted.1,2,5 ALT activity is more markedly elevated in cases with concurrent extrahepatic bile duct obstruction. Serum alkaline phosphatase
(ALP) activity is generally mildly increased except in cats with concurrent extrahepatic bile duct obstruction or pancreatitis,
in which marked increases occur.1 Increases in bilirubin are typically mild to moderate, but may be dramatic with accompanying extrahepatic bile duct obstruction.
Chronic nonsuppurative cholangitis
Nonsuppurative cholangitis, the most common form of feline inflammatory hepatobiliary disease, encompasses several reported
histologic descriptions, including lymphocytic-plasmacytic cholangitis, lymphocytic cholangitis, progressive lymphocytic cholangitis,
and sclerosing cholangitis. It is difficult to determine whether these histologic descriptions represent different diseases
or stages of a single progressive disease process. For ease of discussion, we consider three distinct histologic forms: lymphocytic-plasmacytic
cholangitis, lymphocytic cholangitis, and chronic cholangitis due to fluke infestation.
Lymphocytic-plasmacytic and lymphocytic cholangitis
2A. Lymphocytic-plasmacytic cholangitis. The portal areas and bile ducts are mildly to moderately infiltrated with lymphocytes,
plasma cells, and lesser numbers of neutrophils (hematoxylin-eosin stain; 400X).
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Lymphocytic-plasmacytic cholangitis is associated with mild to severe infiltration of portal areas or bile ducts with lymphocytes
and plasma cells and lesser numbers of neutrophils (Figures 2A & 2B).1,4 In the lymphocytic variant, the inflammatory cells are predominantly lymphocytes with lesser numbers of plasma cells and
neutrophils.4 Bile duct hyperplasia is typically present in both forms. In some cases, bile duct epithelium may become vacuolated and
dropout is observed, resulting in a generalized reduction in the number of medium- and small-size bile ductules on histologic
samples (vanishing bile duct syndrome).1 Depending on chronicity, varying degrees of portal fibrosis to portal bridging fibrosis or periductal fibrosis are noted.1,2,4,7 In some cases, an onion-skin layering of connective tissue develops around small bile ducts.1 This histologic pattern has been described as sclerosing cholangitis and may represent a progression of lymphocytic or lymphocytic-plasmacytic cholangitis or a separate disease entity.
2B. Figure 2A at a higher magnification (hematoxylin-eosin stain; 1,000X).
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The development of lymphocytic or lymphocytic-plasmacytic cholangitis may represent tissue response to chronic, nonseptic
injury,1
although some cases may represent progression from the suppurative form.2 In the latter case, antibiotics may eliminate the initial bacterial cause, but hepatobiliary damage may continue secondary
to self-perpetuating immune reactions to neoantigens released during the initial infection.
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