Low fertility related to 1/29 centric fusion anomaly in cattle.
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Biomedical subjects
G R Ruth
Publications and source records attributed to G R Ruth.
Health and metabolic responses of young calves housed at -30 degrees C to -8 degrees C.
Newborn, male, Holstein calves, were continuously housed for three weeks in calf hutches at 17 degrees C or in a thermal environment which varied rhythmically on a daily basis either between -20 degrees C and -8 degrees C (experiment A) or between -30 degrees C and -18 degrees C (experiment B). Compared to warm-housed calves, cold-housed calves in experiment A had metabolic rates which were significantly higher (p less than 0.001) in a standing position but which were not significantly different (p less than 0.05) in a recumbent position. Recumbent and standing cold-housed calves in experiment B had an increased (p less than 0.05) metabolic rate compared to warm-housed controls. Heat loss was less (p less than 0.05) for recumbent cold-housed calves in experiment B than for standing calves in a thermoneutral environment. Localized subcutaneous hemorrhages of hindlimbs were a consistent necropsy finding among all cold-housed calves. Average daily gains of cold-housed calves were not significantly different from warm-housed controls. Clinical, physiological and pathological findings indicated that cold treatments used in the present study did not cause serious harm to calves. It was concluded that calves housed in properly managed hutches are remarkably cold tolerant.
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Thermal insulation of young calves exposed to cold.
Tissue, external and whole animal insulation values were determined for 12 newborn male Holstein calves continuously housed for two weeks in hutches within environmental chambers in which temperature was maintained at a constant 17 degrees C (three calves) or cycled on a daily basis either between -20 degrees and -8 degrees C (three calves) or between -30 degrees and -18 degrees C (six calves). Three of the six calves at the coldest temperature were outfitted with an insulated coat. The insulated coat provided calves a 52% increase in total insulation. Tissue insulation of cold-housed calves increased 37.2% over the first two weeks of life. It was concluded that the capacity for vasoconstriction improved with age. External insulation did not change significantly except during the first week in cold-housed calves without insulated coats. External insulation values were five to eight times those of tissue insulation values for all treatment groups. This indicated that insulation of structures external to the skin (hair, bedding, ground, etc.) provided most of the insulation for calves.
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Blastomycosis in wild wolves.
Blastomycosis was fatal to a wild wolf in Minnesota, and serologic evidence of blastomycosis was found in a Wisconsin wolf. No unusual movements were detected in the Minnesota animal from October 1983 through October 1985. However, by early December 1985, this wolf was weak and debilitated, and it perished on 14 December after approaching a human residence.
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Histochemical morphologic features of growth cartilages in long bones of pigs of various ages.
Growth cartilages were obtained from humeri, femora, and ulnae of 31 pigs between 1 and 169 days old. On the basis of stain uptake and distribution, distinct layers were identified in articular-epiphyseal cartilage complexes and growth plates. The laminated appearance was dependent on stain uptake by territorial and interterritorial matrices and was more distinct in pigs greater than 15 days old. There was morphologic heterogeneity, which probably represented a functional heterogeneity, among chondrocytes in all layers and zones of both types of growth cartilage. The laminar appearance of growth cartilages and the distribution of different types of cells were similar for all pigs in each age category and for all sites.
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Necropsy of adult cattle.
This article presents a brief overview of some examination techniques commonly used during necropsy of adult cattle. A few common diseases and their typical lesions are described and appropriate laboratory techniques to confirm or help deny the roles of specific agents are mentioned.
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Dyschondroplasias of growth cartilages (osteochondrosis) in crossbred commercial pigs at one and 15 days of age: radiological, angiomicrographical and histological findings.
The age of onset and morphology of the earliest lesions of dyschondroplasias in pigs have not been established. Bones and growth cartilages from pigs were examined for the presence of lesions using radiological, angiomicrographical and histological techniques. Lesions were in 10 of 11 pigs at 15 days of age and 12 of 21 pigs at one day of age, indicating that the condition was congenital. The simplest and apparently earliest lesion was an area of persistent hypertrophied chondrocytes and matrix which extended from the articular-epiphyseal complex or physis into the epiphysis or metaphysis, respectively. Since the prevalence of lesions was high it was considered that the dyschondroplasia may be part of the usual growth pattern of cartilages in contemporary pigs.
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Angiomicrographic investigation of the vessels associated with physes in young pigs.
There is little information available relating to the vasculature of physes of pigs, hence the object of the present study was to establish the distribution of blood vessels in normal physes of pigs at one and 15 days old. By the use of an angiomicrographic technique it was possible to demonstrate that vessels were in two main categories; first, those which entered the physis from the epiphysis and terminated, or branched and then terminated half to two thirds of the distance into the depth of the physis; second, vessels which crossed the full depth of the physis. Since vessels that cross the physis from epiphysis to metaphysis were a frequent feature of normal physes they do not seem to be a congenital defect which predisposes to the development of dyschondroplasias in young pigs.
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Dyschondroplasias, including osteochondrosis, in boars between 25 and 169 days of age: histologic changes.
Microscopic sections of physeal and articular-epiphyseal (A-E) cartilages from major limb bones of 60 boars between 25 and 169 days of age were examined. The objectives in this study were to determine the age of onset and pathogenesis of osteochondrosis, a defect of endochondral ossification. Lesions regarded as typical of osteochondrosis were associated with physes of pigs from 25 days of age, indicating an earlier age of onset than has generally been documented. Two morphologically distinct lesions were observed, but both had areas with increased depth of the zone of hypertrophying chondrocytes. Some lesions were repairing. With increasing age of the pigs, the number of involved physes increased in each of 6 different age groups up to 169 days. Lesions associated with physes were observed in boars younger than those with lesions associated with A-E complexes. A few pigs at, or older than, 53 days of age, had osteochondrosis-like lesions involving epiphyseal growth cartilages. However, a dyschondroplasia different from osteochondrosis and typified by chondrolysis was more frequently associated with A-E complexes of pigs at or greater than 79 days of age. The number of affected cartilages and sites with this type of lesion also increased with age. Although osteoarthrosis had not developed in any of the pigs, it is probable that chondrolytic areas were precursors of degenerative joint disease. To date, osteochondrosis has been used to encompass lesions involving physes and A-E complexes. However, in view of the findings in the present study, dyschondroplasia is the preferred term to be used generically and then qualified by morphologic description, since causations may be different.
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Dyschondroplasias, including osteochondrosis, in boars between 25 and 169 days of age: radiologic changes.
Boars in 6 different groups (between 25 and 169 days of age) were examined radiographically to determine the age of onset of lesions associated with the sites of endochondral ossification in limb bones. Although lesions were in histopathologic sections of physes from all groups of pigs, they were not found frequently in radiographs of live animals until boars were more than 100 days old. Microscopic lesions were infrequent in articular-epiphyseal (A-E) complexes of pigs less than 80 days old, and radiographic examination of live animals had limited value until animals were greater than 100 days old. Radiographs of slabs of bone were useful in the detection of physes with lesions in all age groups and A-E complexes with lesions in boars 100 days of age or older. So that the accuracy of radiographic examination of live animals for the diagnosis of dyschondroplasias could be evaluated, a comparison was made between the numbers of growth cartilages with lesions as determined by radiologic examination of live animals, radiographic examination of slabs of bone, and light microscopy (examination of tissue sections). Only 21% of the lesions associated with physes and 22% of the lesions associated with A-E complexes were detected in radiographs of bones of live pigs. The authors concluded that the latter method was inaccurate for the identification of dyschondroplastic foci. Identification of lesions by examination of radiographs of slabs of bone was only slightly more accurate, since 33% of physes and 23% of A-E complexes which had lesions were found. Potential errors in evaluation of radiographs were discussed.(ABSTRACT TRUNCATED AT 250 WORDS)
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Bovine protoporphyria: documentation of autosomal recessive inheritance and comparison with the human disease through measurement of heme synthase activity.
Protoporphyria is an autosomal dominant disease in man in which protoporphyrin accumulated because of a defect in heme synthase (ferrochelatase) activity. A disease has been described in cattle that has the same manifestations as does the human disease. We measured heme synthase activity in sonicates of cultured skin fibroblasts and whole liver homogenates from animals with protoporphyria, their unaffected parents, and normal cattle in order to examine the mode of inheritance and compare it with human protoporphyria. The mean activity (+/- SEM) in fibroblasts from the three groups was 2.0 +/- 0.4, 47 +/- 12, and 149 +/- 10 pmol heme formed/mg protein per hr, respectively, consistent with autosomal recessive inheritance. Similarly, the levels of heme synthase activity in livers of the parents were intermediate to those of normal animals and of animals with protoporphyria. When compared with normal human fibroblasts and liver, the specific activity of heme synthase in normal bovine tissue was significantly higher. These studies indicate that manifestations of protoporphyria do not occur in cattle unless the animal is homozygous for the gene defect, whereas in humans, the heterozygous condition is sufficient. This is probably because the specific activity of heme synthase in cells of heterozygous animals is not reduced to a level that significantly alters heme metabolism.
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Eosinophilic myositis in a slaughtered heifer.
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Screening for genetic diseases: principles and practice.
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Animals↗
Trichophyton mentagrophytes dermatophytosis in wild fox.
Dermatophytosis caused by a zoophilic varient of Trichophyton mentagrophytes was diagnosed in a litter of eight captured wild red fox (Vulpes fulva). The animals had widespread partial alopecia and scattered crusty foci 2 to 3 cm in diameter on the skin. Treatment with 7 mg/kg/body weight/day of griseofulvin in the feed effectively controlled the infection.
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Fatal thrombocytopenic hemorrhagic diathesis associated with dapsone administration to a dog.
Dapsone was given for six days to a dog with chronic skin disease. The dog then became weak and anorectic, and it vomited and had purpura caused by severe thrombocytopenic hemorrhagic diathesis. Despite treatment, the dog died a week later. There were clinical and pathologic evidence that the dog's platelets and megakaryocytes had been destroyed during the first few days of dapsone therapy. It was concluded that the syndrome was dapsone-induced and that thrombocytopenia should be considered among the adverse reactions to dapsone in the dog.
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Malignant catarrhal fever in bison.
Malignant catarrhal fever was diagnosed in 3 herds of American bison (Bison bison) in South Dakota from 1973 to 1976. Clinical signs included depression, nasal and ocular discharge, conjunctivitis and keratitis, and diarrhea. Herd morbidity ranged from 3 to 53.8%, and mortality was 100%. At necropsy, ulcerative lesions were found throughout the alimentary tract, trachea, and bronchi. Microscopically, necrotizing vasculitis without thrombosis was found in virtually every organ examined.
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Ultrastructural alterations in nutritional cardiomyopathy of selenium-vitamin E deficient swine. I. Fiber lesions.
Cardiomyopathy was produced in 38 weanling swine by feeding a semisynthetic diet deficient in selenium and vitamin E for 13 to 59 days. Pigs were killed for morphologic studies of the cardiac lesions at sequential times after development of the deficiency disease. Gross examination disclosed hydropericardium and scattered pale streaks and patches of necrosis in the myocardium, especially the left ventricle. Histopathologically, the lesions were scattered throughout the heart but were most severe in the atria. Ultrastructurally, the damaged fibers had many features of myofibrillar degeneration with hypercontraction bands, myofibrillar lysis, and mitochondrial swelling, disruption, and mineralization. Numerous macrophages appeared to have passed through focal disruptions in the external laminae of the muscle cells and engulfed sarcoplasmic and nuclear debris. Stromal collapse and mild fibrosis persisted as residual lesions in scattered areas of myocardium in pigs with long term deficiency. Although vascular lesions were present in the hearts of selenium and vitamin E deficient pigs, it was concluded that the fiber alterations developed independently of the vascular changes. The pathogenesis of this cardiomyopathy induced by nutritional deficiency is thought to be related to lack of protection by the selenoenzyme, glutathione peroxidase, and the antioxidant, vitamin E, from lipoperoxidative damage.
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