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Biomedical subjects

S Tzipori

Publications and source records attributed to S Tzipori.

At least 109 records · Page 6Linked to original sources

Haemorrhagic necrotising enteritis in foals associated with Clostridium perfringens.

Two foals aged 35 and 48 h from 2 Thoroughbred studs died several hours after developing clinical signs of depression, severe haemorrhagic diarrhoea and dehydration. Both foals had an acute haemorrhagic enteritis extending from the anterior jejunum to the terminal ileum which was characterised histologically by villus necrosis. Necrotic villi were surrounded by large numbers of rod-shaped Gram positive bacteria. Clostridium perfringens was recovered from the intestines of both foals and the isolates were considered to be C. perfringens type C. Other cases of diarrhoea were also observed in foals of the same age on these 2 studs, but the aetiology of these was not determined.

Animals↗

Enteropathogenic Escherichia coli enteritis: evaluation of the gnotobiotic piglet as a model of human infection.

The pathogenicity of classical enteropathogenic Escherichia coli strains of human origin was investigated in gnotobiotic piglets. One to two day old piglets in groups of four were infected perorally with approximately 10(8) colony forming units of one of eight enteropathogenic E coli strains or a non-pathogenic control strain. Animals were necropsied 24 or 48 hours after infection and their intestines were subjected to histological examination, quantitative bacterial culture and estimation of lactase activity. Four enteropathogenic E coli strains caused mild to moderate diarrhoea in nine of the 16 piglets inoculated with them. Piglets given two of these strains later became moribund. One enteropathogenic E coli strain caused a severe illness unaccompanied by diarrhoea. Inflammation of the intestinal mucosa occurred with all eight enteropathogenic E coli strains, but not with the control strain. Pathological changes were most pronounced in the distal ileum and colon and adherent bacteria were seen on the surface of the inflamed mucosa. The extent of the inflammatory response in infected piglets for the most part paralleled the severity of the clinical signs, the degree of bacterial colonisation and the reduction in lactase activity. Electron microscopic examination of tissue from piglets infected with three different strains showed that bacterial adherence to the apical plasma membrane of epithelial cells was accompanied by distinctive ultrastructural changes. These included degeneration of the microvillous brush border, together with cupping and pedestal formation of the plasma membrane at sites of bacterial attachment. The same changes have been seen in naturally occurring enteropathogenic E coli diarrhoea in humans and rabbits. The combined clinical and pathological findings indicate that the neonatal gnotobiotic piglet is a suitable model of infection with enteropathogenic E coli.

Animals↗

Attachment of E. coli-bearing K88 antigen to equine brush-border membranes.

Equine small intestinal brush-border membranes, from 40 adult horses were tested in vitro for the presence of receptors for the Escherichia coli adhesive antigens K88ab, K88ac and K99. Only K88-positive strains of E. coli adhered strongly to horse brush-border membranes. In contrast, a K88-negative mutant strain J2, 2 K99-positive strains and 3 E. coli strains isolated from foals failed to adhere to horse brush-border membranes. Purified K88ac pili when reacted with equine brush-border membranes inhibited to a great extent the adhesion of K88-positive E. coli. Similarly, K88-positive E. coli previously reacted with K88 antibody, did not attach to equine brush-border membranes. Oral inoculation of 4 newborn foals with strains of K88-positive enterotoxigenic E. coli, producing either heat-stable or heat-labile enterotoxin, caused diarrhoea in 1 animal.

Adhesiveness↗

Streptococcus durans: an unexpected enteropathogen of foals.

Streptococcus durans was isolated from a foal with profuse watery diarrhea and caused a similar syndrome when inoculated into foals via the orogastric route. The most consistent and striking histological feature was the extensive colonization of the mucosal surface of the small intestine by S. durans. Associated mucosal changes were mild to modeate, and brush border lactase and alkaline phosphatase production were depressed. S. durans also induced acute diarrhea in young gnotobiotic piglets. Mucosal changes were mild and, as with foals, the mucosal surface of the small intestine was colonized by the organism.

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Colitis in sheep due to a Campylobacter-like bacterium.

Epidemic diarrhoea was observed in approximately 2,000 of 6,700 sheep on 9 farms. The disease, called weaner colitis, caused mortality of 1%, while morbidity varied from 20 to 75%. Colon contents from affected sheep were inoculated into 17 sheep, 13 of which developed diarrhoea 5 to 7 days after inoculation. Naturally and experimentally infected sheep had mild, erosive typhlitis and colitis. Microscopic examination of washed scrapings of colonic mucosa from all affected sheep revealed masses of curved bacteria that were not seen in controls. Electron microscopic examination showed similar bacteria adherent to colonic epithelium of an experimentally infected sheep. Curved, motile bacteria were isolated from 2 naturally occurring cases. One isolate was inoculated into 9 sheep, 2 of which developed diarrhoea. The other isolate was given to 4 sheep without observable effect. The curved bacteria grew only on media containing blood, in an atmosphere of approximately 10% air, 10% CO2 and 80% H2. They were Gram-negative, with a polar flagellum at one or both ends, they did not ferment glucose or give a positive catalase reaction. It is suggested that these bacteria are a new Campylobacter species and that they play a major role in the aetiology of weaner colitis.

Animals↗

Experimental cryptosporidiosis in calves: clinical manifestations and pathological findings.

Twenty-two calves between one and 20 days old were infected orally or by contact with cryptosporidia. Calves were maintained as either specific pathogen free, colostrum fed or sucking and were inoculated with either a bacteria free or a contaminated cryptosporidium preparation. Enteritis was characterised by depression, anorexia and diarrhoea and cryptosporidium oocysts were excreted during the clinical course of the illness. In the initial stages of the disease, cryptosporidium infestation was found throughout the small intestine; in the later stage the large intestine was also affected. Villous atrophy and fusion was present at small intestinal sites infected with cryptosporidia and lactase levels were depressed. No lesions were seen in infected large intestinal mucosa. Although the incubation period was longest (five to seven days) in calves infected by contact, there were few differences in the clinical course of disease or the pathological findings between any of the infected calves.

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Intestinal changes associated with rotavirus and enterotoxigenic Escherichia coli infection in calves.

Newborn calves inoculated with rotavirus, enterotoxigenic Escherichia coli (ETEC) serotype 020:K' x 106':K99:HNM, either alone or in combination, became depressed, anorectic, diarrhoeic and dehydrated. ETEC did not adhere to the intestine although there was extensive proliferation in the lumen. Only slight mucosal changes were induced by ETEC and the activity of membrane bound lactase remained normal. More severe mucosal damage and a decrease in lactase activity were found in newborn calves inoculated with either rotavirus or rotavirus and ETEC in combination. The most severe clinical illness was found in calves inoculated with both rotavirus and ETEC. Calves inoculated at 1 week of age with either rotavirus or ETEC remained clinically normal. Rotavirus infection produced slight mucosal changes and a reduction of lactase activity. In contrast, colostrum-fed or suckling calves up to 2 weeks old inoculated with both rotavirus and ETEC became clinically affected, showed severe mucosal damage and decreased lactase activity. There was no bacterial adhesion to the intestinal mucosa as observed by immunofluorescent labelling and light microscopy.

Animals↗

Cryptosporidiosis in hospital patients with gastroenteritis.

Among 884 hospital patients with gastroenteritis, 36 (4.1%) were excreting Cryptosporidium oocysts in their stools; only 5 of the 36 patients were also excreting other enteropathogens, while none of 320 hospital patients without gastroenteritis were excreting Cryptosporidium oocysts. Children were more commonly infected with Cryptosporidium (4.8%) than were adults (1.6%). The prevalence of infection was higher (7%) during the summer period of February-May 1981 than in the remainder of the observation period to the beginning of June 1982 (1.9%). The most common clinical manifestation of gastroenteritis in Cryptosporidium-infected patients was diarrhea, lasting from 3 to over 14 days, accompanied by vomiting, anorexia, and abdominal pain. The results show that a small proportion of patients with gastroenteritis are infected with Cryptosporidium, and the importance of the infection needs to be examined.

Adolescent↗

The clinical manifestation and pathogenesis of enteritis associated with rotavirus and enterotoxigenic Escherichia coli infections in domestic animals.

Rotavirus and enterotoxigenic Escherichia coli (ETEC) are enteropathogens each capable of inducing diarrhoea in some animal species and man. Unstressed young animals develop an age-related resistance to infection with either rotavirus or ETEC which differs for each animal species. The effects of experimental infection of calves, lambs, foals and piglets with rotavirus and ETEC given either alone or in combination, have been examined. In general, dual infections tended to lengthen the period of age susceptibility and increase the severity of gastroenteritis, compared to infection with either agent alone. ETEC caused little or no pathological changes in the small intestine while rotavirus induced moderate inflammatory, morphological and physiological changes including reduced activity of membrane-bound digestive enzymes. In dual infections, mucosal lesions were more severe than those seen after rotavirus infection and ETEC proliferation in the lumen of the small intestine was greater than in animals infected with ETEC alone. Two distinct mechanisms of diarrhoea, presumably, were involved; net fluid hypersecretion into the lumen of the gut mediated by ETEC enterotoxin(s), and brush border maldigestion and malabsorption which was caused by rotavirus infection of the small intestine.

Animals↗

Enterocolitis in piglets caused by Cryptosporidium sp. purified from calf faeces.

Twelve gnotobiotic piglets were dosed with a bacteria-free calf faecal homogenate which contained Cryptosporidium oocysts. The infection induced severe enterocolitis in piglets when inoculated at 1 day of age, moderate diarrhoea at 7 days of age and a subclinical infection at 15 days of age. In piglets aged 3 days or less, the entire intestine was extensively infected with Cryptosporidium and the mucosa was severely damaged. In piglets 7 days of age or older, the upper small intestine was sparsely infected with the organisms, but the ileum and the large bowel were heavily infected with associated mucosal damage.

Aging↗

Enteritis in foals induced by rotavirus and enterotoxigenic Escherichia coli.

Colostrum-deprived, colostrum-fed or suckling foals were orally inoculated with foal rotavirus and enterotoxigenic Escherichia coli derived from a calf. Neither agent given alone caused diarrhoea in foals aged 1 or 2 days, although with rotavirus, 2 of the 3 inoculated foals became depressed 3 days after inoculation and all 3 were excreting rotavirus in the faeces. Inoculation of both agents induced diarrhoea in colostrum-deprived, colostrum-fed or suckling foals aged up to 16 days. There was an apparent age-related resistance to diarrhoea which developed between 2 and 3 weeks of age. It was related to failure of rotavirus to establish apparent infection in older foals and was independent of preinoculation maternal antibody.

Animals↗

Experimental colibacillosis in gnotobiotic piglets exposed to 3 enterotoxigenic serotypes.

Three strains of enterotoxigenic Escherichia coli (ETEC) (064:KSNT, K88ac; 020:KSNT, K88ac and 08:K85ab, K99) originally cultured from outbreaks of diarrhoea in piglets a few hours old, were administered orally to gnotobiotic piglets. There was a marked age-related difference in the clinical response to infection between the 3 strains although they all produced heat-stable toxin. All 3 strains produced severe clinical signs of depression, anorexia, vomiting, diarrhoea, followed by dehydration and death in one-day-old piglets. In piglets infected at 3 days of age the two K88+ ETEC caused diarrhoea and death but the K99+ ETEC induced moderate diarrhoea only. In piglets infected at 7 days of age, the 064 strain produced severe diarrhoea and death, and 020 strain caused mild diarrhoea in 3 of 6 piglets with one death while the 08 strain caused no illness. Pathological changes in the intestinal tract associated with these infections were minimal, or absent. Immunofluorescent staining with homologous hyperimmune sera demonstrated adherence of the 3 ETEC strains to the brush border of small intestinal epithelial cells. Fluorescing organisms were observed in all infected piglets irrespective of the severity of clinical signs but the degree and extent of colonisation varied with the age of the piglets and the infecting strain. This may explain the difference in clinical response between the 3 strains.

Animals↗

Experimental cryptosporidiosis in laboratory mice.

Eight strains of laboratory mice were susceptible to subclinical infections with Cryptosporidium sp. at 1 to 4 days of age, but only a transient infection could be established at 21 days of age or older. Immunosuppression of 21-day-old mice failed to render them more susceptible to infection. Laboratory storage conditions for Cryptosporidium sp. were investigated by titration in 1- to 4-day-old mice. Storage by freezing with a variety of cryoprotectants was unsuccessful, but storage at 4 degrees C in phosphate-buffered saline or 2.5% potassium dichromate was possible for 4 to 6 months.

Aging↗

Experimental infection of lambs with Cryptosporidium isolated from a human patient with diarrhoea.

An inoculum containing Cryptosporidium oocysts obtained from an adult human patient with acute transient diarrhoea induced enteritis in two newborn specific pathogen free lambs. Three days after inoculation the lambs became depressed and diarrhoeic, their milk intake was reduced and Cryptosporidium oocysts were detected in their faeces. Mucosal changes observed in the small intestine of one infected lamb were consistent with but less severe than those induced experimentally in lambs by cryptosporidia isolated from calves and lambs.

Animals↗

Intestinal lesions in specific-pathogen-free lambs associated with a cryptosporidium from calves with diarrhea.

Small and large intestines of seven specific pathogen-free lambs infected with cryptosporidia from calves with diarrhea were examined by scanning and transmission electron microscopy and by light microscopy. The small intestine was infected in all the lambs, and the cecum and colon in three. Small intestinal alterations were severe villous atrophy and dilatation of the crypts of Lieberkühn. Epithelial cross-bridging between contiguous villi caused much villous fusion. Epithelial cells constituting the bridges were connected by desmosomal junctions, and were continuous with the epithelial coverings of the associated villi. The lamina propria was heavily infiltrated with neutrophil leukocytes. Infected crypts in cecum and colon were dilated and devoid of mucus-secreting cells, while the ridges between crypts were hypertrophied, and the lamina propria was infiltrated by neutrophils. Cell vegetations with adherent bacteria were present in the surface intestinal epithelium of two lambs infected for 11 and 14 days, respectively. No adherent bacteria were seen in any site in lambs killed up to six days post-inoculation.

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