Debridement and retention of the prosthesis was the initial treatment modality in 30 patients with 33 Staphylococcus aureus prosthetic joint infections (PJIs) who presented to the Mayo Clinic between 1980 and 1991. Treatment failure, defined as relapse of S. aureus PJI or occurrence of culture-negative PJI during continuous antistaphylococcal therapy, occurred in 21 of 33 prosthetic joints. The 1-year and 2-year cumulative probabilities of treatment failure were 54% (95% confidence interval [CI], 36%-71%) and 69% (95% CI, 52%-86%), respectively. A median of 4 additional surgical procedures (range, 1-9) were required to control the infection in the 21 prosthetic joints for which treatment failed. Prostheses that were debrided >2 days after onset of symptoms were associated with a higher probability of treatment failure than were those debrided within 2 days of onset (relative risk, 4.2; 95% CI, 1.6-10.3). These data suggest that debridement and retention of the prosthesis as the initial therapy for PJI due to S. aureus is associated with a high cumulative probability of treatment failure and that the probability of treatment failure may be related to the duration of symptoms.
Human streptococci that belong to Streptococcus dysgalactiae subspecies equisimilis (SDSE) have long been known under the name of beta-hemolytic groups C and G streptococci. Extensive taxonomic studies during the past years have distinguished most of the veterinary pathogens belonging to Lancefield groups C and G from those of human origin. After being considered nonpathogenic for many years, SDSE is now recognized as an important bacterial pathogen. The clinical spectrum of diseases caused by this species closely resembles Streptococcus pyogenes infections, including the occurrence of poststreptococcal sequelae. In accordance with these observations, many of the virulence factors present in S. pyogenes can also be found in SDSE strains. High nucleotide-sequence identities in virulence genes and the association of these genes with mobile genetic elements support the hypothesis of extensive horizontal gene-transfer events among streptococcal species of the pyogenic group. Recent epidemiological studies have shown increasing numbers of invasive SDSE infections, often among immunocompromised patients, and suggest that this species will probably gain even more clinical importance in the near future. For a better understanding of the changing epidemiology and pathogenicity of SDSE, an increased awareness of these microorganisms as human pathogens and proper identification are mandatory.
Beta‐haemolytic streptococci are important human and animal pathogens: their genetic traits that are associated with the ability to infect human hosts remain, however, unclear. The surface protein, Lmb, mediates the adherence of Streptococcus agalactiae to human laminin. For further analysis of the corresponding gene, the adjacent genomic regions were sequenced. Lmb is localized on a putative composite transposon of 16 kb and is flanked by two copies of a novel insertion sequence element (ISSag2). It harbours the genes scpB and lmb, which are 98% identical with the respective genes of Streptococcus pyogenes. Analysis of the distribution of these genes and ISSag2 among 131 streptococcal strains revealed that all of the human isolates, but only 20% (12 of 61) of the animal isolates, contained scpB and lmb or their homologues. To investigate if the putative transposon can be mobilized, an erythromycin resistance marker was incorporated into the lmb gene of S. agalactiae. Screening for mutant strains with a regained susceptibility for erythromycin identified strains with a deletion of scpB, lmb, and one copy of ISSag2. We hypothesize that a horizontal gene transfer caused the exchange of scpB and lmb and that the ability of S. pyogenes, S. agalactiae and group C and G streptococcal strains to colonize or infect human hosts is dependent on their presence.
Despite an anticipated selective pressure, the prevalence of emm1 among isolates from throat infections in northwestern Germany remains high, but does not reflect the predominance of emm1 among invasive isolates in Germany.
The efficacy of treatment with a combination of ampicillin, imipenem, and vancomycin was compared with that of two-drug combinations or monotherapy in a model of experimental endocarditis using a strain of Enterococcus faecium with high-level resistance to vancomycin and moderate intrinsic resistance to ampicillin and imipenem. In vitro time-kill synergy studies demonstrated bactericidal synergistic activity only for the triple combination. In vivo, monotherapy with vancomycin was not effective. Treatment with either ampicillin or imipenem alone or in combination with vancomycin resulted in <4 log10 reduction in colony-forming units (cfu) per gram of vegetation. The combination of ampicillin with imipenem was highly active (an additional 5 log10 reduction in cfu per gram of vegetation compared with the most active single agent), but efficacy was not increased by the addition of vancomycin to ampicillin and imipenem. Therapy with the combination of ampicillin and imipenem may be effective for some strains of multidrug-resistant enterococcal infections.
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