Orthopaedic-implant infections by Escherichia coli: molecular and phenotypic analysis of the causative strains.

OBJECTIVES: Little is known about Escherichia coli Orthopaedic Implant Infections (OII) pathogenesis. Thus, we compared 30 clinical strains isolated in this context with 30 clinical strains of faecal origin, in order to identify phenotypic and genetic features related to E. coli OII. METHODS: Phylogenetic analysis and detection of 19 virulence genes were performed by PCR. Ability to form biofilm was studied using the crystal violet reference method and the innovative BioFilm Ring Test(®). RESULTS: Most of the OII isolates (56.7%) belonged to the virulence-associated phylogenetic group B2, but did not present a specific set of virulence factors. S fimbriae was the only adhesin significantly associated with OII isolates. Isolates varied greatly in their ability to form biofilm but OII isolates did not produce significantly more biofilm in vitro than isolates of faecal origin, whatever the method used. CONCLUSIONS: Neither a specific pathogenic signature nor an increased ability to form biofilm in vitro was detected in E. coli strains isolated from OII. Nevertheless, genetic properties of these isolates could provide a clue to their origin. Hence, we found that virulence factors of uropathogenic strains and urological disorders were frequently detected among our OII cohort.

Association of glycoprotein B and immediate early-1 genotypes with human leukocyte antigen alleles in renal transplant recipients with cytomegalovirus infection.

BACKGROUND: Numerous risk factors for cytomegalovirus (CMV) infection or disease, or both, such as serostatus of donor and recipient, immunosuppressive regimen, or intensity of viral load, have been identified in renal transplant recipients. Additional parameters may be involved, notably, genetic variability of both host and virus, which could modulate the efficacy of the immune response. METHODS: Active CMV infection was analyzed retrospectively in 634 renal transplant recipients, according to human leukocyte antigen (HLA)-A, HLA-B, and HLA-DR alleles; CMV serostatus; presentation of the disease; and variations in the coding sequences of glycoprotein (g) B and IE1 proteins. RESULTS: Active infection occurred in 141 of 634 patients: seropositivity of the donor and the recipient were identified as risk factors. Patients carrying the HLA-A11, HLA-A32, or HLA-DR11 allele developed active infection more frequently, whereas none of the patients with the HLA-B16 or HLA-B55 allele was actively infected. Significant independent associations between some genotypes and particular HLA alleles were observed: gB1 was more frequent in the HLA-A24 or HLA-B7 context and underrepresented in patients with HLA-DR11; gB2 was more frequent in HLA-A32 or HLA-DR11 carriers; and an increased frequency of gB3 was observed in the HLA-A29 context. Considering the IE1-2 genotype, increased frequency was noted for HLA-A3 carriers, whereas this type was underrepresented for patients with the HLA-DR11 allele. CONCLUSION: Data strongly suggest that differential presentation of polymorphic gB or IE peptides by HLA molecules or differential recognition by host CD8+ and CD4+ T lymphocytes, or both, should modulate immunologic response and then CMV pathogenesis in renal transplant patients.