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S. maltophilia: A Multi-Resistant Nosocomial Pathogen
Abstract & Commentary
By Robert R. Muder, MD, Hospital Epidemiologist, Pittsburgh VA Medical Center, Section Editor, Hospital Epidemiology, is Associate Editor for Infectious Disease Alert.
Dr. Muder does research for Aventis and Pharmacia.
Stenotrophomonas maltophilia (formerly known as Pseudomonas maltophilia, Xanthomonas maltophilia) is a motile, gram-negative bacillus that is widely distributed in nature, particularly in water and soil. It rarely causes disease in healthy hosts, but it can be a particularly troublesome pathogen in highly compromised, hospitalized patients. The most serious infections caused by S. maltophilia are catheter-related bacteremia and pneumonia.1 Central venous catheters are the most frequent source of bacteremia; malignancy, neutropenia, and receipt of broad spectrum antimicrobial therapy are notable risk factors. S. maltophilia bacteremia often presents as "breakthrough" bacteremia, that is, occurring while the patient is receiving antimicrobials.
The other typical infection caused by S. maltophilia is hospital-acquired pneumonia, particularly in patients receiving mechanical ventilation; pneumonia is the second most frequent source of bacteremia. It should be noted, however, that S. maltophilia often colonizes the sputum of ventilated patients without pneumonia; differentiating infection from colonization in a patient with underlying pulmonary pathology may be problematic. Approximately 10% of patients with cystic fibrosis are colonized with S. maltophilia; the incidence of colonization increases with the duration of the illness. It is not clear that colonization of cystic fibrosis is itself an independent predictor of disease severity.
S. maltophilia may cause infection at a variety of other sites. Ocular infections, including keratitis and endophthalmitis, may occur after ophthalmologic surgery. Soft tissue infections occur after contamination of wounds with soil. Among hospitalized patients, isolation of S. maltophilia from wounds typically represents colonization rather than infection. A notable exception are neutropenic patients, in whom S. maltophilia may cause severe soft tissue infection, often with associated bacteremia.2 S. maltophilia is an occasional cause of endocarditis in patients with prosthetic heart valves or a history of intravenous drug abuse.3
Treatment of S. maltophilia infection is problematic due to the organism's intrinsic resistance to multiple classes of antimicrobials.4 It possesses two separate βeta-lactamases, a zinc containing penicillinase and a cephalosporinase. Nearly all isolates of S. maltophilia are highly resistant to carbapenems. Resistance to third generation cephalosporins and anti-pseudomonal penicillins is variable. Interestingly, many isolates are susceptible to ticarcillin/clavulanate, but nearly all are resistant to piperacillin/tazobactam.
S. maltophilia isolates frequently have drug efflux pumps that mediate resistance to multiple classes of antimicrobials, including βeta-lactams, aminoglycosides, and quinolones. Susceptibility to the latter two classes of agents is highly variable. MICs to newer agents, such as moxifloxacin and gatifloxacin, tend to be lower than to older agents, such as ciprofloxacin and levofloxacin. Historically, trimethoprim-sulfamethoxazole has been highly active against S. maltophilia. Recent surveillance data show an increase in resistance,5 so that susceptibility of trimethoprim-sulfamethoxazole can't be assumed. Limited data indicate that S. maltophilia is usually susceptible to tigecycline, although clinical experience is lacking.
In vitro studies have identified a number of antimicrobial combinations with synergistic activity against S. maltophilia. Trimethoprim/sulfamethoxazole and ticarcillin/clavulanate are synergistic, and may demonstrate in vitro synergy, even if the isolate is resistant to both combinations. Synergy between quinolones and third generation cephalosporins has also been documented.
As S. maltophilia tends to cause infection in highly compromised patients, and is often resistant to multiple classes of agents, appropriate therapy can be challenging. Although data from clinical trials is lacking, observational data from series of patients with bacteremia suggests that multi-drug treatment is associated with lower mortality than single agent treatment.4 Candidates for multi-drug therapy include neutropenic patients, patients with bacteremia, and patients with hospital-acquired pneumonia. Combination therapy should consist of one βeta-lactam agent, such as a third generation cephalosporin or ticarcillin/clavulanate (NOT piperacillin/tazobactam) plus either trimethoprim/sulfamethoxazole or a quinolone. The choice of individual agents should be based on the results of in vitro testing. Tigecycline is an option if high level resistance or allergy to other agents exists.
Less severe infection, such as UTI or uncomplicated soft tissue infection, can usually be managed with a single agent. Trimethoprim-sulfamethoxazole is the preferred agent if the isolate is susceptible. It is probably best to avoid quinolone monotherapy since emergence of quinolone resistance on therapy can occur.