Jaundice caused by primary common bile duct lymphoma of a cat.

A 10-year-old American Shorthair cat presented with anorexia and jaundice, and echogenic evaluation revealed diffuse thickening of the common bile duct (CBD) wall. An exploratory laparotomy was conducted, the lesion was evaluated as difficult to remove, and the cat was euthanized and autopsied. Histologically, round neoplastic cells proliferated in the mucosa of the CBD and infiltrated the hepatic lobe, pancreas, and duodenum. Immunohistochemistry revealed that the neoplastic cells were positive for cytoplasmic-CD3 and granzyme B, and TCR-gamma clonal rearrangement was detected. Based on these findings, the neoplasia was diagnosed as a primary CBD lymphoma originating from cytotoxic T or natural killer cells. To the best of our knowledge, this is the first reported case of feline primary CBD lymphoma. Although rare, lymphoma of the CBD should be considered in cats with jaundice and thickening of the CBD.

Differential diagnoses in 83 dogs with icterus / Diagnósticos diferenciais em 83 cães com icterícia

Icterus (jaundice) is a yellowish pigmentation resulting from the depositing of bilirubin in tissues due to its high plasmatic concentration. The pathogenesis of icterus includes metabolic changes or obstructed bilirubin excretion and it is classified as pre-hepatic, hepatic and post-hepatic. This study aimed to evaluate and classify different causes of icterus in dogs during post mortem examination. These dogs were examined from 2014 to 2017, using macroscopic and histologic exams as well as ancillary tests. Eighty-three dogs were examined macroscopically and microscopically. They were separated into groups of icterus types: 24 (28.9%) dogs had pre-hepatic icterus, 45 (54.2%) had hepatic, 13 (15.7%) pre-hepatic and hepatic and one (1.2%) had post-hepatic icterus. Many factors were identified as a cause of icterus, including infectious agents (51/83), neoplasms (13/83), hepatic degeneration (11/83), chronic hepatic diseases (6/83), and obstructive causes (1/87). Among the infectious causes, leptospirosis, ehrlichiosis and disorders suggestive of septicemia were diagnosed. Neoplasms associated with icterus were cholangiocarcinoma, hemangiosarcoma and lymphoma. Other causes of icterus included degenerative diseases, such as lipidosis and glycogen degeneration. Hepatic fibrosis (cirrhosis) as a chronic disease and cholelithiasis also produced icterus. PCR was performed to confirm leptospirosis and ehrlichiosis. Samples of total DNA were used to amplify a fragment of a gene from Leptospira interrogans and Ehrlichia canis. In some dogs, co-infection of these agents was detected. The classification and identification of icterus etiologies in dogs is very important due to the number of diseases with this alteration, where ante mortem diagnosis is not always easily performed when some of these conditions are present.(AU)

Icterícia é a pigmentação amarelada decorrente da deposição de bilirrubina em tecidos devido à elevada concentração plasmática. A patogênese da icterícia inclui alterações no metabolismo ou na excreção de bilirrubina, sendo classificada em pré-hepática, hepática ou pós-hepática. O objetivo desse estudo foi identificar, avaliar e classificar as causas de icterícia em cães necropsiados de 2014 a 2017, associando as lesões macroscópicas, histológicas e exames complementares. Foram avaliados macro- e microscopicamente 83 cães com diferentes intensidades de icterícia. Os cães foram separados em grupos de acordo com o tipo de icterícia: 24 (28,9%) cães com icterícia pré-hepática, 45 (54,2%) cães com icterícia hepática, 13 (15,7%) com icterícia pré-hepática e hepática e um (1,2%) com icterícia pós-hepática. Foram identificadas várias etiologias associadas à icterícia, dentre elas pode-se destacar, agentes infecciosos (51/83), neoplasmas (13/83), processos degenerativos (11/83), crônicos (6/83) e obstrutivos (1/83). Dentre as causas infecciosas, destacam-se a leptospirose, a erliquiose e as lesões sugestivas de septicemia. Entre os neoplasmas associados com icterícia destacaram-se o colangiocarcinoma, hemangiossarcoma e linfoma. Outras causas de icterícia incluiriam os processos degenerativos como as degenerações gordurosa e glicogênica. Fibrose hepática (cirrose) e colelitíase foram também diagnosticados como causa de icterícia. A PCR foi utilizada para o diagnóstico confirmatório de leptospirose e erliquiose. Amostras de DNA total foram utilizadas para amplificar um fragmento dos genes de Leptospira interrogans e de Ehrlichia canis. Em alguns cães foi detectada co-infecção por estes agentes. A classificação e a identificação das causas de icterícia em cães são relevantes devido ao grande número de doenças que apresentam essa alteração, muitas vezes sem diagnóstico ante mortem.(AU)

Cutaneous toxoplasmosis in an immunosuppressed dog / Toxoplasmose cutânea em um cão imunosuprimido

A seven-year-old female spayed Schnauzer was presented with cutaneous ulcerated nodular lesions shortly after the beginning of an immunosuppressive treatment for immune-mediated hemolytic disease. Cytology was performed and a great number of neutrophils and banana-shaped organisms were observed. Biopsy showed a neutrophilic and histiocytic dermatitis and panniculitis with myriads of intralesional bradyzoites cysts and tachyzoites. PCR analysis was positive for Toxoplasma gondii and negative for Neospora caninum. Immunohistochemistry confirmed intralesional T. gondii antigens. This study reports a rare case of cutaneous toxoplasmosis in an immunosuppressed dog...

Uma cadela Schnauzer, castrada, de sete anos apresentou lesões cutâneas nodulares ulceradas pouco tempo após início de tratamento imunossupressor para doença hemolítica imunomediada. Foi realizado exame citológico, e um grande número de neutrófilos e estruturas em forma de banana foi observado. Biópsia mostrou dermatite e paniculite neutrofílica e histiocítica com miríades de taquizoítos e cistos de bradizoítos intralesionais. PCR foi positivo para Toxoplasma gondii e negativo para Neospora caninum. Imuno-histoquímica confirmou antígenos de T. gondii intralesionais. Este trabalho relata um caso raro de toxoplasmose cutânea em um cão imunossuprimido...

Aspectos anatomopatológicos da leptospirose em cães: 53 casos (1965-2011) / Pathological aspects of leptospirosis in dogs: 53 cases (1965-2011)

Os aspectos anatomopatológicos da leptospirose foram estudados em 53 cães que tiveram diagnóstico definitivo confirmado por imuno-histoquímica do tecido renal. Na necropsia, as principais lesões observadas incluíram icterícia (79,2%) e hemorragia (75,5%), principalmente no pulmão (56,6%). Alterações macroscópicas hepáticas (56,6%) e renais (50,9%) foram frequentes e caracterizavam-se principalmente por descolorações (30,2% e 32,1% respectivamente), acentuação do padrão lobular hepático (26,4%) e estriações brancas na superfície de corte dos rins (22,6%). Lesões extrarrenais de uremia ocorreram na metade dos casos (50,9%). Hepatomegalia (11,3%), nefromegalia (9,4%) e irregularidade da superfície capsular dos rins (3,8%) foram menos comuns. Na histologia dos rins (n=53), as lesões encontradas (98,1%) foram quase que exclusivamente agudas ou subagudas (96,2%) e caracterizavam-se por graus variados de nefrose tubular (86,8%) e nefrite intersticial não supurativa (60,4%), com evidente dissociação degenerativo-inflamatória. Na histologia do fígado (n=42), as lesões encontradas (97,6%) eram constituídas principalmente por dissociação dos cordões de hepatócitos (78,6%), colestase intra-canalicular (33,3%) e necrose hepática (31%). Lesões reativas, como hipertrofia das células de Kupffer, leucocitostase sinusoidal e infiltrado inflamatório mononuclear nos espaços porta, foram vistas em muitos casos (42,8%). Na histologia do pulmão (n=28), hemorragia (85,7%) e edema (57,1%) alveolares foram muito prevalentes. Neutrófilos e macrófagos nos espaços alveolares (35,7%) e neutrófilos no interior de pequenos vasos pulmonares (17,9%) também foram achados frequentes. Os resultados aqui demonstrados devem servir de alerta aos patologistas veterinários brasileiros, pois a apresentação anatomopatológica da leptospirose canina em nossa região (Região Central do Rio Grande do Sul, Brasil) não se modificou nos últimos 50 anos, mantendo-se semelhante àquela descrita internacionalmente até a década de 1980, mas muito diferente do que é atualmente reconhecido para os Estados Unidos, o Canadá e parte da Europa Ocidental. Recomendamos que os critérios histopatológicos para o diagnóstico da leptospirose canina devem incluir a presença concomitante de nefrite tubulointersticial aguda ou subaguda, hepatite reativa não específica e lesão alveolar difusa, incluindo hemorragia alveolar difusa com capilarite, em um cão que durante a necropsia demonstre icterícia, hemorragias e lesões extrarrenais de uremia na ausência de esplenomegalia.

The pathological aspects of canine leptospirosis were studied in 53 dogs with a conclusive diagnosis of the disease, as confirmed by immunohistochemistry on renal tissue. Main necropsy lesions included icterus (79.2%) and hemorrhage (75.5%), mainly in the lungs (56.6%). Gross hepatic (56.6%) and renal (50.9%) changes were frequently found and were characterized mainly by discoloration (respectively 30.2% and 32.1%), accentuation of hepatic lobular pattern (26.4%) and white streaks in the cut surface of kidneys (22.6%). Extrarenal lesions secondary to uremia occurred in half of the cases (50.9%). Enlarged livers (11.3%), and kidneys (9.4%), and rough renal capsular surfaces (3.8%) were less common findings. In the histopathology of the kidneys (n=53), the encountered lesions (98.1%) were almost exclusively acute or subacute (96.2%) and were characterized by varying degrees of tubular nephrosis (86.8%) and non-suppurative interstitial nephritis (60.4%), with evident degenerative-inflammatory dissociation. In the histopathology of the liver (n=42), the encountered lesions (97.6%) consisted mainly of hepatocellular dissociation (78.6%), intracanalicular cholestasis (33.3%) and hepatocellular necrosis (31%). Reactive lesions, such as Kupffer cell hypertrophy, sinusoidal leucocytostasis and inflammatory mononuclear infiltrate within portal triads were observed in several cases (42.8%). In the histopathology of the lung (n=28), alveolar hemorrhage (85.7%) and edema (57.1%) were rather frequent lesions. Neutrophils and macrophages in the alveolar spaces (35.7%) and neutrophils within small pulmonary vessels (17.9%) were also frequent findings. The findings stemming from the current study should serve as an alert for Brazilian veterinary pathologists, since the pathological presentations of canine leptospirosis in this region (Central Region of the State of Rio Grande do Sul, Brazil) did not change in the last 50 years, and is still similar to that described worldwide up to the decade of 1980's, but rather different from that currently recognized in the United States, Canada and part of West Europe. We recommend that the histopathological criteria for the diagnosis of canine leptospirosis should include the concomitant occurrence of acute or subacute tubulointerstitial nephritis, non specific reactive hepatitis and diffuse alveolar damage, including diffuse alveolar hemorrhage with capillaritis, in a dog which at necropsy had presented icterus, hemorrhage and extrarenal lesions of uremia without splenomegaly.

Suspected choledochal cyst in a domestic shorthair cat.

A 9-year-old female neutered domestic shorthair cat was presented with a history of polyphagia, weight loss and inappropriate urination. Clinical examination revealed jaundice and a mid-cranial abdominal mass. Further investigations revealed a large extra-hepatic cyst originating from the biliary tract (choledochal cyst). Concurrent chronic, active neutrophilic cholangitis and chronic lymphoplasmacytic pancreatitis were also noted. Surgical drainage, subtotal resection and omentalisation of the cyst, along with supportive medical management, were successful in relieving the clinical signs.

Infectious canine hepatitis in red foxes (Vulpes vulpes) in the United Kingdom.

The pathological findings are described in three cases of infectious canine hepatitis in free-ranging red foxes (Vulpes vulpes) in England. The foxes died after short periods of clinical illness. Mild jaundice and hepatic congestion were evident grossly. On histopathological examination, intranuclear inclusion bodies were visible in hepatocytes, in association with hepatocyte dissociation and necrosis, as well as in renal glomeruli, renal tubular epithelial cells and vascular endothelial cells. Canine adenovirus type 1 (CAV-1) was isolated from all three foxes. In a serological study, antibodies to CAV-1 were detected in tissue fluid extracts taken from 11 of 58 (19 per cent) frozen red fox carcases from England and Scotland.

Retrospective study of 28 cases of cholecystoduodenostomy performed using endoscopic gastrointestinal anastomosis stapling equipment.

Medical records were reviewed of 24 dogs and four cats that underwent cholecystoduodenostomy to relieve extrahepatic biliary obstruction. These procedures had been performed using a 30-mm endoscopic gastrointestinal anastomosis stapler. At presentation, most animals had clinical signs of vomiting and anorexia, and total bilirubin was elevated in both dogs (n=21) and cats (n=4). Pancreatitis (n=13), cholangiohepatitis (n=7), and neoplasia (n=6) were the most common underlying conditions. Sixteen dogs and two cats survived to their 2-week reevaluation. The most common cause of death was euthanasia (n=9) secondary to neoplasia (n=4), peritonitis (n=3), or respiratory arrest (n=2).

A mouse model provides evidence that genetic background modulates anemia and liver injury in erythropoietic protoporphyria.

Erythropoietic protoporphyria is an inherited disorder of heme biosynthesis caused by partial ferrochelatase deficiency, resulting in protoporphyrin (PP) overproduction by erythrocytes. In humans, it is responsible for painful skin photosensitivity and, occasionally, liver failure due to accumulation of PP in the liver. The ferrochelatase deficiency mouse mutation is the best animal model available for human erythropoietic protoporphyria. The original description, based on mice with a BALB/cByJCrl genetic background, reported a disease resembling the severe form of the human disease, with anemia, jaundice, and liver failure. Using congenic strains, we investigated the effect of genetic background on the severity of the phenotype. Compared with BALB/cByJCrl, C57BL/6JCrl mice developed moderate but increasing anemia and intense liver accumulation of PP with severe hepatocyte damage and loss. Bile excretory function was not affected, and bilirubin remained low. Despite the highest PP concentration in erythrocytes, anemia was mild and there were few PP deposits in the liver in SJL/JOrlCrl homozygotes. Discriminant analysis using six hematologic and biochemical parameters showed that homozygotes of the three genetic backgrounds could be clustered in three well-separated groups. These three congenic strains provide strong evidence for independent genetic control of bone marrow contribution of PP overproduction to development of liver disease and biliary PP excretion. They provide a tool to investigate the physiological mechanisms involved in these phenotypic differences and to identify modifying genes.

Challenging diagnosis--icterus associated with a single perforating duodenal ulcer after long-term nonsteroidal antiinflammatory drug administration in a dog.

A dog developed icterus, vomiting, and anorexia 2 wk after orthopedic surgery and treatment with meloxicam for approximately 1 y. Exploratory laparotomy revealed a single perforated duodenal ulcer. The most likely cause of the hyperbilirubinemia was intrahepatic cholestasis resulting from peritonitis associated with the perforation.

Extrahepatic biliary tract obstruction: a retrospective study of 45 cases (1983-1993).

The medical records of 41 dogs and four cats with either surgical or postmortem confirmation of extrahepatic biliary tract obstruction were reviewed. Clinical signs of icterus, vomiting, anorexia, or a combination of these signs were exhibited by 100% of cases. Elevated serum bilirubin was documented in 37 of 41 dogs and two of four cats (86.6%). The predominant, underlying, pathological process was extraluminal obstruction of the biliary tract due to pancreatitis (19 of 45 cases; 42.2%) or neoplasia (11 of 45 cases; 24.4%). Biliary tract surgery was performed in 29 cases, of which 12 (41.3%) recovered. Animals diagnosed with extrahepatic biliary tract obstruction had a relatively good long-term prognosis, provided they were not compromised substantially due to severe necrotizing pancreatitis or neoplasia.

Diseases associated with spontaneous feline leukemia virus (FeLV) infection in cats.

More than 2000 cats sent for necropsy in order to provide a diagnosis were investigated immunohistologically using paraffin sections for the presence of a persistent infection with feline leukemia virus (FeLV). The spectrum of neoplastic and non-neoplastic diseases associated significantly with FeLV infection was determined statistically. Three-quarters of the cats with persistent FeLV infections died of non-neoplastic diseases and about 23% died of tumors, nearly exclusively those of the leukemia/lymphoma disease complex. A strong association with liver degeneration, icterus and a FeLV-associated enteritis was found in addition to the known association with non-neoplastic diseases and conditions such as anemia, bacterial secondary infections and respiratory tract inflammations due to the immunosuppressive effect of FeLV, hemorrhages and feline infectious peritonitis. Surprisingly, diseases and conditions like feline infectious panleukopenia, enteritis (of other types than FeLV-associated enteritis and feline infectious panleukopenia), glomerulonephritis, uremia and hemorrhagic cystitis were not associated with persistent FeLV infection. Another unexpected finding was that most pathogenic infectious agents demonstrated in the cats were not FeLV-associated either. Thus, immunosuppression due to FeLV infection seems to make the animals susceptible to certain pathogenic infectious agents, but not to the majority.

Feline hepatic disease.

Species differences in anatomy, physiology, and biochemistry lead to many dissimilarities between the canine and feline liver. Major differences exist in the interpretation of liver function tests, the significance of biochemical jaundice, the consequences of anorexia, and the efficiency of hepatic metabolic systems. Biochemical alterations in total bilirubin, ALT, and SAP may indicate the presence of disease in the feline liver. It is, however, impossible to make accurate diagnoses without liver biopsy. A liver biopsy can provide a diagnosis and prognosis and can guide the therapeutic plan. The feline hepatic diseases most frequently seen in our hospital are hepatic lipidosis, cholangiohepatitis complex, toxic hepatopathy, and hepatic neoplasia. Less common diseases of the feline liver include extrahepatic biliary obstruction, portacaval vascular anomalies, hepatic parasites, hepatic cysts, and diaphragmatic hernia. Systemic diseases that can effect the liver of cats are feline infectious peritonitis, multicentric lymphosarcoma, myeloproliferative diseases, hemolytic anemia, infectious panleukopenia, and systemic fungal infections.

Comparative veterinary hematology: a bird's eye view.

A comparative look at veterinary hematology in the class Mammalia is presented to acquaint the medical technologist with a new dimension in clinical pathology. Aspects of clinical hematology, such as erythrocyte and leukocyte morphologies, dynamics, and diseases, are discussed.

Extrahepatic biliary carcinomas in Asiatic bears.

Extrahepatic biliary carcinomas occurred in 2 Asiatic bears at the National Zoological Park in Washington, D.C. The tumors were associated with ascites in both cases and jaundice in 1 and metastasized widely. Neither bear had gallstones. Microscopically, the tumors were infiltrative, scirrhous adenocarcinomas that produced varying amounts of mucin. A genetic predisposition and change from the natural diet were factors proposed to contribute to the development of this neoplasm.

Phenazopyridine toxicosis in the cat.

Severe illness developed after the oral administration of several drugs, including large doses of phenazopyridine (100 mg TID for 4 days) to a cat with dysuria and hematuria. Hemolysis and icterus were evident in blood serum and plasma after day 4 of drug administration, and many hemolyzed red blood cell "ghosts" containing Heinz bodies were observed on a stained blood smear. The cat became anemic and died within 48 hours after the last dose was administered. In an attempt to confirm a cause-and-effect relationship between drug administration and disease, 100 mg of phenazopyridine was given TID (65 mg/kg/day) for 3 days to a clinically normal cat. Nearly 50% of the hemoglobin was oxidized to methemoglobin during the course of phenazopyridine administration. Lower dosages of phenazopyridine (10 and 20 mg/kg/day) for longer periods of administration to 2 other clinically normal cats did not result in illness or anemia; however, the number and size of Heinz bodies and blood methemoglobin content were increased. Evidence of hepatic injury was observed in the clinically affected cat and in 2 of the experimental cats. The relationship between hepatic injury and toxic signs was not determined. Combination products recommeneded for treatment of cystitis in man often contain phenazopyridine. Such products should be avoided in cats unless a safe, effective dosage for phenazopyridine can be established.

The excretion of phylloerythrin and bilirubin by calves and sheep.

Under general anaesthesia the common bile duct was ligated in two sheep and two calves. Occlusion of the duct was permanent and was followed by portal fibrosis, proliferation of bile ducts and intrahepatic bile stasis. Mild hepatic cell damage was accompanied by the release of glutamate dehydrogenase, sorbitol dehydrogenase and arginase into serum. The release of gamma-glutamyl transpeptidase was slower but more continuous. One sheep and one calf developed peritonitis associated with the leakage of bile from a biopsy wound in the live. One of these animals and the other two on which biopsy was not performed became photosensitised on exposure to sunlight. The concentration of phylloerythrin was high in serum and urine. All animals became jaundiced and the increased concentration of bilirubin in serum and urine was mainly direct reacting, ie, conjugated with glucuronic acid.