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S Tzipori

Publications and source records attributed to S Tzipori.

At least 91 records · Page 5Linked to original sources
PubMed1989

Studies on attenuation of rotavirus. A comparison in piglets between virulent virus and its attenuated derivative.

The development of rotavirus vaccines against acute gastroenteritis for human infants has been accorded a very high priority. Several vaccine candidates all of which are live cultivated strains of animal origin have been tested in humans. However the nature of attenuation of these viruses for humans is unknown. In this study we have attenuated a pig rotavirus by 15 sequential passages in cell culture after which the virus no longer causes diarrhoea in piglets. The pathogenesis of infection of the attenuated rotavirus strain (AT/76 P15) in gnotobiotic piglets was compared with that of the virulent parent strain (AT/76). The pattern of virus replication in the small intestine was judged by histology, disaccharidase assay, immunoperoxidase labelling of gut sections using group A specific rotavirus antibody, and rotavirus antigen assay of gut contents. The parent strain caused variable but extensive infection that resulted in the complete destruction of mature small intestinal enterocytes and villous contraction within 3 days. Membrane bound digestive enzymes were lost, and profound watery diarrhoea and dehydration resulted in causing piglets to become moribund. In contrast attenuated virus appeared to propagate at a much slower pace. Fewer infected epithelial cells were detected at any one time. Destruction of enterocytes was never extensive enough to cause marked mucosal changes in histology. Membrane bound digestive enzymes remained near normal levels and there was little or no diarrhoea. Virus replication ceased after 6 days. It is concluded that attenuation of the porcine rotavirus strain studied was associated with its decreased ability to propagate in enterocytes after adaption to culture.

Animals↗
PubMed1989

Nature and distribution of mucosal lesions associated with enteropathogenic and enterohemorrhagic Escherichia coli in piglets and the role of plasmid-mediated factors.

Bacterial attachment-effacement (att-eff) is emerging as an important virulence characteristic common to both enteropathogenic Escherichia coli (EPEC) and enterohemorrhagic E. coli (EHEC). The contribution of the plasmid-encoded EPEC adherence factor to the production of mucosal lesions and diarrhea was investigated in gnotobiotic piglets. Bacterial att-aff in the intestinal mucosa of piglets infected with plasmid-cured EPEC strain E2348/69 (O127) was indistinguishable from that in piglets infected with the parent strain, but the distribution of lesions was different; it occurred in the small intestines of 6 of 7 piglets infected with the parent strain compared with only 2 of 11 (P = 0.006) infected with the plasmid-cured strain. Plasmid-encoded factors in EPEC and EHEC strains did not appear to contribute to bacterial competition with normal gut microflora. Of 13 strains belonging to five EPEC serogroups, O55, O142, O26, O119, and O111, 3 fulfilled the criteria for EHEC (2 O26 and 1 O111). There were three distinct patterns of bacterial association with the intestinal mucosa of infected piglets. (i) EHEC strains caused bacterial att-eff associated with extensive destruction of surface and glandular epithelia in the large intestines with little or no inflammatory response. (ii) Some EPEC strains caused severe diarrhea which correlated with the extent of bacterial att-eff in the proximal small intestine, disruption of the epithelial cell membrane, and inflammation. It is suggested that, with respect to virulent strains, this degree of involvement determines the clinical outcome. Mildly pathogenic strains (O127 and O119), in which bacterial att-eff was restricted to the distal halves of the small and large intestines, caused little or no diarrhea. In such strains, nonimmune host factors (smaller, poorly feeding, and lethargic piglets) tended to play a determining role with regard to the degree of involvement of the small intestine and hence the clinical outcome. (iii) One strain (O55) caused illness and mucosal damage which could not be accounted for by the sparse bacterial att-eff observed in the gut. Instead, bacteria penetrated into and proliferated in the lamina propria, undermining the villous tips in the small intestine. Bacterial att-eff was the most important virulence factor in most of the strains examined, but plasmid-mediated factors facilitated bacterial adhesion in the small intestine, which may explain the reduced pathogenicity of the plasmid-cured variant of strain E2348/69 for human volunteers.

Animals↗
PubMed1988

Studies in gnotobiotic piglets on non-O157:H7 Escherichia coli serotypes isolated from patients with hemorrhagic colitis.

A number of verotoxin-producing Escherichia coli strains isolated from sporadic cases of hemorrhagic colitis in the United States over the last 5 yr were shown to belong to serogroups other than O157:H7-the serotype originally implicated in this disease. Experimental infection of gnotobiotic piglets with five such strains (0111:NM, 0145:NM, 045:H2, 04:NM, and Ound:NM) caused diarrhea resulting from mucosal lesions in the cecum and colon that were indistinguishable from those previously described in piglets infected with E. coli O157:H7. This suggests that, as with other categories of pathogenic E. coli, several serotypes cause hemorrhagic colitis in humans. The five E. coli strains that were compared with one O157:H7 strain and with an enteropathogenic calf strain (serotype 05:NM) caused a spectrum of disease ranging from moderate diarrhea (O157:H7) to severe illness (including septicemia and death) (0111:NM). Characteristic lesions, which were identical for all seven pathogenic strains, included bacterial attachment, effacement of the microvillus border, and dissolution of the cell membranes of surface and glandular epithelium, resulting in complete cell destruction. Some piglets exhibited neurologic signs of convulsions and ataxia. It is concluded that a number of E. coli serotypes, in addition to O157:H7, fulfill the present limited criteria for enterohemorrhagic E. coli, which include association with hemorrhagic colitis, production of one or more verotoxins, possession of a large plasmid (50-70 megadaltons), and induction of distinct mucosal lesions in the large bowel of gnotobiotic piglets.

Animals↗
PubMed1988

Development and protective efficacy of a recombinant-DNA derived fimbrial vaccine against enterotoxic colibacillosis in neonatal piglets.

A vaccine containing Escherichia coli fimbriae produced by recombinant-DNA techniques was tested in controlled challenge trials and in commercial piggeries experiencing neonatal enterotoxic colibacillocis. In the challenge trials, piglets suckling vaccinated sows were significantly protected from diarrhoea and colonization of the small intestine by enterotoxigenic E. coli. High titres of anti-fimbrial IgG antibody were detected in the serum and colostrum of vaccinated sows and in serum of their piglets. In the field trials, prevalence of diarrhoea and preweaning mortality due to diarrhoea were greatly reduced in piglets suckling vaccinated sows.

Animals↗
PubMed1988

Cryptosporidiosis in perspective.

In this review I have examined the vast literature which has accumulated on Cryptosporidium, particularly in the past 3 years, in an attempt to highlight areas in which progress has been made in relation to the organism and the disease, and to indicate areas in which knowledge is still lacking. Since 1982, a global effort by scientists and clinicians has been directed towards determining the nature of the disease in humans and the relative contribution of cryptosporidiosis to gastroenteritis. From published data, the incidence of diarrhoea is 1-5% in most developed countries, and 4-7% in less developed countries, when measured throughout the year and in all age groups. The frequency of cryptosporidiosis is highest in children aged between 6 months and 3 years, and in particular locations (e.g., day-care centres) and at particular times of the year. Although susceptibility to infection is life-long, one suspects that the lower prevalence among older children and adults is due to immunity acquired from frequent exposure. Other important factors contributing to higher prevalence are the season--it is more frequent in a wet, warm climate--association with travel to particular destinations, poor hygiene, intimate contact with certain animals, and congregation of large numbers of young previously unexposed children in day-care centres. The association between cryptosporidiosis and giardiasis presumably results from the existence of a common source of infection. The immune status of the host appears to be a major determinant of whether the infection is self-limiting or persistent. It is clear that both branches of the immune system are required for complete recovery, since T-lymphocyte dysfunction or hypogammaglobulinaemia can both lead to persistent illness. Chronic diarrhoea and malabsorption attributed to cryptosporidiosis also occur in the absence of evidence of immune defect. The importance of respiratory tract infection in humans, other than in the terminal stages of chronic illness, requires investigation. The infection has now been identified in all classes of vertebrates; it has been observed in all domestic animals including pets, and a wide range of wildlife including birds. Cryptosporidiosis seems to cause diarrhoea in young ruminants, less frequently in pets. In birds the parasite has been observed in the gastrointestinal tract, without ill effect, and in the respiratory tract, in which clinical symptoms of variable severity have been described. The mucosal response of the gastrointestinal tract to infection appears to vary among mammals and may be the key to the variable clinical manifestations observed.(ABSTRACT TRUNCATED AT 400 WORDS)

Acquired Immunodeficiency Syndrome↗
PubMed1988

Cerebral infection with Escherichia coli O157:H7 in humans and gnotobiotic piglets.

Escherichia coli O157:H7 was isolated from a fatal case of haemorrhagic colitis with haemolytic uraemic syndrome and neurological symptoms. This strain induced diarrhoea and neurological symptoms including incoordination, ataxia, and convulsions in piglets after oral inoculation. Similar neurological signs were seen in piglets inoculated intraperitoneally with bacterial extracts containing a shiga-like toxin that is elaborated by the bacteria. Histological examination of the brains from these piglets showed vascular damage and small infarcts confined to the cerebellum. Comparable lesions were also seen in the brain of the child from whom E coli O157:H7 was isolated. We suggest that the cerebral changes in the piglets and in the patient were caused by the shiga-like toxin elaborated by E coli O157:H7. The shiga-like toxin is thought to cause neurological abnormalities by damage to cerebral blood vessels rather than by a direct effect on the neurones.

Animals↗
PubMed1987

Role of a 60-megadalton plasmid and Shiga-like toxins in the pathogenesis of infection caused by enterohemorrhagic Escherichia coli O157:H7 in gnotobiotic piglets.

Enterohemorrhagic Escherichia coli (EHEC) of serotype O157:H7 has two putative virulence factors: (i) a fimbrial adhesin, specified by a 60-megadalton (MDa) plasmid, and (ii) bacteriophage-specified cytotoxin(s), known as Shiga-like toxin (SLT) or verotoxin. The contribution of these factors to the pathogenesis of EHEC-induced disease in gnotobiotic piglets was examined. The bacterial strains included the following: two EHEC strains and their corresponding plasmid-cured derivatives; another EHEC isolate and its derivative which had spontaneously lost the ability to produce SLT; one E. coli K-12 transconjugatant containing a 60-MDa plasmid from an EHEC strain; two K-12 strains into which an SLT-producing phage had been transduced (one of these strains also carried a 60-MDa EHEC-derived plasmid); and the parent K-12 strain. Each strain was fed to four piglets, which were observed for diarrhea and examined for development of characteristic mucosal lesions 3 or 5 days after inoculation. All 24 piglets inoculated with the three EHEC strains and their respective derivatives (two plasmid cured and one SLT negative) showed the typical mucosal lesions of bacterial attachment: effacement of microvillous border and cell membrane dissolution culminating in destruction of surface and glandular epithelium in the cecum and colon. No such lesions were observed in 12 piglets inoculated with three strains of E. coli K-12, including the strain which carried both the 60-MDa plasmid and a phage which specified production of SLT. Moderate to severe diarrhea was observed in 16 piglets inoculated with two EHEC strains and their derivatives (one plasmid cured and one SLT negative). The third EHEC strain and its plasmid-cured derivative produced fewer typical mucosal lesions and no diarrhea. The reason for the reduced virulence of this strain was not clear. These results demonstrate that neither the 60-MDa plasmid nor the capacity to produce SLT is essential for expression of virulence by E. coli O157:H7 in gnotobiotic piglets.

Animals↗
PubMed1987

In vitro and in vivo pathogenicity of Plesiomonas shigelloides.

Epidemiologic evidence suggests that Plesiomonas shigelloides is an enteric pathogen. We conducted in vitro, animal, and volunteer studies on P. shigelloides isolates from patients with diarrhea. Five strains gave a negative keratoconjunctivitis reaction in guinea pigs and did not invade HeLa cells. Genetic probes for heat-stable enterotoxins related to those of enterotoxigenic Escherichia coli and for gene sequences common to the invasiveness plasmids of Shigella spp. and enteroinvasive E. coli were negative. Heat-labile enterotoxins were not found when a modified GM1-enzyme-linked immunosorbent assay was used. Rabbits did not develop diarrhea but were transiently colonized when inoculated with up to 10(11) P. shigelloides CFU using the reversible intestinal tie adult rabbit diarrhea model. A very large plasmid (between 118 and 312 megadaltons) was found in all isolates. Strain P012 was cured of its plasmid by novobiocin. This strain, but not its cured derivative, invaded the mucosa of the distal ileum of gnotobiotic piglets given 10(10) CFU. At a lower inoculum (10(9) CFU), strain P012 induced inflammation of the colonic mucosa and diarrhea at day 6. The same isolate was fed to 33 healthy volunteers in doses of 1 X 10(3) to 4 X 10(9) CFU. Thirty-six percent of the volunteers shed the organism, but none became ill. These data are only weakly supportive of a role for P. shigelloides in diarrheal illness and suggest the need for more studies with other strains to better understand its pathogenicity.

Animals↗
PubMed1986

Remission of diarrhoea due to cryptosporidiosis in an immunodeficient child treated with hyperimmune bovine colostrum.

A boy aged 6 months who presented with poor weight gain, diarrhoea, and infection with Pneumocystis carinii was found to have congenital hypogammaglobulinaemia, which did not improve despite monthly treatment with intravenous gammaglobulin. At the age of 3 years and 2 months he developed severe vomiting and diarrhoea due to cryptosporidiosis, which failed to respond to conventional treatment. Infusion of hyperimmune bovine colostrum produced against parasite antigen, given by nasogastric tube, was started after symptoms had persisted for three weeks. His vomiting and diarrhoea resolved within five days of treatment, and oocysts were no longer seen in the stools after eight days. Later, however, he developed a rare complication, and oocysts were found in the common bile duct. Hyperimmune bovine colostrum may be useful in the treatment of many patients with immunodeficiency disorders.

Agammaglobulinemia↗
PubMed1985

The pathogenesis of Yersinia enterocolitica infection in gnotobiotic piglets.

Yersinia enterocolitica is an important cause of enteritis and mesenteric adenitis in many countries. However the pathogenesis of the disease caused by this organism has not been fully elucidated. Most isolates from clinical material possess two independent properties associated with virulence whose relative contribution to the development of disease is not known. These are the ability to penetrate the intestinal wall, which is thought to be controlled by a plasmid gene, and the production of heat-stable enterotoxin, which is controlled by a chromosomal gene. In this study, we infected neonatal gnotobiotic piglets with strains of Y. enterocolitica expressing these two properties in various combinations. The suitability of the piglet model was shown in experiments in which piglets fed virulent Y. enterocolitica serogroup O3 developed a clinical illness related to the size of the inoculum, which was accompanied by intestinal lesions similar to those reported in naturally and experimentally infected people and animals. The results confirmed the key role of a 47 X 10(6)-mol. wt plasmid in the pathogenicity of Y. enterocolitica, but suggested that penetration of the intestinal wall may be governed by chromosomal rather than plasmid-borne genes. No role for enterotoxin in the pathogenesis of yersiniosis was shown, although there was evidence that enterotoxin may promote intra-intestinal proliferation of Y. enterocolitica, thus favouring increased shedding of bacteria and encouraging their spread between hosts.

Animals↗