Postanesthetic death in a cat with myopathy.

There are few reports of naturally occurring muscular dystrophy in domestic animals. Herein, we describe a case of muscular dystrophy in a 4-year-old neutered male American domestic shorthair cat that died unexpectedly following anesthesia for an elective surgical procedure. Macroscopic muscular hypertrophy and histologic evidence of myofiber size variation, mineralization, myofiber degeneration, and necrosis were compatible with a diagnosis of muscular dystrophy. Extensive endomysial fibrosis was noted histologically in the diaphragm. A complete absence of dystrophin protein in Western blot confirmed the diagnosis of Duchenne muscular dystrophy. Immunofluorescence microscopy revealed reduced levels of dystrophin-associated proteins and an upregulation of utrophin at the sarcolemma. Anesthetic deaths can occur in dystrophin-deficient cats, and therefore muscular dystrophy and the associated cardiomyopathy should be considered in the differential diagnoses for perianesthetic death in cats.

Neoplasms and pigmentation of thyroid glands in F344 rats exposed to 2,4-diaminoanisole sulfate, a hair dye component.

2,4-Diaminoanisole sulfate was fed at dietary levels of 0.12% (low dose) or 0.5% (high dose) to groups of 50 male and 50 female inbred F344 rats for 78 weeks. By 107 weeks after the initial exposure, 58% of the male rats and 42% of the female rats administered the high dose had thyroid neoplasms, whereas only 7--8% of the controls developed them. Follicular cell carcinomas were the primary type of neoplasm induced. None of the controls had these tumors. The carcinomas, which were papillary, cystic, or solid, were highly invasive but did not metastasize. A brown pigment was present as granules primarily in thyroid follicular cells in all exposed rats. The amount of pigment as determined by an image-analyzing computer revealed that the cross-sectional area occupied by the pigment granules and the optical density of the granules were dose related.

Natural infection of a horse with Fascioloides magna.

A 25-year-old Quarterhorse mare was euthanized for a variety of medical reasons. At necropsy, 7 liver flukes, identified as Fascioloides magna, were recovered from the liver. This is the first report of F. magna in a horse.

Morphology of nasal cavity neoplasms in F344 rats after chronic feeding of p-cresidine, and intermediate of dyes and pigments.

p-Cresidine was administered in the feed at either of two concentrations (0.5 and 1.0 percent) to groups of 50 male and 50 female F344 rats for 104 weeks. Fifty animals of each sex were placed on test as controls and fed only the basic laboratory diet. All animals were observed for up to 2 weeks after discontinuation of treatment. In treated rats of both sexes, statistically significant numbers of adenomas, adenocarcinomas and squamous cell carcinomas were diagnosed in the nasal cavity. Most of the neoplasms were seen in the high dose male and female rats. 22 male rats (49%) showed poorly differentiated adenocarcinomas infiltrating the skull and brain. Only two male rats (4%) had a squamous cell carcinoma, whereas 8 female rats (17%) had squamous cell carcinomas and 14 female rats (30%) were diagnosed as having adenocarcinomas of the nasal cavity. In the 4 neoplasms studied ultrastructurally, features characteristic of adenocarcinomas were identified. Cells were arranged around central lumina lined with microvilli. The luminal edges of cells were linked together by junctional complexes. Cytoplasmic differentiation was generally poor, with ribosomes and polyribosomes being the predominant organelles. Neurogenic features were rare and difficult to identify due to unsatisfactory fixation. In one of the tumors, areas of squamous differentiation were found. The cells constituting such areas contained prominent bundles of tonofilaments which are characteristic of early squamous metaplasia.

Acquired B lymphocyte deficiency and chronic enterocolitis in a 3-year-old quarter horse.

This case report describes a 3-year-old American Quarter Horse with acquired immunodeficiency. Clinical signs included chronic diarrhea due to Salmonella typhimurium and bacterial pneumonia. Characterization of the immunodeficiency involved in vivo phytohemagglutinin (PHA) intradermal testing, in vitro lymphocyte proliferation in response to concanavalin A, immunofluorescence flow cytometry data on blood lymphocytes, serum protein electrophoresis and immunoglobulin (Ig) quantification. A diagnosis of B lymphocyte deficiency with resulting deficiencies in serum IgG, IgA and IgM and a concurrent decrease in T cell function was made based on these tests. Postmortem examination revealed no evidence of lymphosarcoma. This case represents a variation of young adult-onset B cell deficiency not previously described in the literature.

Hepatic and pulmonary pathology of experimental Fascioloides magna infection in guinea pigs.

The guinea pig was used to study the pathology of Fascioloides magna, an important pathogen for sheep. Although flukes migrated freely through various tissues in infected guinea pigs, the most serious lesions occurred in the liver and lungs. The sequential development of lesions indicated that flukes first invaded the quadrate lobe of the liver and subsequently migrated to other liver lobes and tissues. Six weeks post-infection, there was a marked drop in the recovery of flukes from the liver along with a dramatic increase in pulmonary involvement. Much of the hepatic and pulmonary pathology in infected animals was secondary to extensive vascular lesions caused by migrating flukes. In the liver, vascular lesions predominantly involved the portal and hepatic veins. Thrombophlebitis and locally extensive necrosis, resembling infarction, were observed. Vascular lesions in the lungs occurred in the pulmonary arteries leading to thrombosis and haemorrhagic infarction. Discovery of a fluke in a pulmonary artery, along with the pattern of hepatic and pulmonary lesions, suggested that flukes probably used the cardiovascular system as a pathway for dissemination. Death in fluke-infested guinea pigs was most often associated with severe pulmonary lesions. The nature and distribution of fluke-induced lesions observed in this study demonstrate that the guinea pig is a suitable animal model for Fascioloides magna infection in sheep.

AA amyloid-associated gastroenteropathy in a horse.

Systemic amyloidosis involving the digestive tract is described in an 11-year-old Morgan stallion. The disease was characterized clinically by weight loss, ptyalism, anaemia, persistent mature neutrophilia, hypoalbuminaemia and hypergammaglobulinaemia. The D-xylose absorption test indicated malabsorption. Necropsy revealed oral, oesophageal and gastric ulcers and reddened segments of small bowel mucosa with scant haemorrhages. Microscopically, amyloid deposits were found throughout all tissue layers of the digestive tract, except the serosa. Deposits of amyloid were most apparent in the small bowel mucosa and submucosal arteries. Amyloid was also present in the spleen and lymph nodes and to a lesser extent in the liver, kidneys, lungs, pancreas and bone marrow. All amyloid deposits gave the typical histochemical reaction for AA amyloid with the KMnO4-Congo red stain procedure and immunohistochemical cross-reactivity was demonstrated with antisera to both canine and bovine protein AA by the peroxidase-antiperoxidase technique. The cause of the amyloidosis was not identified, although the haematological and serological data were compatible with an underlying chronic inflammatory process.

Immunohistochemical morphometry of pancreatic endocrine cells in diabetic, normoglycaemic glucose-intolerant and normal cats.

The anatomical distribution and volume fractions of pancreatic A cells (glucagon), B cells (insulin) and D cells (somatostatin) were evaluated by an immunoperoxidase technique in 6 diabetic cats, 6 normoglycaemic glucose-intolerant cats and 6 normal control cats. Islets lacking A cells were observed in some sections from the right lobe of the pancreas which correlated with a significantly lower A cell volume fraction in the right pancreatic lobe. Endocrine cell volume fractions in normoglycaemic glucose-intolerant cats were not significantly different from controls. Thus, a reduction in B cell volume fraction was not necessary for the occurrence of impaired glucose tolerance in these cats. However, the reduction of B cell volume fraction in the 2 normoglycaemic glucose-intolerant cats with insular amyloidosis may in part explain the more severely impaired glucose tolerance previously observed in these cats. Insular amyloidosis in our feline diabetics, as in human type II diabetics, was associated with a significant decrease in A and B cell volume fractions. In both human type II and feline diabetes mellitus, however, the reduction in B cell mass does not appear sufficient alone to lead to diabetes mellitus. Therefore, amyloid replacement of functional endocrine cells does not appear to be the primary diabetogenic event in feline diabetes mellitus, but may contribute to progression of the condition due to loss of functional B cell reserves. We thus postulate that a B cell defect precedes deposition of islet amyloid and that these amyloid deposits may thus provide an important biochemical clue to specific B cell derangements occurring in adult-onset diabetics.

Diphallia in a mixed-breed dog with multiple anomalies.

Complete diphallia was detected in a six-month-old Poodle cross dog. Duplication of the urinary bladder, right renal hypoplasia, bifurcation of the descending colon and bilateral cryptorchidism were also present. The left urethra was patent, and emptied the left urinary bladder; the right urethra ended blindly at a point 2.5 cm from the tip of the right penis. The left urinary bladder was joined medially to a right urinary bladder with no interbladder communication; however, the right bladder opened caudally into a blind sac which drained into the left prostatic urethra. Pyelonephritis of the left kidney was present, and was suspected to be due to ascending bacterial infection of the right urinary bladder and the right segment of the bifurcated descending colon, which terminated at the apex of the right urinary bladder. Diphallia and associated urogenital anomalies are reviewed.

Intramedullary spinal cord metastasis in the dog.

Intramedullary spinal cord metastasis (ISCM) was diagnosed in three dogs with signs of myelopathy. The clinicopathologic features of ISCM in these and previously reported cases in the veterinary and human literature were compared. Myelopathic signs associated with ISCM may be the initial clinical manifestation of malignancy or may develop in the patient with known malignancy. Pain, a frequent manifestation of extradural compressive myelopathy, is not a consistent feature of ISCM. Survey spinal radiographs are usually unrewarding and cerebrospinal fluid (CSF) abnormalities nonspecific. Myelography is indicated to differentiate intramedullary lesions from more common extradural compressive lesions. Myelographic interpretation may be difficult, and intramedullary tumors must be differentiated from spinal cord edema or hemorrhage. Evidence of widely disseminated malignancy should increase suspicion for ISCM; hemangiosarcoma and lymphosarcoma should be considered the most likely histologic types. CSF cytology may be helpful in the diagnosis of patients with lymphosarcoma. Prognosis is poor due to the frequent presence of disseminated disease, although temporary response to corticosteroid therapy may be achieved. More aggressive therapeutic approaches, such as spinal irradiation and microsurgical resection of metastases, have been advocated in humans but have not been reported in the dog. Although it is an uncommon complication of systemic malignancy, ISCM should be considered in the differential diagnosis of myelopathy in the dog.

Intracranial lesions in dogs with hemangiosarcoma.

A retrospective analysis of 85 dogs with hemangiosarcoma (HSA) that underwent complete necropsy, including gross examination of the brain, was conducted. Grossly identifiable intracranial lesions were present in 17 dogs. Twelve of 85 dogs (14.2%) had brain metastases. Four of 85 dogs (4.7%) had hemorrhagic lesions and/or ischemic necrosis without identifiable tumor. One dog had a primary central nervous system tumor. Signs of intracranial disease were present in six of 85 dogs (7.1%) with HSA; four had brain metastases and two had nonneoplastic lesions. Metastases had a propensity for cerebrum and gray matter. Dogs with brain metastases had more widely disseminated disease than dogs without brain metastases (P less than 0.001). Dogs with pulmonary metastases were at greater risk for developing brain metastases than dogs without pulmonary metastases (odds ratio = 8.31). Although thoracic radiography accurately identified ten of 12 dogs (83%) with pulmonary metastases, too few cases were available to assess the applicability/accuracy of thoracic radiography in predicting the presence or absence of brain metastases in dogs with malignancy and signs of intracranial disease.

Idiopathic hypereosinophilic syndrome in 3 Rottweilers.

Three Rottweilers with marked peripheral eosinophilia and infiltration of the liver, spleen, lungs, and bone marrow with eosinophils were diagnosed with idiopathic hypereosinophilic syndrome (IHES). Mean serum immunoglobulin E concentrations were markedly high. On cytogenetic analysis, no evidence of karyotypic abnormalities was found in bone marrow aspirates. Despite an extensive search, no underlying cause for the eosinophilia could be identified. In this study, cytogenetic analysis and measurement of serum IgE concentrations were used to differentiate IHES and eosinophilic leukemia.

Evaluation of serum and seminal plasma markers in the diagnosis of canine prostatic disorders.

Serum and seminal plasma concentrations or activities of acid phosphatase (AP), prostate specific antigen (PSA), and canine prostate specific esterase (CPSE) were measured in normal dogs, dogs with benign prostatic hyperplasia (BPH), dogs with bacterial prostatitis, and dogs with prostatic carcinoma to determine if these assays would be of value in differentiating dogs with prostatic carcinoma from normal dogs, and dogs with other prostatic disorders. In addition, tissue sections of prostatic adenocarcinomas were stained with antiprostatic AP, anti-CPSE, and anti-PSA antibodies to determine if these would be suitable immunohistochemical markers of prostatic carcinoma. Prostate-specific antigen was not detected in canine serum or seminal plasma. Serum and seminal AP activities did not differ significantly between normal dogs and those with prostatic diseases, or among dogs with different prostatic disorders. Serum CPSE activities were significantly higher in dogs with BPH than in normal dogs. Mean serum CPSE activities in dogs with BPH, bacterial prostatitis, and prostatic carcinoma were not significantly different from each other. Slight to moderate immunohistochemical staining of canine prostatic adenocarcinomas was noted for prostatic AP and PSA; most tumors did not stain for CPSE. These results show that proteins of prostatic origin appear in the serum of dogs as a result of prostatic pathology, especially BPH. Canine prostatic adenocarcinoma does not appear to be associated with significant increases in CPSE or AP activities, possibly because of down-regulation of these enzymes by prostatic carcinoma cells. It is also possible that failure to detect significant differences resulted from limited statistical power for some groups and pairwise analyses because of the small number of dogs evaluated.

Experimentally induced canine toxocariasis: laboratory examinations and pathologic changes, with emphasis on the gastrointestinal tract.

Eght dogs were orally superinfected for 1 month with 50,000 embryonated Toxocara canis ova. Results of laboratory examinations during inoculation and for 2 weeks postinoculation revealed moderate leukocytosis, marked absolute eosinophilia, hypoalbuminemia, increased concentrations of serum glutamic pyruvate transaminase, and in 2 dogs, precipitating humoral antibodies. Other changes were moderate ascites, hepatomegaly, lymphadenopathy, and focal lesions (0.5 to 3.0 mm) in liver, lung, kidney, intestine, abdominal lymph node, heart, diaphragm, and spleen. Microscopically, focal eosinophilic gastroenteritis was produced. Eosinophils and globule leukocytes were increased throughout the intestinal mucosa. Eosinophil-infiltrated and granulomatous lesions were in the same organs listed as having focal lesions, as well as in the pancreas. The importance of serum beta-globulin content as a potential diagnostic tool was emphasized, and the experimentally induced infection was compared with naturally occurring eosinophilic gastroenteritis in the dog.

Pathophysiologic effects of experimentally induced Fascioloides magna infection in sheep.

The pathophysiologic responses of 13 sheep inoculated orally with 100 metacercariae of Fascioloides magna were monitored for 4 months after inoculation. There were no differences in weight gains between these and a number of noninoculated control sheep throughout the experiment. Complete blood cell counts showed an increase only in the absolute number of eosinophils. Serum preparations (2 times a week) from 7 inoculated and 7 noninoculated sheep did not identify any significant changes in alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase, and gamma-glutamyl transferase activities. There were no changes in total bilirubin, BUN, creatinine, inorganic phosphorus, calcium, albumin, chloride, potassium, and sodium values. Four months after they were inoculated, all sheep were necropsied, and flukes were recovered. Gross lesions attributed to fluke migration were found in the liver and portal lymph nodes, diaphragm, lungs, kidneys, and spleen. Microscopically, liver lesions in inoculated sheep occurred in the portal areas, veins, and Glisson's capsule and were characterized by both active and chronic forms of inflammation. Abundant infiltrates of eosinophils and plasma cells often marked the portal areas. Endophlebitis, with or without thrombosis, was the predominate vascular lesion. The flukes recovered varied greatly in size (6.5 to 48.0-mm long) and demonstrated some sexual development, but none was sexually mature.

Feline mammary hypertrophy/fibroadenoma complex: clinical and hormonal aspects.

Abnormal mammary enlargement, characterized microscopically by hyperplasia of both epithelial and mesenchymal tissues, was studied in 26 cats which were mostly young, sexually intact females. Clinicopathologic data indicated that mammary hypertrophy was likely progesterone-dependent. Administration of progestins preceded this condition in 5 cats, 4 of which were neutered. Serum progesterone concentrations (6.7 ng/ml) were increased in 1 of the 3 cats tested. Estrogen receptors were not found in the cytosols or nuclei of mammary tissues in the 2 cats studied. However, there were convincing 4S [3H]progesterone or 5S [3H]R5020 binding peaks which were suppressible by nonlabeled progestins. Progesterone receptors were measured at 14.9 and 8.6 fm/mg of protein, respectively. The apparent influence of progesterone, whether present as exogenous therapy in the male or female or as endogenous steroid of ovarian origin, has thus been demonstrated directly and indirectly in cats with mammary hypertrophy.

Influence of modified protein diets on electrolyte, acid base, and divalent ion balance in dogs with experimentally induced chronic renal failure.

The influence of a maintenance diet (44.4% dry weight protein) and 2 reduced protein diets (8.2 and 17.2% dry weight protein) on acid-base, electrolyte, and divalent ion balance of dogs with experimentally induced chronic renal failure was studied for 40 weeks. Moderate-to-severe hyperchloremic metabolic acidosis developed in dogs fed the 8.2% protein diet, but not in the groups fed the 17.2% and 44.4% protein diets. Serum sodium and potassium concentrations were not altered significantly by the diets. Mean serum calcium concentrations increased significantly in the 3 groups after renal failure was induced; however, serum calcium concentration generally did not exceed the normal range. Dogs fed reduced protein diets had smaller serum magnesium and phosphorus concentrations than did the dogs fed the maintenance diet. Microscopic alterations in bone morphology consistent with canine renal osteodystrophy were not detected after 40 weeks of renal failure in dogs fed the 17.2% and 44.4% protein diets. Examination of skull radiographs of the dogs prepared 40 weeks after renal failure was induced revealed that the lamina dura dentes were visible in all groups. It was concluded that the 8.2% protein diet was of therapeutic benefit in management of altered divalent ion metabolism in dogs with chronic renal failure. However, the high frequency of concomitant acidosis indicated that appropriate alkalinization therapy should be included with this diet. Adverse effects of feeding the 17.2% protein diet were not detected. However, it was less effective than the 8.2% protein diet in minimizing development of hypermagnesemia and skeletal changes consistent with renal osteodystrophy.

Influence of modified protein diets on the nutritional status of dogs with induced chronic renal failure.

The influence of a canine maintenance diet containing 44.4% protein (dry weight) and 2 reduced-protein renal-failure diets containing 8.2% or 17.2% protein (dry weight) on the nutritional status of dogs with induced chronic renal failure was evaluated for 40 weeks. Nutritional status was assessed by changes in serially determined body weights, hindlimb circumferences, serum protein concentrations, complete blood cell counts, serum cholesterol concentrations, glucose tolerance tests, and blood glucose concentrations. Evidence of suboptimum nutritional status was observed in dogs fed the 8.2% or 44.4% protein diets, but not in dogs fed the 17.2% protein diet. Only a small reduction in hindlimb circumference developed in dogs fed the 17.2% protein diet. Reduced body weight and hindlimb circumference and normocytic normochromic anemia developed in dogs fed the 44.4% protein diet. Reduced body weight and hindlimb circumference, hypoalbuminemia, hypoproteinemia, hypercholesterolemia, and normocytic normochromic anemia developed in dogs fed the 8.2% protein diet. A beneficial effect of moderate dietary protein restriction (17.2% protein) on the nutritional status of the dogs was observed. In contrast, excessive intake or restriction of dietary protein was associated with detrimental effects.

Progesterone receptors in feline mammary adenocarcinomas.

Estradiol and progesterone receptors were measured in tumor cytosols from 3 intact and 4 neutered female cats with spontaneously occurring mammary adenocarcinomas. Serum from 2 of the intact cats which had been in estrus 4 and 4 to 6 weeks before tumor excision contained progesterone concentrations of 16.2 and 2.2 ng/ml, respectively; serum progesterone in the other cats was less than 2 ng/ml. Estradiol receptors were not detected in any cytosols. Progesterone receptors were detected in all of the cytosols, in concentrations ranging from 4.0 to 11.7 (mean = 7.2) fmol/mg of protein. Scatchard plot analysis of tumor cytosol from an 8th cat with mammary adenocarcinoma revealed presence of high affinity progesterone binding with a dissociation constant (Kd) of 3.47 nM. Tumor receptor content could not be correlated with stage of the estrous cycle nor with whether the cat was intact or neutered.

Influence of reduced protein diets on morbidity, mortality, and renal function in dogs with induced chronic renal failure.

The influence of a maintenance diet containing 44.4% dry weight protein and 2 reduced protein diets containing 8.2% and 17.2% dry weight protein on morbidity, mortality, and renal function of dogs with induced chronic renal failure was studied for 40 weeks. The diets differed in mineral and electrolyte composition in addition to differences in protein, carbohydrate, and fat content. Dogs fed the 44.4% protein diet had a higher mortality (6 of 11) than did dogs fed the 8.2% (1 of 6) or 17.2% (0 of 6) protein diets. Dogs fed the 44.4% protein diet died of uremic complications. An occlusive portal vein thrombus caused death of the nonsurvivor fed the 8.2% protein diet. Clinical signs of uremia were detected only in nonsurvivors fed the 44.4% protein diet. Surviving dogs fed the maintenance diet were less active and had poorer hair than did dogs fed reduced protein diets. Inulin clearance rate and urinary protein excretion were lower in most dogs fed reduced protein diets than in dogs fed the maintenance diet. Despite the greater decrease in renal function, serum urea nitrogen concentrations were markedly lower in dogs fed the 8.2% and 17.2% protein diets than in dogs fed the 44.4% protein diet. Seemingly, the reduced protein renal failure diets were of benefit in preventing or reducing morbidity and mortality associated with the uremic syndrome and in reducing serum urea nitrogen concentrations as compared with that of the higher protein diet. The potential benefits of dietary protein restriction in dogs with chronic renal failure prevailed over potential adverse affects of excessive protein consumption.