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Review
. 2007 Aug;75(8):3688-95.
doi: 10.1128/IAI.01730-06. Epub 2007 May 14.

Mellowing out: adaptation to commensalism by Escherichia coli asymptomatic bacteriuria strain 83972

Per Klemm  1 , Viktoria Hancock, Mark A Schembri
Affiliations
Review

Mellowing out: adaptation to commensalism by Escherichia coli asymptomatic bacteriuria strain 83972

Per Klemm et al. Infect Immun. 2007 Aug.
No abstract available

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Figures

FIG. 1.
FIG. 1.
The E. coli ABU strain 83972 carries the fim, foc, and pap clusters, encoding type 1, F1C, and P fimbriae, respectively. However, all three gene clusters have accrued mutations that destroy their function, rendering 83972 incapable of expressing functional fimbriae on the surface of the cell (30, 56). The three fimbrial systems have been incapacitated in quite different ways (as indicated in gray). (A) The type 1 system has been inactivated by a major deletion encompassing 4.25 kb of the fim gene cluster. (B) The F1C system has been inactivated by point mutations in the fimbrial transport system, affecting the focD gene encoding the usher protein, making it impossible for the fimbrial components to reach the cell surface. (C) The P system has been made nonfunctional by the introduction of point mutations in the papG gene: 83972 can produce P fimbriae, but these are unable to bind to their cognate receptor.
FIG. 2.
FIG. 2.
Comparison of two prototypic UTI E. coli strains, the UPEC strain CFT073 and the ABU strain 83972. (A) Behavior of the prototype strains in the human UT. (B) Properties of the two strains. UPEC CFT073 was isolated from the blood of a patient with acute pyelonephritis, and its entire genome has been sequenced (72). The properties of E. coli 83972 were compiled from several studies (18, 30, 54, 56, 57).
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