The structure of the sternal bursa of turkeys.

The sternal bursa developed as a microscopically recognizable synovial sac in turkeys at about 4 1/2 to 6 weeks of age. In birds 12 weeks old it was difficult to delineate the bursa grossly although microscopically it was a definite structure. After 12 weeks, the walls of the bursa were thick enough that the limits of the sac could be determined grossly. The synovial membrane was in the subcutis, and microscopically was a vascular band of loose to dense connective tissue of variable thickness. Laterally the membrane was folded so that in cross section it appeared as a tonguelike projection of variable length into the cavity. The lining cells centrally were flat fibroblasts while laterally they were cuboidal, particularly over the lateral folds. In older turkeys the cuboidal lining cells were sometimes stratified.

Tissue changes in enlarged sternal bursas of turkeys.

Enlarged sternal bursas evident in turkeys beyond 12 weeks of age were examined grossly and microscopically in 169 turkeys 3 to 26 weeks old. Grossly, the enlarged sternal bursas were sacs of varied size and wall thickness containing fluid in amounts from a fraction of a milliliter up to 70 ml. The fluid was usually the consistency of serum but was sometimes viscid, and in infected bursas it would be purulent. Its color varied from amber to red to dark brown depending on the amounts of and the changes in the blood pigments. The synovial membranes were smooth and glistening and of variable thicknesses. Strands or cords of the synovial membrane of variable thickness and number extended from side to side of the sac. Microscopically, the synovial membrane was focally thickened in the small bursas and generally thickened in the larger bursas. The thickening was the result of an increase in the very cellular fibrous tissue and in the number and size of blood vessels. The lining cells were flat fibrocytes one cell thick in the smaller bursas, and round stratified cells in the larger bursas. In infected bursas, mononuclear and heterophilic infiltration occurred. Hemorrhaging occurred quite often, the result of trauma to the highly vascular synovial membrane.

Clinical signs and bone changes associated with phosphorus deficiency in beef cattle.

For 10 years, 42 female Herefords (as they progressed from weanling calves to aged cows) were fed diets individually, with phosphorus (P) content being the only variable. During growth and the first 3 gestations, clinically evident differences were not associated with 2 dietary treatments (approx 12 and 38 g of P/day). During the next 2 gestations (2 years), half the cows from each original treatment group were fed less than 6 g of P (n = 21 cows, 11 from the group fed 12 g of P/day and 10 from the group fed 38 g of P/day) daily. The other half were fed diets supplying approximately 8 g of P (n = 11 cows fed 12 g of P/day) and 35 g of P (n = 10 cows fed 38 g of P/day) daily. During the last 3 years of the experiment, all remaining cows were fed diets containing 12 g (n = 19 cows originally fed 12 g) or 19 g (n = 17 cows originally fed 38 g) of P/day. Cows fed diets containing less than 6 g of P/day developed an insidious and subtle complex syndrome characterized by weight loss, rough hair coat, abnormal stance, and lameness. Spontaneous fractures occurred in the vertebrae, pelvis, and ribs. In severely affected cows, fractures did not heal properly. Some bones were demineralized markedly, and the cortical surfaces were porous, chalky white, soft, and fragile. Osteoid tissue was not properly mineralized. Radiography revealed diminished bone density (osteoporosis), cortical thinning, and resorption of trabeculae. Time-related availability of dietary P initiated excessive turnover of bone, with resultant structural changes and impaired function.(ABSTRACT TRUNCATED AT 250 WORDS)

Hereditary multiple exostoses: clinicopathologic features of a comparative study in horses and man.

Investigation of hereditary multiple exostoses in horses under controlled research conditions for 10 years and epidemiologic studies that have spanned up to five generations of human families contain notable similarities. The present study demonstrated that a single dominant autosomal gene is responsible for hereditary multiple exostoses in horses and man. Affected individuals transmit this trait to approximately 50% of their progeny, whereas nonaffected individuals do not transmit the condition to their offspring. The tumors in affected horses are most often present at birth. They tend to be bilaterally symmetrical and vary in size, shape, and texture. Those on the legs generally do not appear to enlarge as the animal matures, but others, notably those on the ribs and scapulae, enlarge until skeletal maturity, Histologically, the tumors appear as typical ostosteochondromas in both horse and man. Sarcomatous transformations have not yet been detected after 10 years in horses, although such changes are occasionally reported in the similar disease condition in man. The remarkable similarities of hereditary multiple exostoses in the horse to that in man provide an opportunity for comparative biomedical study.

Relationship of cheek tooth abrasion to fluoride-induced permanent incisor lesions in livestock.

Teeth from cattle, sheep, and horses that ingested various fluoride intakes and teeth from field studies of these species plus deer, elk, and bison were examined for abnormalities. Approximately 99,000 animals in 322 herds were examined for fluorosis. From field studies, 988 cattle of various ages and with different degrees of dental fluorosis were slaughtered and necropsied. The severity of fluoride-induced mottling, hypoplasia, and abnormal abrasion of paired permanent incisor teeth was correlated with abrasion of premolar and molar (cheek) teeth that form and mineralize at approximately the same age. Severe irregular wear of cheek teeth impaired mastication and resulted in poor utilization of feed and unthriftiness. Excessive amounts of fluoride during tooth formation and mineralization induce characteristic dental changes. Offspring from the fluoride-affected animals did not have discernible fluoride-induced lesions in the deciduous teeth.

Dietary phosphorus for beef cows.

Hereford heifers (48 initially) were individually fed variable amounts of dietary phosphorus (P) from weaning through their 8th gestation. During phase I, 2 groups (24 cows each) were given 20.6 to 38.1 g of P/day and 6.0 to 12.1 g of P/day (increasing as animals grew). During phase II (the 4th gestation), half of the animals from each group were maintained with the same respective diets, and the other half were given 5.1 to 6.6 g of P/day. Within 6 months, animals given 5.1 to 6.6 g of P/day gradually developed signs of P deficiency. Clinical signs of deficiency and lesions included general unthriftiness, body weight loss, reduced feed consumption, reluctance to move, abnormal stance, spontaneous bone fractures, and finally, impaired reproductive performance. Cows given 7.8 to 8.9 g of P/day in diet 2 during phase II did not develop discernible clinical signs of P deficiency. Cows that were given 5.1 to 6.6 g of P/day apparently regained their health and reproductive capability when fed 11.7 to 12.6 or 17.1 to 20.5 g of P/day. The data indicate that bones serve as an effective storage source of P and support and buffer body needs until there is serious depletion of skeletal P. These results indicate that common recommendations for dietary P, such as those outlined by the National Research Council (17.5 g of P/day over the entire year for cows weighing 450 kg), exceed the basic requirements for beef cattle; 12 g of P/day is adequate for 450-kg beef cows.

Clinical effects of low dietary phosphorus concentrations in feed given to lactating dairy cows.

Thirty-four Holstein cows, pregnant with their second calf, were individually fed diets containing 3 concentrations of phosphorus (P): 24 cows for 12 months and 10 cows for 7.5 months of lactation. Cows were randomly allotted to the specific dietary groups 2 months before expected parturition. The 3 dietary concentrations of P were 0.24%, 0.32%, and 0.42% in diet. Cows given 0.24% P in diets produced significantly less milk than did cows in the other groups. Other clinical signs of P deficiency in the cows fed the diet with 0.24% P included loss of body weight, decreased feed consumption, and lower inorganic serum P concentration 2 to 10 weeks after parturition. There were no significant differences in the variables measured between cows given dietary P concentrations of 0.32% and 0.42%. There was no evidence of hemoglobinuria after parturition. Reproductive performance did not differ significantly, although the trend was in favor of the cows fed the diet with 0.24% P.

Effects of diets containing sodium fluoride on mink.

Mink (Mustela vison) kits still nursing, and adult male mink were fed diets containing various levels of fluorine (as NaF) to determine the effects on health, growth and pelt quality. Different groups were fed diets containing 25.5 (control), 46.0, 111.5 or 287.0 ppm fluorine (on a wet basis) for 7-8 mo. Gross, radiographic and microscopic changes were seen in bones from some animals ingesting the higher levels of fluorine. Chemical analyses for fluorine generally reflected levels ingested. Fluorine caused no detectable differences in pelt quality. After data were evaluated, tolerance levels in the feed of not more than 50 ppm fluorine for breeding stock and 100 ppm fluorine for animals being raised only for pelts are recommended.

Fluoride toxicosis in wild ungulates.

To compare the occurrence of chronic fluoride toxicosis in wild and domestic animals in selected areas of Utah, Idaho, Montana, and Wyoming, deer, elk, and bison bones and teeth were collected for evaluation. Vegetation and drinking water samples also were collected, so that potential sources of fluoride could be evaluated. Deer, elk, and bison were found to be susceptible to the adverse effects of ingestion of excessive amounts of fluoride. Teeth and bones were primarily affected with characteristic lesions. Pathognomonic soft tissue changes were not observed. The animals had been exposed to a variety of sources of excessive fluoride, including water high in fluoride, forages contaminated by industrial effluents that were high in fluoride, vegetation contaminated with high fluoride-content soil by rain splash or wind, or a combination of these sources. Waters high in fluoride, especially from geothermal springs and wells, often contained appreciable amounts of various soluble salts. Evidence accumulated from specimens collected throughout the aforementioned states indicated that there are areas where chronic fluoride toxicosis is a problem for wildlife. These areas were where natural sources of fluorine (especially geothermal waters) provided amounts for ingestion that exceed species tolerance limits or were near certain industrial operations.

Hereditary multiple exostosis. A comparative genetic evaluation in man and horses.

Comparative studies are being conducted on hereditary multiple exostosis in man and the horse. In both, there is an unquestionable inheritance pattern of a typical single, dominant, autosomal gene. Those who carry the gene have a one-half chance of transmitting it to each offspring, whereas, those who do not carry the gene do not transmit this abnormality to their progeny. The lesions are clinically and histologically similar; no persistent chromosomal irregularities have been associated with the abnormality in either man or the horse and no single evidence of malignancy in either man or animal has been detected in this study to date.

Hereditary multiple exostosis. A comparative human-equine-epidemiologic study.

Hereditary multiple exostosis (HME), a bone tumor first described by Virchow, has been studied over a period of 15 years on a comparative basis. The horse, an excellent biomedical model for this physically deforming multiple bone tumor in man, has been utilized in this study. The etiology, hereditary pattern, potential for malignancy and other aspects of this strange affliction need additional clarification. This in-depth study of 261 individuals from 144 families was compared with that of 55 horses bearing the HME trait, selectively bred and studied over the same period. Important information has been collected and evaluated about this condition that is suspect of being frequently missed diagnostically, with a higher incidence in humans that recognized. Continuing development studies of offspring of the original study participants; sarcomatous transformation monitoring; and recently developed genetic techniques should add to our understanding of this puzzling hereditary condition.