scholarly journals Bacterial contamination of the small intestine of infants with enteropathogenic Escherichia coli and other enteric infections: a factor in the aetiology of persistent diarrhoea?

BMJ ◽  
1986 ◽  
Vol 292 (6530) ◽  
pp. 1223-1226 ◽  
Author(s):  
M E Penny ◽  
D G Harendra de Silva ◽  
A S McNeish
2020 ◽  
Vol 40 (3) ◽  
pp. 165-169
Author(s):  
Hugo P. Lopes ◽  
Gisllany A. Costa ◽  
Ana C.L.Q. Pinto ◽  
Leandro S. Machado ◽  
Nathalie C. Cunha ◽  
...  

ABSTRACT: Enteropathogenic Escherichia coli (EPEC) and Shigatoxigenic E. coli (STEC) strains are among the major pathotypes found in poultry and their products, which are capable of causing human enteric infections. Colistin has been claimed the drug of choice against diseases caused by multidrug-resistant Gram-negative bacteria (MDRGN) in humans. The mcr-1 gene was the first plasmidial gene that has been described to be responsible for colistin resistance and has also been detected in birds and poultry products. Our study aimed to detect the mcr-1 gene in enteropathogenic strains of E. coli in order to evaluate the resistance to colistin in broilers. The material was obtained from 240 cloacal samples and 60 broiler carcasses. The strains were isolated by the conventional bacteriological method and by the virulence genes, which characterize the enteropathogenic strains and resistance, and the samples were detected by polymerase chain reaction (PCR). Of the 213 isolated strains of E. coli, 57 (26.76%) were characterized as atypical EPEC and 35 (16.43%) as STEC. The mcr-1 gene was found in 3.5% (2/57) of the EPEC strains and 5.7% (2/35) of the STEC strains. In this study, it was possible to confirm that the mcr-1 resistance gene is already circulating in the broiler flocks studied and may be associated with the pathogenic strains.


2021 ◽  
Author(s):  
S. Iakhno ◽  
S.S. Hellestveit ◽  
Ö.C.O. Umu ◽  
L.T. Bogevik ◽  
C.P. Åkesson ◽  
...  

1AbstractEnterotoxigenic Escherichia coli (ETEC) F4+: O149 is a causative agent for the development of post-weaning diarrhoea (PWD) in pigs that contributes to production losses. Yeast cell wall components used as a feed additive can modulate gut immunity and help protect animals from enteric infections. This work investigated how a novel yeast diet with high inclusion of yeast proteins (40% of crude protein) affected the course of ETEC mediated diarrhoea in weaner piglets from a farm with or without a history of post-weaning diarrhoea. We found that immune response to F4ab ETEC infection and appetite of the animals were altered by high inclusion C. jadinii yeast. The results indicate that the novel diet can support the diseased animals either directly through the effect of yeast beta-glucans and mannans or indirectly through the promotion of small intestine lactobacilli or both.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Charles R. Midgett ◽  
Kacey Marie Talbot ◽  
Jessica L. Day ◽  
George P. Munson ◽  
F. Jon Kull

AbstractEnteric infections caused by the gram-negative bacteria enterotoxigenic Escherichia coli (ETEC), Vibrio cholerae, Shigella flexneri, and Salmonella enterica are among the most common and affect billions of people each year. These bacteria control expression of virulence factors using a network of transcriptional regulators, some of which are modulated by small molecules as has been shown for ToxT, an AraC family member from V. cholerae. In ETEC the expression of many types of adhesive pili is dependent upon the AraC family member Rns. We present here the 3 Å crystal structure of Rns and show it closely resembles ToxT. Rns crystallized as a dimer via an interface similar to that observed in other dimeric AraC’s. Furthermore, the structure of Rns revealed the presence of a ligand, decanoic acid, that inhibits its activity in a manner similar to the fatty acid mediated inhibition observed for ToxT and the S. enterica homologue HilD. Together, these results support our hypothesis that fatty acids regulate virulence controlling AraC family members in a common manner across a number of enteric pathogens. Furthermore, for the first time this work identifies a small molecule capable of inhibiting the ETEC Rns regulon, providing a basis for development of therapeutics against this deadly human pathogen.


1986 ◽  
Vol 27 (2) ◽  
pp. 235-242
Author(s):  
Berit Κ. Djønne ◽  
Eivind Liven

2021 ◽  
Vol 9 (3) ◽  
pp. 522
Author(s):  
Lyudmila V. Gromova ◽  
Elena I. Ermolenko ◽  
Anastasiya L. Sepp ◽  
Yulia V. Dmitrieva ◽  
Anna S. Alekseeva ◽  
...  

In recent years, great interest has arisen in the use of autoprobiotics (indigenous bacteria isolated from the organism and introduced into the same organism after growing). This study aimed to evaluate the effects of indigenous bifidobacteria on intestinal microbiota and digestive enzymes in a rat model of antibiotic-associated dysbiosis. Our results showed that indigenous bifidobacteria (the Bf group) accelerate the disappearance of dyspeptic symptoms in rats and prevent an increase in chyme mass in the upper intestine compared to the group without autoprobiotics (the C1 group), but significantly increase the mass of chyme in the colon compared to the C1 group and the control group (healthy animals). In the Bf group in the gut microbiota, the content of opportunistic bacteria (Proteus spp., enteropathogenic Escherichia coli) decreased, and the content of some beneficial bacteria (Bifidobacterium spp., Dorea spp., Blautia spp., the genus Ruminococcus, Prevotella, Oscillospira) changed compared to the control group. Unlike the C1 group, in the Bf group there was no decrease in the specific activities of maltase and alkaline phosphatase in the mucosa of the upper intestine, but the specific activity of maltase was decreased in the colon chyme compared to the control and C1 groups. In the Bf group, the specific activity of aminopeptidase N was reduced in the duodenum mucosa and the colon chyme compared to the control group. We concluded that indigenous bifidobacteria can protect the microbiota and intestinal digestive enzymes in the intestine from disorders caused by dysbiosis; however, there may be impaired motor function of the colon.


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