Portal vein and aortic thromboses in a Siberian husky with ehrlichiosis and hypothyroidism

A six-year-old, neutered male Siberian husky was presented for euthanasia for end-stage liver disease. Examination of the dog raised questions regarding the severity of the condition. It had presented to the referring veterinarian with polyuria, polydipsia and weight loss. Blood tests at that time revealed elevated liver enzymes and hypoalbuminaemia. Cirrhosis was presumptively diagnosed, based on an ultrasound examination, which showed ascites with a normal liver. The dog had a history of hypothyroidism, which was controlled with levothyroxine. Physical examination revealed cachexia. A second abdominal ultrasound examination was performed and revealed portal vein and aortic thromboses. Tick titres showed a positive Ehrlichia canis titre of 1:640. Skin biopsies showed lymphoplasmacytic vasculitis. Doxycycline and aspirin treatment was initiated, and the clinical signs resolved. The authors concluded that the thrombi were primarily caused by chronic ehrlichiosis, based on the clinical findings and the response to treatment.     

Hepatocellular carcinoma and suspected splenic hemangiosarcoma in a potbellied pig

A 10-year-old, lethargic, potbellied pig presented with signs of abdominal discomfort and a palpable abdominal mass. Laparotomy revealed a 20 cm diameter mass on the spleen and smaller masses on the omentum and liver. After euthanasia and histologic examination of the hepatic mass, the diagnosis was hepatocellular carcinoma.     

Resolution of skin lesions and long-term survival in a dog with superficial necrolytic dermatitis and liver cirrhosis

A nine-year-old, neutered female Shetland sheepdog was presented with crusted, ulcerative skin lesions affecting the footpads, commissures of the lips and the lateral canthi of the eyes. Histopathological examination of skin biopsies revealed changes consistent with superficial necrolytic dermatitis and biochemical analysis demonstrated elevated liver enzymes. Abdominal radiography revealed a small liver which, on ultrasonography, appeared diffusely mottled and showed changes suggestive of periportal fibrosis. On exploratory laparotomy, the pancreas appeared normal, but the liver was small and had multiple nodules throughout the parenchyma. This appearance was confirmed as cirrhosis on histopathological examination. The dog was placed on a hepatic support diet and treated with colchicine, essential fatty acid supplementation and raw egg yolks. After four weeks, the skin lesions had resolved and the dog remained free of clinical signs over a 22-month follow-up period.     

Focal fatty liver in a heifer: utility of ultrasonography in diagnosis

A 30-month-old Holstein heifer presented with a history of decreased appetite and respiratory signs. Sonographic examination of the liver incidentally revealed an area of increased echogenicity between the portal vein and the gallbladder. The lesion was nonspherical and had no mass effect or displacement of the adjacent vessels. Its boundaries, to the liver, were geographic. The liver specimen was histologically compatible with a diagnosis of focal fatty liver change (FFLC). The sonographic features of focal fatty infiltration of the liver are characteristic. Recognition of the ultrasonographic data is important to differentiate FFLC from other lesions.     

Death associated with parenteral administration of copper disodium edetate in calves

Copper disodium edetate in recommended doses was apparently responsible for the deaths of one calf and clinical signs of toxicosis in 5 others on one farm, and 7 deaths and clinical signs of toxicosis in a number of others on another ranch. Signs of hyperexcitability, hypermetria, hindlimb weakness, head pressing, depression, and opisthotonos occurred 6 to 24 hours after injections and preceded death by 1 to 2 days. Necropsy and histologic examination revealed massive liver necrosis. High blood concentrations of liver enzymes in affected cattle that did not die indicated that they had liver damage. High blood concentration of iron in cattle that died indicated possible interaction of copper and iron.     

Tyzzer's disease in kittens with familial primary hyperlipoproteinaemia

The clinical signs, gross pathology and histopathological findings of three kittens with Tyzzer's disease are described. The three affected kittens were also hyperlipoproteinaemic, being offspring of a hyperlipoproteinaemic sire and a normolipoproteinaemic dam. Two kittens showed clinical signs of acute hepatic disease with severe icterus. Necropsy revealed multiple focal lesions in the liver, myocardium and intestines. Histological examination confirmed the presence of organisms resembling Bacillus piliformis in viable hepatocytes adjacent to necrotic liver tissue. Apart from the hyperlipoproteinaemia no predisposing ‘stress’ factors were identified.     

Presumptive trimethoprim-sulfadiazine-related hepatotoxicosis in a dog.

Administration of trimethoprim-sulfadiazine in a dog was associated with vomiting, inappetence, and icterus, and high values of alanine transaminase, aspartate transaminase, alkaline phosphatase, gamma-glutamyltransferase, and total bilirubin concentration. The clinical signs and biochemical abnormalities resolved after discontinuation of the treatment. Histologic examination of sections from a liver biopsy specimen revealed moderate, predominantly portal hepatitis with cholestasis.     

Mycobacterium infection in a gray-cheeked parakeet

A gray-cheeked parakeet, approximately 3 years of age, was submitted for necropsy. Clinical signs included diarrhea, decreased feed consumption, fluffing of feathers, shivering, weight loss, and limping. Necropsy revealed enlargement and pale discoloration of the spleen and intestines. The liver contained multifocal pale foci. Granulomas, some of which had necrotic centers, were present along the subserosa of the intestinal tract. Microscopic examination revealed diffuse granulomatous splenitis, enteritis, and multifocal granulomatous hepatitis. Numerous acid-fast bacteria were demonstrated in the spleen, liver, and intestine.     

Fatal coxiellosis in Swainson's Blue Mountain Rainbow Lorikeets (Trichoglossus haematodus moluccanus)

Three Swainson's Blue Mountain Rainbow Lorikeets (Trichoglossus haematodus moluccanus), ranging from 6 to 8 months of age, presented with lethargy, emaciation, and progressive neurologic signs. The first one died 24 hours after the onset of clinical signs, and the other two were euthanized 10 to 14 days after the onset of progressive neurologic disease. Clinical signs in these lorikeets included head pressing, hemiparesis, seizures, obtunded mentation, weakness, and lethargy. Two of the lorikeets had hepatomegaly, and one had splenomegaly on gross examination. Histopathology revealed disseminated microgranulomas in the liver, spleen, and brain, and lymphohistocytic perivascular encephalitis and cephalic vasculitis. Electron microscopic examination of macrophages in brain lesions revealed spherical to rod-shaped prokaryotic organisms with a trilaminar cell wall. Molecular analysis revealed a novel species of Coxiella. This is believed to be the first report of a Coxiella sp. causing disease in a lorikeet.     

An unusual presentation of suspected oedema disease of swine in Kenya

From a group of 11 recently weaned pigs, 4 were reported to be sick. Clinical examination of the sick pigs revealed marked dyspnoea, bluish-red discolouration of the skin, incoordination and difficulty in walking. Bacteriological examination of the gut contents of 2 pigs that had died earlier yielded pure cultures of haemolytic Escherichia coli. Post mortem examination of the remaining 2 pigs that died subsequently revealed progressive pulmonary collapse. One of these also showed subcutaneous oedema of the head and marked oedema of the mesentery of the spiral colon and oedema of the brain. Microscopically there was pulmonary alveolar collapse and degenerative changes in the liver. On the basis of the clinical signs, isolation of haemolytic E. coli and the post mortem findings, a diagnosis of oedema disease was made.     

Yersinia pseudotuberculosis Infection in a Cat

A diagnosis of Yersinia pseudotuberculosis in a cat was established by microbiological and histological means. Clinical signs were general malaise, anorexia and vomition. Significant laboratory findings included a serum glutamicpyruvic transaminase elevation and the presence of urine bilirubin and urobilinogen. Histological examination of liver biopsies revealed numerous varying-sized foci of caseation necrosis containing large numbers of Gram-negative coccobacilli. Bacteriological techniques, treatment and control measures are discussed.     

Colchicine treatment in a dog with hepatoportal fibrosis

A two-year-old female spayed English setter with hepatic encephalopathy was found to have hepatoportal fibrosis and acquired portosystemic shunts on laparotomy and liver biopsy. The dog was treated symptomatically with a low-protein diet, lactulose and metronidazole, while colchicine was given as antifibrotic therapy. There was a gradual improvement in clinical signs and liver function until 30 months after first presentation, when the dog developed severe haematuria caused by renal infarction of unknown aetiology. Post mortem examination revealed hepatic fibrosis to be unchanged. This case illustrates that long term survival may be possible in canine hepatoportal fibrosis and suggests that colchicine may be effective in improving liver function and slowing progression of hepatic fibrosis.     

Hepatoencephalopathy and hypocalcemia in a miniature horse mare.

A pregnant, miniature horse mare had clinical signs of hepatoencephalopathy and concurrent hypocalcemia. The signs included dullness, inappetence, blindness, head pressing, weakness, muscle fasiculations, uveitis, and urinary incontinence. Hepatic dysfunction and hypocalcemia were confirmed by serum biochemical analysis. The mare was treated successfully with a continuous infusion of Ringer solution, calcium gluconate, dextrose, B-complex vitamins, sodium ampicillin, and flunixin meglumine; topical administration of ophthalmic ointments; and decompression of the urinary bladder. Histologic examination of a liver biopsy specimen revealed acute hepatic necrosis, which likely was associated with administration of a vaccine of equine origin 2 months earlier.     

Ultrasonographic findings in three cows with chronic ragwort (Senecio alpinus) poisoning

Three cows with regwort (Senecio alpinus) poisoning were examined clinically, haematologically and ultrasonographically, and biopsy specimens of the liver were examined histologically. At the end of the study, the cows were euthanased and examined postmortem. The major clinical signs included severely disturbed general demeanour and behaviour, and severe diarrhoea. One cow was photosensitive. The activities of liver enzymes and the concentration of bilirubin were high in all of the cows. In two of the cows, ultrasonographic examination revealed a heavy accumulation of abdominal fluid, which was diagnosed as non-inflammatory ascites. In all the cows, the liver parenchyma was heterogeneous, and cows 1 and 2 had multiple echogenic foci 5 to 10 mm in diameter. In cow 3, the facies diaphragmatica of the liver appeared irregular in outline owing to the presence of nodules which were approximately 5 cm in diameter. The liver was also greatly enlarged and extended almost to the linea alba ventrally and beyond the reticulum cranially. All the cows had portal hypertension and the portal vein was dilated, resulting in oedema of the walls of the gall bladder, the small intestines and the omentum. The diameter of the caudal vena cava was reduced as a result of the impaired hepatic circulation. Histological examination of liver biopsy specimens revealed severe hepatic fibrosis in all the cows.     

Hepatic capillariasis in captive ring-tailed lemurs (Lemur catta)

A female ring-tailed lemur (Lemur catta) and her two cubs held in a zoo in Chile exhibited signs of severe hepatic insufficiency. In spite of supportive treatment, the three animals died a few days after the onset of signs. Postmortem examination revealed ascites and fibrotic lesions in the liver of all the individuals. Histologically, the liver of two of them showed a severe parasitic ova infection and lipidosis, the morphologic characteristics of the parasitic ovas were consistent with Capillaria hepatica (syn. Calodium hepatica) eggs. To the authors' knowledge, this is the first clinical case report of hepatic capillariasis in prosimians, and its implications are discussed.     

Ataxia and weakness as uncommon primary manifestations of hepatic encephalopathy in a 15‐year‐old trotter gelding

A 15‐year‐old trotter gelding was evaluated because of an acute onset of ataxia in all 4 limbs. There was no known history of trauma. The gelding showed grade 2/5 ataxia in all 4 limbs, which was localised after clinical neurological examination to the cervical vertebral spinal cord. Initial therapy consisted of oral anti‐inflammatory doses of prednisolone and antimicrobial treatment with potentiated sulphonamides. The ataxia progressed to grade 3/5 at Day 10 of hospitalisation. Additionally, the horse was slightly depressed and showed spontaneous yawning during examination. Facial sensation was blunted. Blood chemistry revealed a marked elevation of liver specific enzymes and blood ammonia levels. Transcutaneous abdominal ultrasonography revealed hepatomegaly. Due to a guarded prognosis, the horse was subjected to euthanasia. At necropsy the left lateral liver lobe was markedly enlarged and showed a firm texture, whereas the cranial part and the right and quadratic liver lobe displayed a severe and diffuse atrophy. Histopathologically, the left lateral liver lobe revealed a moderate to severe cirrhosis with a severe, diffuse hepatocellular iron‐accumulation. Increased numbers of Alzheimer type II astrocytes in the cerebral cortex and cerebral white matter vacuolisation were indicative for encephalopathy. These findings were interpreted as haemosiderosis and cirrhosis of the liver with consecutive hepatic encephalopathy. Aetiologically, haemosiderosis should be considered as a cause of liver cirrhosis with consecutive hepatic encephalopathy. Although hepatic encephalopathy in horses usually presents with predominating cerebral signs, it has to be taken into account as a differential diagnosis in cases of acute onset generalised ataxia.     

Concurrent multiple myeloma and mast cell neoplasia in a 13‐year‐old castrated male Maine Coon cat

A 13‐year‐old, castrated male Maine Coon cat was presented to Oklahoma State University Boren Veterinary Medical Teaching Hospital for yearly echocardiographic examination monitoring hypertrophic cardiomyopathy (HCM) diagnosed in 2003. Physical examination revealed a heart murmur and premature beats, likely related to HCM, but was otherwise unremarkable. A biochemistry profile revealed a hyperglobulinemia (6.3 g/dL). Cytologic examination of fine‐needle aspirates from liver and spleen revealed increased numbers of plasma cells and mast cells, confirmed with subsequent histologic examination. Immunohistochemistry (IHC) for c‐kit in the spleen and liver showed mast cells predominantly exhibiting type I staining pattern, with moderate numbers exhibiting type II pattern in spleen, and scattered cells exhibiting type II and III patterns in liver. Bone marrow cytology and core biopsy documented approximately 22% plasma cells. Cutaneous masses on the cat's left shoulder and right carpus were cytologically confirmed mast cell tumors. Serum protein electrophoresis with immunofixation confirmed an IgG monoclonal gammopathy. This is an example of 2 hematologic neoplasms occurring simultaneously in a cat. Concurrent pathologies may be overlooked if a single disease is diagnosed and suspected of causing all clinical signs. Both neoplasms were well differentiated, and neoplastic cells could have easily been interpreted as a reactive population had a full workup not been performed. Missing either diagnosis could result in a potentially lethal outcome. Eleven months after diagnoses, the cat was clinically doing well following a splenectomy and oral prednisolone and chlorambucil chemotherapy. Globulins decreased to 4.9 g/dL.     

Disseminated lymphoma with large granular lymphocyte morphology diagnosed in a horse via abdominal fluid and transtracheal wash cytology

A 22‐year‐old Tennessee Walking Horse mare was presented to the Auburn University Large Animal Teaching Hospital with a 3‐day history of lethargy, anorexia, and mild signs of colic. The mare had a several‐month history of weight loss and refractory cough. Physical examination revealed an increased respiratory rate, and crackles and wheezes were heard on thoracic auscultation. Thoracic ultrasonographic examination showed disseminated, minor, bilateral comet tail‐like lesions on the parietal pleural surfaces. Abdominal ultrasonographic examination was unremarkable. Trans‐rectal palpation revealed a firm small colon impaction with concomitant diarrhea. Laboratory data were characterized by a very pronounced acute inflammatory leukogram with severe neutropenia and significant left shift, evidence of hepatocellular damage/necrosis, cholestasis, and possibly mixed metabolic alkalosis and acidosis. On cytologic evaluation of a peritoneal fluid sample, there were many large granular lymphocytes (LGL). Large numbers of LGL were also observed on cytologic examination of a subsequent transtracheal wash. The final cytologic interpretation was disseminated lymphoma with LGL morphology. Due to worsening of the clinical signs and poor prognosis, the mare was euthanized. On necropsy and in histopathologic examination, disseminated lymphoma with LGL morphology was noted in a mesenteric lymph node, lungs, liver, spleen, kidneys, and right dorsal colon. Lymphoma with LGL morphology is rarely diagnosed in the horse. This report provides unique cytologic findings of a case of disseminated lymphoma with LGL morphology in a horse, confirmed with histopathologic evaluation.     

Hepatic capillariasis (Capillaria hepatica) in porcupines (Erethizon dorsatum) in Pennsylvania.

Tissues of 53 adult porcupines (Erethizon dorsatum) from Pennsylvania were obtained for histopathologic examination. Hepatic capillariasis was recorded in 9% of the porcupines. An additional 11% of the liver sections showed lesions that were compatible with migration by Capillaria hepatica. Because only 1 section of the liver per animal was examined microscopically, the documented prevalence of C. hepatica in Pennsylvania is considered conservatively low. However, this condition was subclinical, because none of the infected animals showed clinical signs, and none revealed severe pathologic changes in the affected livers. This seems to be the only report of C. hepatica in porcupines.     

Peliosis hepatis and hemoperitoneum in a dog with diphacinone intoxication

Objective: To describe the clinical course of a dog presented with peliosis hepatis and hemoperitoneum in concert with anticoagulant rodenticide intoxication.
Case summary: A 7.75-year-old spayed female Shetland Sheepdog presented with clinical signs consistent with hypovolemia, hemoperitoneum, and a history of bright green stool 3 days before the onset of clinical signs. Initial packed cell volume/total solids were consistent with acute hemorrhage. A coagulation profile showed prolongation in activated clotting time and prolongation of both prothrombin and activated partial thromboplastin time, suggesting abnormal coagulation. Abdominal hemorrhage persisted in the face of normalization of the hemodynamic status and coagulation profile, and treatment with Vitamin K₁. Abdominal ultrasound revealed multiple patchy hypoechoic areas throughout the caudate liver lobe. An exploratory laparotomy was performed 24 hours after presentation and revealed the caudate liver lobe as the source of the hemorrhage. Histopathologic examination of a specimen of the liver was consistent with peliosis hepatis. Toxicologic testing identified diphacinone levels in the blood consistent with anticoagulant rodenticide intoxication. Postoperative recovery was uneventful, and within 48 hours the dog was discharged. The dog returned to full function and a hepatic ultrasound performed 15 months postoperatively showed no significant abnormalities.
New or unique information provided: Exposure to anticoagulant rodenticides may be associated with the development of peliosis hepatis in dogs.