While foot infections in persons with diabetes are initially treated empirically, therapy directed at known causative organisms may improve the outcome. Many studies have reported on the bacteriology of diabetic foot infections (DFIs) over the past 25 years, but the results have varied and have often been contradictory. A number of studies have found that Staphylococcus aureus is the main causative pathogen (12,34,35), but two recent investigations reported a predominance of gram-negative aerobes (20, 47). The role of anaerobes is particularly unclear, because in many studies specimens were not collected or cultured properly to recover these organisms. Among those that did use appropriate methods, some report that anaerobes play a minimal role (2,7,15,21,46), while others suggest that Bacteroides fragilis is the predominant anaerobe isolated (1,3,17,57).These discrepancies could be partly due to differences in the causative organisms occurring over time, geographical variations, or the types and severity of infection included in the studies (1,20,47,51). In addition, some studies used a relatively small number of specimens, failed to report recent or concomitant antibiotic therapy, did not ensure that the specimen collection techniques would exclude superficial or colonizing organisms, or even make clear whether or not the wound was clinically infected. Also, laboratory processing of the samples may have been inadequate to grow anaerobes or fastidious organisms, and protocols that classify potential pathogens (e.g., coagulase-negative staphylococci [CoNS] or Corynebacterium species) as colonizers may have been used (4,46,49).While S. aureus and beta-hemolytic streptococci are widely recognized as pathogens in early DFIs, the role of other frequently isolated organisms is less clear to both the clinician and the microbiology laboratory. Previous studies have shown that when optimal specimen collection, transport, and culture techniques are used, multiple organisms are usually recovered from DFIs (6,14,23,29,30,45,55). Furthermore, some studies suggest that the interactions of organisms within these polymicrobial mixtures lead to the production of virulence factors, such as hemolysins, proteases, and collagenases, as well as short-chain fatty acids, that cause inflammation, impede wound healing, and contribute to the chronicity of the infection (5,52,53,56). In such mixtures, biofilms that impede the penetration of antimicrobial agents into the infected site may also form (25). Thus, the presence of multiple species can have important clinical implications that should not be overlooked (5, 23).
During the 12-year period from 1993 to 2004, antimicrobial susceptibility profiles of 74,394 gram-negative bacillus isolates recovered from intensive care unit (ICU) patients in United States hospitals were determined by participating hospitals and collected in a central location. MICs for 12 different agents were determined using a standardized broth microdilution method. The 11 organisms most frequently isolated were Pseudomonas aeruginosa (22.2%), Escherichia coli (18.8%), Klebsiella pneumoniae (14.2%), Enterobacter cloacae (9.1%), Acinetobacter spp. (6.2%), Serratia marcescens (5.5%), Enterobacter aerogenes (4.4%), Stenotrophomonas maltophilia (4.3%), Proteus mirabilis (4.0%), Klebsiella oxytoca (2.7%), and Citrobacter freundii (2.0%). Specimen sources included the lower respiratory tract (52.1%), urine (17.3%), and blood (14.2%). Rates of resistance to many of the antibiotics tested remained stable during the 12-year study period. Carbapenems were the most active drugs tested against most of the bacterial species. E. coli and P. mirabilis remained susceptible to most of the drugs tested. Mean rates of resistance to 9 of the 12 drugs tested increased with Acinetobacter spp. Rates of resistance to ciprofloxacin increased over the study period for most species. Ceftazidime was the only agent to which a number of species (Acinetobacter spp., C. freundii, E. aerogenes, K. pneumoniae, P. aeruginosa, and S. marcescens) became more susceptible. The prevalence of multidrug resistance, defined as resistance to at least one extended-spectrum cephalosporin, one aminoglycoside, and ciprofloxacin, increased substantially among ICU isolates of Acinetobacter spp., P. aeruginosa, K. pneumoniae, and E. cloacae.Gram-negative bacilli (GNB) are a common cause of sepsis, pneumonia, urinary tract infections, and postsurgical infections in patients in acute care hospitals (14, 24). Antimicrobial resistance among GNB is increasing worldwide (21). This is a major public health problem and a cause for both substantial morbidity and mortality among hospitalized patients. A direct correlation has been shown between resistance of GNB and patient mortality, cost of patient care, and length of stay in the hospital (3,22,26,28). The problem of GNB resistance is of particular concern in the intensive care unit (ICU) setting.The most important determinant in the successful management of infections in patients in the ICU is prompt institution of effective empirical antimicrobial therapy; inappropriate empirical therapy affects both patient mortality rates and patient time spent in the ICU (12, 17). Optimizing empirical therapy requires knowledge of likely antimicrobial resistance patterns. With the aim of tracking resistance rates among GNB as the causes of infection in patients in U.S. ICUs, Merck Research Laboratories (Merck & Co., Upper Gwynedd, PA) established a multicenter laboratory-based surveillance program in 1993. Two previous reports from this investigation were published in 1996 and 2003 (13, 20). The current report describes the ...
Nosocomial primary BSI due to S. aureus significantly prolongs the hospital stay. Primary nosocomial BSIs due to MRSA result in an approximate threefold increase in direct cost, compared with those due to MSSA.
Ertapenem is more effective than cefotetan in the prevention of surgical-site infection in patients undergoing elective colorectal surgery but may be associated with an increase in C. difficile infection. (ClinicalTrials.gov number, NCT00090272 [ClinicalTrials.gov].).
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