Neuronal-visceral GM1 gangliosidosis in a dog with beta-galactosidase deficiency.

A 9-month-old dog with a history of progressive motor dysfunction was shown to have a deficiency in brain beta-galactosidase activity. The canine disease, like that of children with GM1 gangliosidosis, is characterized by accumulation of GM1 ganglioside in the brain, liver, and spleen, and membranous cytoplasmic bodies in neurons. The dog's pedigree suggests an autosomal recessive pattern of inheritance.

Association of magnesium deficiency with the blood pressure-lowering effects of calcium.

The role of dietary calcium and magnesium in the development of hypertension was studied in nine groups, each consisting of nine spontaneously hypertensive rats aged 8-31 weeks. The animals were fed AIN 76A semi-purified diets varying in calcium (0.075, 0.5 and 2.5%) and magnesium (0.01, 0.05 and 0.75%) concentrations according to a 3 x 3 factorial design. Dietary calcium and systolic blood pressure were inversely related, significantly (P less than 0.05) after 12 weeks. Total and ultrafilterable serum calcium concentrations were also significantly negatively correlated with blood pressure (r = -0.46; P = 0.001 and r = -0.57; P = 0.001, respectively). Repeated measures analysis of variance indicated that dietary magnesium had no effect on systolic blood pressure, and no calcium x magnesium interaction on blood pressure was observed. Signs of magnesium deficiency, calcium deposits in the kidneys, and histological lesions were observed in groups on a high-calcium diet receiving normal and low levels of magnesium. Thus a lowering of blood pressure by calcium supplementation, without concomitant magnesium supplementation, was accompanied by biochemical and histological abnormalities in this animal model.

Streptococcus suis infection in swine: a retrospective study of 256 cases. Part I. Epidemiologic factors and antibiotic susceptibility patterns.

A retrospective study of 256 cases of naturally acquired Streptococcus suis infections in swine submitted to the Indiana Animal Disease Diagnostic Laboratory from 1985 to 1989 was performed to determine the epidemiologic factors and antibiotic susceptibility patterns associated with S. suis serotypes 1-8 and 1/2. A standardized computer form was used to record the history, signalment, and clinical signs obtained from the records of selected cases and the microscopic lesions identified after review of the histopathology slides for each case. A computer statistics package (SAS) was used to evaluate the data. Although the number of recovered S. suis isolates increased in the fall and winter months, most serotypes were readily isolated throughout the year; only serotypes 1, 4, 7, and 1/2 increased in frequency of isolation in the fall, winter, and spring months. The majority (61.1%) of infected pigs in this study were < 12 weeks of age. More than 75% of pigs infected with serotypes 1, 6, 7, and 1/2 were < 12 weeks of age. There was extensive overlap in the age distributions for pigs with each serotype, and statistically significant differences for most serotypes were not observed. Fifty percent of pigs infected with S. suis serotypes 1 and 1/2 were 3-10 weeks of age, 50% of pigs infected with serotype 2 were 6-14 weeks of age, and 50% of pigs infected with serotypes 3, 4, 5, 7, and 8 were 2-16 weeks of age. Isolates of S. suis were not uniformly susceptible to penicillin, and a large percentage of isolates were resistant to many antibiotics in common usage.(ABSTRACT TRUNCATED AT 250 WORDS)

Streptococcus suis infection in swine: a retrospective study of 256 cases. Part II. Clinical signs, gross and microscopic lesions, and coexisting microorganisms.

A retrospective study of 256 cases of naturally acquired Streptococcus suis infections in swine submitted to the Indiana Animal Disease Diagnostic Laboratory from 1985 to 1989 was undertaken to describe the clinical signs, lesions, and coexisting organisms associated with S. suis serotypes 1-8 and 1/2. Infected pigs generally had clinical signs and gross lesions referable to either the respiratory system or to the central nervous system (CNS), but not both. Neurologic signs were inversely related to gross lesions in the respiratory tract (R2 = -0.19, P = 0.003), as were respiratory signs and gross lesions in the CNS (R2 = -0.19, P = 0.003). Suppurative bronchopneumonia was the most common gross lesion observed (55.2%, overall). Fibrinous and/or suppurative pleuritis, epicarditis, pericarditis, arthritis, peritonitis, and polyserositis were also reported. In 68% of the pigs, other bacteria in addition to S. suis were isolated. Escherichia coli (35.0%) and Pasteurella multocida (30.0%) were the most commonly recovered bacterial agents. Mycoplasma and viral agents were identified less often, and their role in the development of streptococcosis was difficult to assess. In pigs infected with serotypes 2-5, 7, 8, and 1/2, suppurative meningitis with suppurative or nonsuppurative encephalitis, suppurative bronchopneumonia, fibrinopurulent epicarditis, multifocal myocarditis, and cardiac vasculitis were the most common microscopic lesions observed, whereas pigs infected with serotype 1 generally presented with suppurative meningitis and interstitial pneumonia. Microscopic lesions were morphologically similar among serotypes and were also similar to those reported with other pyogenic bacteria.(ABSTRACT TRUNCATED AT 250 WORDS)

A sudden death syndrome induced in poults and chicks fed diets containing Fusarium fujikuroi with known concentrations of moniliformin.

A sudden death syndrome was induced in chicks and poults fed diets containing Fusarium fujikuroi, formulated to contain 0-330 mg/kg moniliformin (M) with or without the maximum recommended therapeutic concentration of monensin. Lesions of monensin toxicosis were not observed. Clinical signs were referable to cardiac dysfunction (sudden death, dyspnea, cyanosis, depression). Poults and chicks dying early in the study had no gross lesions or had lesions of right ventricular dilation. Treated poults and chicks dying late in the study or euthanatized at termination of the study had lesions of bilateral myocardial hypertrophy, usually concentric. Absolute heart weights and relative heart weights, expressed as a percentage of body weight, were significantly greater in treated birds than controls (P < 0.05), whereas body weights were significantly less (P < 0.05). Microscopically, lesions progressed from acute myocardial degeneration to necrosis, fibrosis, and hypertrophy. Ultrastructural findings were consistent with the gross and microscopic lesions. Serum pyruvate concentrations were a useful indicator of M-induced cardiotoxicosis. Concentrations of serum pyruvate increased with increased concentration of dietary M, but were not affected by addition of monensin to the diet. In chicks ingesting 40-300 mg/kg M, serum pyruvate concentrations were significantly greater (P > 0.05) than those in controls (controls, 0.28 +/- 0.08 mmol/liter; exposed 0.38 +/- 0.11-0.55 +/- 0.13 mmol/liter). Poults ingesting 80-330 mg/kg M had significantly greater serum pyruvate concentrations than controls (controls 0.33 +/- 0.09 mmol/liter; exposed 0.43 +/- 0.13-1.00 +/- 0.006 mmol/liter). The Vetronics System was used to evaluate electrocardiographic alterations in a limited number of chicks and poults surviving to the end of the feeding trial. Electrocardiographic alterations in poults and chicks fed diets containing > or = 40 mg/kg and > or = 160 mg/kg M, respectively, were consistent with ventricular hypertrophy, myocardial injury, and hypoxia. Electrocardiographic alterations were more striking in poults than in chicks. Altered myocardial metabolism due to M toxicosis, in conjunction with the unusual susceptibility of domestic poultry to altered cardiac metabolism, is believed to be the cause of the organ-specific lesions in these birds. These findings suggest that cardiac injury with subsequent alterations in cardiac electrical conductance may be a cause of the sudden deaths observed in poultry chronically intoxicated with dietary M.

Experimentally induced thiamine deficiency in beagle dogs: pathologic changes of the central nervous system.

Brain and spinal cord were examined in twenty-two 2- to 5-month-old Beagle dogs fed a purified thiamine-deficient ration for 84 +/- 42 (range, 32 to 134) days. Eleven dogs were used as principals, 6 were pair-fed controls, and 5 were controls fed ad libitum. Thiamine at 300 micrograms/kg of body weight was administered IM to control groups once a week. Lesions occurred in 2 topographic patterns in the brain of 8 of the principals. In pattern I, only the caudal colliculi were involved. In pattern II, the suprasplenial gyri of the cerebral cortex and the claustra, caudal colliculi, cerebellar nodulus, and medial vestibular nuclei were commonly involved. In both patterns I and II, gray matter was primarily involved, and in bilateral structures, the 2 sides were affected. Lesions were not limited to a given cerebral lamina or layer of the cerebellum, whereas sulcal areas were relatively spared, and the cingulate gyri were completely spared. Microscopic appearance of the lesions varied greatly among locations and individual principals. Collectively, regressive and reparative changes indicated that there was a progressive process which began with spongiosis and ended with tissue necrosis. These included hydropic vacuolation of the neuropil and myelin sheaths followed by demyelination, neuronal cell body necrosis, hypertrophy and hyperplasia of endothelial cells, necrosis of glia, neutrophil infiltration, disintegration of neuropil, and, finally, accumulation of lipid-containing phagocytes. Axonal degeneration was variable. Neuronal necrosis in the brain stem was characterized by acute swelling and lysis and by shrinkage of the cell body in cerebral and cerebellar cortex and basal ganglia.

Experimentally induced thiamine deficiency in beagle dogs: clinical observations.

Twenty-three 2- to 5-month-old Beagle dogs were fed a purified thiamine-deficient ration (2 to 3 micrograms of thiamine/100 g of ration) at a rate of 40 to 70 g/kg of body weight/day depending on age. Eleven dogs were used as principles, 6 as pair-fed controls, and 6 as ad libitum-fed controls. Controls were treated once a week with an IM dose of 300 micrograms of thiamine hydrochloride/kg of body weight. Three stages of clinical disease occurred in the principals: (i) an initial short (18.0 +/- 7.9 days) stage of induction, during which the dogs usually grew suboptimally, but were otherwise healthy, (ii) an intermediate stage of preliminary clinical signs of deficiency, characterized by a variable period (58.5 +/- 37.0 days) of progressive inappetance, failure to grow, loss of body weight, and coprophagia, and (iii) a terminal stage, which, in most dogs, was abrupt in onset and short (7.6 +/- 6.0 days) and consisted of either a neurologic syndrome or sudden unexpected death syndrome. Eight of the principals developed the neurologic syndrome characterized by anorexia, emesis, CNS depression, paraparesis, sensory ataxia, torticollis, circling, exophthalmos, tonic-clonic convulsions, profound muscular weakness, recumbency, and then died. Common reflex abnormalities included exaggerated patella reflex, proprioceptive and supporting reflex deficits, induced torticollis and ventroflexion of head, and absent eye menace (blink) reflex. Three other principals developed the sudden unexpected death syndrome. Common signs of deficiency were inappetance and paresis. Two were found dead and 1, with severe ECG abnormalities (including elevation of ST segment and tall or deeply inverted T waves), was killed.

Adrenal and hepatic calcium stearate crystal deposits in dogs fed a thiamine-deficient diet.

The nature and histologic environment of birefringent crystals found incidentally at necropsy in the liver and adrenal glands of dogs fed a thiamine-deficient diet were studied. The crystals were identified as calcium stearate by ultrastructural and x-ray microdiffraction techniques. Crystals were observed intracellularly within cytoplasmic vacuoles and extracellularly within sinusoids. Generally, crystals were also observed in pair-fed controls that were given a purified diet (equal in weight to that consumed by the thiamine-deficient animals) plus supplemental thiamine. Crystal deposits were found in trace amounts in a few of the ad libitum-fed controls. Although thiamine deficiency may be involved in promoting crystal deposition in the adrenal cortex, calcium stearate crystal formation within the adrenal glands and the liver appears unrelated to dietary thiamine deficiency per se, but is probably related to deficiency of an unidentified nutrient in the purified thiamine-deficient diet.

Acute vitamin D2 (ergocalciferol) toxicosis in horses: case report and experimental studies.

Acute accidental vitamin D2 (ergocalciferol) toxicosis was diagnosed in a 6-month-old foal with extensive lesions of soft tissue mineralization. In an experimental study, three 18-month-old horses were given ergocalciferol per os at a rate of 9,300, 22,200, or 47,200 IU/kg of body weight/day for 21 days. Clinical signs or lesions were not seen in horses given the low and intermediate doses, whereas the horse receiving the highest dose developed clinical signs and lesions similar to those noted in the foal. Signs included depression, loss of appetite, weakness, limb stiffness with impaired mobility, and cessation of growth or weight loss. Gross and histologic lesions of mineralization of various soft tissues, especially of the endocardium and wall of large blood vessels, were seen in the foal and the horse given the high dose. Marked, persistent, hyperphosphatemia (7.0 to 13.0 mg of P/dl of serum) developed in each horse. The horse given the intermediate dose remained normocalcemic. Horses given the low and high doses became hypercalcemic (13.6 to 14.5 mg of Ca/dl of serum), but serum calcium concentrations varied from day to day and both horses were normocalcemic at necropsy (12.4 to 12.7 mg of Ca/dl of serum). Distal metacarpal bone ash concentrations of calcium, phosphorus, and magnesium of the foal were mg/g of bone ash) 400.5, 180.5, and 5.30, respectively. In the horses, treatment with ergocalciferol also had no significant effect on serum magnesium (1.88 to 2.18 mg/dl of serum) or distal metacarpal bone ash concentrations of calcium (352.5 to 362.5 mg/g of bone ash), phosphorus (182.5 to 184.0 mg/g of bone ash), or magnesium (5.48 to 6.02 mg/g of bone ash).

Acute vitamin D3 toxicosis in horses: case reports and experimental studies of the comparative toxicity of vitamins D2 and D3.

Acute vitamin D toxicosis was diagnosed in 2 horses fed a grain ration containing 1,102,311 IU of cholecalciferol (vitamin D3)/kg (500,000 IU/lb) for about 30 days. Horse 1 died acutely with extensive mineralization of cardiovascular and other soft tissues. Horse 2, which had severe clinical signs and clinicopathologic changes of toxicosis, was treated with nonsteroidal antiinflammatory drugs and recovered in about 6 months. In an experimental study, the toxicity of ergocalciferol (vitamin D2) and cholecalciferol was compared in 2 horses (No. 3 and 4) given the respective vitamins at a daily dosage of 33,000 IU/kg of initial (day 0) body weight for 30 days. Except for slight loss in body weight (8%) during the 1st few days of treatment, horse 3 remained clinically normal. Horse 4 developed limb stiffness and tachycardia, became anorectic, weak, and recumbent, lost 29% of body weight, and had polydipsia and polyuria. Horses 2, 3, and 4 developed persistent hyperphosphatemia. Horse 2 remained normocalcemic whereas horses 3 and 4 became hypercalcemic by day 28. In horse 3, serum vitamin D2 metabolite concentrations on days 0, 1, 14, and 26 were: vitamin D2 (ng/ml) = less than 5.0, 5.7, 71.4, and 188.0; 25-hydroxy-vitamin D2 (ng/ml) = less than 5.0, less than 5.0, 43.1, and 117.5; and 1,25-dihydroxy-vitamin D (pg/ml) = 19.7, 23.2, 25.0, and 45.7, respectively. In horse 4, serum vitamin D3 metabolite concentrations on the same days were: vitamin D3 (ng/ml) = less than 5.0, 110.0, 1,049.0, and 887.0; 25-hydroxy-vitamin D3 (ng/ml) = less than 5.0, 18.9, 201.0 and 182.0; and 1,25-dihydroxy-vitamin D (pg/ml) = 21.5, 18.9, 25.2, and 21.6, respectively. Urine of horses 2 and 4 became acidic (pH 6). Horses 2, 3, and 4 became hyposthenuric, but the decrease in urine specific gravity (sp gr) in horse 3 occurred only after 3 weeks of treatment and was only moderate (sp gr, 1.018 to 1.021) and nonprogressive. Hyposthenuria was evident in horse 4 on day 4 (sp gr, 1.028), and was progressive and marked (sp gr, days 28 to 32: 1.006 to 1.009). Urine sp gr of horse 2 ranged from 1.002 to 1.007. Fractures were demonstrated radiographically and histologically in the costochondral junctions of horses 3 and 4. Mineralization of cardiovascular and other soft tissues developed in horses 3 and 4, with lesions being more severe and having a wider tissue distribution in horse 4.

Bacillus piliformis infection (Tyzzer's disease) in a calf.

A 1-week-old Jersey bull calf with a history of diarrhea, weakness, and lethargy was submitted for necropsy. Principal macroscopic findings were enteritis and multifocal necrotizing hepatitis. Histologically and ultrastructurally, organisms with characteristics of Bacillus piliformis were associated with the foci of necrosis in the liver.

Hereditary junctional mechanobullous disease in a foal.

Mechanobullous disease was diagnosed in a male Belgian foal that had sloughed hooves at 30 hours and at 6 and 12 days of age. Histologic and electron microscopic studies disclosed that lesions were the result of separation of the basal epithelial cell layer from the lamina densa of the basement membrane zone along the lamina lucida. Results of immunofluorescence on tissue specimens were negative for immunoglobulin deposition. The breeding history of the foal's dam indicated that the foal was produced from breeding of the mare to its full sibling stallion. This same mare had produced a female foal, sired by a different stallion, which also had sloughed hooves during the first 2 weeks of life and had similar histologic and electron microscopic changes. This newly recognized disease of horses most closely resembles junctional-type epidermolysis bullosa described in human beings.

Giant cell tumor of soft parts in six horses.

Giant cell tumor of soft parts was diagnosed in 6 horses 3 to 12 years old (mean, 6.8 +/- 3.5 years): 3 Quarter Horse geldings, 2 Standardbred mares, and 1 Standardbred stallion. The neoplasms developed as raised, solitary masses, approximately 1 to 4 cm in diameter, which were firmly attached to subcutaneous tissue of the neck (1 horse), shoulder (1 horse), thigh (2 horses), or stifle (2 horses). Excision was followed by local recurrence in 3 horses within 1 to 1 1/2 months. The neoplasms were firm and cut with resistance. On cut surface, they were white, with mottled red hemorrhagic areas.

Naturally-occurring Tyzzer's disease (Bacillus piliformis infection) in horse foals.

Spontaneous Tyzzer's disease is described in quarter horse foals which died suddenly with no clinical history of apparent illness. Significant gross findings included icterus, focal paletan areas in the liver and catarrhal entercolitis. Focal dark red lesions were present in the small intestine of one foal, and the mesenteric lymph nodes of another were enlarged and hyperemic. Histopathologically, the liver showed multiple discrete and confluent foci of necrosis, fatty change, sinusoid congestion and haemorrhage. Bundles of intracytoplasmic bacilli were demonstrated in hepatocytes at the margin of liver lesions using special stains. Infiltration of the portal triads with inflammatory cells and biliary duct hyperplasia and degeneration were also observed. Lesions in the intestine were characterised by mucosal necrosis with inflammatory cell infiltration, increased mucus production, submucosal lymphoid hyperplasia and, in one foal, submucosal haemorrhage. Necrosis of lymph follicles, congestion and haemorrhage were also present in the spleen and mesenteric lymph nodes.

Influence of magnesium deficiency on horse foal tissue concentraion of Mg, calcium and phosphorus.

1. The effects of feeding with a purified magnesium-deficient diet (--Mg, 7-8 mg Mg/kg) on horse foal blood serum and tissue concentrations of Mg, calcium and phosphorus were studied, and the results compared with histopathological findings. 2. Serum concentrations of Ca and P were unaffected by feeding with the --Mg diet, whereas serum Mg concentrations decreased from a mean initial (day o) concentration of 0.78 mmol/l to 0.53 mmol/l 7 d after foals were placed on the -Mg diet, and then continued to decrease at a slower rate. 3. Aorta concentrations of Ca and P, but not Mg, were positively correlated with the period of time foals were given the -Mg diet, verifying histopathological findings. Results for both aorta Ca and P analyses and histopathological studies indicated that mineralization of the aorta began approximately 30-35 d after foals were placed on the -Mg diet. 4. Feeding with the -Mg diet had no significant, analytically detectable effect on brain, liver, kidney, lung, spleen, skeletal or cardiac muscle concentrations of Ca, P or Mg, although microscopic evidence of mineralization was seen in some of these tissues from foals given the Mg diet for 71-180 d. 5. A significant negative correlation was found between bone ash concentrations of Mg (rib, metacarpus and metatarsus) and the length of time foals were fed on the Mg diet. Bone ash concentrations of Ca and P were, however, unchanged. 6. Low serum Mg values and negative correlations between the bone ash concentration of Mg and the period of time foals were fed on the -Mg diet supplemented with 390 mg. Mg as MgO/kg were interpreted as suggesting that either this level of Mg supplementation is marginal for the growing foal, or that the Mg in MgO is not readily available to the growing foal.