Progressive lymphocytic cholangitis in the cat

A distinct type of liver disease is described in 21 cats. It is characterized morphologically by monolobular fibrosis, lymphocytic infiltrates which surround and permeate bile ducts and proliferation of bile ductules of varying intensity. The most common clinical signs are ascites, jaundice and hypergammaglobulinaemia. The condition appears to progress through an active stage of intense lymphocytic infiltration and proliferation of bile ductules to a stage of progressive monolobular fibrosis which results in distortion of liver architecture. The rate of progression is very variable. The condition differs from that of ascending or suppurative cholangitis described in the cat and bears only superficial resemblances to various forms of cholangitis in man and other species. At present the aetiology is unknown but it is suggested that genetic and immunological factors may predispose certain animals to produce hepatic lesions after exposure to a variety of environmental factors.     

Duck circovirus induces a new pathogenetic characteristic,primary sclerosing cholangitis

Primary sclerosing cholangitis (PSC) is a chronic, cholestatic liver disease of unknown cause. In the study, we found that duck circovirus (DuCV) induces PSC in natural and reproductive cases. PSC in DuCV naturally infected ducks was investigated by PCR and histopathology. A model of PSC was developed in one-day old duck by infection of DuCV. Effects on serum levels of liver enzymes and histology were evaluated, and DuCV tropism for bile duct in liver was analyzed by immuohistochemistry. Pathology observation of natural or reproductive DuCV infected ducks showed that the lesion of liver were characterized by cholangiocytic injuries and progressive fibrous obliteration of the biliary tree associated with lymphocytes infiltration. ALT, AST, ALP, GGT, ALB, TBIL and TP were significantly increased in serum of DuCV infected ducks. DuCV showed higher tropism for epithelial cells of bile duct than other cells in PSC.     

Suppurative cholangitis in cats

Suppurative cholangitis in 5 aged cats was characterized clinically by weight loss, depression, dehydration, icterus, and fever. The major abnormal laboratory findings were a severe left shift of WBC and a high, conjugated bilirubin concentration consistent with an inflammatory process and cholestasis. Gross pathologic findings included periductal biliary fibrosis (4 cats), periductal pancreatic fibrosis (2 cats), cholelithiasis (2 cats), deformation of the gallbladder (2 cats), and chronic interstitial pancreatitis (2 cats). Histopathologic findings in all cases were portal hepatic fibrosis, biliary hyperplasia, and suppurative exudate within dilated intrahepatic biliary ducts. Weight loss and portal fibrosis were suggestive of chronic, intermittent illness. The pathogenesis appeared to involve invasion of the bile duct by enteric bacteria. Cholangitis was observed to occur in association with pancreatitis, cholelithiasis, or anatomic abnormalities of the biliary tract.     

Choledochal cyst with secondary cholangitis,choledochitis, duodenal papillitis,and pancreatitis in a young domestic shorthair cat

Choledochal cysts, congenital segmental dilations of the common bile duct, have been reported in few cats, and histologic characterization is lacking. A 20-mo-old spayed female domestic shorthair cat was presented because of vomiting and weight loss. There was progressive elevation of liver enzyme activity (ALT > ALP, GGT) and hyperbilirubinemia. Diagnostic imaging identified focal cystic dilation of the common bile duct, dilation and tortuosity of adjacent hepatic ducts, and a prominent duodenal papilla. A choledochal cyst was suspected, and the animal was euthanized. On postmortem examination, there was a 2-cm, firm, thickened, cystic dilation of the common bile duct, patent with adjacent ducts. Histologically, the cyst wall was expanded by fibroblasts, collagen, and lymphoplasmacytic inflammation. Adjacent bile ducts were markedly dilated and tortuous, with lymphoplasmacytic inflammation and papillary mucosal hyperplasia that extended to the major duodenal papilla. There was chronic neutrophilic cholangitis, suggesting bacterial infection and/or disturbed bile drainage, extrahepatic obstruction, and lymphoplasmacytic pancreatitis with ductular metaplasia. Prominent lymphoid follicles within biliary ducts and duodenum suggested chronic antigenic stimulation. Choledochal cysts can be associated with chronic neutrophilic cholangitis, extrahepatic obstruction, choledochitis, duodenal papillitis, and pancreatitis, and should be a differential for increased hepatic enzymes and hyperbilirubinemia in young cats.     

Congenital dilatation of the bile ducts (Caroli's disease) in young dogs

We describe 8 young dogs with congenital dilatation of the intra- and extrahepatic bile ducts and diffuse cystic kidney disease, compatible with Caroli's disease in humans. The dogs were referred between 1980 and 2000 because of chronic disease at an age of 6 months to 3 years. These dogs included 3 Collies, 2 Frisian Stabyhouns, 2 Jack Russell Terriers, and 1 mixed-breed dog. The most common signs were vomiting (6/6), polyuria and polydipsia (4/6), and anorexia (4/6). Ascites was a common finding (4/6). Clinicopathologic abnormalities were available for 6 dogs. All had increased plasma alkaline phosphatase activity and fasting bile acids: increased alanine aminotransferase activity and urea and creatinine concentrations were present in 50% of dogs. Ultrasound examination of the liver showed severely dilated bile ducts without evidence of obstruction, and calcification in all cases but 1. Postmortem examination revealed severe dilatation of the larger intra- and extrahepatic bile ducts. The common bile duct and gall bladder were normal, and the bile system was patent. The ducts contained a clear viscid fluid often with calcified material. Microscopically, marked portal fibrosis was present, often with abnormally structured dilated bile ducts lined with columnar or cuboid epithelium and regularly small calcifications. The lesion was complicated by ascending cholangitis in 1 dog. The kidneys showed marked cortical and medullary fibrosis with a diffuse radial cystic pattern; only slight renal fibrosis was found in the oldest dog. Seven dogs were euthanized without treatment; the oldest dog was alive and well 5 months after diagnosis and was maintained on a protein-restricted diet.     

Enterococcus hirae enteropathy with ascending cholangitis and pancreatitis in a kitten

A 2-month-old female Persian cat that had been showing episodes of anorexia and diarrhea for the previous 4 weeks was presented in shock and died 2 days later. Numerous Gram-positive cocci were located along the brush border of small intestinal villi, without significant inflammatory infiltration. Similar bacteria were present within hepatic bile ducts and pancreatic ducts and were associated with suppurative inflammation and exfoliation of epithelial cells. Culture of the liver and lung yielded bacteria identified as Enterococcus hirae. Fecal culture from an asymptomatic adult female from the same cattery also yielded large numbers of E. hirae. To our knowledge, this is the first report of E. hirae enteropathy in a cat and the first report of ascending cholangitis and ductal pancreatitis caused by an Enterococcus spp.     

Hepatic trematodiasis in a Ganges River dolphin

Hepatic trematodiasis caused by Cyclorchis campula was diagnosed in a juvenile Ganges River dolphin that had been in captivity at an aquarium for approximately 1 year. Histopathologic findings were severe chronic suppurative cholangitis, hyperplasia of the bile duct epithelium, and periductal fibrosis associated with fluke infection of the large bile ducts.     

A case of recovery from canine destructive cholangitis in a Miniature Dachshund

A 7-year-old Miniature Dachshund presented with severe chronic jaundice and elevated liver enzymes. Destructive cholangitis was diagnosed according to histopathological findings of remarkable ductopenia with inflammatory infiltrates and fibrosis in the portal areas. Supportive therapy with prednisolone, high-dose ursodeoxycholic acid, human placental extract and antibiotics was tried, and the patient showed recovery of clinical signs 3 months after diagnosis. A second liver biopsy was performed about 1 year after initial diagnosis, and bile duct restoration was confirmed with continuous inflammation around portal areas and inside the lobules. Although we could not determine which treatment was effective in this case, destructive cholangitis in dogs may be recoverable with long-term supportive therapies.     

Congenital polycystic kidney in a white-tailed deer (Odocoileus virginianus).

Polycystic kidney and liver disease was seen in a stillborn white-tailed deer (Odocoileus virginianus) fawn. Bilaterally enlarged kidneys were characterized by severe dilatation of all renal tubules. Glomeruli were sparse, small, and located within a dilated Bowman's capsule. The liver was characterized by marked periportal fibrosis, biliary hyperplasia, and bile duct ectasia with dilated ducts containing inspissated bile. The presentation and morphology of this case are most similar to autosomal recessive polycystic disease in humans.     

Cellular proliferation of bile ductules and gamma-glutamyl transpeptidase in livers and sera of young cattle following a single infection with Fasciola hepatica

During the course of experimental single infection with Fasciola hepatica in calves, the origin of the increased concentration of gamma-glutamyl transpeptidase (gamma-GT) found to be present in the serum during the biliary stage of the disease, was studied. The enzyme originates from the liver after flukes have caused intermittent and selective cholestasis in the bile-duct system. The enzyme which normally is present in the bile ducts can under these circumstances enter the surrounding interstitial tissues through broken-up junctions of the bile drainage system or be added to these from proliferating bile-ductule epithelium. The multiplication of bile-ductule cells can be looked upon as a neogenesis of cholangioles, which becomes essential when newly formed perilobular connective tissues prevent restoration of the anatomical connections of the bile capillaries with the biliary tree. The connective tissue growth is induced by bile fluid. An initially regional perilobular fibrosis is eventually distributed diffusely through the liver by migration of flukes. The continued and extending fibrosis is due to the constant recurrence of intermittent and selective cholestasis. The transient occlusions of branches of the bile ducts are very likely to be attributable to persistent cholangitis. The growth of connective tissues has a considerable effect on the gain in weight of the liver.     

Cellular proliferation of bile ductules and gamma‐glutamyl transpeptidase in livers and sera of young cattle following a single infection with Fasciola hepatica

Summary

During the course of experimental single infection with Fasciola hepatica in calves, the origin of the increased concentration of gamma‐glutamyl transpeptidase (γ‐GT) found to be present in the serum during the biliary stage of the disease, was studied.

The enzyme originates from the liver after flukes have caused intermittent and selective cholestasis in the bile‐duct system. The enzyme which normally is present in the bile ducts can under these circumstances enter the surrounding interstitial tissues through broken‐up junctions of the bile drainage system or be added to these from proliferating bile‐ductule epithelium. The multiplication of bile‐ductule cells can be looked upon as a neogenesis of cholangioles, which becomes essential when newly formed perilobular connective tissues prevent restoration of the anatomical connections of the bile capillaries with the biliary tree. The connective tissue growth is induced by bile fluid. An initially regional perilobular fibrosis is eventually distributed diffusely through the liver by migration of flukes.

The continued and extending fibrosis is due to the constant recurrence of intermittent and selective cholestasis. The transient occlusions of branches of the bile ducts are very likely to be attributable to persistent cholangitis. The growth of connective tissues has a considerable effect on the gain in weight of the liver.     

Anatomicopathological study of vascular and biliary systems using cast samples of Fasciola-infected bovine livers

In 117 livers with fascioliasis, this study was focused on the number of Fasciola, the number and intrahepatic localization of affected hepatic ducts and bile ducts, and the degree of fibrosis in the hepatic segments and bile ducts. The degree of pathological changes in bile ducts caused by fascioliasis was classified into five levels. The site of Fasciola habitation was most often the hepatic ducts of the porta hepatis: it was the left hepatic duct in 101 livers and the right hepatic duct in 88 livers. Casts were prepared by infusing synthetic resin into the hepatic arterial, portal, hepatic venous and biliary systems of 15 bovine livers with fascioliasis and then examined. In the left lobe, quadrate lobe, and caudate process where atrophic fibrosis was noted, the bile ducts became rod-shaped by losing branches, and the samples resembled dead branches of liver. Portal branches were thinned or completely terminated with marked fibrosis. Fine and irregular newly formed bile ducts not parallel with portal branches were observed in livers with markedly chronic fascioliasis. Distal portal branches in the right lobe, caudate lobe, and papillary process showed hypertrophic proliferative changes. The arterial system was generally well developed in thickened walls of bile ducts and formed vascular beds, and surrounded the bile ducts as tubes. In livers with severe fibrosis, capillaries were markedly developed and resembled glass cotton.     

Congenital dilatation of the large and segmental intrahepatic bile ducts (Caroli's disease) in two Golden retriever littermates

Two, sibling, male Golden retriever puppies, 13 weeks of age, were presented with congenital biliary cysts of the liver involving both hepatic and segmental bile ducts, as well as bilateral polycystic kidney disease. Ultrasonography of the livers of both pups demonstrated segmental cystic lesions that were contiguous with the bile ducts. Histopathology revealed cystic ectatic bile duct hyperplasia and dysplasia with variable portal fibrosis in the liver, while in the kidneys there were radially arranged, cylindrically dilated cysts of the collecting ducts, which extended through the medulla and cortex. This pathology was compatible with that of congenital dilatation of the large and segmental bile ducts (Caroli's disease) described in humans, dogs and rats. In humans Caroli's disease has an autosomal recessive inheritance pattern, while in rats activation of the MEK5/ERK cascade initiates the biliary dysgenesis of Caroli's disease in this species. However, the exact mode of inheritance and pathogenesis of Caroli's disease in dogs is as yet unknown. Previous reports on congenital hepatic cystic diseases of the dog have described Caroli's disease like lesions in various breeds, but these are believed to be the 1st reported cases in the Golden retriever breed.     

Pathogenesis of aleutian mink disease. VII. Chronic hepatitis with bile duct proliferation]

Aleutian disease is a chronic persistent viral infection of mink characterized by hypergammaglobulinema, generalized plasmacytosis, sclerosing glomerulonephritis, polyarteritis, and plasma cell hepatitis with bile duct proliferation. The development of hepatic lesions was studied both light- and electron-microscopically in mink experimentally infected with Aleutian disease virus. Fifteen normal and 99 mink experimentally infected with Aleutian disease virus were used. Experimental mink were killed in intervals from 3 weeks to 23 months after infection, and liver sections were processed for both light- and electron-microscopic studies. Experimentally infected mink developed portal and intralobular lymphocytic and plasmacytic infiltrates in the liver 3 weeks after infection. Four to five weeks after infection there was evidence of early bile duct proliferation that began as an outgrowth of the portal bile ducts. Three to five months after infection a marked bile duct proliferation was present in some of the portal triads and adjacent liver lobules; but there was no tendency of these lesions to progress into biliary cirrhosis. Ultrastructural characteristics of proliferating bile duct cells were marked deformation, formation of multiple cell layers, reduction in the number of microvilli and desmosomes, and infiltration of the epithelial cells by lymphoid cells and plasmacytes. The hepatic lesions either develop by direct virus stimulation or by the deposition of virus-antibody complexes.     

Histopathologic features, immunophenotyping, clonality, and eubacterial fluorescence in situ hybridization in cats with lymphocytic cholangitis/cholangiohepatitis

Feline lymphocytic cholangitis is a poorly characterized disease complex with respect to histologic lesions, immunophenotype, and etiopathogenesis. Seventy-eight cases of feline lymphocytic cholangitis (n = 51) and feline hepatic lymphoma (n = 27) were reviewed using standardized histopathology, immunophenotyping (B cell and T cell), polymerase chain reaction for T-cell receptor (TCR) gene rearrangement, and fluorescence in situ hybridization (FISH) for eubacteria. Five histopathologic features in cases of lymphocytic cholangitis assisted in its differentiation from hepatic lymphoma: bile duct targeting (n = 32, 62.7%), ductopenia (n = 9, 17.6%), peribiliary fibrosis (n = 37, 72.5%), portal B-cell aggregates (n = 36, 70.6%), and portal lipogranulomas (n = 38, 74.5%). The majority of lymphocytic cholangitis cases (n = 35, 68.6%) were T cell predominant; 15 (29.4%) had an equal mix of B cells and T cells, and 1 (1.9%) had a B cell-predominant infiltrate; 66.6% of hepatic lymphoma cases were T-cell lymphomas. TCR clonality results were unexpected, with 17.1% of cases of lymphocytic cholangitis having clonal or oligoclonal populations and with T-cell lymphomas having variable TCR clonality (63.6% clonal or oligoclonal, 36.3% polyclonal). The majority of lymphocytic cholangitis (n = 32 of 36, 88.8%) and all hepatic lymphoma cases had no detectable eubacteria using FISH. As demonstrated here, bile duct targeting, ductopenia, peribiliary fibrosis, portal B-cell aggregates, and portal lipogranulomas are lymphocytic cholangitis features that, along with polyclonal TCR (83%), help differentiate it from hepatic lymphoma. No strong evidence was found implicating in situ bacterial colonization as an etiopathogenesis of lymphocytic cholangitis.     

Changes in the concentrations of bile acids in the plasma of sheep with liver damage

The concentration of total plasma bile acids was measured in normal sheep and in sheep in which liver damage was induced by chronic copper poisoning, ligated bile ducts or induced ketosis. All three treatments produced a rise in total bile acid concentration in plasma which was proportional to the degree of hepatic damage seen histologically and which tended to parallel changes in activity of iditol, and glutamate dehydrogenase and aspartate amino-transferase in plasma. Plasma bile acid concentration was a more sensitive method of detecting these types of liver damage than was the measurement of total plasma bilirubin concentration, and could be used to assess alterations in liver function in sheep.     

Cholangitis in cats: symptoms, cause, diagnosis, treatment, and prognosis

Inflammation of the bile ducts is common in cats. This review article reports on what is currently known about the various types of cholangitis (i.e., cholangitis caused by liver flukes, neutrophilic cholangitis, and lymphocytic cholangitis). Treatment is available for cholangitis caused by liver flukes and for neutrophilic cholangitis, and the prognosis is good. However, the cause of lymphocytic cholangitis is not known and there is currently no evidence-based therapy. Several causes are mentioned in the literature, but more research is needed in order to establish the cause of this disease and to develop an appropriate therapy.     

Photosensitivity in South Africa. VI. The experimental induction of geeldikkop in sheep with crude steroidal saponins from Tribulus terrestris

Geeldikkop was induced in sheep by the oral administration of crude steroidal saponins from Tribulus terrestris. Two of the sheep developed typical lesions of geeldikkop, including birefringent crystalloid material in bile ducts and concentric periductal lamellar fibrosis. The clinical pathological changes in these sheep were also consistent with those of geeldikkop: aspartate transaminase and gamma-glutamyl transferase activities in the sera of both were elevated, and one had bilirubinaemia. A third sheep became photosensitive without typical lesions of geeldikkop in the liver or changes in the activities of liver enzymes before euthanasia. The findings of these trials are consistent with reports from abroad that ovine hepatogenous photosensitization, caused by Agave lechuguilla and Narthecium ossifragum, can be induced with crude saponins from the respective plants.     

Ultrasonographic findings in cattle and buffaloes with chronic hepatic fascioliosis

The purpose of this study was to characterize the ultrasonographic findings in cattle and buffaloes with chronic hepatic fascioliosis. To the best of the author's knowledge, this report is the first to document ultrasonographic findings in buffaloes with chronic hepatic fascioliosis. Ultrasonographic findings included distended gallbladders with either homogenous or heterogeneous contents, edema of the gallbladder walls, which ranged from mild or moderate to severe and bile duct mineralization. In 78% of the buffaloes, there was an ultrasonographic picture of hepatic fibrosis in which heterogeneous and hyperechogenic hepatic parenchymas with multiple echogenic foci were imaged. Other ultrasonographic findings included peritoneal, pleural and pericardial effusions. Two cows and one buffalo were slaughtered and examined postmortem. Hence, it was possible to verify distended gallbladders, edema of the gallbladder wall, calcified bile ducts, cholestasis and hepatic fibrosis by using ultrasonography in the cows and buffaloes with chronic hepatic fascioliosis. The procedure offers a useful supplement to clinical, hematological and biochemical examinations on the diagnosis of this condition.     

Congenital hepatic fibrosis and cystic bile duct formation in Swiss Freiberger horses

Congenital hepatic fibrosis with autosomal recessive or dominant inheritance has been described in humans, cats, piglets, and dogs. In horses, only two cases of congenital hepatic fibrosis have been previously reported. This retrospective study of records from the Institute for Animal Pathology, University of Berne, identified 30 foals with liver lesions compatible with congenital hepatic fibrosis. Anamnestic data revealed clinical signs of severe liver injury in most affected animals. Pathologic examination showed severely enlarged, firm livers with thin-walled cysts. Histologically, the livers showed diffuse porto-portal bridging fibrosis with many small, irregularly formed and sometimes cystic bile ducts. All foals belonged to the Swiss Freiberger breed. Pedigree analysis revealed that the diseased animals could be traced back to one stallion. These results strongly suggest that congenital hepatic fibrosis in Swiss Freiberger horses is a recessively inherited autosomal genetic defect.