Recent reports have revealed the existence of widespread extensively drug-resistant (XDR) P. aeruginosa high-risk clones in health care settings, but there is still scarce information on their specific chromosomal (mutational) and acquired resistance mechanisms. Up to 20 (10.5%) of 190 bloodstream isolates collected from 10 Spanish hospitals met the XDR criteria. A representative number (15 per group) of isolates classified as multidrug-resistant (MDR) (22.6%), resistant to 1 to 2 classes (moderately resistant [modR]) (23.7%), or susceptible to all antibiotics (multiS) (43.2%) were investigated in parallel. Multilocus sequence typing (MLST) analysis revealed that all XDR isolates belonged to sequence type 175 (ST175) ( n = 19) or ST111 ( n = 1), both recognized as international high-risk clones. Clonal diversity was higher among the 15 MDR isolates (4 ST175, 2 ST111, and 8 additional STs) and especially high among the 15 modR (13 different STs) and multiS (14 STs) isolates. The XDR/MDR pattern in ST111 isolates correlated with the production of VIM-2, but none of the ST175 isolates produced acquired β-lactamases. In contrast, the analysis of resistance markers in 12 representative isolates (from 7 hospitals) of ST175 revealed that the XDR pattern was driven by the combination of AmpC hyperproduction, OprD inactivation (Q142X), 3 mutations conferring high-level fluoroquinolone resistance (GyrA T83I and D87N and ParC S87W), a G195E mutation in MexZ (involved in MexXY-OprM overexpression), and the production of a class 1 integron harboring the aadB gene (gentamicin and tobramycin resistance). Of particular interest, in nearly all the ST175 isolates, AmpC hyperproduction was driven by a novel AmpR-activating mutation (G154R), as demonstrated by complementation studies using an ampR mutant of PAO1. This work is the first to describe the specific resistance markers of widespread P. aeruginosa XDR high-risk clones producing invasive infections.

Background. A dramatic decrease in the incidence of invasive pneumococcal disease (IPD) was observed among children and adults in the United States a

Fecal colonization with multiresistant Acinetobacter baumannii was evaluated in 189 consecutive patients in intensive care units (ICUs) during two different 2-month periods (October–November 1993 and May–June 1994). Rectal swabs were obtained weekly from admission to discharge from the ICU. Overall, 77 patients (41%) had multiresistant A. baumannii fecal colonization; colonization was detected in 55(71%) of the patients within the first week of their ICU stay. Clinical infections due to multiresistant A. baumannii occurred more frequently in patients with fecal colonization than in those without fecal colonization (26% vs. S%, respectively; P < .001). The reinforcement of isolation measures between study periods reduced both the number of fecal carriers of multiresistant A. baumannii (from 52% to 31%; P < .01) and the number of patients with multiresistant A. baumannii infections (from 17% to 11%; no statistical significance). The digestive tract of ICU patients could be an important epidemiologic reservoir for multiresistant A. baumannii infections in hospital outbreaks. Further prospective studies should be undertaken to define the relative significance of digestive tract colonization compared with other body site colonizations.