Colangitis Felina
Colangitis Felina
Colangitis Felina
KEYWORDS
Feline Cat Cholangitis Liver Lymphocytic Neutrophilic Inflammation
Fluke
KEY POINTS
Inflammatory liver disease (cholangitis) is common in cats.
Three major forms are recognized: neutrophilic, lymphocytic, and chronic cholangitis. Re-
sults of diagnostic modalities, including hematology, biochemistry, abdominal ultrasound,
and fecal analysis, can assist in ranking differentials.
Liver biopsy and/or bile analysis (cytology and bacterial culture) are necessary for defin-
itive diagnosis.
Empiric antibiotic and other supportive treatments are indicated in clinically unstable
cases of suspected neutrophilic cholangitis in which invasive diagnostics carry an unac-
ceptable risk.
Neutrophilic cholangitis and chronic cholangitis can usually be cured with appropriate
treatment. Lymphocytic cholangitis can be managed and some cats have long survival
times.
INTRODUCTION
Inflammatory liver disease is reported to be the most common, or second most com-
mon, abnormality detected in feline liver biopsies.1,2 Hirose and colleagues2 (2014)
diagnosed inflammatory liver disease in 50% of abnormal biopsies submitted to a
teaching hospital in Japan. In the United States, 25.7% of cases had inflammatory dis-
ease, whereas 49.7% had hepatic lipidosis.1
The term cholangitis to describe inflammatory liver disease is favored over cholan-
giohepatitis. Cholangitis most accurately reflects the histopathological abnormalities
that are centered on the biliary tract with secondary, if any, involvement of the hepatic
parenchyma. The World Small Animal Veterinary Association standardization commit-
tee recognizes 3 forms of feline cholangitis: neutrophilic, lymphocytic, and chronic, the
latter associated with liver fluke.3
This article reviews the etiopathogenesis, clinical findings, risks, and benefits of diag-
nostic investigations, comorbidities, treatment, and outcomes of feline cholangitis.
NEUTROPHILIC CHOLANGITIS
Except in liver fluke endemic regions, neutrophilic cholangitis is the most commonly
reported form in most studies, making up 56.3% to 90% of cases of inflammatory liver
disease.2,4,5
CAUSES
Most cases of neutrophilic cholangitis result from bacterial infection.6,7 Comorbid dis-
ease is common, in particular pancreatitis, either alone or with inflammatory bowel dis-
ease (IBD) in a syndrome known as triaditis, and may increase the risk of ascending
bacterial infection.5,6,8,9 In the cat, the common bile duct and pancreatic duct usually
enter the duodenum together at the major duodenal papilla. Conversely, pancreatitis
and IBD may be a consequence of neutrophilic cholangitis.2
The role of Helicobacter spp in feline neutrophilic cholangitis and/or triaditis is
unclear. Although Helicobacter spp are detected by polymerase chain reaction
(PCR) in the liver and bile of cats with neutrophilic and lymphocytic cholangitis, they
are also detected in cats with noninflammatory liver disease and clinically healthy
cats.4,6,10
SIGNALMENT
HISTORY
A short history of illness, usually less than 2 weeks, is typical.7,12 Common historical
findings include:5,11,12
Lethargy
Inappetence
Anorexia
Vomiting
Diarrhea
Recent weight loss
PHYSICAL EXAMINATION
LABORATORY FINDINGS
Neutrophilia ranges from severe with a left shift and toxic changes to absent. Of
note, neutrophilic cholangitis is not always accompanied by liver enzyme elevations.5
Compared with lymphocytic cholangitis, cases of neutrophilic cholangitis have
higher segmental and band neutrophil counts, as well as increases in alanine amino-
transferase (ALT) activity and total bilirubin.11 Inappetence, dehydration, vomiting,
and diarrhea can precipitate prerenal azotemia, hypokalemia, hyponatremia, and
hypochloremia.
Coagulation times (prothrombin time, activated partial thromboplastin time,
activated clotting time) can be prolonged and must be evaluated before invasive
Table 1
Abnormalities reported in hematology and biochemical analysis in cats with neutrophilic
cholangitis
Abbreviations: ALP, alkaline phosphatase; ALT, alanine aminotransferase; AST, aspartate amino-
transferase; GGT, gamma-glutamyltransferase.
Data from Refs.5,7,11–13
706 Boland & Beatty
diagnostics such as liver biopsy11,13 (see also Cynthia R.L. Webster’s article
“Hemostatic Disorders Associated with Hepatobiliary Disease,” in this issue). Hepatic
dysfunction may result in hyperammonemia and liver function should be evaluated
before anesthesia. Preprandial and postprandial serum bile acid concentrations
may be abnormal or may not be interpretable due to the presence of hyperbilirubine-
mia11 (see also Yuri A. Lawrence and Jörg M. Steiner’s article “Laboratory Evaluation
of the Liver,” in this issue).
Hypocobalaminemia or hypercobalaminemia can be present in cats with neutro-
philic cholangitis and/or in cats with concurrent pancreatitis or IBD.14,15 Elevated feline
pancreas-specific lipase immunoreactivity concentrations raise suspicion for concur-
rent pancreatitis. One study showed that biochemical and hematological parameters
did not assist in identifying concurrent pancreatitis.5
DIAGNOSTIC IMAGING
Imaging findings can support a diagnosis of neutrophilic cholangitis but normal findings
do not exclude the diagnosis. Abdominal radiographs may reveal mild hepatomegaly
or cholecystoliths.11 Abdominal ultrasound may reveal increased thickness and irreg-
ularity of the gall bladder wall, dilation and tortuosity of the cystic and common bile
ducts, diffuse hyperechogenicity of the liver parenchyma, hepatomegaly, hyperechoic
gall bladder contents, gall bladder distention, and choleliths if present (Figs. 2 and
3).5,11,16 Marolf and colleagues16 (2012) found no significant differences in ultrasono-
graphic changes between cats with neutrophilic versus lymphocytic cholangitis.
Ultrasonographic changes associated with concurrent pancreatitis, including hypo-
echogenicity of the pancreas, peripancreatic fluid accumulation, irregular pancreatic
margins, and hyperechoic peripancreatic fat, may be present.5,17 Concurrent IBD
may manifest as intestinal wall thickening with preserved layering.5,18
BACTERIAL CULTURE
Ascending infection via the biliary tree is thought to be the most common route.
Ascending bacterial infection is supported by frequent culture of enteric bacteria
Fig. 2. Ultrasound image from a cat with bacterial cholecystitis and common bile duct
obstruction. The gall bladder is distended with a thickened wall (white arrow) and echo-
genic content. (Courtesy of Dr Joanna Pilton, The University of Sydney, Sydney, Australia.)
Feline Cholangitis 707
Fig. 3. Ultrasound image from a cat with bacterial cholecystitis and common bile duct
obstruction. The common bile duct (CBD) (white arrow) is markedly distended and tortuous,
and has a thickened wall and echogenic intraluminal material. (Courtesy of Dr Joanna Pilton,
The University of Sydney, Sydney, Australia.)
from bile or liver biopsies from affected cats (Box 1).5,8,19–21 A single bacterial species
is cultured from more than 80% of cases, with Escherichia coli being the most com-
mon isolate.5,6,8,12,19,20 Other possible routes of infection include hematogenous
seeding, enteric mucosal translocation, or entry via the portal system.6,8,12,19
Normally, bile in cats is sterile although transient bactibilia with enteric bacteria
has been reported.20,21 Risk factors for the development of persistent biliary infection
include cholelithiasis, biliary tract obstruction, hepatic neoplasia, congenital abnor-
malities, extrahepatic disease (eg, pancreatitis, IBD, triaditis), or pre-existing inflam-
matory liver disease.6,8,20,22
Box 1
Bacteria cultured from bile, liver, and choleliths in cats
Bacteria
Escherichia coli
Enterococcus spp
Enterococcus faecalis
Streptococcus spp
Streptococcus viridans
Clostridium spp
Clostridium perfringens
Bacterioides spp
Salmonella enterica serovar Typhimurium
Pseudomonas spp
Pseudomonas fluorescens
Staphylococcus spp
Acinetobacter spp
Table 2
Diagnostic sample collection for cytology, bacterial culture, and histopathology
Fig. 4. Grossly purulent bile aspirated from the gall bladder of a cat with bacterial cholecys-
titis. (From Brain PH, Barrs VR, Martin P, et al. Feline cholecystitis and acute neutrophilic
cholangitis: clinical findings, bacterial isolates, and response to treatment in six cases. J Fe-
line Med Surg 2006;8:95; with permission.)
implications. Nonbacterial pathogens are rare in feline cholangitis and bile cytology
can assist in identifying these.8
LIVER BIOPSY
Histopathology of liver biopsy samples is required for definitive diagnosis. Biopsy may
not be possible, for example, in unstable or deteriorating patients or if financial
Fig. 5. Diff-Quik stained bile smear showing degenerate neutrophilic inflammation and
pleomorphic bacterial rods and cocci from a cat with bacterial cholecystitis. (From Brain
PH, Barrs VR, Martin P, et al. Feline cholecystitis and acute neutrophilic cholangitis: clinical
findings, bacterial isolates, and response to treatment in six cases. J Feline Med Surg
2006;8:96; with permission.)
710 Boland & Beatty
COMORBIDITIES
TREATMENT
Antibiotics and supportive care are the mainstays of treatment of neutrophilic cholan-
gitis (Table 4).7,11,12
Antibiotic Selection
Antibiotic selection is ideally based on the results of bacterial culture and sensitivity
testing. Empiric antibiotic therapy is required, at least until culture results are received.
Unless cytologic findings support alternate choices, empiric therapy should provide
Table 3
Summary of liver histologic features of neutrophilic, lymphocytic, and chronic cholangitis in
cats
Chronic Cholangitis
Neutrophilic Cholangitis Lymphocytic Cholangitis Associated with Liver Fluke
Portal neutrophilic Moderate to marked Periductal and portal
infiltrates aggregates of small lym- inflammatory infiltrates,
Lower numbers of phocytes infiltrating portal which can extend into the
lymphocytes and plasma areas and around bile hepatic parenchyma (lym-
cells in portal areas ducts phocytes, macrophages,
Neutrophilic infiltrates can Biliary hyperplasia plasma cells, eosinophils,
extend into the hepatic Biliary ductular and neutrophils)
parenchyma proliferation Dilation and adenomatous
Dilated intrahepatic biliary Variable degrees of portal hyperplasia of biliary ducts
ducts fibrosis Periportal and periductal
Neutrophils within biliary Lymphocytes can pene- fibrosis
duct lumens and trate the lumen of biliary Hyperplastic adenomatous
infiltrating duct walls ducts and infiltrate biliary or ulcerative cholecystitis
Bile duct proliferation, epithelium leading to can be present
hyperplasia and epithelial ductopenia Adult liver flukes or eggs
degeneration Lymphocytic infiltrates can are often not identified
Variable degrees of fibrosis extend into the hepatic
Periportal necrosis parenchyma
Fig. 6. Liver biopsy from a cat with chronic neutrophilic cholangitis. There is pronounced
periductal concentric fibrosis with mild edema and biliary hyperplasia. A mixed periportal
inflammatory infiltrate and intraductal neutrophils are present (30 3-diaminobenzidine and
hematoxylin). (Courtesy of Dr Mark Krockenberger, The University of Sydney, Sydney,
Australia.)
Supportive Care
Hospitalization periods range from a few days to a week or more.7 IV fluid therapy is
used for rehydration and correction of electrolyte abnormalities (see Table 4). Hypo-
kalemia should be identified and treated. Analgesia can be safely provided by the use
of opioids. Nonsteroidal anti-inflammatory drugs are contraindicated in cats with
dehydration, inappetence, vomiting, and diarrhea because of the risk of severe
adverse effects such as nephrotoxicity and gastrointestinal ulceration. Antiemetics
and appetite stimulants may be required.33,34 Other medications that may benefit
cats with neutrophilic cholangitis include S-adenosylmethionine, silybin, and urso-
deoxycholic acid (UDCA).35–37
Vitamin K1 deficiency can occur in conditions causing biliary obstruction and can
contribute to coagulation abnormalities in cats with liver disease (see Cynthia R.L.
Webster’s article, “Hemostatic Disorders Associated with Hepatobiliary Disease,” in
this issue). Laboratory assessment of coagulation and/or supplementation of vitamin
K1 should be completed before hepatic sampling. Cats with hypocobalaminemia
should be supplemented. Nutrition may be provided for anorexic cats by the use of
nasoesophageal, esophageal, or gastric feeding tubes.11
Feline Cholangitis
Ptyalism
S-adenosylmethionine Hepatoprotectant Neutrophilic cholangitis 90 mg PO SID —
Reduce inflammation
Reduce apoptosis
Promote cell regeneration
713
714
Boland & Beatty
Table 4
(continued )
Drug Group and
Drug Proposed Action Indication Dose and Route Side Effects
Silybin Hepatoprotectant Neutrophilic cholangitis 9 mg PO SID —
Antioxidant
Free radical scavenger
Anti-inflammatory
Stimulates bile flow and
production of
hepatoprotective bile acids
Ursodeoxycholic acid Bile acid Neutrophilic cholangitis 10–15 mg/kg PO SID —
Increased bile flow Lymphocytic cholangitis
Possible cytoprotective
properties
Prednisolone Glucocorticoid Lymphocytic cholangitis 1 mg/kg SID IV, PO Polyphagia
Anti-inflammatory Polydipsia
Immunosuppressant Polyuria
Skin fragility
Poor fur regrowth
Weight gain
Gastrointestinal ulceration
Diabetes mellitus
Praziquantel Anticestodal antiparasitic Liver fluke 10–25 mg/kg SC or PO SID for 3–5 d Injection site reaction
Gastrointestinal side effects
Abbreviations: CRI, continuous rate infusion; IM, intramuscular; IV, intravenous; SC, subcutaneous.
Data from Refs.7,11,12,30,33–38
Feline Cholangitis 715
COMPLICATIONS
PROGNOSIS
Most cats recover with appropriate treatment and recurrence is rare with reported sur-
vival times of several years.7,11 Concurrent disease may affect long-term outcome in
some cats.11
LYMPHOCYTIC CHOLANGITIS
There are conflicting data regarding the prevalence of lymphocytic cholangitis in cats.
This disease accounted for only 0.17% of cats presenting to a university referral hos-
pital and 6.8% of all cats with inflammatory liver disease in a necropsy study.1,40
However, a recent study of cats in Greece reported a higher prevalence with 18
per 27 symptomatic and 14 per 20 asymptomatic cats having histopathological evi-
dence of cholangitis. Of these, 25 had lymphocytic and 5 had chronic neutrophilic
cholangitis.41 Histologic severity scores were not significantly different between
symptomatic and asymptomatic cats. Possible explanations for this higher preva-
lence may include regional differences, sample size, differences in study design,
and histopathology classification or interpretation. The significance of histopatholog-
ically identified cholangitis in asymptomatic cats is unclear and requires further
investigation.
CAUSES
Fig. 7. Left lateral abdominal radiograph of a cat with a common bile duct (CBD) obstruction
postoperatively. A radiopaque stent (black arrow) is located within the CBD and duodenum.
A Jackson-Pratt abdominal drain (Mila International, Inc, Kentucky) is also present (white
arrow). (Courtesy of Dr Joanna Pilton, The University of Sydney, Sydney, Australia.)
716 Boland & Beatty
SIGNALMENT
Cats of any age, breed, or sex can be affected. Some studies report an increased risk
in young cats and others in older cats.26,40,44 A male predisposition is inconsistently
reported.26,27,40 Persian or Norwegian Forest cats are overrepresented in studies
from the United Kingdom and the Netherlands, respectively.26,40
HISTORY
A protracted history of slowly progressive illness over weeks to months is typical for
lymphocytic cholangitis.26,27,45 In contrast to cats with neutrophilic cholangitis, they
may be bright, alert, and responsive at presentation. Commonly reported historical
findings include:11,26,27,40
Weight loss
Polyphagia
Anorexia
Vomiting
Lethargy
Polydipsia and polyuria
PHYSICAL EXAMINATION
LABORATORY FINDINGS
Table 5
Abnormalities in hematology and biochemical analysis in cats with lymphocytic cholangitis
Affected cats can develop moderate to marked ascites. Abdominal fluid analysis typi-
cally reveals a high protein content with increased globulin levels, small lymphocytes,
nondegenerate neutrophils, and other inflammatory cell types.26,45
DIAGNOSTIC IMAGING
LIVER BIOPSY
Fig. 8. Liver biopsy from a cat with marked chronic lymphocytic cholangitis. There is moder-
ate periductal fibrosis with a variably intense portal lymphocytic infiltrate with widespread
moderate hepatocellular nodular hyperplasia (30 3-diaminobenzidine and hematoxylin).
(Courtesy of Dr Mark Krockenberger, The University of Sydney, Sydney, Australia.)
718 Boland & Beatty
COMORBIDITIES
TREATMENT
PROGNOSIS
Resolution of ascites and median and mean survival times of 26 to 36 months with
treatment are reported in studies with small numbers of cats.11,26,40,45
Liver flukes reported to infect cats are trematodes belonging to the families Dicrocoe-
liidae (Platynosomum spp) and Opisthorchiidae (Opisthorchis spp, Clonorchis spp,
Metorchis spp, and Amphimerus spp). There is lack of consensus on the classification
of individual species, some of which may be synonymous.48,49
Feline Cholangitis 719
DISTRIBUTION
Feline liver fluke infestation has been reported throughout the world with different
regional prevalences.48,49 The Opisthorchiidae family also infect humans who acquire
infection from eating undercooked fish. Cats, as well as many other mammals,
including dogs, may act as reservoir hosts in endemic regions.50,51 Most reports in
the English language of clinical disease in cats describe Platynosomum spp infections.
LIFECYCLE
Trematodes have complex life cycles involving 2 to 4 hosts and many larval stages.
Platynosomum spp fluke lifecycles are incompletely understood but are thought to
involve:48,52
First intermediate host: land snail species ingest eggs and shed sporocysts into
the environment
Second intermediate host: terrestrial isopods (crustaceans) ingest sporocysts
Paratenic host: lizard and amphibian species are infected by eating isopods
Definitive host: cats are infected by eating lizards. The flukes migrate to the liver
and eggs are shed in feces
The Opisthorchiidae fluke life cycles involve:49
First intermediate host: aquatic snail species ingest eggs and shed redia into the
environment
Second intermediate host: fish of the family Cyprinidae are infected when
cercaria penetrate their epithelium
Definitive host: cats are infected by eating raw fish. The flukes migrate to the liver
and eggs are shed in feces
Platynosomum fastosum
Platynosomum spp are found in tropical and subtropical regions where they can cause
lizard poisoning in cats. In endemic regions, the prevalence of P fastosum infestation
can exceed 80% among free roaming cats.48,53–55 The flukes reside in the gall bladder
and biliary ducts causing inflammation and obstruction.
SIGNALMENT
An inconsistent female predisposition has been reported. Free roaming cats more
than 2 years of age are overrepresented.54,56
HISTORY
Most liver fluke infections in cats are asymptomatic.57 If clinical signs occur, historical
findings include chronic or acute28,57–60
Inappetence
Lethargy
Weight loss
Vomiting
Diarrhea
Acute presentations may be associated with extrahepatic biliary obstruction.
Disease severity may be affected by parasite burden, repeated infection, and/or
chronicity.30
720 Boland & Beatty
PHYSICAL EXAMINATION
Physical examination findings include poor body condition, dehydration, jaundice, he-
patomegaly, abdominal pain, and ascites.28,30,57,58,60
LABORATORY FINDINGS
Laboratory findings reported in cats with liver fluke infections are summarized
in Table 6. Most cases for which FIV and FeLV status has been reported are
negative.30,59
Fecal analysis to identify fluke eggs can assist in diagnosis.29,55,61 Negative fecal
analysis does not rule out infection. The accuracy of fecal analysis is influenced by
intermittent shedding of eggs, low parasite burdens, low numbers of eggs per gram
of feces, and the fecal analysis method.29,55,61 Formalin-ether sedimentation is a sen-
sitive technique. Repeated fecal analysis combined with other laboratory and imaging
findings may be required for diagnosis. Fecal PCR tests have been developed for
some liver fluke species.
Köster and colleagues29 (2016) reported that analysis of bile obtained by percuta-
neous ultrasound-guided cholecystocentesis contained a significantly higher fluke
egg count than fecal analysis. This technique may assist in cases if liver fluke infesta-
tion is suspected but not confirmed by fecal analysis.
DIAGNOSTIC IMAGING
COMORBIDITIES
Bacterial cholangitis (Escherichia coli) associated with liver fluke infestation was re-
ported in 6 per 13 cats.29 However, all cats in this study were FIV positive. The inci-
dence of clinically significant bacterial cholecystitis in liver fluke infested cats
requires further investigation. Liver fluke infections have rarely been associated with
cholangiocarcinoma in cats.62
Table 6
Abnormalities in hematology and biochemical analysis reported in liver fluke infections
(Platynosomum spp) in cats
Hematology Biochemistry
Mild nonregenerative anemia Hyperbilirubinemia
Eosinophilia Increased ALT activity
Lymphocytosis Increased ALP activity
Increased AST activity
LIVER BIOPSY
Gross postmortem and exploratory laparotomy findings in cats infected with liver fluke
may include gallbladder distension; wall thickening and necrosis; enlarged bile ducts;
thickened, dilated, and tortuous common bile and cystic ducts; obstruction of the
cystic or common bile duct; presence of liver flukes within the gall bladder and biliary
tree; and mild to moderate hepatomegaly.30,57,58,62
Histopathological features of chronic cholangitis associated with liver fluke infec-
tions are summarized in Table 3.
TREATMENT
PROGNOSIS
Although most cats remain asymptomatic, liver fluke infestation can be fatal.
Opisthorchiidae
Opisthorchiidae (Opisthorchis spp, Clonorchis spp, Metorchis spp, and Amphimerus
spp) occur worldwide and prevalences of 30% to 50% in free roaming cats are com-
mon.50,51 Reports of clinical disease in cats are rare but this may be underreported.
Clinical, laboratory and histopathology findings in cats infected with Opisthorchis
spp, Metorchis spp, Clonorchis spp, and Amphimerus spp mirror those of P fastosum
infections.50,63–65 Treatment with praziquantel is effective.
REFERENCES
1. Gagne JM, Weiss DJ, Armstrong PJ. Histopathologic evaluation of feline inflam-
matory liver disease. Vet Pathol 1996;33(5):521–6.
2. Hirose N, Uchida K, Kanemoto H, et al. A retrospective histopathological survey
on canine and feline liver diseases at the University of Tokyo between 2006 and
2012. J Vet Med Sci 2014;76(7):1015–20.
3. Van den Ingh TSGAM, Cullen JM, Twedt DC, et al. Morphological classification of
biliary disorders of the canine and feline liver. In: Rothuizen J, Bunch SE,
Charles JA, et al, editors. WSAVA standards for clinical and histological diagnosis
of canine and feline liver disease. World Small Animal Veterinary Association
standardization group. Edinburgh (Scotland): Saunders Elsevier; 2006. p. 61–76.
4. Greiter-Wilke A, Scanziani E, Soldati S, et al. Association of Helicobacter with
cholangiohepatitis in cats. J Vet Intern Med 2006;20:822–7.
5. Callahan Clark JE, Haddad JL, Brown DC, et al. Feline cholangitis: a necropsy
study of 44 cats (1986-2008). J Feline Med Surg 2011;13(8):570–6.
6. Twedt DC, Cullen J, McCord K, et al. Evaluation of fluorescence in situ hybridiza-
tion for the detection of bacteria in feline inflammatory liver disease. J Feline Med
Surg 2014;16(2):109–17.
722 Boland & Beatty
7. Brain PH, Barrs VR, Martin P, et al. Feline cholecystitis and acute neutrophilic
cholangitis: clinical findings, bacterial isolates and response to treatment in six
cases. J Feline Med Surg 2006;8:91–103.
8. Peters LM, Glanemann B, Garden OA, et al. Cytological findings of 140 bile sam-
ples from dogs and cats and associated clinical pathological data. J Vet Intern
Med 2016;30:123–31.
9. Weiss DJ, Gagne JM, Armstrong PJ. Relationship between inflammatory hepatic
disease and inflammatory bowel disease, pancreatitis and nephritis in cats. J Am
Vet Med Assoc 1996;209(6):1114–6.
10. Sjödin S, Trowald-Wigh G, Fredriksson M. Identification of Helicobacter DNA in
feline pancreas, liver, stomach, and duodenum: Comparison between findings
in fresh and formalin-fixed paraffin-embedded tissue samples. Res Vet Sci
2011;91:e28–30.
11. Gagne JM, Armstrong PJ, Weiss DJ, et al. Clinical features of inflammatory liver
disease in cats: 41 cases (1983-1993). J Am Vet Med Assoc 1999;214(4):513–6.
12. Hirsch VM, Doige CE. Suppurative cholangitis in cats. J Am Vet Med Assoc 1983;
182(11):1223–6.
13. Shaker EH, Zawie DA, Garvey MS, et al. Suppurative cholangiohepatitis in a cat.
J Am Anim Hosp Assoc 1991;27:148–50.
14. Trehy MR, German AJ, Silvestrini P, et al. Hypercobalaminaemia is associated
with hepatic and neoplastic disease in cats: a cross sectional study. BMC Vet
Res 2014;10(1):1–16.
15. Simpson KW, Fyfe J, Cornetta A, et al. Subnormal concentrations of serum cobal-
amin (vitamin B12) in cats with gastrointestinal disease. J Vet Intern Med 2001;
15(1):26–32.
16. Marolf AJ, Leach L, Gibbons DS, et al. Ultrasonographic findings of feline chol-
angitis. J Am Anim Hosp Assoc 2012;48(1):36–42.
17. Oppliger S, Hartnack S, Reusch CE, et al. Agreement of serum feline pancreas-
specific lipase and colorimetric lipase assays with pancreatic ultrasonographic
findings in cats with suspicion of pancreatitis: 161 cases (2008-2012). J Am
Vet Med Assoc 2014;244(9):1060–5.
18. Daniaux LA, Laurenson MP, Marks SL, et al. Ultrasonographic thickening of the
muscularis propria in feline small intestinal small cell T-cell lymphoma and inflam-
matory bowel disease. J Feline Med Surg 2014;16(2):89–98.
19. Wagner KA, Hartmann FA, Trepanier LA. Bacterial culture results from liver, gall-
bladder, or bile in 248 dogs and cats evaluated for hepatobiliary disease: 1998–
2003. J Vet Intern Med 2007;21:417–24.
20. Sung JY, Leung JWC, Olson ME, et al. Demonstration of transient bacterobilia by
foreign body implantation in feline biliary tract. Dig Dis Sci 1991;36(7):943–8.
21. Sung JY, Olson ME, Leung JWC, et al. The sphincter of Oddi is the boundary of
bacterial colonization of the feline biliary and the gastrointestinal tract. Microb
Ecol Health Dis 1990;3:199–207.
22. Warren A, Center S, McDonough S, et al. Histopathologic features, immunophe-
notyping, clonality, and eubacterial fluorescence in situ hybridization in cats with
lymphocytic cholangitis/cholangiohepatitis. Vet Pathol 2011;48(3):627–41.
23. Eich CS, Ludwig LL. The surgical treatment of cholelithiasis in cats: a study of
nine cases. J Am Anim Hosp Assoc 2002;38:290–6.
24. Mayhew PD, Holt DE, McLear RC, et al. Pathogenesis and outcome of extrahe-
patic biliary obstruction in cats. J Small Anim Pract 2002;43(6):247–53.
25. Savary-Bataille KCM, Bunch SE, Spaulding KA, et al. Percutaneous ultrasound-
guided cholecystocentesis in healthy cats. J Vet Intern Med 2003;17:298–303.
Feline Cholangitis 723
26. Lucke VM, Davies JD. Progressive lymphocytic cholangitis in the cat. J Small
Anim Pract 1984;25:249–60.
27. Day MJ. Immunohistochemical characterization of the lesions of feline progres-
sive lymphocytic cholangitis/cholangiohepatitis. J Comp Pathol 1998;119(2):
135–47.
28. Xavier FG, Morato GS, Righi DA, et al. Cystic liver disease related to high Platy-
nosomum fastosum infection in a domestic cat. J Feline Med Surg 2007;9(1):
51–5.
29. Köster L, Shell L, Illanes O, et al. Percutaneous ultrasound-guided cholecysto-
centesis and bile analysis for the detection of Platynosomum spp.-induced chol-
angitis in cats. J Vet Intern Med 2016;30:787–93.
30. Haney DR, Christiansen JS, Toll J. Severe cholestatic liver disease secondary to
liver fluke (Platynosomum concinnum) infection in three cats. J Am Anim Hosp
Assoc 2006;42(3):234–7.
31. Costa Devoti C, Murtagh K, Batchelor D, et al. Exocrine pancreatic insufficiency
with concurrent pancreatitis, inflammatory bowel disease and cholangiohepatitis
in a cat. Vet Rec Case Rep 2015;3:e000237.
32. Mayhew PD, Weisse CW. Treatment of pancreatitis-associated extrahepatic
biliary tract obstruction by choledochal stenting in seven cats. J Small Anim Pract
2008;49(3):133–8.
33. Batchelor DJ, Devauchelle P, Elliott J, et al. Mechanisms, causes, investigation
and management of vomiting disorders in cats: a literature review. J Feline
Med Surg 2013;15(4):237–65.
34. Quimby JM, Lunn KF. Mirtazapine as an appetite stimulant and anti-emetic in cats
with chronic kidney disease: a masked placebo-controlled crossover clinical trial.
Vet J 2013;197(3):651–5.
35. Center SA, Randolph JF, Warner KL, et al. The effects of S-adenosylmethionine on
clinical pathology and redox potential in the red blood cell, liver, and bile of clin-
ically normal cats. J Vet Intern Med 2005;19(3):303–14.
36. Avizeh R, Najafzadeh H, Razijalali M, et al. Evaluation of prophylactic and thera-
peutic effects of silymarin and N-acetylcysteine in acetaminophen-induced hep-
atotoxicity in cats. J Vet Pharmacol Ther 2010;33(1):95–9.
37. Nicholson BT, Center SA, Randolph JF, et al. Effects of oral ursodeoxycholic acid in
healthy cats on clinicopathological parameters, serum bile acids and light micro-
scopic and ultrastructural features of the liver. Res Vet Sci 1996;61(3):258–62.
38. Plumb DC. Plumb’s veterinary drug handbook. 8th edition. New York: John Wiley
& Sons Inc; 2015.
39. Sergeeff JS, Armstrong PJ, Bunch SE. Hepatic abscesses in cats: 14 cases
(1985–2002). J Vet Intern Med 2004;18:295–300.
40. Otte CMA, Penning LC, Rothuizen J, et al. Retrospective comparison of prednis-
olone and ursodeoxycholic acid for the treatment of feline lymphocytic cholangi-
tis. Vet J 2013;195(2):205–9.
41. Fragkou FC, Adamama-Moraitou KK, Poutahidis T, et al. Prevalence and clinico-
pathological features of triaditis in a prospective case series of symptomatic and
asymptomatic cats. J Vet Intern Med 2016;30(4):1031–45.
42. Otte CMA, Pérez Gutiérrez O, Favier RP, et al. Detection of bacterial DNA in bile
of cats with lymphocytic cholangitis. Vet Microbiol 2012;156(1–2):217–21.
43. Boomkens SY, Kusters JG, Hoffmann G, et al. Detection of Helicobacter pylori in
bile of cats. FEMS Immunol Med Microbiol 2004;42:307–11.
724 Boland & Beatty
44. Otte CMA, Rothuizen J, Favier RP, et al. A morphological and immunohistochem-
ical study of the effects of prednisolone or ursodeoxycholic acid on liver histology
in feline lymphocytic cholangitis. J Feline Med Surg 2014;16(10):796–804.
45. Prasse KW, Mahaffey EA, DeNovo R, et al. Chronic lymphocytic cholangitis in
three cats. Vet Pathol 1982;19(2):99–108.
46. Nakayama H, Uchida K, Lee S, et al. Three cases of feline sclerosing lymphocytic
cholangitis. J Vet Med Sci 1992;54(4):769–71.
47. Weiss DJ, Gagne JM, Armstrong PJ. Characterization of portal lymphocytic infil-
trates in feline liver. Vet Clin Pathol 1995;24(3):91–5.
48. Basu AK, Charles RA. A review of the cat liver fluke Platynosomum fastosum Kos-
sack, 1910 (Trematoda: Dicrocoeliidae). Vet Parasitol 2014;200(1–2):1–7.
49. King S, Scholz T. Trematodes of the family Opisthorchiidae: a minireview. Korean
J Parasitol 2001;39(3):209–21.
50. Aunpromma S, Tangkawattana P, Papirom P, et al. High prevalence of Opis-
thorchis viverrini infection in reservoir hosts in four districts of Khon Kaen Prov-
ince, an opisthorchiasis endemic area of Thailand. Parasitol Int 2012;37(1):60–4.
51. Lin R, Tang J, Zhou D, et al. Prevalence of Clonorchis sinensis infection in dogs
and cats in subtropical southern China. Parasit Vectors 2011;4(0):180.
52. Pinto HA, Mati VLT, de Melo AL. New insights into the life cycle of Platynosomum
(Trematoda: Dicrocoeliidae). Parasitol Res 2014;113:2701–7.
53. Krecek RC, Moura L, Lucas H, et al. Parasites of stray cats (Felis domesticus L.,
1758) on St. Kitts, West Indies. Vet Parasitol 2010;172:147–9.
54. Rodrı́guez-Vivas RI, Williams JJ, Quijao-Novelo AG, et al. Prevalence, abundance
and risk factors of liver fluke (Platynosomum concinnum) infection in cats in
Mexico. Vet Rec 2004;154(22):693–4.
55. Rocha NO, Portela RW, Camargo SS, et al. Comparison of two coproparasitolog-
ical techniques for the detection of Platynosomum spp. infection in cats. Vet Para-
sitol 2014;204(3–4):392–5.
56. Salomão M, Souza-Dantas LM, Mendes-de-Almeida F, et al. Ultrasonography in
hepatobiliary evaluation of domestic cats (Felis catus, L., 1758) infected by Pla-
tynosomum looss, 1907. Int J Appl Res Vet Med 2005;3(3):271–9.
57. Taylor D, Perri SF. Experimental infection of cats with the liver fluke Platynosomum
concinnum. Am J Vet Res 1977;38(1):51–4.
58. Powell KW. Liver fluke infection in a cat. J Am Vet Med Assoc 1970;156(2):218.
59. Barriga OO, Caputo CA, Weisbrode SE. Liver flukes (Platynosomum concinnum)
in an Ohio cat. J Am Vet Med Assoc 1981;179(9):901–3.
60. Soto JA, Villalobos A, Arraga de Alvarado CM, et al. Obstructive biliary cirrhosis
in a cat due to Platynosomum fastosum infection. Revista Cientifica 1991;1(2):
16–9.
61. Ramos RAN, Lima VFS, Monteiro MFM, et al. New insights into diagnosis of Pla-
tynosomum fastosum (Trematoda: Dicrocoeliidae) in cats. Parasitol Res 2016;
115:479–82.
62. Andrade RLFS, Dantas AFM, Pimentel LA, et al. Platynosomum fastosum-
induced cholangiocarcinomas in cats. Vet Parasitol 2012;190:277–80.
63. Watson TG, Croll NA. Clinical changes caused by the liver fluke Metorchis con-
junctus in cats. Vet Pathol 1981;18(6):778–85.
64. Lewis DT, Malone JB, Taboada J, et al. Cholangiohepatitis and choledochectasia
associated with Amphimerus pseudofelineus in a cat. J Am Anim Hosp Assoc
1991;27(2):156–62.
65. Chang HP. Pathological changes in the intrahepatic bile ducts of cats (Felis ca-
tus) infested with Clonorchis sinensis. J Pathol Bacteriol 1965;89(0):357–64.