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Biomedical subjects

W R Kelly

Publications and source records attributed to W R Kelly.

At least 37 records · Page 2Linked to original sources

Effects of the intravenous administration of Clostridium perfringens type D epsilon toxin on young goats and lambs.

Young goats (n = 18) and lambs (n = 10) were compared in respect of the effects of Clostridium perfringens type D epsilon toxin. Toxin produced neurological signs within 0.5-3 h of intravenous injection in (1) all of six kids given doses of 250, 185 or 120 mouse lethal doses 50% (MLD50)/kg body weight, (2) two of the three kids given 60 MLD50/kg, and (3) all of five lambs given 250 or 120 MLD50/kg. Six kids and three lambs given 45, 30 or 15 MLD50/kg, one lamb given 60 MLD50/kg, and three kids and one lamb given saline (controls) all remained clinically normal. Gross post-mortem changes were observed only in the kids and lambs that showed clinical signs. In the kids these changes consisted of severe acute interstitial and alveolar oedema of the lungs. However, only two out of five lambs that presented clinical signs showed pulmonary oedema. No histological changes were observed in the brain of any of the kids inoculated with epsilon toxin. In the brain of four out of the five lambs given doses of 120 or 250 MLD50/kg, there were histological lesions consisting of perivascular proteinaceous oedema and haemorrhages. These results show that kids and lambs are equally susceptible to the intravenous injection of epsilon toxin, but that they differ in the histological response of the central nervous system to the toxin.

Animals↗

Detection of Clostridium perfringens type D epsilon antitoxin in serum of goats by competitive and indirect ELISA.

Indirect and competitive ELISA techniques were developed and their ability to detect antibodies to Clostridium perfringens epsilon toxin in goat serum was compared. Different dilutions of a hyperimmune goat serum, in serum from a colostrum-deprived kid, were used as positive controls, while sera from eleven colostrum-deprived kids were used as negative controls. The epsilon toxin antibodies in the hyperimmune serum were also measured by mouse neutralisation test (MNT). The correlation coefficient between both the indirect ELISA technique and MNT was 0.99, while the same coefficient for the competitive ELISA was 0.98. Both the indirect and competitive ELISAs proved to be rapid, simple, sensitive and specific for detecting antibodies to C. perfringens epsilon toxin in serum of goats.

Animals↗

PCR detection of Clostridium perfringens producing different toxins in faeces of goats.

A polymerase chain reaction (PCR) was used to identify the genes encoding the major toxins of Clostridium perfringens in faeces of goats. When pure cultures of Cl. perfringens types A, B, C, D and E were used as templates in the PCR, amplicons were observed on the agarose gel as bands at approximately the 247 (alpha primers), 1025 (beta primers), 403 (epsilon primers) and 298 (iota primers) bp level of the DNA marker. When used to identify different types of Cl. perfringens in samples artificially spiked with these micro-organisms, the PCR detected as few as 1-1.5 x 10(2) cfu g-1 of the five types of Cl. perfringens tested. The PCR technique allowed the identification and typing of Cl. perfringens strains in faeces of goats, without recourse to other techniques such as the mouse neutralization test.

Animals↗

Form and function of lacunae in the ovary of the laying hen.

BACKGROUND: Spontaneous atresia of large, yolky, ovarian follicles occurs in the chicken and in other species when the stimulus for ovulation ceases. This means that as much as 40 ml of yolk must be resorbed by the ovary if normal ovarian morphology is to be regained. This study examines the process of yolk resorption in the ovarian stroma following bursting atresia. METHOD: Light, transmission, and scanning electron microscopy were used to study the morphology of lacuna spaces and their changes in ovaries of broiler and layer breeds of domestic chicken, both in actively laying birds and in birds undergoing spontaneous or induced follicular atresia. A comparative study was made of the ultrastructural differences between lacuna-lining cells, blood-vessel endothelium, and germinal epithelium of the ovary. RESULTS: Transformation of lacuna-lining cells and peritoneal cells into macrophages occurred after bursting atresia and exposure of these cells to released yolk. Complete atresia of large yolky follicles occurred very quickly. CONCLUSION: The resorption of this large volume of yolk, at least in part, seems to be mediated by the transformed lacuna-lining cells.

Animals↗

In vitro responses of avian monocytes to homologous yolk.

BACKGROUND: Large volumes of yolk are released into stromal lacunae of the avian ovary during bursting atresia. It is broken down by macrophages that accumulate in large numbers in the lacunae in the presence of free yolk. The macrophages may be derived from lacunae-lining cells or from blood monocytes. METHODS: Chicken blood monocytes were isolated from adult laying hens, cultured, and exposed to different concentrations of homologous yolk. Morphological changes were studies by light microscopy and transmission and scanning electron microscopy, and the rate of breakdown of yolk micelles was measured by turbidometry. Tritiated thymidine uptake was used to measure monocyte proliferation rate following exposure to yolk. RESULTS: Following exposure to yolk, the cells rapidly changed from fibroblastlike to macrophagelike cells. The turbidometric results indicated very significant clearing of yolk micelles by the cultured monocytes. These findings were supported by light and transmission and scanning electron microscopy, which showed these cells to be extremely active in engulfing yolk particles. CONCLUSIONS: This process in cultured monocytes is morphologically identical to that observed in previous studies in cells lining the lacunae of ovaries of hens, in which large yolky follicles are undergoing bursting atresia. Therefore, it should serve as a model for studying yolk resorption during this form of atresia.

Animals↗

Enterotoxaemia in goats.

Enterotoxaemia of sheep and goats occurs worldwide, but the condition in goats is poorly understood. The disease in goats is mostly caused by Clostridium perfringens type D, although the role of the toxins of this microorganism in the pathogenesis of the disease is not fully understood. The disease occurs in three forms, peracute, acute and chronic, the cardinal clinical sign of the acute and chronic forms being diarrhoea. The main biochemical alterations are hyperglycaemia and glycosuria, while at necropsy the disease is often characterized by haemorrhagic colitis. The typical histological changes observed in the brain of sheep with enterotoxaemia are not considered to be a common feature of enterotoxaemia in goats. Although the pathogenesis of caprine enterotoxaemia has not yet been properly defined, it is usually accepted that the presence of C. perfringens type D in the small bowel, together with a sudden change to a diet rich in carbohydrates, is the main predisposing factor for the disease. Vaccination seems to be poorly effective in preventing caprine enterotoxaemia, which might be due to the fact that the enteric form of the disease is partially independent of circulating C. perfringens toxin. More studies are needed on caprine enterotoxaemia, especially of its pathogenesis and immunity, in order to develop more efficient control measures for this disease.

Animals↗

Detection by polymerase chain reaction of Clostridium perfringens producing epsilon toxin in faeces and in gastrointestinal contents of goats.

A polymerase chain reaction (PCR) was used to identify the gene-encoding epsilon toxin production in Clostridium perfringens types B and D in faeces and in gastrointestinal contents of goats. The samples were cultured in thioglycollate broth and centrifuged. The upper layer of the pellet was used as a template for PCR, obviating the need for DNA extraction. This technique specifically differentiated Cl. perfringens types B and D from Cl. perfringens types A and C and from Escherichia coli. When used to identify Cl. perfringens type D in samples artificially spiked with the micro-organism, the PCR detected as few as 1.4 x 10(2) cfu g-1 of sample. Gastrointestinal contents and faeces were collected from 20 goats at slaughter and processed by PCR. Several positive results were obtained from the first five goats that were slaughtered and sampled a few days after their arrival at the abattoir, but only a few samples gave positive results during the following weeks, after the goats had been fed a concentrated ration containing monensin. A possible role of this drug in control of enterotoxaemia is suggested.

Animals↗

Pyrrolizidine alkaloidosis in a two month old foal.

A foal, small and jaundiced from birth, succumbed after two months to chronic hepatic damage which was characterised by fibrosis, biliary ductular hyperplasia and the presence of pleomorphic hepatocytes containing either a single large nucleus or multiple nuclei. The fixed liver contained sulfur-bound pyrroles, which are derived from pyrrolizidine alkaloids. During pregnancy the pasture was heavily infested with the pyrrolizidine alkaloid-containing plant, Senecio madagascariensis. The hepatic disease affecting the foal appears to have been initiated by consumption of the alkaloids by the mare during gestation, and to represent a rare case of congenital pyrrolizidine alkaloidosis.

Animals↗

Epizootic mortality of free-living green turtles, Chelonia mydas, due to coccidiosis.

At least 70 wild green sea turtles, Chelonia mydas, died in the Moreton Bay area of southeast Queensland, Australia over 6 wk in spring 1991. Based on the necropsy of 24 turtles, there was a severe enteritis or encephalitis associated with Caryospora cheloniae, a coccidial pathogen previously recorded only in farm-reared Ch. mydas hatchlings. Infection was characterized by the presence of coccidia in extra-intestinal lesions. Oocysts were observed to sporulate, after which sporozoites escaped into seawater to form a novel stellate configuration. We conclude that C. cheloniae is pathogenic for life stages other than hatchling Ch. mydas and that naturally-occurring coccidiosis is a significant disease of free-living Ch. mydas.

Animals↗

Equine neural angiostrongylosis.

Verminous encephalomyelitis due to Angiostrongylus cantonensis larvae was diagnosed in 2 foals at necropsy. The principal clinical feature was tetraparesis, although history and neurological examination revealed progressive and multifocal neurological disease. At presentation, a tentative diagnosis of parasitic larval migration involving the central nervous system (CNS), presumably due to Strongylus vulgaris, was proposed. Dissection of the spinal cord in one case resulted in recovery of intact larvae of both sexes of A. cantonensis. In both foals, histopathology of the brain and spinal cord revealed nematode sections which were consistent with A. cantonensis larvae.

Angiostrongylus↗

Histopathology of melanocytic lesions in goats and establishment of a melanoma cell line: a potential model for human melanoma.

Melanocytic cells from white Angora goats were studied in vivo and in vitro. The histopathology of pigmented areas of skin from the most common sites of melanoma (solar-exposed areas of the ear, face, and perineum) resembled that of the epidermal melanocytes in Hutchinson's melanotic freckle in humans. Seven melanoma biopsies from 6 Angora goats showed histopathological features in common with human melanoma. A melanoma cell line, GM-1, was established in culture from a lymph node metastasis obtained from an animal that had a primary tumor excised and later developed extensive metastatic disease. GM-1 cells were mainly diploid, amelanotic, proliferated rapidly, spontaneously formed vacuolated cells, and were tumorigenic in nude mice. The species of origin of the GM-1 line was confirmed by isozyme profiles. GM-1 cultured cells and the original biopsy both expressed S-100 protein and tyrosinase antigen. Using GM-1 cells as the immunogen, a monoclonal antibody (MoAb 1F1) was derived that reacted strongly with a 116 kDa antigen in 50% of the GM-1 cells, but had little activity with goat fibroblasts (GM-F) or with human melanoma cells. GM-F, on the other hand, yielded more intense staining than GM-1 with an intermediate filament antibody (IFA), reacting with a 58 kDa antigen in both cell lines. The sensitivity of GM-1 to anticancer agents was similar to that of human melanoma cells. The pathology of caprine melanoma and its association with sun-exposed sites in relatively young animals suggest that it may be a suitable model for studying induction of melanoma by natural sunlight.

Animals↗

Hepatotoxicity to dogs of horse meat contaminated with indospicine.

An outbreak of liver disease which killed more than 30 dogs at Alice Springs was associated with feeding meat from horses, some of which had developed Indigofera linnaei poisoning (Birdsville horse disease). Affected livers were small, nodular and yellow. There was associated jaundice, ascites, elevation of alanine aminotransferase levels in serum, a tendency to bleed, and signs of hepatic encephalopathy. Histologically, livers showed periacinar necrosis, collapse and haemorrhage, with severe swelling, vacuolation and cholestasis in remaining hepatocytes. Indospicine, a toxic amino acid found in the genus Indigofera, was detected in samples of suspect horsemeat. Experimental feeding of horsemeat containing 16 mg indospicine/kg for 32 days produced periacinar necrosis and hepatocellular swelling in 2 dogs, although neither died nor showed clinical illness. In another experiment, intakes of as little as 0.13 mg indospicine/kg bodyweight/day for 70 days produced periacinar liver lesions, and indospicine concentrations in serum, muscle and liver rose during this period to 3.9, 7.9 and 17.5 mg/kg, respectively. It was concluded that meat from horses grazing I. linnaei can be hepatotoxic for dogs, and that this toxicity may be related to its indospicine content.

Amino Acids↗