Biomedical subjects
Publications and source records attributed to S M Dennis.
What should you do if you observe a defective calf in a herd? Our suggestion is to seek qualified help to examine and diagnose the condition. Parentage should be verified by blood typing. But, most important, you can keep cattle genetically clean by having your clients report all defects in calves to their breed association and artificial insemination centers.
A variety of structural and functional congenital defects affecting the central nervous system of cattle have been identified. This article discusses specific defects of the central nervous system. Spastic and paralytic, metabolic, and storage diseases are reviewed.
Almost all types of congenital duplication described in humans have been observed in food animals, and a number are illustrated in this article. Congenital duplications, especially conjoined symmetric twins, are relatively common defects in cattle. The incidence is less in sheep and in hogs, and they appear to be rare in goats. In cattle, cranial duplication is predominant; this is in contrast to caudal duplication in sheep and hogs. These differences among species are interesting and may explain why congenital duplications appear more frequently in cattle than in other domestic animals. Based on the number of eyes and ears, classification criteria for cranial duplications are proposed. The cause of congenital duplications is not known.
With increasing incrimination of viruses, plants, and drugs as causes of ovine congenital defects, concerted efforts are required to identify environmental teratogens. Expanding knowledge of congenital defects requires studying as many defective lambs as possible; recording and documenting; detailed diagnostic examinations; genetic analyses and chromosomal examinations, whenever possible; and field investigations. Adopting standardized classification, terminology, and diagnostic procedures should improve descriptions, diagnoses, and interdisciplinary exchange of information. That, in turn, should improve our knowledge of and diagnosis of congenital defects of sheep in the future. Finally, veterinary clinicians and diagnosticians are encouraged to take an interest in congenital defects and teratology.
Congenital brain defects in cattle are usually obvious at birth, but detection may depend on the nature and extent of the defect. The cause may be genetic or environmental, or the cause may be unknown. Many central nervous system defects are inherited as a simple autosomal recessive trait and may have a significant economic impact on purebred and commercial cattle operations. A common structural defect of genetic nature is internal hydrocephalus. A functional defect of simple autosomal recessive inheritance is bovine progressive degenerative myeloencephalopathy. The most significant teratogenic agents causing central nervous system defects are prenatal viral infections such as bovine virus diarrhea and bluetongue viruses. Many other defects of the central nervous system are reviewed.
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Brachygnathia superior and generalized diarthrodial degenerative joint disease were seen in 17 related, purebred Angus calves ranging in age from 2 days to 4 months. Craniometrical studies revealed decreased maxillary and palatine bone lengths and increased cranial, skull, and facial indices. Radiological evaluation of major appendicular joints demonstrated lipping of the joint margins with osteophyte formation, sclerosis of subchondral bone, and narrowing of joint spaces. Synovial fluid evaluation indicated joint degeneration but no etiologic agent. Rheumatoid factor analysis of plasma was negative. Grossly, all major appendicular joints were defective including the atlanto-occipital articulation. Lesions ranged from loss of surface luster to erosions and deep ulcers with eburnation of the subchondral bone and secondary proliferative synovitis. Histological changes were degeneration of the articular cartilage matrix, chondrocyte necrosis, flaking and fibrillation, chondrone formation, erosions and ulcers of the articular cartilage with subchondral bone sclerosis, vascular invasion with fibrosis, and chronic, nonsuppurative, proliferative synovitis. Growth plates had defective chondrocyte proliferation and hypertrophy with aberrant ossification of calcified cartilaginous matrix. Histochemical analysis of cartilage and bone failed to incriminate which component was defective, glycosaminoglycan or collagen, but indicated different distribution or absence of one or the other. Genealogic studies revealed a genetic basis for the new defect.
In a 14-year study of calves with cardiac defects, 36 had 78 congenital cardiac defects: ectopia cordia cervicalis (n = 10 defects), common aortic trunk (n = 3 defects), dextraposed aorta (n = 8 defects), duplicated major trunks (n = 1 defect), hypoplastic aorta (n = 2 defects), interventricular septal defect (n = 11), interatrial septal defect (n = 2), left ventricular hypoplasia (n = 10), patent ductus arteriosus (n = 5), patent foramen ovale (n = 5), right ventricular hypoplasia (n = 10), cor triloculare biatriatum (n = 1), endocardial fibroelastosis with calcification (n = 3), and valvular hematomas (n = 7). All septal defects were high in location and ranged from 5 to 35 mm in diameter. One calf with a septal defect also had bilateral microphthalmia.
The effects of lasalocid, monensin and thiopeptin on the total number and the generic composition of rumen protozoa were determined in vivo and in vitro. Feeding lasalocid or monensin to cattle on either high grain or high roughage diets reduced total protozoal counts. Addition of lasalocid or monensin (6 to 48 micrograms ml-1) to the in vitro rumen fermentation resulted in marked reduction in protozoal numbers. The inhibition was dose dependent. Thiopeptin had no effect on rumen protozoa either in vivo or in vitro. Among the protozoal types, holotrichs (Dasytricha, Isotricha and Charonina) were unaffected by either lasalocid or monensin. Among the entodiniomorphs, Entodinium, Diplodinium and Ophryoscolex were more sensitive than the other types. Ophryoscolex purkynei was more sensitive to monensin than to lasalocid. Protozoal inhibition by lasalocid and monensin was transient because prolonged antibiotic feeding resulted in the selection of a resistant population in the rumen of cattle.
Sequential pathological changes were studied for 9 days after inoculating Actinobacillus seminis in the mammary gland of sheep. The inoculated mammary glands became enlarged (2 to 4 times normal), turgid or consolidated and contained creamy or greenish-yellow viscid contents. A seminis was isolated from all inoculated udders at necropsy. Microscopically, the reaction in the udder to A. seminis may be divided into 4 overlapping phases; acute purulent, subacute purulent, necrotising, and proliferative. It was concluded that A. seminis was pathogenic for the ovine mammary gland, the clinical and pathological findings were nonspecific, and that A. seminis could survive within ovine mammary tissue for at least 9 days after inoculation.
Lesions induced by inoculation of Brucella ovis into the epididymis were compared in rams previously vaccinated with B. ovis bacterin and unvaccinated rams. Inoculation of killed B. ovis did not produce significant lesions in either group whereas prior vaccination exacerbated epididymal lesions following inoculation of live B. ovis. Increased numbers of neutrophils, macrophages and lymphocytes were present in the interstitium and neutrophilic infiltration of the epididymal duct epithelium and intraepithelial cyst formation was more prominent. The inflammatory response surrounding extravasated spermatozoa was more severe in vaccinated rams but it was not determined if the response was directed at spermatozoa or intermixed brucellae, or both.
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A solid-phase, indirect, enzyme-linked immunosorbent assay (ELISA) was compared with the microtitre complement fixation test for detecting Brucella ovis antibodies in 220 ram sera. The ELISA was more sensitive than the complement fixation test; it demonstrated antibodies in 11 sera from known infected or vaccinated rams that were complement fixation test negative. No false positives were recorded with the ELISA and, in 36 sera positive to both tests, the ELISA titres were consistently higher than the corresponding complement fixation test titres.
Cultures of Streptococcus bovis and mixed populations of rumen bacteria were used to investigate the concentration of ATP and rumen bacterial numbers at various stages of growth. ATP, extracted with Tris buffer, was analyzed using the firefly luciferin-luciferase bioluminescent reaction. ATP concentrations of S. bovis and mixed cultures of rumen bacteria significantly correlated with live cell counts during the log phase of growth but not during the stationary phase. The average cellular ATP concentration of rumen bacteria was calculated to be 0.3 fg of ATP per cell. Studies done with in vivo artificial rumen apparatus revealed that the protozoal contribution to rumen fluid ATP pool size was much more substantial than was the bacterial contribution. The rumen fluid ATP concentration was greater in cattle with protozoa than in those that were defaunated. Differences in ATP concentration due to size differences of ciliate protozoa were observed. Due to the unbalanced distribution of ATP in rumen microbes, ATP appears to be an unsuitable indicator of rumen microbial biomass.
Two rumen-fistulated Holstein heifers were fed three protein-free semipurified diets: 70% roughage, 30% concentrate; 50% roughage, 50% concentrate; and 30% roughage, 70% concentrate. Wheat straw was the roughage, and the concentrate was a pelleted mixture of corn starch, dextrose, fat, urea, vitamins, and minerals. Each animal received the three dietary treatments in a randomized complete block design. On days 1, 3, and 5 following a 21-day adaptation, rumen fluid samples were taken before feeding and at 1, 2, 3, 4, and 5 h after feeding. Total protozoa concentrations for low, medium, and high concentrate diets were 1.5, 2.5, 4.1 X 10(5)/ml. Dasytricha concentrations were not affected by diet, but Entodinium, Diplodinium, Isotricha, Epidinium, and Ophryoscolex increased with increases of the concentrate proportion of the diets. Entodinium, the predominant protozoa with all diets, increased as concentrate proportion of the diet increased. In a second experiment the two heifers from Experiment 1 were fed semipurified diets that contained either urea or soybean meal as the nitrogen source. There were larger populations of Dasytricha and Isotricha when the diet contained soybean meal, and larger populations of Charon, Entodinium, and total protozoa when the diet contained urea. In both experiments, holotrichs were highest 1 to 2 h after feeding, and entodiniomorphs were highest before feeding and 4 to 6 h after feeding. An active protozoan population can exist in the rumen of cattle fed diets virtually devoid of natural protein, and protozoa are influenced by energy and nitrogen source.
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A total of 252 rodents were trapped in the environs of Ahmadu Bello University, Zaria, over a two-year period, of which 221 were brown field rats (Arvicanthus niloticus). Only these were found positive (4.5%). Titers were detected against Leptospira interrogans, serovars australis, icterohaemorrhagiae, tarassovi and hardjo. All positive sera except one reacted against a single serovar. Eight isolates were obtained from field rats: five were serovar australis, one ballum and two unidentified. Five isolates were recovered from 74 bovine kidneys examined: one was serovar pyrogenes and four unidentified. One unidentified isolate failed to react with any of the 16 screening leptospira antisera and another was tentatively considered to be serovar ballum. Two isolates, one ballum and one unidentified, were recovered from the Kubani stream waters. No leptospira was isolated from piggery sewage effluents collected at Kano and Kaduna. It is suggested that serovar ballum be included in any screening battery for leptospirosis in man and animals in Nigeria.