The prevalence of antimicrobial resistance among uropathogens causing acute uncomplicated cystitis in young women

Four hundred and fifty-two urine isolates from women with acute uncomplicated cystitis and a positive urine culture presenting to a sexually transmitted disease clinic were collected during 1989–1991, and 213 specimens were collected over 1995–1997. The predominant species was Escherichia coli, representing 68% of the isolates; others included Staphylococcus saprophyticus (8%), Group B streptococci (7%), Proteus spp. (6%), Klebsiella spp. (4%) and Enterococcus spp. (3%). More than 10% of the E. coli isolates were resistant to ampicillin, cephalothin, tetracycline and trimethoprim–sulfamethoxazole (TMP–SMX ) during both study periods, with the greatest increase in resistance to ampicillin and TMP/SMX between the two periods. Six hundred and four urinary tract infection isolates, including 83% E. coli, 7% S. saprophyticus, 3% Klebsiella spp. 2% Proteus spp., 2% enterococci, 1% Enterobacter spp. and 2% other organisms, were collected from women with acute cystitis attending a university student health service during 1995. Among E. coli isolates, 25% were resistant to ampicillin, 24% to tetracycline and 11% to TMP–SMX. Resistance to fluoroquinolones was essentially absent among gram-negative pathogens. Continued evaluation of susceptibility patterns of pathogens causing acute uncomplicated cystitis to traditional as well as new antimicrobials in well defined populations is necessary to ascertain the optimal empiric therapy

Prevalence of Mycoplasma Genitalium Determined by DNA Probe in Men with Urethritis

The prevalence of urethral infection with Mycoplasma genitalium was determined by use of a DNA probe in 203 men attending a sexually transmitted disease clinic. M genitalium was detected in 3 (14%) of 21 with acute gonococcal urethritis; 3 (10%) of 30 with acute chlamydia-positive non-gonococcal urethritis (NGU); 4 (13%) of 31 with acute chlamydia-negative NGU; 10 (27%) of 37 with persistent or recurrent NGU; and 10 (12%) of 84 with no urethritis. The organism was more prevalent in homosexual (11 [30%] of 37) than in heterosexual men (19 [11%] of 166; p = 0.009). These data do not support an important aetiological role for M genitalium in acute urethritis, but suggest that it may account for some cases of NGU that become persistent or recurrent. The higher prevalence of urethral infection in homosexual men suggests that M genitalium may reside in the gastrointestinal tract

Differential stability and trade-off effects of pathoadaptive mutations in the Escherichia coli FimH adhesin

FimH is the tip adhesin of mannose-specific type 1 fimbriae of Escherichia coli, which are critical to the pathogenesis of urinary tract infections. Point FimH mutations increasing monomannose (1M)-specific uroepithelial adhesion are commonly found in uropathogenic strains of E. coli. Here, we demonstrate the emergence of a mixed population of clonally identical E. coli strains in the urine of a patient with acute cystitis, where half of the isolates carried a glycine-to-arginine substitution at position 66 of the mature FimH. The R66 mutation induced an unusually strong 1M-binding phenotype and a 20-fold advantage in mouse bladder colonization. However, E. coli strains carrying FimH-R66, but not the parental FimH-G66, had disappeared from the patient's rectal and urine samples collected from 29 to 44 days later, demonstrating within-host instability of the R66 mutation. No FimH variants with R66 were identified in a large (>600 strains) sequence database of fimH-positive E. coli strains. However, several strains carrying genes encoding FimH with either S66 or C66 mutations appeared to be relatively stable in the E. coli population. Relative to FimH-R66, the FimH-S66 and FimH-C66 variants mediated only moderate increases in 1M binding but preserved the ability to enhance binding under flow-induced shear conditions. In contrast, FimH-R66 completely lost shear-enhanced binding properties, with bacterial adhesion being inhibited by shear forces and lacking a rolling mode of binding. These functional trade-offs may determine the natural populational instability of this mutation or other pathoadaptive FimH mutations that confer dramatic increases in 1M binding strength. Copyright © 2007, American Society for Microbiology. All Rights Reserved