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Background: Enterotoxigenic Escherichia coli (ETEC) commonly cause diarrhea in children living in developing countries and in travelers to those regions. ETEC are characterized by colonization factors (CFs) that mediate intestinal adherence. We assessed if bovine colostral IgG (bIgG) antibodies against a CF, CS17, or antibodies against CsbD, the minor tip subunit of CS17, would protect subjects against diarrhea following challenge with a CS17-expressing ETEC strain., Methods: Adult subjects were randomized (1:1:1) to receive oral bIgG against CS17, CsbD, or placebo. Two days prior to challenge, subjects began dosing 3 times daily with the bIgG products (or placebo). On day 3, subjects ingested 5 × 109 cfu ETEC strain LSN03-016011/A in buffer. Subjects were assessed for diarrhea for 120 hours postchallenge., Results: A total of 36 subjects began oral prophylaxis and 35 were challenged with ETEC. While 50.0% of the placebo recipients had watery diarrhea, none of the subjects receiving anti-CS17 had diarrhea (P = .01). In contrast, diarrhea rates between placebo and anti-CsbD recipients (41.7%) were comparable (P = 1.0)., Conclusions: This is the first study to demonstrate anti-CS17 antibodies provide significant protection against ETEC expressing CS17. More research is needed to better understand why anti-CsbD was not comparably efficacious. Clinical Trials Registration. NCT00524004., (Published by Oxford University Press for the Infectious Diseases Society of America 2019.)

Introduction: Enterotoxigenic Escherichia coli (ETEC) causes diarrhoea by producing heat-labile (LT) or heat-stable (ST) enterotoxins after colonizing the small intestine by means of colonization factors (CFs). Although detection of the toxins is sufficient for verification of ETEC isolates, toxin-positive strains may be further analyzed for the presence of CFs. Antibiotics may shorten the duration of diarrhoea caused by ETEC, but the rapid emergence of resistant strains limits their usefulness. Methodology: ETEC isolates collected 10 years apart were compared for the prevalence of toxin types, CFs and antibiotic resistance. DNA/DNA hybridization with digoxigenin (DIG)-labeled probes was used for the detection of toxin types, and CF-typing was performed by DNA hybridization using DIG-labeled probes for cfaD and CS6 with slide agglutination. Disk diffusion was used to determine antibiotic resistance. The presence of class 1 integrons was detected by PCR. Results: ST-positive isolates were the most prevalent among the isolates from 1988, but a significant shift towards LT-gene carriage was observed in the 1998 group. CFA/I and CFA/IV were the most common CF types within both groups. The most prevalent resistance patterns among these isolates were ACSTSXT followed by ASTSXT and ASSXT. Conclusion: Our study of the two groups of isolates showed that the rate of LT and ST gene carriage, as well as antibiotic resistance markers, has changed in the ten years separating the two bacterial populations. These variations show the importance of monitoring pathogenic bacteria to obtain a near realistic picture of the circulating bacterial pathogens. [ABSTRACT FROM AUTHOR]

We analyzed a randomly selected group of 30 diffusely adherent (DAEC), 30 enteropathogenic, 30 enteroaggregative, and five Shiga toxin-producing Escherichia coli strains isolated from children with diarrhea. Enterotoxigenic E. coli (ETEC) colonization factors (CFs) were evaluated by a dot-blot assay using 21 CF-specific monoclonal antibodies. Out of 95 non-ETEC strains, three DAEC were found to express coli surface antigen 20 (CS20). No other E. coli expressed CFs. We confirmed the three CS20-positive strains as ETEC-negative by repeat PCR and as toxin-negative by ganglioside-GM1-enzyme-linked immunosorbent assay. To our knowledge, this is the first study that has identified currently recognized CFs in non-ETEC diarrheagenic E. coli strains identified using molecular methods. CFs may be an unrecognized relevant adherence factor in other E. coli, which may then play a role in pathogenesis and the immune response of the host. [ABSTRACT FROM AUTHOR]