Surveillance for Antimicrobial Susceptibility among Clinical Isolates of Pseudomonas aeruginosa and Acinetobacter baumannii from Hospitalized Patients in the United States, 1998 to 2001

Abstract

Pseudomonas aeruginosa and Acinetobacter baumannii are the most prevalent nonfermentative bacterial species isolated from clinical specimens of hospitalized patients. A surveillance study of 65 laboratories in the United States from 1998 to 2001 found >90% of isolates of P. aeruginosa from hospitalized patients to be susceptible to amikacin and piperacillin-tazobactam; 80 to 90% of isolates to be susceptible to cefepime, ceftazidime, imipenem, and meropenem; and 70 to 80% of isolates to be susceptible to ciprofloxacin, gentamicin, levofloxacin, and ticarcillin-clavulanate. From 1998 to 2001, decreases in antimicrobial susceptibility (percents) among non-intensive-care-unit (non-ICU) inpatients and ICU patients, respectively, were greatest for ciprofloxacin (6.1 and 6.5), levofloxacin (6.6 and 3.5), and ceftazidime (4.8 and 3.3). Combined 1998 to 2001 results for A. baumannii isolated from non-ICU inpatients and ICU patients, respectively, demonstrated that >90% of isolates tested were susceptible to imipenem (96.5 and 96.6%) and meropenem (91.6 and 91.7%); fewer isolates from both non-ICU inpatients and ICU patients were susceptible to amikacin and ticarcillin-clavulanate (70 to 80% susceptible); and <60% of isolates were susceptible to ceftazidime, ciprofloxacin, gentamicin, or levofloxacin. From 1998 to 2001, rates of multidrug resistance (resistance to at least three of the drugs ceftazidime, ciprofloxacin, gentamicin, and imipenem) showed small increases among P. aeruginosa strains isolated from non-ICU inpatients (5.5 to 7.0%) and ICU patients (7.4 to 9.1%). From 1998 to 2001, rates of multidrug resistance among A. baumannii strains isolated from non-ICU inpatients (27.6 to 32.5%) and ICU patients (11.6 to 24.2%) were higher and more variable than those observed for P. aeruginosa. Isolates concurrently susceptible, intermediate, or resistant to both imipenem and meropenem accounted for 89.8 and 91.2% of P. aeruginosa and A. baumannii isolates, respectively, studied from 1998 to 2001. In conclusion, for aminoglycosides and most ␤-lactams susceptibility rates for P. aeruginosa and A. baumannii were constant or decreased only marginally (<3%) from 1998 to 2001. Greater decreases in susceptibility rates were, however, observed for fluoroquinolones and ceftazidime among P. aeruginosa isolates.

Antimicrobial susceptibility patterns among bacteria isolated from intensive care units of the largest teaching hospital at the northwest of Iran

“…The overall resistance rate of antimicrobials was higher in the current study than in other reports (Gunseren et al, 1999;Mendes et al, 2005;Styers et al, 2006;Patzer, Dzierzanowska, Turner, 2002;Gonlugur et al, 2004;Karlowsky et al, 2003). Moreover, the resistance rate to cephalosporins (79.5%-87.8%) was comparable to that in Iran (Hadadiet al, 2008), but higher than reported in foreign studies (Gunseren et al, 1999;Al-Lawati, Crouch, Elhag, 2000;Glupczynski et al, 2001;Patzer, Dzierzanowska,Turner, 2002;Gonlugur et al, 2004;Karlowsky et al, 2003;Meric et al, 2005).…”

Molecular Detection of the VirulentExoUGenotype ofPseudomonas aeruginosaIsolated from Infected Surgical Incisions

“…The results were interpreted according to guidelines recommended by the Clinical and Laboratory Standards Institute [15]. Multi-drug-resistant (MDR) P. aeruginosa isolates were defined as resistant to at least three of the following antibiotics: Cefotaxime or cefepime, imipenem, gentamicin, or levofloxacin [16].…”

Genetic Environments of the rmtA Gene in Pseudomonas aeruginosa Clinical Isolates

“…Aminoglycosides are clinically effective agents for treating infections caused by P. aeruginosa as well as other gram-negative bacilli. However, multidrug resistance is rapidly emerging in P. aeruginosa, whose spectrum of resistance often includes aminoglycosides as well as broad-spectrum ␤-lactams and fluoroquinolones (15). The most frequently encountered molecular mechanism for aminoglycoside resistance in P. aeruginosa is the production of aminoglycoside-modifying enzymes such as plasmid-dependent acetyltransferase (AAC), adenylyltransferase (AAD), and phosphotransferase (APH) (6,17,23).…”