Staphylococcus aureus nasal carriage is a well-defined risk factor of infection with this bacterium. The increased risk of S. aureus infection in nasal carriers is supported by the fact that the strains isolated from both colonization and infection sites are indistinguishable in most of the cases. Persistent nasal carriage seems to be associated with an increased risk of infection and this status could be defined now in clinical routine by using one or two quantitative nasal samples. There is evidence for supporting the detection of nasal carriage of S. aureus in patients undergoing cardiac surgery and in those undergoing hemodialysis in order to implement decolonization measures. More studies are needed to determine which carriers have the highest risk of infection and why decolonization strategies failed to reduce S. aureus infection in some other groups of patients.
Legionella viability was monitored during heat shock treatment at 70°C by a flow cytometric assay (FCA). After 30 min of treatment, for 6 of the 12 strains tested, the FCA still detected 10 to 25% of cells that were viable but nonculturable (VBNC). These VBNC cells were able to produce ATP and to be resuscitated after culture on amoebae.
15 August 2003 in The Journal of Infectious Diseases
In this study, we systematically investigated the resistance mechanisms to β-lactams, aminoglycosides, and fluoroquinolones of 120 bacteremic strains of Pseudomonas aeruginosa . Pulsed-field gel electrophoresis genotyping showed that 97 of these strains were represented by a single isolate, 10 by 2 and 1 by 3 clonally related isolates, respectively. Seventy-five percent (90 out of 120) of the bacteremic P. aeruginosa strains displayed a significant resistance to one or more of the tested antimicrobials (up to 11 for 1 strain). These strains were found to harbor a great diversity of resistance mechanisms (up to 7 in 1 strain), leading to various levels of drug resistance. Interestingly, 11 and 36% of the isolates appeared to overproduce the MexAB-OprM and MexXY-OprM efflux systems, respectively. Altogether, our results show that P. aeruginosa may accumulate intrinsic (overproduction of cephalosporinase AmpC, increased drug efflux, fluoroquinolone target mutations, and deficient production of porin OprD) and exogenous (production of secondary β-lactamases and aminoglycoside-modifying enzymes) resistance mechanisms without losing its ability to generate severe bloodstream infections. Consequently, clinicians should be aware that multidrug-resistant P. aeruginosa may remain fully pathogenic.