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editorial
. 1999 Jan;12(1):180–181. doi: 10.1128/cmr.12.1.180

Diarrhea-Associated Diffusely Adherent Escherichia coli

Chantal Le Bouguénec 1
PMCID: PMC88912  PMID: 10375277

This letter is in response to the recently published review by Drs. Nataro and Kaper (9). Although I appreciate the enormity of compiling such a manuscript on a subject as wide as that of intestinal pathogenic Escherichia coli, I would like to clarify a number of points.

My comments relate to the section on diffusely adherent E. coli. Studies have shown that the daa gene cluster, which was described in 1989 and codes for the fimbrial F1845 adhesin, has the same genetic organization as and is closely related to the afa gene clusters, which code for the afimbrial adhesins (AFA) and were first described in 1985 (1–3, 7). I do not agree that a reliable PCR assay has yet to be developed for the afa/daa operons; in fact, such an assay has already been described (8). This assay has already been used in several studies to demonstrate the association of afa-positive strains with diarrhea (4, 5). In the review by Nataro and Kaper (9), the authors describe the use of a 700-bp daa fragment as a probe for the detection of afa/daa; neither the size of the fragment nor the cited reference is correct. Indeed, the daa probe defined by Bilge et al. consisted of a 380-bp fragment internal to the daaC gene (1).

We determined the nucleotide sequence of the afa operon, and based on this sequence we have proposed that the afaB and afaC genes are involved in the biogenesis of the adhesive structure by coding for a chaperone and an usher (2). It was only based on similarities to afaB and afaC that the daaB and daaC genes were allocated similar functions. It is disappointing that a function was attributed to daa genes without reference to our work (see Fig. 5 and page 184 of reference 9). While the afaD/daaD gene is described in the review as a “cryptic” gene, we have also recently published work that suggests a role for AfaD (3, 6). We found that AfaD is an invasin mediating the internalization of adherent bacteria into epithelial cells (6), a finding which illustrates that the afa/daa gene clusters are unique in encoding products which regulate both the adhesion of bacteria to epithelial cells and the invasion of these cells.

REFERENCES

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Clin Microbiol Rev. 1999 Jan;12(1):180–181.

AUTHORS’ REPLY

James P Nataro 1, James B Kaper 1

It is unfortunate that Dr. Le Bouguénec feels that her work has not been appropriately cited in our review. In no way did we intend to disparage Dr. Le Bouguénec or her excellent work characterizing the Dr adhesins of Escherichia coli. However, we offer the following points in defense of our discussion of diffusely adherent E. coli (DAEC).

Of the six categories that we discussed in the review, DAEC has the least claim to human pathogenicity. Indeed, of the six categories, only DAEC has not been proven to be truly pathogenic by virtue of human volunteer studies or outbreak investigations. For this reason alone, our treatment of this E. coli category is much more superficial than those devoted to the other E. coli categories. Indeed, the nature of DAEC is confused further by the findings of Dr. Le Bouguénec that the DA adhesin F1845 and the AFA adhesins, originally implicated as uropathogenic adherence factors, are closely related and that the so-called DA probe (derived from the appropriately referenced F1845 daaC gene) cross-reacts with genes encoding the AFA. Thus, Dr. Le Bouguénec’s data appropriately call into question several classical epidemiologic studies, given that data specifically implicating AFA-positive E. coli as diarrheal pathogens are quite insufficient. The apparent overlap between uropathogenic and diarrheagenic E. coli strains suggests that the afa/daa gene cluster is probably not truly useful in the diagnosis of diarrheal pathogens and that other, as yet undescribed virulence factors that are specific for diarrheagenic DAEC would be more appropriate tools for diagnosis. It should be noted that the PCR assay proposed for DAEC is subject to the same uncertainties as the DA probe. We anticipate that in the near future, Dr. Le Bouguénec and others will identify molecular targets that are appropriate for DAEC diagnosis and detection. We expect that further reviews by us and others will highlight such developments.

With regard to other points of Dr. Le Bouguénec’s letter, we agree that her work was instrumental in attributing a function to the daa genes, but we stand by our three chosen references for our discussion of F1845. Dr. Le Bouguénec points out that a function was not attributed to the afaD gene of AFA-III, with which she has done excellent work. However, since we do not as yet consider the AFA-III factor to be a diarrhea-related adhesin, we chose not to discuss this work. Moreover, Dr. Le Bouguénec’s data implicate the AfaD product as a putative invasin, yet there are no data suggesting that DAEC is invasive in vivo or that hers or other “prototype” DAEC strains are in fact pathogenic at all.

In a review of this magnitude, it is impossible to fully discuss all aspects of each E. coli pathotype. Accordingly, an effort was made to emphasize categories of proven and emerging importance. We hope that authors whose work was not covered in extensive detail understand this perspective.

Articles from Clinical Microbiology Reviews are provided here courtesy of American Society for Microbiology (ASM)

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