Fimbrial Colonization Factor Research Articles

RISK OF DIARRHEA DURING THE FIRST YEAR OF LIFE ASSOCIATED WITH INITIAL AND SUBSEQUENT COLONIZATION BY SPECIFIC ENTEROPATHOGENS

The incidence of colonization by enteropathogenic, enterotoxigenic, enteroinvasive, and enterohemorrhagic Escherichia coli (detected by DNA hybridization with specific radiolabeled probes), Salmonella sp., Shigella sp., Campylobacter jejuni, and rotavirus was related to the presence of diarrhea in a cohort of 75 rural infants followed longitudinally during the first year of life. The study was carried out between August 1985 and February 1987 in the village of Lugar Sobre la Tierra Blanca, in the state of Morelos, 180 km southwest of Mexico City. Intestinal colonization by specific enteropathogens was followed with fecal cultures taken every fortnight and every time a child had diarrhea. Pathogens isolated from cultures taken in the 48 hours prior to the initiation of the diarrheal episode were considered to be associated with the disease. Diarrhea was detected in 82% of the children with initial isolation of enterohemorrhagic E. coli and in 64% of the children with enteropathogenic E. coli or Shigella sp. The risk of diarrhea associated with the initial isolation of other pathogens was lower, at 41% for rotavirus and approximately 25% for enterotoxigenic E. coli, Salmonella sp., and C. jejuni. Initial colonization by the enteropathogens studied, whether or not they were associated with diarrhea, prevented disease, but not colonization by the same organism, when the children were reinfected during the first year of life. Enteropathogenic E. coli adherence factor, human or porcine heat-stable enterotoxins, fimbrial colonization factor antigens, and Shiga-like toxins I and II were important pathogenic characteristics related to the presence of diarrhea and to protection against subsequent infection by the same organisms.

Towards a live oral vaccine against enterotoxigenic Escherichia coli of swine.

A live oral vaccine has been developed against scouring induced in piglets by enterotoxigenic Escherichia coli (ETEC). An attenuated strain of Salmonella typhimurium, G30, has been used as a vector for plasmids encoding the production of the fimbrial colonization factors of porcine ETEC. Initial studies with clones expressing K88 or K99 fimbriae have shown them to be well tolerated when administered orally in very high doses. The clones elicited serum, colostral and milk antibodies to the fimbrial antigens, and a challenge trial indicated that such responses were sufficient to ensure the passive transfer of protective immunity to suckling piglets. The possible advantages of this approach are discussed.

Identification of a new fimbrial structure in enterotoxigenic Escherichia coli (ETEC) serotype O148:H28 which adheres to human intestinal mucosa: a potentially new human ETEC colonization factor.

Three important fimbrial colonization factor antigens (CFAs) designated CFA/I, CFA/II, and E8775 were identified originally in some human enterotoxigenic Escherichia coli (ETEC) strains because of their mannose-resistant hemagglutination properties. To identify CFA, in strains lacking mannose-resistant hemagglutination properties we exploited the ability of human ETEC strains to adhere to human proximal small intestinal mucosa. ETEC strain B7A (O148:H28) was selected for study because it belongs to an epidemiologically important serotype and does not produce a known CFA, and yet it is known to be pathogenic and cause diarrheal disease in human volunteers. Results of an human enterocyte adhesion assay indicated that some bacteria in cultures of B7A produced adhesive factors. To select for such bacteria, cultured human duodenal mucosal biopsy samples were infected with B7A for up to 12 h, after which time a large percentage of the mucosal surface became colonized by bacteria. A new fimbrial structure morphologically distinct from CFA/I, CFA/II, and E8775 fimbriae and consisting of curly fibrils (approximately 3 nm in diameter) was readily identified when bacteria were subcultured from the mucosa and examined by electron microscopy. Identical fimbriae were produced by ETEC strain 1782-77 of the same serotype. Identification of these fimbriae only on bacteria subcultured from human intestinal mucosa strongly suggests that they promote mucosal adhesion of ETEC serotype O148:H28 and thus represent a potentially new human ETEC CFA.

Classification of pathogenic Escherichia coli according to serotype and the production of virulence factors, with special reference to colonization-factor antigens.

Multiple criteria are required to classify Escherichia coli isolates according to pathogenic grouping. There are three groups associated with intestinal illness. Acute watery diarrhea is the hallmark of enterotoxigenic E. coli, the majority of which belong to a small set of specific serotypes harboring plasmids encoding for the production of heat-stable enterotoxin and/or heat-labile enterotoxin and also for a fimbrial colonization-factor antigen. Bacterial dysentery is caused by specific, nonmotile Shigella-like E. coli serogroups identifiable by the property of tissue invasiveness. Specific virulence factors have not been defined for the traditional enteropathogenic E. coli serogroups, although the ability to colonize and overgrow the intestine appears to be of primary importance in this group. E. coli associated with extraintestinal infections generally belong to serogroups and serotypes other than those noted above; the virulence factors of these E. coli include polysaccharide capsular antigens, hemolysin, and fimbrial colonization factors that are antigenically complex and different from those of the enterotoxigenic E. coli.

Detection of enterotoxigenic Escherichia coli colonization factor antigen I in stool specimens by an enzyme-linked immunosorbent assay.

An enzyme-linked immunosorbent assay (ELISA) was employed to detect and quantitate the fimbrial colonization factor antigen (CFA/I) of enterotoxigenic Escherichia coli in stool specimens obtained from adult cases of diarrhea in which CFA/I-positive E. coli was the known causative agent. The inhibition method, or blocking technique, was used. In this method, a standardized dilution of human anti-CFA/I serum was preincubated with dilutions of stool extract before transfer to CFA/I-coated microtiter plate wells, and then ELISA was performed with alkaline phosphatase-conjugated anti-human immunoglobulin. CFA/I purified from E. coli strain H-10407 (O78:H11) was used. Acute-phase diarrheal stool specimens were found to contain approximately 3.0 mg of antigen (mean value) per g stool, whereas control (CFA/I-negative) specimens contained insignificant amounts (less than 0.03 mg/g) of antigen. Also, CFA/I was detected in culture fluids of CFA/I positive enterotoxigenic E. coli belonging to a variety of serotypes and was undetectable in similar preparations from P-strains (spontaneous CFA/I-negative derivatives) of the same test cultures. Equivalent results were obtained in ELISA tests by using bacterial cells taken from isolated colonies grown on CFA agar. These results indicate that the ELISA technique will be useful for the diagnosis of diarrhea caused by CFA/I-positive enterotoxigenic E. coli.

Fimbrial colonization factor CFA/1 protein from human enteropathogenic Escherichia coli strains : Purification, characterization and N-terminal sequence

FEBS LettersVolume 108, Issue 1 p. 107-110 Full-length articleFree Access Fimbrial colonization factor CFA/1 protein from human enteropathogenic Escherichia coli strains Purification, characterization and N-terminal sequence Per Klemm, Per Klemm Institute of Biochemical Genetics, University of Copenhagen, Øster Farimagsgade 2A, DK-1353 København K, DenmarkSearch for more papers by this author Per Klemm, Per Klemm Institute of Biochemical Genetics, University of Copenhagen, Øster Farimagsgade 2A, DK-1353 København K, DenmarkSearch for more papers by this author First published: December 01, 1979 https://doi.org/10.1016/0014-5793(79)81188-6Citations: 25AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL References 1 J.C.G. Ottow, Ann. Rev. Microbiol., 29, (1975), 79– 108. 2 J.N. Robertson, P. Vincent, M.E. Ward, J. Gen. Microbiol., 102, (1977), 169– 177. 3 D.G. Evans, D.J. Evans, W.S. Tjoa, H.L. Dupont, Infect. Immun., 19, (1978), 727– 736. 4 J.H. Freer, A. Ellis, T. Wadström, C.J. Smyth, FEMS Microbiol. Lett., 3, (1978), 277– 281. 5 R.J. Gross, A. Cravioto, S.M. Scotland, T. Cheasty, B. Rowe, FEMS Microbiol. Lett., 3, (1978), 231– 233. 6 I. Ørskov, F. Ørskov, Med. Microbiol. Immunol., 163, (1977), 99– 110. 7 D.G. Evans, R.P. Silver, D.J. Evans, D.G. Chase, S.L. Gorbach, Infect. Immun., 12, (1975), 656– 667. 8 D.J. Evans, D.G. Evans, Infect. Immun., 8, (1973), 322– 328. 9 D.G. Evans, D.J. Evans, H.L. Dupont, J. Infect. Dis., 136, (1977), S118– S123. 10 P.R. Eng, C.O. Parkers, Anal. Biochem., 59, (1974), 323– 325. 11 P. Klemm, F. Poulsen, M.K. Harboe, B. Foltmann, Acta Chem. Scand., 30, (1976), 979– 984. 12 R. Zeeuws, A.D. Strosberg, FEBS Lett., 85, (1978), 68– 72. 13 W. Gaastra, P. Klemm, J.M. Walker, F.K. de Graaf, FEMS Microbiol. Lett., 6, (1979), 15– 18. 14 F.R. Mooi, F.K. de Graaf, FEMS Microbiol. Lett., 5, (1979), 17– 20. 15 M.A. Hermodson, K.C.S. Chen, T.M. Buchanan, Biochemistry, 17, (1978), 442– 445. 16 L.O. Frøholm, K. Sletten, FEBS Lett., 73, (1977), 29– 32. 17 W. Paranchych, L.S. Frost, M. Carpenter, J. Bacteriol., 134, (1978), 1179– 1181. Citing Literature Volume108, Issue1December 01, 1979Pages 107-110 ReferencesRelatedInformation