Of the 44 isolates of type III from invasive episodes, 24 were cultured from blood, 18 were recovered from cerebrospinal fluid (CSF), and 1 each was grown from joint fluid and pulmonary secretions collected by tracheal aspiration. The 19 isolates from asymptomatic neonates were collected from the umbilicus (16 isolates), rectum (2 isolates), and throat (1 isolate). The sample also included isolates of types I (n = 8), lb (n = 16), Ic (n = 14), Ic/Il (n = 6), and II (n = 11) collected during disease episodes in 15 states, primarily from blood or cerebrospinal fluid. In addition, nine isolates from cases of bovine mastitis in France were examined: types Ia (n = 2), lb (n = 2), Ic (n = 4), and II (n = 1).The actual frequencies of recovery of the various serotypes from invasive episodes are not accurately reflected by the numbers of isolates in the collection studied. Non-type-Ill isolates were greatly overrepresented among the invasive isolates, strictly for purposes of genetic comparison. The human isolates were obtained from collections previously characterized for neuraminidase production and other phenotypes (13)(14)(15)(16)(17)(18)(19)(20)(21)(22). No non-type-Ill carrier isolates were analyzed.Many of the type III isolates obtained from humans were coded by S.J.M. for blind analysis in the laboratory ofR.K.S.Abbreviation: ET, electrophoretic type. 4731The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.
There is no standard method for the diagnosis of prosthetic joint infection (PJI). The contribution of 16S rRNA gene PCR sequencing on a routine basis remains to be defined. We performed a prospective multicenter study to assess the contributions of 16S rRNA gene assays in PJI diagnosis. Over a 2-year period, all patients suspected to have PJIs and a few uninfected patients undergoing primary arthroplasty (control group) were included.
To determine the extent to which the vagina, endocervix, and amniotic fluid screen the Escherichia coli strains responsible for neonatal infections, we studied the genetic relationships among 105 E. coli strains isolated from all of the ecosystems involved in this infectious process. Twenty-four strains were isolated from the intestinal flora, and 25 strains were isolated from the vaginas of pregnant women. Twenty-seven strains were isolated from the amniotic fluid, blood, and cerebrospinal fluid (CSF) of infected neonates. The intraspecies genetic characteristics of all of the isolates were determined by random amplified polymorphic DNA (RAPD) analysis, PCR ECOR (E. coli reference) grouping, and PCR virulence genotyping. A correlation was found between the intraspecies distributions of the strains in the A, B1, B2, and D ECOR groups and in the two major RAPD groups (I and II). Nevertheless, the distribution of the E. coli strains in the RAPD groups according to their anatomical origins was more significant than their distribution in the ECOR groups. This may be explained by the existence of an E. coli subpopulation, defined by the RAPD I group, within the ECOR B2 group. This RAPD I group presents a major risk for neonates: 75% of the strains isolated from patients with meningitis and 100% of the strains isolated from patients with bacteremia were in this group. The vagina and the amniotic fluid are two barriers that favor colonization by highly infectious strains. Indeed, only 17% of fecal strains belonged to the RAPD I group, whereas 52% of vaginal strains and 67% of amniotic fluid strains belonged to this subpopulation. The ibeA and iucC genes were significantly associated with CSF strains, whereas the hly and sfa/foc genes were more frequent in blood strains. These findings could serve as a basis for developing tools to recognize vaginal strains, which present a high risk for neonates, for use in prophylaxis programs.
In order to improve our understanding of the colonization of the pulmonary tract of cystic fibrosis (CF) patients by Pseudomonas aeruginosa, 162 isolates from five different ecological origins were studied. The genetic features of each isolate were determined by random amplification of polymorphic DNA (RAPD) and by searching for eight virulence genes (six known virulence genes, algD, lasB, toxA, plcH, plcN and exoS, and two genes encoding putative neuraminidases, nan1 and nan2). Five RAPD groups were identified. Most of the CF isolates were distributed equally in three of these groups (RA, RB and RC). The CF isolates in RB were related to isolates from a wide variety of origins. The CF isolates in RA were related to a population composed of 65 % of the non-CF isolates from pulmonary tract infections. RC was mainly composed of CF isolates that were related to 30 % of isolates from plants. All genes except exoS and nan1 were present in all isolates. The exoS and nan1 virulence factor genes were most prevalent in CF isolates. exoS, which encodes exoenzyme S, was present in 94 % of CF isolates but also in 80 % of non-CF isolates from pulmonary tract infections. nan1, which encodes a putative neuraminidase, was found in 82 . 5 % of the isolates from group RC, which was composed largely of CF isolates. In conclusion, three major genogroups of P. aeruginosa isolates, each of which exhibits peculiar genetic features, are able to colonize CF patients. This may have different consequences on the outcome of pulmonary disease.
Ninety-seven epidemiologically unrelated strains of Listeria monocytogenes were investigated for their sensitivities to quaternary ammonium compounds (benzalkonium chloride and cetrimide). The MICs for seven serogroup 1/2 strains were high. Three came from the environment and four came from food; none were isolated from human or animal samples. All 97 strains carried the mdrL gene, which encodes a multidrug efflux pump, and the orfA gene, a putative transcriptional repressor of mdrL. The absence of plasmids in four of the seven resistant strains and the conservation of resistance after plasmid curing suggested that the resistance genes are not plasmid borne. Moreover, PCR amplification and Southern blot hybridization experiments failed to find genes phylogenetically related to the qacA and smr genes, encoding multidrug efflux systems previously described for the genus Staphylococcus. The high association between nontypeability by phages and the loss of sensitivity to quaternary ammonium compounds are suggestive of an intrinsic resistance due to modifications in the cell wall.
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