Solitary nonepitheliotropic T-cell lymphoma in a dog

A 7-year-old male Golden Retriever with swelling of the rostral bridge and right wing of the nasal areas, sneezing, and inspiratory difficulty was referred to a neighbor veterinarian. Except for those in the nasal area, no lesions were noted during routine physical examination. The mass occupying the nasal cavity was not observed radiographically. Punch biopsy of the affected lesions revealed nonepitheliotropic lymphoma. Immunohistochemical staining for CD3 antigen was positive. The dog was diagnosed with solitary nonepitheliotropic T-cell lymphoma. Local radiotherapy and systemic chemotherapy with doxorubicin were instituted and resulted in total clinical remission. The dog has remained disease free for 30 months.     

Pathological features of proteinuric nephropathy resembling Alport syndrome in a young Pyrenean Mountain dog

The renal biopsy tissue from a 9-month-old, male Pyrenean Mountain dog with renal disorder and severe proteinuria was examined. Ultrastructural examination revealed multilaminar splitting and fragmentation of the glomerular basement membrane (GBM) and diffuse podocyte foot process effacement. Immunofluorescent staining for α(IV) chains revealed presence of α5(IV) and complete absence of α3(IV) and α4(IV) chains in the GBM. Immunohistochemistry also revealed decreased and altered expression of nephrin and podocin in the glomeruli compared with normal canine glomeruli. These results suggested that the glomerular disease of the present case might be consistent with canine hereditary nephropathy resembling human Alport syndrome caused by genetic defect of type IV collagen, and indicated possible contribution of podocyte injury to severe proteinuria in this case.     

Natural remission of nephrotic syndrome in a dog with immune-complex glomerular disease.

A nephrotic syndrome caused by immune-complex glomerular disease was diagnosed in a 4-year-old male Great Dane. The syndrome was characterized by proteinuria, hypoproteinemia, hypoalbuminemia, hypercholesterolemia, and subcutaneous edema. Renal biopsy revealed segmental membranous glomerular disease. The edema underwent complete remission 18 days after admission. Two months after admission, there was no clinical or laboratory evidence of glomerular disease. Periodic reevaluation of the dog during the next 2 years revealed recurrence of proteinuria, but no other clinical or laboratory abnormalities. Serial renal biopsies revealed persistence, but no appreciable increase, in the severity of the segmental membranous glomerular disease. The natural course of the nephrotic syndrome and immune-complex glomerular disease has been associated with unpredictable variability. It was concluded that the widespread use of corticosteroid or immunosuppressant therapy in dogs with immune complex glomerular disease should be withheld until the natural course of the disease has been evaluated in a significant number of patients and until the results of well-controlled clinical studies confirm or deny their therapeutic value.     

Fatal systemic phaeohyphomycosis caused by Ochroconis gallopavum in a dog (Canis familaris)

A 5-year-old Shetland Sheepdog was presented with a history of weakness, ataxia, anemia, thrombocytopenia, and occasional seizures. The dog had been treated for 6 months with prednisone for inflammatory bowel disease. A positive titer for Ehrlichia canis was detected 6 months before referral. The initial physical examination revealed a weak, laterally recumbent dog with pale mucous membranes. Neurologic examination revealed multiple neurologic deficits. A complete blood cell count (CBC) revealed normochromic, normocytic, nonregenerative anemia; lymphopenia; thrombocytopenia; and neutrophilic and monocytic leukocytosis. Urinalysis revealed proteinuria, with a specific gravity of 1.045. The dog was unresponsive to treatment and died. At necropsy, there was severe serofibrinous peritonitis and pleuritis, with randomly scattered dark brown necrotic foci present in multiple organs, including liver, spleen, kidney, and pancreatic lymph node. Histologically, there were extensive regions of parenchymal necrosis surrounded by neutrophils admixed with epithelioid macrophages, lymphocytes, and pigmented fungal organisms. Numerous brown, 2 to 6 microm in diameter, septate, branching hyphae, subsequently identified as Ochroconis gallopavum (formerly Dactylaria constricta var. gallopava), were observed.     

Renal amyloidosis in related English foxhounds

Renal amyloidosis was diagnosed in six related English foxhounds from two separate hunting kennels. There was no apparent age or sex predilection. All the dogs had clinical and laboratory findings compatible with renal disease. The onset of clinical signs was acute in all cases with death or euthanasia in five of the six affected dogs occurring within one week of presentation. The remaining dog was treated with diuresis which produced a temporary improvement. Histological examination of renal tissue from affected dogs identified the presence of both glomerular and interstitial amyloid, which was confirmed by immunohistochemical staining to be of the reactive type (amyloid A). There were occasional sclerosed glomeruli or glomeruli with thickened Bowman's capsules, in addition to interstitial and periglomerular infiltration with a predominance of plasma cells and lymphocytes and secondary changes including tubular eosinophilic casts. Renal papillary necrosis was identified in three dogs. One hound had concurrent multicentric lymphoma. Pedigree analysis of the affected dogs revealed that four individuals shared a common great grandsire and that the same dog was the grand-sire of a further case. Pedigree analysis of five additional dogs from one of the kennels, all of which had clinical signs of acute renal failure but from which renal tissue was not available, revealed a close relationship to those foxhounds with confirmed renal amyloidosis.     

Bronchogenic cyst in a German shepherd dog

Intermittent episodes of fever, severe dyspnoea and cyanosis were observed in a two-and-a-half-year-old male German shepherd dog. The clinical signs were of sudden onset but disappeared within eight hours, in five almost identical episodes over a period of 40 days. Radiological examination of the thorax revealed a large rounded area of radiolucency surrounded by a thin radiopaque structure. The lesion increased in volume between examinations, but otherwise remained similar in appearance. It could not be confirmed from the radiographs whether the structure was situated in lung tissue or mediastinum. Bronchoscopic examination revealed no abnormal findings and there was no bacterial growth from samples taken 30 days after the onset of symptoms. A large, vesicular structure, partly adherent to the mediastinum, was surgically removed from the left cranial lung lobe. The structure was 8 to 10 cm in diameter and partly filled with mucoid pink fluid. Histological examination revealed that the wall contained traces of bronchial epithelial cells. On bacteriological examination of the fluid, Gram-positive, mucus-forming bacteria were present. The definitive gross pathological and histopathological diagnosis was a bronchogenic cyst which had developed secondarily to bronchiectasis. Bronchitis and peribronchitis were also identified. The dog recovered well after surgery and, at the time of writing, was in active duty as a police dog, showing no signs of respiratory illness.     

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.     

RENAL CORTICAL HYPOPLASIA IN A DOG

A case of renal cortical hypoplasia in a Cocker Spaniel bitch is presented. The dog, under clinical observation between the ages of 15 to 26 months, was found to have advancing chronic renal insufficiency. Necropsy examination revealed a markedly hypoplastic renal cortex with a reduced number of glomeruli, some dilated Bowman's capsules, small glomerular tufts, and early interstitial nephritis and fibrosis characteristic of renal cortical hypoplasia.     

Diagnosis of systemic cryptococcosis by fecal cytology in a dog

A 3-year-old Boxer was presented with progressive diarrhea, vomiting, and lethargy of 5-months duration. The dog had watery black feces, a mature neutrophilia, and microcytic anemia. Cytologic evaluation of a direct fecal smear stained with Wright's-Giemsa revealed numerous encapsulated, narrow-based, budding organisms consistent with Cryptococcus sp. Pyogranulomatous inflammation and Cryptococcus organisms also were observed in ultrasound-guided fine-needle aspirates of the small intestine and mesenteric lymph nodes, and in histologic sections of colonic biopsies obtained by endoscopy. Multifocal chorioretinitis by fundic examination was consistent with systemic mycosis, and the reciprocal antigen titer (1600) on a cryptococcal antigen latex agglutination test for Cryptococcus neoformans was markedly increased. Using immunohistochemistry, the organism was identified further as C neoformans var. grubii (C neoformans var. neoformans serotype A). After 3 weeks of antifungal treatment, ultrasound examination revealed urinary bladder wall thickening, and Cryptococcus organisms were found in a urine sediment preparation. After 4 months of treatment, the dog was clinically normal and had no abnormal findings on CBC, serum biochemistry, urinalysis, or fecal cytology; however, the antigen titer remained unchanged, mesenteric lymphadenomegaly and jejunal wall thickening were still evident, and cytologic evaluation of fine-needles aspirates of the jejunal wall revealed budding Cryptococcus organisms. Intestinal involvement in dogs with cryptococcosis is rare, and diagnosis by fecal cytology has not been documented previously.     

Urethral haemangiosarcoma in a boxer

A seven-year-old, entire female boxer presented with a history of restless behaviour and inappetence. Physical examination revealed that the dog was listless and had a hunched gait. Neurological examination was normal. Abdominal ultrasonography revealed a 4 cm x 4 cm mass in the cranial pelvic canal. Neurological abnormalities were detected three days after presentation, and progressed from proprioceptive deficits to loss of deep pain sensation in the pelvic limbs over a two-day period. The dog was euthanased and postmortem examination revealed that the pelvic mass was a urethral haemangiosarcoma with metastasis to the second lumbar vertebra. This case is unusual as urethral tumours are usually transitional cell carcinomas and frequently present with signs of dysuria.     

Renal microcirculatory and correlated histologic changes associated with dirofilariasis in dogs

Nine 7-month-old Beagle dogs were inoculated with 200 third-stage larvae of Dirofilaria immitis. The development of cardiac disease secondary to heartworm infection was confirmed by thoracic radiography, echocardiography, and angiography with blood pressure measurements. The only indication of renal disease was mild-to-moderate proteinuria. The dogs were euthanatized approximately 18 months after inoculation. The mean microfilarial count in blood at the time of euthanasia was 88,700/ml, with a mean of 89 adult heartworms in the vena cavae, heart, and pulmonary arteries. The kidneys were perfused for microangiographic and correlative histologic examination of the intrarenal microvasculature and associated renal morphologic features. Angiograms of whole kidneys from 6 dogs revealed attenuation or truncation of the major renal vessels. Microangiograms of all kidney slices revealed attenuation in the microangiographic appearance of the glomerular capillaries. Histologic examination of all kidney slices revealed mild-to-intense, diffuse, chronic interstitial nephritis and generalized membranoproliferative glomerulonephritis. Microfilariae were observed within the glomerular capillaries and the medullary vessels. The microangiographic changes correlated with and were explained in part by the histologic changes in the renal parenchyma.     

Biliary cystadenoma in a Maltese dog: clinical and diagnostic findings

A 14-year-old Maltese dog presented for complete medical examination due to intermittent vomiting and diarrhea observed during the previous two days. A single, solitary, lobulated cystic mass was observed in the liver upon ultrasonographic and computed tomographic examination. After surgical hepatic resection to remove the mass, histological examination revealed a multilocular cyst lined by cuboidal to columnar epithelial cells, which is consistent with biliary cystadenoma. Here, we report the clinical, clinicopathological, histopathological, and diagnostic imaging findings of biliary cystadenoma in a dog.     

Multisystemic infection with an Acanthamoeba sp in a dog

CASE DESCRIPTION-A 10-month-old Boxer was evaluated for fever and signs of cervical pain. CLINICAL FINDINGS-Physical examination revealed lethargy, fever, and mucopurulent ocular and preputial discharge. On neurologic examination, the gait was characterized by a short stride. The dog kept its head flexed and resisted movement of the neck, consistent with cervical pain. Clinicopathologic findings included neutrophilic leukocytosis, a left shift, and monocytosis. Cervical radiographs were unremarkable. Cerebrospinal fluid analysis revealed neutrophilic pleocytosis and high total protein content. On the basis of signalment, history, and clinicopathologic data, a diagnosis of steroid-responsive meningitis-arteritis was made. TREATMENT AND OUTCOME: The dog was treated with prednisone (3.2 mg/kg [1.45 mg/lb], PO, q 24 h), for 3 weeks with limited response. Consequently, azathioprine (2 mg/kg [0.9 mg/lb], PO, q 24 h) was administered. Three weeks later, the dog was evaluated for tachypnea and lethargy. Complete blood count revealed leukopenia, neutropenia, and a left shift. Thoracic radiography revealed a diffuse bronchointerstitial pattern. The dog subsequently went into respiratory arrest and died. On histologic evaluation, amoebic organisms were observed in the lungs, kidneys, and meninges of the brain and spinal cord. A unique Acanthamoeba sp was identified by use of PCR assay. CLINICAL RELEVANCE: This dog developed systemic amoebic infection presumed to be secondary to immunosuppression. The development of secondary infection should be considered in animals undergoing immunosuppression for immune-mediated disease that develop clinical signs unrelated to the primary disease. Although uncommon, amoebic infection may develop in immunosuppressed animals. Use of a PCR assay for identification of Acanthamoeba spp may provide an antemortem diagnosis.     

An experimental model of chronic renal disease in dogs by infusion of microspheres into the renal arterial circulation

The feasibility of renal arterial infusion of nonbiodegradable microspheres as a model of chronic renal disease in dogs was evaluated. Resin-coated, styrene-divinyl benzene copolymer microspheres were infused into the kidneys of healthy adult Beagles by direct injections of both renal arteries in a single surgical procedure. Injections of 25-microns diameter microspheres had minimal effect on either the clinical status or serum values of the dogs. Histologic examination revealed the majority of the microspheres lodged within the capillary beds of the glomeruli, and little change to the kidneys. However, injections of 50-microns diameter microspheres caused significant increases in serum concentrations of urea nitrogen and creatinine. Histologically, the larger microspheres obstructed afferent arterioles and small arteries, which caused diffuse glomerular necrosis and nephron damage. With doses ranging from 1 to 3 million microspheres/dog, a correlation between the quantity of microspheres injected and severity of renal damage was observed. The optimal dose for producing a model of moderate renal disease was determined to be 1.8 million microspheres/dog (0.9 million microspheres/kidney). During long-term studies, microsphere-injected dogs fed a moderately restricted protein ration remained relatively azotemic, compared with control dogs on the identical ration. During the 5-month postsurgical period, the serum urea nitrogen concentration averaged 18.41 +/- 1.59 mg/dl (mean +/- SE) for the microsphere-injected dogs vs 9.31 +/- 0.38 for the control dogs (P less than 0.001). Similarly, the mean serum creatinine value was significantly higher (P = 0.020) for the microsphere-injected dogs, compared with the controls (1.23 +/- 0.12 mg/dl vs 0.94 +/- 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)     

Progressive Langerhans' cell histiocytosis in a puppy

A 8-month-old, female miniature Dachshund dog was presented for the complaint of pruritic, generalized, multiple nodules and plaques. Two months previously, a nodule on the left pinna was excised and diagnosed as a cutaneous histiocytoma. One month post-excision, a nodule reappeared at the same site and, shortly thereafter, additional nodules developed. Histopathological examination revealed a diffuse proliferation of histiocytic cells, which reacted strongly to antibodies for vimentin and lysozyme. Immunophenotypic analysis showed that most of the cells expressed CD1a, CD1c, CD11c, CD18, CD45 and MHC class II markers. Electron microscopic examination revealed cytoplasmic filopodia and paracrystalline structures. These findings indicated that the cells originated from Langerhans' cell. The disease progressed despite glucocorticoid therapy and griseofulvin was administered as an immunomodulating drug. All lesions resolved completely after 7 weeks of griseofulvin treatment. The dog, however, died three months later after discontinuation of griseofulvin therapy and a necropsy was not performed. It is considered that the present canine dermatosis corresponds with a severe form of Langerhans' cell histiocytosis in humans rather than canine cutaneous histiocytoma.     

Systemic histiocytosis in a Bernese mountain dog

Systemic histiocytosis was diagnosed at post mortem examination in a three-year-old Bernese mountain dog born in the United Kingdom. The dog presented with a progressive nodular skin disease, chemosis and periocular swelling occurring over six months. It was unresponsive to topical corticosteroids, antibiotics and oral azathioprine. Elective euthanasia was performed. Post mortem examination revealed extensive histiocytic infiltration of the skin, subcutis and skeletal muscles, particularly of the head.     

Pericardial effusion associated with metastatic disease from an unknown primary tumor in a dog

A 6.5-year-old, spayed female Siberian husky presented with signs of cardiac tamponade and weakness. Pleural, pericardial, and abdominal effusion were identified with radiographs and ultrasound. Pericardiocentesis relieved signs of tamponade, and the dog was clinically improved. Pericardial effusion recurred, and pericardiectomy was performed. Histopathological examination of excised tissues failed to reveal evidence of infectious or neoplastic disease. After pericardiectomy, clinically apparent thoracic effusion persisted. The dog was euthanized, and postmortem histopathological examination revealed emboli of metastatic carcinoma cells in the epicardium. The location of intrathoracic disease in this dog made antemortem diagnosis difficult, if not impossible.     

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.     

Myeloproliferative disease with megakaryocytic predominance in a dog with occult dirofilariasis

A 7-year-old male German Shepherd dog with a history of lethargy, weight loss and severe anemia was referred to the University of Florida Veterinary Medical Teaching Hospital for examination. Abnormal laboratory findings included a normocytic and normochromic anemia, thrombocytosis, eosinophilia, basophilia and hyperproteinemia. An increased pulmonary density in the caudal lung lobes was observed on thoracic radiographs. Bone marrow aspiration and core biopsy revealed a hypercellular bone marrow with increased numbers of unidentified blast cells and bizarre megakaryocyte proliferation. Circulating microfilariae were not present in the blood, but serum examined by immunofluorescence was strongly positive for antibodies against Dirofilaria immitis microfilariae. A diagnosis of myeloproliferative disease with megakaryocytic predominance and occult dirofilariasis was made.     

Effects of a Specific Thromboxane Synthetase Inhibitor on Development of Experimental Dirofilaria immitis Immune Complex Glomerulonephritis in the Dog

Twelve Beagle dogs were immunized with aqueous-soluble Dirofilaria immitis antigens, and subsequent to at least fivefold increases in serum antibody titer, 6 mg of homologous antigen was infused into the left renal artery. Six dogs were treated once daily starting the day of infusion with 0.75 mg/kg of 1-benzylimidazole (1-BIM) in saline. Six control dogs were given saline only. Light, immunofluorescent, and transmission electron microscopic examinations of renal tissue from control dogs, 10 days after antigen infusion, showed a mesangioproliferative glomerulonephritis in the left kidney with polymorphonuclear leukocyte (PMNL) infiltration and fibrin deposition. Immunoglobulin (Ig) G, M, C3, and Dirofilaria antigen deposits were observed in a segmental granular pattern. Mesangial, subendothelial, and intramembranous electron dense deposits were observed, and anti-Dirofilaria antibodies were demonstrated in kidney eluates from each dog. Administration of 1-BIM had no significant effect on IgG, IgM, C3, or antigen deposits, electron dense deposits, or concentration of antibody in kidney eluates. However, 1-BIM-treated dogs had less glomerular cell proliferation, periodic acid-Schiff (PAS) positive glomerular staining, PMNL infiltration, and fibrin deposition. These data suggest that thromboxane is an important mediator in the development of immune complex glomerulonephritis, and that in certain circumstances, inhibition of thromboxane synthesis may be an effective therapy for immune complex glomerulonephritis in the dog.