3. small Anim. Pract.

(1975) 16, 163-172

Jaundice in the cat associated with inflammation

of the biliary tract and pancreas
D . F. K E L L Y , * D . G. B A G G O T T , ? AND
C. J. G A S K E L L t
* Department of Pathology, The Medical School, University of Bristol,
University Walk, Bristol BS8 ITD. t Department of Veterinary Medicine,
School of Veterinary Science, University of Bristol, Langford, Bristol BS18 7DU

ABSTRACT
A 7-year-old Siamese cat had recurrent episodes of pyrexia, anorexia,
weight loss and jaundice. There was biochemical evidence of hepatic
damage and hyperbilirubinaemia. At necropsy there was catarrhal and
fibrosing inflammation of the biliary ducts, gall bladder and pancreas. The
lesion was probably a sequel to ascending infection of the biliary and pan-
creatic ducts. Although this combination of lesions is not uncommon in
cats, associated clinical disease appears to be infrequent.

INTRODUCTION
Jaundice is relatively uncommon in the cat and current textbooks give little in-
formation on the causes and pathogenesis of icterus (Catcott, 1964; Joshua, 1965;
Wilkinson, 1966). This paper describes a case of recurrent pyrexia and jaundice
associated with biliary obstruction due to inflammatory disease of the gall bladder
and bile ducts.

CASE R E P O R T
A 7-year-old entire male Siamese cat was referred in August, 1973 with a history
of intermittent vomiting and progressive weight loss over the preceding 4 months.
I n 1972 the cat had recovered from an ‘enteritis-like’ condition accompanied by
jaundice and weight loss. In May 1973 the cat was again unwell, with inappetence,
weight loss and episodes of vomiting. Treatment a t this time with Vitamin A and
corticosteroids was followed by marked improvement. The animal continued to
lose weight, however, and 2 weeks later the vomiting recurred and became more

C. J. Gaskell is supported by a Scholarship from the Feline Advisory Bureau.

163
164 D . F . K E L L Y et al.

marked. Radiography of the abdomen and exploratory laparotomy revealed no

gross abnormality. The cat was treated with corticosteroids and penicillin over
the following 6 weeks; it remained bright although weight loss continued and
occasional vomiting occurred.
On examination at the University of Bristol in August, 1973 the cat was de-
pressed, emaciated and jaundiced. Haematological examination revealed neutro-
philia with a shift to the left. The serum glutamic pyruvic transaminase (SGPT)
level was raised. The serum alkaline phosphatase (SAP) and blood glucose levels
were within normal limits. Abdominal radiographs were again unremarkable.
Treatment with oxytetracycline, vitamins and fluids subcutaneously over a period
of 10 days produced slight clinical improvement and the cat again began to eat
and drink. Further biochemical examination showed a rise in SGPT levels, and
haematological examination revealed a fall in the packed cell volume and red
blood cell count. Serum amylase level on one occasion was within normal limits;
at another time it was slightly raised, 2500 IU/ml. T h e pertinent laboratory data
are summarized in the table.
An exploratory laparotomy revealed gross abnormality of the pancreas and
biliary tract. The cat was killed under general anaesthesia.

PATHOLOGY
Post-mortem jndings
The cat was emaciated (body weight 2230 gm) and had distinctly icteric mucous
membranes and subcutaneous tissues. Yellow discolouration was also present in
TABLE
1. Laboratory Data on a Siamese cat with recurrent pyrexia and
jaundice

Haematological values* Normal values t

WBC ( x I03/cu mm) 50.0; 34.6; 45.4 13.9 i 5.2
Differential Count (yo)
Bands 3; 2 0.9+ 0.8
Polymorphs 91; 94 60.4 & 14.8
Eosinophils 2; 1 8.8k 2.4
Lymphocytes 3; 2 28.2 f 2.2
Monocytes 1; 1 1.7k 1.8
Biochemical values*
SGPT (mU/ml) 90; 150; 190 < 20
SAP (KA unitslml) 15; 10; 12 < 15
Serum total bilirubin (mg %) 4.1 < 0.2
Serum Amylase (IU/ml) 1500; 2500 800-2000
Plasma glucose (mg yo) 60; 55 60-90
Blood urea (mg %) 50 30-60
~ ~~~ ~~~~~

* Obtained between 11 and 4 days before euthanasia. t Haematological

normal values from Penny, Carlisle & Davidson ( 1970).
 JAUNDICE IN T H E C A T 165

FIG. 1. Posterior surface of the liver. The gall bladder is enlarged and the bile duct is
dilated and tortuous. The gall bladder has been opened to show the thickened wall.
There is fine nodularity of the surface of the pancreas. x 1.5.

internal organs. T h e most striking gross changes were in the liver and pancreas.
The liver was of normal size with a smooth capsule and normal firm cut sur-
faces. The gall bladder was grossly dilated and its thickened wall was tense and
fluctuating (Fig. 1). The gall bladder was lined by thick, pale, granular mucous
membrane and the contents were mucinous and pale. T h e main bile duct was
both dilated and tortuous; its internal appearance was similar to that of the gall
bladder. There was no evidence of extra-hepatic obstruction of the bile duct. T h e
contents of the main bile ducts were turbid and viscous. The surface of the pan-
creas was unusually pale and had accentuated nodularity ; cut surfaces were firm,
pale and nodular. An unrelated incidental finding was focal renal cortical scar-
ring, similar to that described by Lucke ( 1968).

Histopathologicaljindings
The mucosa of the gall bladder was thrown into high folds by oedematous con-
166 D . F. K E L L Y et al.

FIG.2. Wall of the gall bladder showing cholecystitis. T h e rnucosa forms high folds a n d
there is diffuse infiltration of the oedematous connective tissue by inflammatory cells.
H & Ex 165.

nective tissue in which there were diffuse accumulations of neutrophilic leucocytes,

plasma cells and globule leukocytes (Fig. 2). Inflammatory cells were present
throughout the thickness of the oedematous wall and there was a patchy fibrinous
exudate on the serosal surface of the gall bladder. Neutrophils were also within
the lumen of the gall bladder where they were mixed with mucous secretion.
Histological changes in the liver were centred on the portal areas. Bile ducts
were dilated and neutrophils were present within the lumen, epithelium and ad-
jacent connective tissue around the ducts (Fig. 3 ) . There was marked peribiliary
fibrosis. Proliferation of bile ducts was also a feature (Fig. 4).Bile plugs were
present in parenchymal canaliculi, especially in the centrilobular areas.
The accentuated nodularity of the pancreas was associated with interlobular
 J A U N D I C E I N T H E CAT 167

FIG.3. Liver. In this portal area there are dilated bile ducts. Their lumina are filled with
inflammatory exudate. H & E x 67.

fibrosis. Oedematous young fibrous connective tissue was very conspicuous and
frequently extended into the intralobular areas of the gland. Neutrophils and
lymphocytes were scattered throughout the pancreatic fibrous tissue (Fig. 5 ) .
Pancreatic ducts were dilated; some contained eosinophilic secretion and neutro-
phils (Fig. 6). Globule leucocytes were often seen beneath the ductal epithelial
cells.
The pathological diagnosis was cholecystitis, cholangitis and interstitial pan-
creatitis.
168 D . F . K E L L Y et al.

FIG.4. Liver showing cholangitis. There is proliferation of bile ducts and peribiliary
fibrosis. Lymphocytes are present in the portal connective tissue and the lumen of the
central bile duct contains neutrophils. H & E x 165.
 J A U N D I C E I N THE CAT 169

FIG.5 . Pancreas. There is marked inflammation and fibrosis of the interlobular and in-
tralobular tissue. The ducts are dilated and inflammatory cells are present within their
lumina. H & E x 67.

C
170 D . F. K E L L Y et al.

FIG. 6. Pancreas. A dilated interlobular duct contains secretion and neutrophils. The
duct is surrounded by lymphocytes and oedematous fibrous tissue. H & E x 165.

DISCUSSION
The early clinical signs in this animal were non-specific and, beyond inferring the
presence of intra-abdominal disease, did not suggest a firm diagnosis. The recur-
rence ofjaundice, however, suggested that the cat should be examined for evidence
of liver disease. Consistent elevation of SGPT levels indicated the presence of
hepatocellular injury and the marked elevation of serum total bilirubin confirmed
the clinical impression of jaundice. I n the absence of evidence of a haemolytic
process it was assumed that the hyperbilirubinaemia was of obstructive or hepato-
toxic origin. SAP levels were within the normal range, but because there is con-
siderable renal excretion of alkaline phosphatase in the cat (Wilkinson, 1962) an
obstructive jaundice was not excluded. This contrasts with the situation in the dog
 JAUNDICE IN THE CAT 171

where elevation of the level of SAP, in the absence of bone disease, is a useful in-
dication of biliary obstruction (Kaneko & Cornelius, 1970). The significance of
the levels of serum amylase is uncertain. Present information suggests a wide range
of normal values (Table 1) ; the second value of 2500 IU/mlpossiblyreflectsleakage
of enzyme from pancreatic acinar cells damaged by the inflammatory process. The
presence of an active inflammatory process in the biliary tract and pancreas iz
reflected by the persistent neutrophilia.
The histopathological features of the inflammatory lesions in the gall bladder,
biliary ducts and pancreas are consistent with a reaction to ascending infection of
the biliary and pancreatic ducts from the duodenum. T h e portal peribiliary fibro-
sis is indicative of the chronicity of the process and suggests the possibility that
previous infection may have produced the earlier clinical episodes in 1972. Periods
of apparent clinical improvement may have been due to partial resolution of the
cholangitis with relief of luminal obstruction. Concomitant inflammation of the
biliary and pancreatic ducts is a not uncommon necropsy finding in the cat (Jubb
& Kennedy, 1970) and may be seen as an incidental post-mortem finding in cats
used in toxicological testing (D. F. Kelly, unpublished observations). Inflamma-
tion of the two duct systems might be expected to be common, as the pancreatic
and biliary ducts fuse before entering the duodenum. The morbid anatomical
features of the pancreatic lesion in this case correspond with the description of
interstitial pancreatitis (Jubb & Kennedy, 1970).
Although the lesions described appear to be common in cats, clinical disease
associated with inflammatory change of the biliary and pancreatic ducts is not
commonly recognized. Joshua (1965) mentioned a 64-year-old cat with recurring
episodes of jaundice apparently following a bacterial infection; the cat was re-
ported to have nodular hyperplasia and focal inflammation ofthe pancreas. Her case
appears to resemble the one described in this paper. Wilkinson (1966) refers to
feline biliary cirrhosis as a sequel to obstruction and inflammation of the biliary
system and states that it is usually associated with jaundice. It is possible that
ascending duct infection may result in self-limiting clinical episodes similar to
those described in this paper. The common post-mortem lesions of interstitial pan-
creatitis and cholangitis or their sequel (biliary cirrhosis) may represent the healed
stage of infection. These clinical and pathological observations are presented SO
that clinicians may consider the possibility of disease of the biliary and pancreatic
ducts in cats with otherwise unexplained pyrexia, weight loss and jaundice.

REFERENCES
E.J. (1964)Feline Medicine and Surgery, 1st edn, p. 389. American Veterinary Publications,
CATCOTT,
Santa Barbara, California.
JOSHUA,J.O. (1965) The Clinical Aspects of Some Diseases ofcats, p. 86. William Heinemann, London.
JUBB, K.V.F. & KENNEDY, P.C. (1970) Pathology of Domestic Animals, 2nd edn, vol. 2, p. 268.
Academic Press, New York.
172 D. F. K E L L Y et al.

KANEKO, J.J. & CORNELIUS, C.E. (1970) Clinical Biochemistry of Domestic Animals. 2nd edn, vol. 1,
p. 210. Academic Press, New York.
LUCKE, V.M. (1968) 3. Path. Bact. 95, 67.
PENNY,R.H.C., CARLISLE, C.H. & DAVIDSON, H.A. (1970) B . Vet.3. 126, 459.
WILKINSON, G.T. (1966) Diseases of the Cat, p. 84. Pergamon Press, Oxford.
WILKINSON, J.H. (1962) An Introduction to Diagnostic Enzymology, p. 88. Arnold, London.