Gastric dilatation and enterotoxemia in ten captive felids.

CASE DESCRIPTION 10 large felids at 8 facilities were determined or suspected to have developed gastric dilatation with or without enterotoxemia over a 20-year period. Four felids were found dead with no premonitory signs. CLINICAL FINDINGS 4 felids (2 male snow leopards [Uncia uncia], 1 male Amur tiger [Panthera tigris altaica], and 1 male Sumatran tiger [Panthera tigris sumatrae]) were found dead or died before they could be evaluated. Six felids had hematemesis (1 male and 1 female African lion [Panthera leo] and 1 male jaguar [Panthera onca]) or abdominal distention and signs of lethargy with or without vomiting (1 male African lion, 1 male Malayan tiger [Panthera tigris jacksoni], and 1 female Sumatran tiger). Gastric dilatation was radiographically and surgically confirmed in the male Malayan and female Sumatran tigers and the jaguar. TREATMENT AND OUTCOME In 3 felids with an antemortem diagnosis, the gastric dilatation resolved with decompressive laparotomy but then recurred in 1 felid, which subsequently died. Three others died at various points during hospitalization. Although Clostridium perfringens type A was recovered from 3 of the 5 felids for which microbial culture was performed, and 2 felids had a recent increase in the amount fed, no single factor was definitively identified that might have incited or contributed to the gastric dilatation. CLINICAL RELEVANCE Gastric dilatation was a life-threatening condition in the large felids of this report, causing sudden death or clinical signs of hematemesis, abdominal distention, or vomiting. Even with rapid diagnosis and surgical decompression, the prognosis was poor. Research is needed into the factors that contribute to this emergent condition in large felids so that preventive measures might be taken.

Focal symmetrical encephalomalacia in sheep / Encefalomalacia focal simétrica em ovino

Focal symmetrical encephalomalacia (FSE) is the most prominent lesion seen in the chronic form of enterotoxemia by Clostridium perfringens type D. This paper reports FSE in sheep in Brazil. Six deaths occurred within a seven days period in a flock of 70, four to 30-month-old Santa Inês sheep in the state of Paraíba in the Brazilian semiarid. The flock was grazing a paddock of irrigated sprouting Cynodon dactylon (Tifton grass), and supplemented, ad libitum, with a concentrate of soybean, corn and wheat. Nervous signs included blindness and recumbence. A 19 month-old sheep was examined clinically and necropsied after a clinical course of three days. Gross lesions were herniation of the cerebellar vermis and multifocal, bilateral, symmetric brownish areas in the internal capsule, thalamus and cerebellar peduncles. Histologic lesions were multifocal, bilateral malacia with some neutrophils, swelling of blood vessels endothelium, perivascular edema, and hemorrhages. The flock was vaccinated, before the outbreak, with only one dose of Clostridium perfringens type D vaccine. Two factors are suggested to be important for the occurrence of the disease: insufficient immunity due to the incorrect vaccination; and high nutritional levels by the supplementation with highly fermentable carbohydrates.

Encefalomalacia focal simétrica (EFS) é a lesão mais proeminente vista nas formas subaguda ou crônica da enterotoxemia por Clostridium perfringens tipo D. Este trabalho relata EFS em ovinos no semiárido do estado da Paraíba. Seis ovinos morreram, em um período de sete dias, dentro de um rebanho de 70 animais, da raça Santa Inês, entre 4-30 meses de idade, que pastavam em piquete de Cynodon dactylon (capim Tifton), que estava rebrotando. Os ovinos eram suplementados com um concentrado de soja, trigo e milho. Os sinais nervosos incluíam cegueira e decúbito lateral. Um ovino de 19 meses de idade foi examinado clinicamente e necropsiado, depois de um curso clínico de 3 dias. Macroscopicamente foram observadas herniação do cerebelo e áreas acastanhadas, multifocais, simétricas e bilaterais na cápsula interna, tálamo e pedúnculo cerebelar. Histologicamente observou-se malacia, bilateral e simétrica, com alguns neutrófilos, tumefação das células endoteliais dos vasos sanguíneos, edema perivascular e hemorragia. O rebanho foi vacinado, antes do surto, com umaúnica dose de vacina para Clostridium perfringens tipo D. Dois fatores são sugestivos quanto a importância da ocorrência da enfermidade: imunidade insuficiente devida à vacinação incorreta; e altos níveis nutricionais da suplementação com carboidratos altamente fermentáveis.

Eimeria macusaniensis associated lesions in neonate alpacas dying from enterotoxemia.

Histopathological analysis of 108 intestine samples (103 grossly affected ileum and 5 jejunum) taken from Clostridium-induced neonatal alpaca (Vicugna pacos) enterotoxemia mortalities collected in the Departments of Arequipa, Puno and Cusco of southern Peru during the 2005-2008 birth seasons (January-March), revealed the presence of large numbers of both asexual and sexual stages of Eimeria macusaniensis in 33/108 (30.55%) of the samples with moderate to severe necrotized and/or hemorrhagic enteritis. It is proposed that damage to the mucosa produced by coccidial infections may facilitate overgrowth of Clostridium perfringens with toxin production leading to fatal enterotoxemia.

Sudden death of feedlot cattle.

Sudden deaths or the sudden death syndrome are perceived as major concerns in cattle feedlots because most of these deaths occur in cattle near market weight. Etiology and preventive measures are poorly defined. The current literature indicates that sudden deaths are associated most commonly with digestive upsets. Death is thought to be the result of interactions between factors including acidosis, bloat, and endotoxemia. Trauma, peracute interstitial pneumonia, and other identifiable events are specifically defined but relatively uncommon. Enterotoxemia is of questionable significance as a cause of sudden deaths.

Caprine enterotoxaemia associated with cerebral microangiopathy.

Cerebral microangiopathy is described in naturally occurring clostridial enterotoxaemia in two goats. The two cases were selected from the files of two diagnostic laboratories in Australia, on the basis that the clinical syndrome and history were consistent with a diagnosis of enterotoxaemia, and that the diagnosis was confirmed by the identification of epsilon toxin in the intestinal contents. The lesions consisted of acute perivascular proteinaceous exudate in the brain and bilaterally symmetrical foci of encephalomalacia were observed in one of the goats. These brain lesions confirm that Clostridium perfringens type D enterotoxaemia may produce histologically detectable brain changes in goats.

An outbreak of enterotoxaemia caused by Clostridium perfringens type D in goats in Patagonia.

Forty-four of a flock of 117 angora goats in the Rio Negro province of Argentina died within four days. Most of the animals died shortly after the onset of clinical signs, but in a few the clinical course lasted for several days. Post mortem the small and large intestines were filled with watery contents, blood and fibrin clots, and there were numerous ulcers on the mucosa. Small areas of malacia were observed histologically in the brain. Clostridium perfringens type D in pure culture was isolated from the kidneys and gut contents of the affected animals. Epsilon toxin was identified by the mouse seroneutralisation test in the supernatant solution from cultures of these isolates and in the intestinal contents of the affected animals. Heavy infestations with coccidia, nutritional and environmental stress, and an anthelmintic overdose were possible predisposing factors for the outbreak.

Participation of calcium ion on depletion mechanism of liver glycogen by purified glucocorticoid antagonizing factor released in blood during endotoxemia.

The present study was conducted by the use of purified glucocorticoid antagonizing factor (GAF) released in blood of endotoxemic mice to determine whether or not the factor (GAF and Ca2+) may play a possible role of mediator in depletion mechanism of liver glycogen in endotoxemia. The liver glycogen level in 2 hr after injection with GAF plus cortisone-treated mice was markedly lower than that in cortisone alone-treated mice. However, the administration of trifluoperazine or verapamil markedly increased glycogen levels in liver of GAF plus cortisone-injected mice. On the other hand, when the mice fed a calcium-free diet were injected with GAF plus cortisone, there was merely a significant difference in liver glycogen level as compared to cortisone alone-treated mice. The level of Ca2+ in liver cytosol fraction in cortisone-treated mice was higher 2 hr after GAF injection than that in the cortisone alone-treated one. The phosphorylase a activity in liver 2 hr after injection of GAF plus cortisone did not show a significant difference as compared to that in mice treated with cortisone alone. However, the activity ratio of glycogen synthase enzyme (synthase I synthase I + D) was decreased in GAF plus cortisone-treated mice as compared to that in cortisone alone-treated mice. These findings suggest that there are participations of Ca2+ and mediator GAF released from reticuloendothelial system (RES macrophages in glucoregulation of endotoxemia. Thus, it may be speculated that intracellular Ca2+ may mediate glycogenesis rather than glycogenolysis in the depletion mechanism of liver glycogen during GAF-poisoning.

[Infectious diarrhea]. / Infektiöse Diarrhöe.

Due to the growth in tourism, infectious diarrhea is no longer a problem of warm developing countries but a common condition encountered by the general practitioner. In this review the authors summarize the etiology, pathophysiology and clinical picture of the disease, and outline the diagnostic and therapeutic approach.

[Old and new data on diarrhetic diseases in childhood I. Etiology and pathophysiology]. / Alte und neue Erkenntnisse zu den Durchfallerkrankungen im Kindesalter. I. Atiologie und Pathophysiologie

Etiology and Pathophysiology. The present article is a comprehensive review of recent research results in the field of acute diarrhea. The most important new idea in contrast to older views is that almost all acute diarrheas are associated with a disturbance of intestinal bacterial homeostasis: overgrowth of the small intestine with apathogenic or pathogenic organisms is followed by changes in intestinal metabolism with increase in intestinal water and electrolyte secretion. Anaerobic organisms cause by enzymatic deconugation and dydroxylation of bile acids secretion of fluid into the small intestine and inhibition of fluid absorption from the large intestine. 10-OH-fatty acids, which are formed intraluminally by enzymatic hydroxylation of long-chain unsaturated fatty acids from the diet by similar anaerobic organisms, produce profuse secretion of fluid into the small intestine. The ability of numerous strains of E. coli to produce enterotoxin, which has a qualitatively similar action to cholera toxin, is now considered to be a major cause of infantile diarrhea. The separation of two completely different pathophysiologic mechanisms of E. Coli, the enterotoxic and the enteroinvasive action which are determined by extranuclear chromosomal material, is an important result of recent research. Overgrowth of the small intestine with different bacteria is followed by loss of actiivity of lactase, and later of all disaccharidases in the intestinal mucosa.