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Clinical Microbiology Reviews, January 1999, p. 180-181, Vol. 12, No. 1
0893-8512/99/$00.00+0
LETTERS TO THE EDITOR
Diarrhea-Associated Diffusely Adherent Escherichia
coli
LETTER
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
| 1.
|
Bilge, S. S.,
C. R. Clausen,
W. Lau, and S. L. Moseley.
1989.
Molecular characterization of a fimbrial adhesin, F1845, mediating diffuse adherence of diarrhea-associated Escherichia coli to HEp-2 cells.
J. Bacteriol.
171:4281-4289[Abstract/Free Full Text].
|
| 2.
|
Garcia, M.-I.,
A. Labigne, and C. Le Bouguénec.
1994.
Nucleotide sequence of the afimbrial-adhesin-encoding afa-3 gene cluster and its translocation via flanking IS1 insertion sequences.
J. Bacteriol.
176:7601-7613[Abstract/Free Full Text].
|
| 3.
|
Garcia, M.-I.,
P. Gounon,
P. Courcoux,
A. Labigne, and C. Le Bouguénec.
1996.
The afimbrial adhesive sheath encoded by the afa-3 gene cluster of pathogenic Escherichia coli is composed of two adhesins.
Mol. Microbiol.
19:683-693[Medline].
|
| 4.
|
Germani, Y.,
E. Bégaud,
P. Duval, and C. Le Bouguénec.
1996.
Prevalence of enteropathogenic, enteroaggregative, and diffusely adherent Escherichia coli among isolates from children with diarrhea in New Caledonia.
J. Infect. Dis.
174:1124-1126[Medline].
|
| 5.
|
Germani, Y.,
E. Bégaud,
P. Duval, and C. Le Bouguénec.
1997.
An Escherichia coli clone carrying the adhesin-encoding afa operon is involved in both diarrhoea and cystitis in twins.
Tr. R. Soc. Trop. Med. Hyg.
91:573.
|
| 6.
|
Jouve, M.,
M.-I. Garcia,
P. Courcoux,
A. Labigne,
P. Gounon, and C. Le Bouguénec.
1997.
Adhesion to and invasion of HeLa cells by pathogenic Escherichia coli carrying the afa-3 gene cluster are mediated by the AfaE and AfaD proteins, respectively.
Infect. Immun.
65:4082-4089[Abstract].
|
| 7.
|
Le Bouguénec, C.,
M.-I. Garcia,
V. Ouin,
J.-M. Desperrier,
P. Gounon, and A. Labigne.
1993.
Characterization of plasmid-borne afa-3 gene cluster encoding afimbrial adhesins expressed by Escherichia coli strains associated with intestinal and urinary tract infections.
Infect. Immun.
61:5106-5114[Abstract/Free Full Text].
|
| 8.
|
Le Bouguénec, C.,
M. Archambaud, and A. Labigne.
1992.
Rapid and specific detection of the pap, afa, and sfa adhesin-encoding operons in uropathogenic Escherichia coli strains by polymerase chain reaction.
J. Clin. Microbiol.
21:137-144.
|
| 9.
|
Nataro, J. P., and J. B. Kaper.
1998.
Diarrheagenic Escherichia coli.
Clin. Microbiol. Rev.
11:142-201[Abstract/Free Full Text].
|
| | | | |
Chantal Le Bouguénec
Pathogénie Bactérienne des Muqueuses
Institut Pasteur
28 rue du Dr. Roux
75724 Paris Cedex 15, France
|
AUTHORS' REPLY
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.
| | | | |
James P. Nataro
James B. Kaper
Departments of Medicine and Microbiology & Immunology
University of Maryland School of Medicine
Baltimore, Maryland
|
Clinical Microbiology Reviews, January 1999, p. 180-181, Vol. 12, No. 1
0893-8512/99/$00.00+0
This article has been cited by other articles:
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(2001). Characterization of AfaE Adhesins Produced by Extraintestinal and Intestinal Human Escherichia coli Isolates: PCR Assays for Detection of Afa Adhesins That Do or Do Not Recognize Dr Blood Group Antigens. J. Clin. Microbiol.
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