title: Comparison of the contributions of heat-labile enterotoxin and heat-stable enterotoxin b to the virulence of enterotoxigenic Escherichia coli in F4ac receptor-positive young pigs.
abstract: In swine, the most common and severe enterotoxigenic Escherichia coli (ETEC) infections are caused by strains that express K88 (F4)(+) fimbriae, heat-labile enterotoxin (LT), heat-stable enterotoxin b (STb), and enteroaggregative E. coli heat-stable toxin 1. Previous studies based on a design that involved enterotoxin genes cloned into a nontoxigenic fimbriated strain have suggested that LT but not STb plays an important role in dehydrating diarrheal disease in piglets <1 week old and also enhances bacterial colonization of the intestine. In the present study, we compared these two toxins in terms of importance for piglets >1 week old with a study design that involved construction of isogenic single- and double-deletion mutants and inoculation of 9-day-old F4ac receptor-positive gnotobiotic piglets. Based on the postinoculation percent weight change per h and serum bicarbonate concentrations, the virulence of the STb(-) mutant (Delta estB) did not significantly differ from that of the parent. However, deletion of the LT genes (Delta eltAB) in the STb(-) mutant resulted in a complete abrogation of weight loss, dehydration, and metabolic acidosis in inoculated pigs, and LT complementation restored the virulence of this strain. These results support the hypothesis that LT is a more significant contributor than STb to the virulence of F4(+) ETEC infections in young F4ac receptor-positive pigs less than 2 weeks old. However, in contrast to previous studies with gnotobiotic piglets, there was no evidence that the expression of LT enhanced the ability of the F4(+) ETEC strain to colonize the small intestine.
authors.affiliation: Department of Veterinary & Biomedical Sciences, University of Nebraska-Lincoln, Lincoln, NE 68583, USA.
authors.forename: Joseph
authors.initials: J
authors.lastname: Erume
authors.forename: Emil M
authors.initials: EM
authors.lastname: Berberov
authors.forename: Stephen D
authors.initials: SD
authors.lastname: Kachman
authors.forename: Michael A
authors.initials: MA
authors.lastname: Scott
authors.forename: You
authors.initials: Y
authors.lastname: Zhou
authors.forename: David H
authors.initials: DH
authors.lastname: Francis
authors.forename: Rodney A
authors.initials: RA
authors.lastname: Moxley
mesh_terms: D000818:Animals; D001427:Bacterial Toxins / Q000235:genetics / Q000633:toxicity*; D003967:Diarrhea / Q000382:microbiology / Q000473:pathology / Q000662:veterinary*; D054307:Enterotoxigenic Escherichia coli / Q000472:pathogenicity*; D004768:Enterotoxins / Q000235:genetics / Q000633:toxicity*; D004927:Escherichia coli Infections / Q000382:microbiology / Q000473:pathology / Q000662:veterinary*; D029968:Escherichia coli Proteins / Q000235:genetics / Q000633:toxicity*; D005260:Female; D017353:Gene Deletion; D005856:Germ-Free Life; D008297:Male; D011971:Receptors, Immunologic / Q000378:metabolism; D013552:Swine; D013553:Swine Diseases / Q000382:microbiology / Q000473:pathology*; D014774:Virulence
chemical_list: D001427:Bacterial Toxins; D004768:Enterotoxins; D029968:Escherichia coli Proteins; D011971:Receptors, Immunologic; C034151:heat stable toxin (E coli); C037872:pili, bacterial receptor; C027538:heat-labile enterotoxin, E coli