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Biomedical subjects

D G Butler

Publications and source records attributed to D G Butler.

18 recordsLinked to original sources
PubMed1992

Clinical signs, treatment, and postmortem lesions in dairy goats with enterotoxemia: 13 cases (1979-1982).

Enterotoxemia attributable to Clostridium perfringens type D in goats is difficult to diagnose because of a lack of specific clinical signs or postmortem lesions, on which to base the diagnosis. This report describes the clinical signs, postmortem lesions, and clinical responses to treatment and vaccination in 4 goat herds, in which a diagnosis of enterotoxemia was confirmed. Four clinical cases had the diagnosis confirmed on the basis of signs of diarrhea or sudden death and the isolation of C perfringens and epsilon toxin from the feces at the time of admission. The 10 necropsy cases were diagnosed on the basis of the isolation of C perfringens (not typed) or epsilon toxin from the intestinal contents of goats that died with clinical signs compatible with enterotoxemia and without lesions associated with a second serious disease. Enterocolitis was the most consistent lesion reported at necropsy in the 10 goats with enterotoxemia. Ovine enterotoxemia vaccines were of limited value in preventing enterotoxemia. These observations imply that naturally induced enterotoxemia in goats involves a different pathophysiologic mechanism than that associated with enterotoxemia in sheep.

Animals↗
PubMed1992

Experimental infection of severe combined immunodeficient beige mice with Mycobacterium paratuberculosis of bovine origin.

Severe combined immunodeficient beige mice were inoculated orally and intraperitoneally with a bovine strain of Mycobacterium paratuberculosis to explore their potential as laboratory animal models in the study of paratuberculosis (Johne's disease). Control animals were similarly inoculated with heat-killed M. paratuberculosis. In the mice inoculated intraperitoneally, focal lesions and acid-fast bacilli were first detected in the livers (4 weeks postinfection) and later in the spleens and intestines of the test but not the control animals. No bacteria were seen in the hearts, kidneys, or lungs. At 12 weeks postinfection, all test mice had significant losses in body weight compared with those in controls (P less than 0.05), a characteristic sign of bovine paratuberculosis. Tumor necrosis factor alpha was not detected in the serum. Histologic lesions were seen in the intestines, livers, and spleens of the animals in the orally inoculated test group after 26 weeks of infection. Our results suggest that the severe combined immunodeficient beige mouse may be a useful model for the investigation of paratuberculosis and cachexia and the evaluation of antimycobacterial drugs.

Animals↗
PubMed1979

Determinants of diarrhea in viral enteritis. The role of ion transport and epithelial changes in the ileum in transmissible gastroenteritis in piglets.

To understand mechanisms of viral diarrhea further, we studied ileal ion transport in vitro in relation to mucosal changes and epithelial differentiation in transmissible gastroenteritis in piglets, an invasive viral enteritis thought to involve mainly proximal intestine. In infected pigs, at the height of diarrhea, short-circuited ileal epithelium failed actively to transport Na+ and Cl-, and there was a defect of glucose-mediated Na+ transport. The Cl- secretory response to theophylline remained intact. Conductance measurements indicate that paracellular permeability may be reduced and transcellular transport may be altered. A mucosal lesion was observed at the time of the transport changes, characterized by villus blunting, crypt hyperplasia, and immature crypt-type enterocytes on the villus epithelium, deficient in disaccharidase and (Na+, K+)ATPase activity but rich in thymidine kinase. Consideration of the major determinants of diarrhea in this invasive enteritis must take into account not only altered mucosal function and differentiation but also the extent of intestinal involvement, including the ileum, a major site of fluid absorption in the intestine.

Animals↗
PubMed1978

Chronic enteritis associated with the malabsorption and protein-losing enteropathy in the horse.

Chronic granulomatous enteritis associated with weight loss and hypoproteinemia was identified in 2 horses. Both horses continued to have normally formed feces. Malabsorption of carbohydrate and lipid, with concomitant gastrointestinal protein loss was demonstrated in 1 case. One horse was treated symptomatically and gained 108 kg. In both cases, principal gastrointestinal lesions were partial to total villus atrophy and transmural mononuclear leukocytosis, with lymphocytes and histiocytes predominating. The cause of the condition was not identified in either case.

Animals↗
PubMed1977

Human rotavirus enteritis induced in conventional piglets. Intestinal structure and transport.

To better understand the pathogenesis of infantile viral gastroenteritis, we studied Na+ and Cl- fluxes in vitro in short-circuited jejunal epithelium from 8-10-day-old piglets after infection with a standard dose of human rotavirus given via nasogastric tube. 11 infected piglets, all of whom became ill, were compared with 9 uninfected, healthy litter-mates. When killed 72 h after infection, intestinal villi were shorter and crypts deeper (P less than 0.025) in duodenum, upper jejunum, and mid-small intestine, but not ileum in infected piglets. Virus antigen was seen by fluorescence microscopy in occasional jejunal villus tip cells in only four infected piglets and no controls at 72 h. Net Na+ and Cl- fluxes did not differ from noninfected litter-mate controls under basal conditions, but response to glucose was blunted in infected piglets (P less than 0.001). Theophylline stimulated net Cl- secretion in both infected and control animals, and cyclic AMP concentration in isolated jejunal villus enterocytes did not differ significantly. In isolated jejunal villus enterocytes of infected piglets, thymidine kinase activity increased (P less than 0.001), and sucrase activity decreased (P less than 0.001). We conclude that in this invasive enteritis caused by a major human viral pathogen, glucose-coupled Na+ transport is impaired in the jejunum at a time when the villus epithelium shows enzyme characteristics of crypt epithelium, and when little or no virus is present. These findings are identical to those occurring in an invasive coronavirus enteritis of piglets but differ markedly from those seen with enterotoxigenic diarrhea.

Animals↗
PubMed1977

Transmissible gastroenteritis: sodium transport and the intestinal epithelium during the course of viral enteritis.

Sodium transport, mucosal structure, and epithelial enzymes were studied in piglets killed 10, 25, 40, 72, or 144 hr after infection with a standard dose of transmissible gastroenteritis virus. Glucose-stimulated Na transport measured in short-circuited jejunal epithelium and suspensions of villous enterocytes became progressively more abnormal during the first 40 hr, but recovered completely by 144 hr. As Na transport deteriorated, jejunal mucosal villi shortened and crypts deepened; cells isolated from the villi became more crypt-like in their enzyme profile, with high levels of thymidine kinase and low levels of sucrase activity 40 hr after infection. At 40 hr, when diarrhea is severe, little if any virus has been found in the epithelium. Our data suggest that the relatively undifferentiated crypt type enterocytes on the villi constitute an important determinant of altered Na transport and diarrhea in this invasive viral enteritis.

Animals↗
PubMed1976

Viral gastroenteritis: recent progress, remaining problems.

Infants and young children are particularly susceptible to a recently identified viral enteritis which is highly contagious and seems both common and universal. In this disease, virus invades the upper intestinal epithelium, causing acute diarrhoea with early fever and vomiting. We studied a similar disease in pigs, infecting three-week-old animals with transmissible gastroenteritis virus (TGE), which also invades the upper intestinal epithelium. In this model, diarrhoea is massive 16-40 hours after infection, when stools contain increased electrolytes but no excess of sugar. In the jejunum of intact pigs at the 40-hour stage we found altered Na+ and water flux, decreased mucosal activities of disaccharidases and Na+, K+-ATPase, but normal adenylate cyclase activity. At the same stage the response of Na+ flux to glucose was blunted in jejunal epithelium studied in Ussing short-circuit chambers and in suspensions of villous cells; Cl- flux responded normally to theophylline, and thymidine kinase and sucrase activities of cells isolated from jejunal villi were similar to those found in crypt cells. Probably by 40 hours after infection most virus has been shed from the mucosa. Viral diarrhoea clearly differs from enterotoxigenic diarrhoea. Consideration of its pathogenesis must take into account the dynamic nature of the mucosal epithelium and the factors governing differentiation of enterocytes as they migrate from crypt to villus. Sufficient information is available now to characterize one specific and apparently prevalent viral enteritis in man and to identify additional viral enteritides. There is hope that preventative therapy can be developed. Our understanding of the mechanisms of viral diarrhoea is limited, but the availability of an animal model and the promise of others makes us optimistic that these deficiencies can be remedied. Greater understanding of the pathogenesis of viral diarrhoea should better the active therapy of affected infants and children.

Animals↗
PubMed1976

The andrenocortical homolog in the lake sturgeon, acipenser fulvescens rafinesque.

The adrenocortical homolog in the chondrostean fish, Acipenser fulvescens, is confined within yellow corpuscles located at the dorsal junction of the two kidneys near the cardinal veins. The concentration and distribution of this tissue in chondrosteans appear to be a condition intermediate between that of cyclostomes and teleosts. The homology of this tissue to adrenocortical tissue of higher vertebrates is demonstrated in its delta5-3beta-hydroxysteroid dehydrogenase activity and the ultrastructure of the cells. The cells contain large lipid droplets and an abundance of smooth endoplasmic reticulum and mitochondria. The abundance of smooth endoplasmic reticulum, a large Golgi apparatus and an extensive elaboration of the plasma membrane suggest the high degree of steroidogenic activity of these cells. Apposed plasma membranes make contacts through the unique cell contacts described in the adrenocortical cells of mammals (Friend and Gilula, '72). The Golgi apparatus is described as a most conspicuous component of the cytoplasm and is presented as further evidence for the important involvement of this organelle in corticosteroidogenesis in vertebrates. These morphological observations are discussed in relation to the known secretory products of this tissue in the sturgeon, and it is suggested that there is a need for further examination of the corticosteroids produced by lower vertebrates.

Adrenal Glands↗
PubMed1976

Transmissible gastroenteritis. Mucosal ion transport in acute viral enteritis.

Ion transport in the jejunal mucosa of 14-to 16-day-old piglets with severe diarrhea 40 hr after infection with transmissible gastroenteritis (TGE) virus was studied. In infected pigs Na+ transport failed to respond normally to glucose when studied either in Ussing short-circuited chambers or in suspensions of enterocytes isolated selectively from jejunal villi. Theophylline, 10mM, added to the chambers produced the same brisk electrical responses and increments in net Cl- secretion in tissue from both infected and control groups. A defect in glucose-stimulated Na+ absorption in the acute stage of a viral enteritis has been identified which probably contributes to the impaired lumen-to-extracellular fluid flux of Na+ found previously in the jejunum of intact TGE-infected pigs. The mechanisms causing diarrhea in this invasive viral enteritis differ from those causing toxigenic diarrhea.

Acute Disease↗