Multidrug-resistant Pseudomonas aeruginosa producing PER-1 extended-spectrum serine-beta-lactamase and VIM-2 metallo-beta-lactamase.

MA. The isolation of strains of rickettsiae of the spotted fever group in Israel and their differentiation from other members of the group by immunofluorescence methods. Scand J Infect Dis 1974;6:53-62. 7. Beati L, Finidori JP, Gilot B, Raoult D. Comparison of serologic typing, sodium dodecyl sulfate-polyacrylamide gel electrophore-sis protein analysis, and genetic restriction fragment length polymorphism analysis for identification of rickettsiae: characterization of two new rickettsial strains. gene comparison, a new tool for phylogenetic analysis, and its application for the rickettsiae. Int J Syst Bacteriol 1997;47:252-61. 9. Fournier PE, Roux V, Raoult D. Phylogenetic analysis of spotted fever group rickettsiae by study of the outer surface protein rOmpA. Laboratory diagnosis of rickettsioses: current approaches to diagnosis of old and new rickettsial diseases. To the Editor: In Pseudomonas aeruginosa, secondary beta-lactamases with extended substrate specificity can be responsible for acquired resistance to the most powerful antipseudomonal beta-lactams, such as expanded-spectrum cephalosporins and carbapenems (1). A number of these enzymes have been described, including extended-spectrum serine-beta-lactamases (ESBLs) of groups 2be and 2d (e.g., PER-1 and various OXA-type enzymes) (2,3) and metallo-beta-lactamases of group 3 (e.g., IMP-1 and the recently described VIM-1 and VIM-2 enzymes) (2,4,5). The secondary ESBLs can degrade penicillins, expanded-spectrum cepha-losporins, and monobactams (but not carbapenems) and are often susceptible to serine-beta-lactamase inhibitors (1-3). The secondary metallo-beta-lactamases, on the other hand, are notable for their carbapenemase activity and can degrade virtually all beta-lactams except monobactams, while being resistant to the currently available inhibitors (1,2,5,6). On March 2000, a multidrug-resistant P. aeruginosa (isolate VA-182/00) was isolated in pure culture from a bronchial washing of a 58-year-old patient with multiple myeloma. The patient had been admitted 15 days earlier to the Varese University Hospital with a diagnosis of pneumonia and had been treated with ciprofloxacin (0.5 g twice a day) plus piperacillin (2 g three times a day) for 12 days, and then with imipenem/cilastatin (0.5 g three times a day). No cultures of respiratory tract specimens were done earlier in hospitalization. Multiple myeloma had been diagnosed in 1997, and the patient had been treated with multiple cycles of antiproliferative chemotherapy and had received autolo-gous peripheral blood stem cell transplantation. According to clinical records, P. aeruginosa had not been isolated previously during this patient's protracted illness. In vitro susceptibility testing showed that the P.cin and levofloxacin (MICs, >32 µg/mL). Only piperacillin and piperacillin/tazobactam had MIC values slightly lower than the breakpoints …