INTRODUCTION — Stenotrophomonas (Xanthomonas) maltophilia is a multidrug-resistant gram-negative bacillus that is an opportunistic pathogen [1-4], particularly among hospitalized patients. S. maltophilia infections have been associated with high morbidity and mortality in severely immunocompromised and debilitated individuals.
The clinical features and management of S. maltophilia infections are discussed here. The general approach to gram-negative bacillary bacteremia, catheter-associated bloodstream infections, and hospital-acquired pneumonia are discussed elsewhere. (See "Gram-negative bacillary bacteremia in adults" and "Intravascular non-hemodialysis catheter-related infection: Treatment" and "Treatment of hospital-acquired and ventilator-associated pneumonia in adults".)
MICROBIOLOGY — S. maltophilia is a ubiquitous, aerobic, non-fermentative, gram-negative bacillus that is closely related to the Pseudomonas species [5]. The name signifies "a unit feeding on few substrates," based on the Greek roots stenos (narrow), trophos (one who feeds), and monas (a unit). Maltophilia means "affinity for malt," based on the Greek roots maltum (malt) and philia (affinity).
S. maltophilia is an obligate aerobe that grows well on commonly used laboratory media, including blood and MacConkey agars. It is lactose nonfermenting, oxidase-negative, and catalase-positive and can be reliably identified in the laboratory using standard biochemical tests. In addition, it is accurately identified by commercially available automated identification systems [4]. Matrix-assisted laser desorption/ionization (MALDI) identification of Stenotrophomonas is not yet standard for many microbiology laboratories.
S. maltophilia was first isolated in 1943 and, at the time, was named Bacterium bookeri. It was later classified within the genus Pseudomonas, then Xanthomonas, and then finally Stenotrophomonas in 1993 [4,6,7]. S. maltophilia is the only species of Stenotrophomonas known to infect humans [7], whereas its closest genetic relatives are plant pathogens [7,8]. It is frequently isolated from soil, water, animals, plant matter, and hospital equipment [4,9-21]. S. maltophilia has inherent ability to adhere to foreign materials and form a biofilm, rendering protection from host defenses as well as antimicrobial agents [18,19,22-26]. Factors contributing to this behavior include its positively charged surface and fimbrial adhesions [7,22-24,26-28].
In addition, S. maltophilia has intrinsic or acquired resistance mechanisms to several antibiotic classes. Resistance to beta-lactams is conferred by two inducible beta-lactamases, a zinc-containing penicillinase (L1) and a cephalosporinase (L2) [21,29-32]. An aminoglycoside acetyl-transferase confers resistance to aminoglycoside antibiotics [33-39]. Temperature-dependent changes in the outer membrane lipopolysaccharide (LPS) structure have been associated with added resistance to aminoglycoside antibiotics [18,40-43]. In addition, many strains of S. maltophilia possess efflux pumps, which confer further resistance to multiple antibacterial classes [39,44-47]. (See 'Efficacy of antibiotic options' below.)
There are uncertainties regarding the optimal approach to in vitro susceptibility testing given discrepancies between results of various methods [48-51]. The US Clinical and Laboratory Standards Institute (CSLI) has published disc-diffusion minimal inhibitory concentration (MIC) breakpoints for trimethoprim-sulfamethoxazole, minocycline, and levofloxacin and broth dilution MIC breakpoints for ticarcillin-clavulanic acid, ceftazidime, minocycline, levofloxacin, and chloramphenicol [18,49,52,53]. Etest may be used for evaluation of ceftazidime, minocycline, and chloramphenicol susceptibility. There are no MIC interpretive criteria for tetracycline or tigecycline, although susceptibility to tigecycline is assumed using interpretive criteria for Enterobacteriaceae [54]. In contrast, the European Committee on Antimicrobial Susceptibility Testing (EUCAST) has only published breakpoint criteria for trimethoprim-sulfamethoxazole [55].
EPIDEMIOLOGY — The reported incidence of S. maltophilia infections ranges from 7.1 to 37.7 cases per 10,000 discharges [4,39,48,56]. The incidence seems to be increasing as the population of patients at risk increases [1,4,49,57-59]. This increase is probably due to advances in the treatment of malignancy, increased use of invasive devices, and widespread use of broad-spectrum antibiotics.
Risk factors associated with S. maltophilia infection include admission to an intensive care unit (ICU), HIV infection, malignancy, cystic fibrosis, neutropenia, mechanical ventilation, central venous catheters, recent surgery, trauma, and previous therapy with broad-spectrum antibiotics [1,2,4,20,21,48,57,58,60]. S. maltophilia infections are typically hospital-acquired; even in community-acquired infections, most affected individuals have significant healthcare exposure or predisposing comorbidities (eg, prior trauma, immunocompromising condition, indwelling devices) [61].
A number of outbreaks of S. maltophilia have been described involving adult ICU patients [62-64], hematologic malignancy and bone marrow transplant recipients [65,66], hemodialysis patients [67], and neonates [68,69]. Patient exposure to contaminated tap water has been the suspected etiology in many outbreaks [64,66,68]. In addition, a number of outbreaks and pseudo-outbreaks have been associated with failures in endoscope reprocessing [70-74].
DISEASE ASSOCIATIONS — Pneumonia and bacteremia are the most common manifestations of infection [2,4,39,49,50,75-78].
Pulmonary infection — S. maltophilia pneumonia is usually hospital-acquired and most frequently occurs in mechanically ventilated patients. Compared with pulmonary colonization, infection is associated with underlying immunosuppression [79]. Clinical and radiographic findings are generally similar to those seen with other infectious causes of hospital-acquired pneumonia. However, in patients with hematologic malignancies, a syndrome of rapidly progressive and frequently fatal hemorrhagic pneumonia associated with S. maltophilia infection has been increasingly reported [9,80,81].
S. maltophilia is a recognized pathogen for cystic fibrosis patients in the United States, with overall prevalence rates similar to those of nontuberculous mycobacteria [82]. S. maltophilia infection correlates with decline in lung function in adult and pediatric cystic fibrosis patients; however, causality has not been determined [83,84]. (See "Cystic fibrosis: Antibiotic therapy for chronic pulmonary infection", section on 'Other pathogens'.)
Bacteremia — Most cases of S. maltophilia bacteremia are associated with indwelling catheters [3,85,86]. As an example, in a study of 207 oncology patients with a central venous catheter and S. maltophilia bloodstream infection, 73 percent of infections were deemed to be catheter-related, 22 percent were secondary (mainly from a pulmonary source), and 5 percent were thought to be primary and non-catheter related [85]. Many catheter-related S. maltophilia bloodstream infections are polymicrobial. Relapse of catheter-associated bacteremia, even up to 200 days after treatment of the initial infection, is also described and has been associated with prolonged neutropenia and catheter retention [87].
Other sources of bacteremia include the gastrointestinal tract or severe mucositis in patients with profound neutropenia [85,88]
Other manifestations — Less common manifestations of S. maltophilia infections include endocarditis, mastoiditis, peritonitis, meningitis, soft tissue infection, wound infection, urinary tract infection, and ocular infection [2,4,39,49,50,76-78,89]. Stenotrophomonas can also cause cutaneous manifestations, which may reflect metastatic infection or local infiltration [90,91]. Reported skin manifestations include cellulitis, infected ulcers, and ecthyma gangrenosum.
DIAGNOSIS OF INFECTION — S. maltophilia can be readily identified on culture of relevant clinical specimens. Growth of S. maltophilia from normally sterile sites (such as blood, pleural fluid, or peritoneal fluid) should be interpreted to represent true infection. However, since S. maltophilia can adhere to the mucosal surfaces of the upper airway and large bronchi and may colonize these areas without causing infection, it is important to differentiate colonization from true infection due to S. maltophilia, particularly from respiratory isolates.
In patients with clinical evidence of pneumonia (eg, new pulmonary infiltrate, decreased oxygenation, and fever and/or leukocytosis), cultures growing S. maltophilia (with or without other concurrent respiratory pathogens) from respiratory sites should be interpreted to be consistent with true infection.
In the absence of consolidation on chest radiography and other clinical signs of pulmonary infection, a positive respiratory tract isolate of Stenotrophomonas probably represents colonization rather than invasive disease. In a retrospective review of 92 patients presenting with acute respiratory symptoms and subsequently found to have respiratory cultures positive for S. maltophilia, there was no measurable impact of antibiotic therapy in the absence of chest radiograph consolidation [92].
Additionally, clinicians must use caution when interpreting culture data obtained from non-sterile sites such as indwelling urinary catheters, surgical drains, and vascular catheter hubs, given the organism's propensity to colonize foreign materials. In these situations, the assessment for clinical evidence of infection (eg, fever, leukocytosis, localized pain) is critical. In the absence of bacteremia or evidence of infection in other sterile sites (such as pleural fluid, peritoneal fluid), such culture findings may be presumed to reflect colonization rather than infection.
TREATMENT
Indications — S. maltophilia infections should be treated with antibiotics promptly given that delay in appropriate treatment can contribute to significant mortality. Whether isolation of S. maltophilia from a clinical specimen represents true infection rather than colonization warrants careful assessment, as colonization should not be treated and inappropriate antibiotic use contributes to added adverse effects and selection for resistant organisms. Distinguishing between infection and colonization is discussed elsewhere. (See 'Diagnosis of infection' above.)
In cases in which the distinction between infection and colonization is uncertain (eg, in a patient who is known to have airway colonization with S. maltophilia and subsequently develops clinical evidence of pneumonia), we recommend initiation of treatment for S. maltophilia until additional clinical information is available. After 48 to 72 hours, we re-evaluate the need for continued S. maltophilia therapy in such patients. We do not typically include S. maltophilia coverage in empiric treatment of pneumonia or for sepsis in critically ill patients or immunocompromised patients without prior evidence of S. maltophilia colonization.
Efficacy of antibiotic options — S. maltophilia is a multidrug-resistant organism, so antibiotic options are limited and clinical data are limited regarding optimal therapy. Trimethoprim-sulfamethoxazole (TMP-SMX) is the treatment of choice as it has the most reliable in vitro activity against S. maltophilia [93-95]. As an example, in a surveillance study of gram-negative organisms isolated from patients hospitalized with pneumonia between 2009 and 2012, susceptibility to TMP-SMX was documented for 96 percent of the 302 S. maltophilia isolates from United States hospitals and 98 percent of the 192 isolates from European hospitals [93]. Additionally, observational studies and case series report favorable clinical outcomes when TMP-SMX is used [57,96]. However, some patients are unable to tolerate TMP-SMX due to hypersensitivity reaction, drug toxicity, or other adverse reaction. Furthermore, in vitro resistance to TMP-SMX among S. maltophilia isolates has been increasingly reported, particularly in patients with cystic fibrosis [49,75,97,98].
Fluoroquinolones, in particular levofloxacin, are potential alternatives to TMP-SMX [94]. In the surveillance study discussed above, 75 to 84 percent of S. maltophilia pulmonary isolates were susceptible to levofloxacin [93]. Additionally, small retrospective studies have suggested similar clinical outcomes (microbiologic cure, clinical success, and short-term mortality rates) in S. maltophilia infection with fluoroquinolone versus TMP-SMX monotherapy [96,99]. However, in vitro studies raise concern about the potential selection of resistant mutants during treatment with fluoroquinolones [100,101]. Although data suggest that moxifloxacin may have similar in vitro activity as levofloxacin against S. maltophilia [102], there are no Clinical and Laboratory Standards Institute (CLSI) defined breakpoints for moxifloxacin. Therefore, it is our practice to preferentially use levofloxacin rather than moxifloxacin for treatment of S. maltophilia infections.
Minocycline and tigecycline also have low minimal inhibitory concentrations among S. maltophilia isolates [93,94,103], and each has been shown in small retrospective studies to be associated with clinical outcomes that are comparable to those with TMP-SMX [104,105]. However, low serum drug levels of tigecycline, which limit its utility for bloodstream infections, and concerns about higher mortality rates associated with tigecycline compared with other agents for pneumonia treatment dampen enthusiasm for this agent.
Pre-clinical data suggest that cefiderocol appears to have reliable in vitro activity against S. maltophilia, but clinical data are limited [106,107]. In a trial of cefiderocol for the treatment of multidrug-resistant gram-negative bacilli infections, only 5 patients with S. maltophilia infection (pneumonia) were included, and S. maltophilia-specific outcomes were not reported [108,109].
Ticarcillin-clavulanic acid had been proposed as an alternate therapeutic agent, although rates of in vitro resistance are reported to be as high as 55 percent [18,39,110], and the drug is unavailable in most countries (including the United States and Canada). Resistance rates to ceftazidime are also relatively high [94], and only 20 percent of isolates resistant to TMP-SMX and levofloxacin in one study were susceptible to ceftazidime-avibactam, using CLSI breakpoints for ceftazidime alone [111]. Polymyxins (eg, colistin sulfate) have variable rates of in vitro activity against S. maltophilia.
Otherwise, S. maltophilia has high rates of resistance, either through intrinsic or acquired mechanisms, to other beta-lactams, aztreonam, aminoglycosides, fosfomycin, and carbapenems. Resistance to carbapenems should be presumed regardless of susceptibility testing results.
Because of the high rates of resistance to many antibiotic classes, there has been interest in the potential for synergistic activity with combination regimens. Thus far, clinical data regarding benefit of combination therapy are limited, and so its role remains uncertain. In one prospective study of patients with S. maltophilia bacteremia, receipt of two or more of TMP-SMX, a third generation cephalosporin, and an extended-spectrum penicillin was associated with lower mortality rates compared with receipt of just one [57]. The evidence for combination therapy resides predominantly in in vitro studies. Several have reported in vitro synergy for various combinations of antibiotics including TMP-SMX plus ceftazidime, TMP-SMX plus ticarcillin-clavulanic acid, and ticarcillin-clavulanic acid plus ciprofloxacin [112-114].
Approach to antibiotic selection — TMP-SMX (administered as 15 mg/kg/day of the TMP component in three or four divided doses, adjusted for renal function) is the treatment of choice [7], and we usually use this for empiric (ie, prior to the availability of susceptibility testing results) and directed therapy (if the isolate is susceptible) of S. maltophilia infections. For empiric therapy of S. maltophilia infections in severely ill patients, patients with neutropenia or other immunocompromising condition, and patients with persistent signs and symptoms despite seemingly appropriate therapy, we suggest addition of a second active agent (eg, levofloxacin or ceftazidime based on local antibiogram and patient factors such as allergies) until susceptibility results are known.
For patients who cannot use TMP-SMX because of hypersensitivity or other expected drug toxicity, we use levofloxacin or ceftazidime, again based on knowledge of the local antibiogram and patient-specific factors such as allergies and/or need for coverage of additional pathogens, for empiric therapy. If the isolate is susceptible to levofloxacin, it is appropriate to continue levofloxacin as directed therapy of S. maltophilia, particularly if there is a polymicrobial infection and levofloxacin is treating other identified pathogens. If the isolate is susceptible to other beta-lactams (eg, ceftazidime), these are also reasonable alternatives if TMP-SMX cannot be used.
If the isolate is susceptible to TMP-SMX but not to fluoroquinolones or any beta-lactams, we favor rapid desensitization for patients who have an immunoglobulin E mediated hypersensitivity reaction to TMP-SMX (see "Rapid drug desensitization for immediate hypersensitivity reactions") [7,115]. Otherwise, potential alternatives include minocycline, tigecycline, and colistin, each of which are associated with particular adverse effects. Cefiderocol may have activity, but clinical data are limited. Consultation with an expert in infectious diseases is advised.
Evidence supporting this approach to antimicrobial selection is discussed elsewhere. (See 'Efficacy of antibiotic options' above.)
Duration of therapy — The duration of therapy depends on the site of the infection; 14 days of therapy is appropriate for bacteremia and 7 days of therapy is appropriate for hospital-acquired pneumonia in an immunocompetent host, as long as there has been evidence of clinical improvement. Longer durations of therapy (10 to 14 days) are often used in immunocompromised hosts. (See appropriate topic reviews for discussion regarding the duration of therapy for specific infections).
Although data have suggested that a seven-day course of antibiotics is appropriate for uncomplicated gram-negative bacillary bacteremia, S. maltophilia infections were not well represented in those studies. (See "Gram-negative bacillary bacteremia in adults", section on 'Duration and route of therapy'.)
Other management issues — In addition to antimicrobial treatment, certain infections may warrant additional interventions, such as catheter removal or wound debridement. As an example, for catheter-associated blood stream infections, removal of the catheter is important in reducing the rate of relapse [87]. (See "Intravascular non-hemodialysis catheter-related infection: Treatment", section on 'Selecting a catheter management strategy'.)
PROGNOSIS — S. maltophilia infections have been associated with high morbidity and mortality in severely immunocompromised and debilitated individuals.
Overall, mortality estimates range from 21 to 69 percent [58,116-118]. However, the actual mortality attributed to these infections when controlling for other variables is unclear. Retrospective analyses have sought to identify independent risk factors associated with mortality in patients infected with S. maltophilia; in one retrospective cohort study, admission to an intensive care unit and delay in effective treatment were found to be independent risk factors for mortality [2].
PREVENTION — Infection control and antibiotic stewardship measures are important to minimize the incidence of S. maltophilia infections and for reducing emergence of resistant strains. These measures include appropriate use of antibiotics, avoidance of prolonged or unnecessary use of foreign devices, and adherence to hand hygiene practices. Strict hand hygiene and contact isolation procedures have been utilized to reduce clonal spread in the intensive care unit setting [119]. (See "Infection prevention: Precautions for preventing transmission of infection".)
SUMMARY AND RECOMMENDATIONS
●Stenotrophomonas maltophilia is a multidrug-resistant gram-negative bacillus that is an opportunistic pathogen associated with high morbidity and mortality in severely immunocompromised and debilitated individuals. Risk factors associated with Stenotrophomonas infection include admission to an intensive care unit, HIV infection, malignancy, cystic fibrosis, neutropenia, mechanical ventilation, central venous catheters, recent surgery, trauma, and previous therapy with broad-spectrum antibiotics. (See 'Microbiology' above and 'Epidemiology' above.)
●Pneumonia (usually hospital-acquired) and bacteremia (often associated with an indwelling catheter) are the most common manifestations of S. maltophilia infection. Less common manifestations include endocarditis, mastoiditis, peritonitis, meningitis, soft tissue infection, wound infection, urinary tract infection, and ocular infection. (See 'Disease associations' above.)
●Growth of S. maltophilia from normally sterile sites (such as blood, pleural fluid, or peritoneal fluid) should be interpreted to represent true infection. In patients with clinical evidence of pneumonia, cultures growing S. maltophilia from respiratory sites should be interpreted to be consistent with infection, but in its absence, S. maltophilia growth probably represents colonization rather than invasive disease. Similarly, interpretation of culture data obtained from non-sterile sites (eg, indwelling catheters or drains) must take into account the organism's propensity to colonize foreign material without causing infection. (See 'Diagnosis of infection' above.)
●For empiric and directed therapy of S. maltophilia infections, we suggest trimethoprim-sulfamethoxazole (TMP-SMX) (Grade 2C). For empiric treatment of patients who are severely ill with S. maltophilia infections, who have an immunocompromising condition, or who have persistent symptoms despite TMP-SMX, we also suggest adding a second agent (such as levofloxacin or ceftazidime) until susceptibility results are available (Grade 2C). If a patient cannot use TMP-SMX because of hypersensitivity or other expected drug toxicity, we use levofloxacin or ceftazidime for empiric therapy; either of these is also an acceptable alternative for directed therapy if the isolate is susceptible. (See 'Approach to antibiotic selection' above and 'Efficacy of antibiotic options' above.)
●The duration of therapy depends on the site of the infection; 14 days of therapy is appropriate for bacteremia and 7 days of therapy is usually appropriate for hospital-acquired pneumonia in an immunocompetent host. Certain infections may warrant additional interventions, such as catheter removal or wound debridement. (See 'Duration of therapy' above and 'Other management issues' above.)
●Infection control measures are important to minimize the incidence of S. maltophilia infections and for reducing emergence of resistant strains. These measures include judicious use of antibiotics, avoidance of prolonged or unnecessary use of foreign devices, and adherence to hand hygiene practices. (See 'Prevention' above and "Infection prevention: Precautions for preventing transmission of infection".)
1 : Factors associated with mortality in patients with bloodstream infection and pneumonia due to Stenotrophomonas maltophilia.
2 : Independent predictors for mortality in patients with positive Stenotrophomonas maltophilia cultures.
3 : Clinical characteristics and prognostic factors of patients with Stenotrophomonas maltophilia bacteremia.
4 : Microbiological and clinical aspects of infection associated with Stenotrophomonas maltophilia.
5 : Stenotrophomonas (Xanthomonas) maltophilia as an emerging opportunistic pathogen in association with HIV infection: a 10-year surveillance study.
6 : Stenotrophomonas (Xanthomonas) maltophilia as an emerging opportunistic pathogen in association with HIV infection: a 10-year surveillance study.
7 : Stenotrophomonas maltophilia: an emerging opportunist human pathogen.
8 : The complete genome, comparative and functional analysis of Stenotrophomonas maltophilia reveals an organism heavily shielded by drug resistance determinants.
9 : Fatal pulmonary hemorrhage in patients with acute leukemia and fulminant pneumonia caused by Stenotrophomonas maltophilia.
10 : Relapsing pyrogenic reactions due to Xanthomonas maltophilia in a dialysis patient with a long-term central venous catheter.
11 : Meningitis due to Xanthomonas maltophilia.
12 : Successful treatment of multi-resistant Stenotrophomonas maltophilia meningitis with ciprofloxacin in a pre-term infant.
13 : Stenotrophomonas maltophilia: an unusual cause of biliary sepsis.
14 : Septic prepatellar bursitis caused by Stenotrophomonas (Xanthomonas) maltophilia.
15 : Cutaneous infections with Stenotrophomonas maltophilia in patients using immunosuppressive medication.
16 : Infrequently encountered Pseudomonas species causing infection in humans.
17 : Nosocomial infections due to Xanthomonas maltophilia (Pseudomonas maltophilia) in patients with cancer.
18 : Antimicrobial therapy for Stenotrophomonas maltophilia infections.
19 : Pseudomonas maltophilia infections in man.
20 : Nosocomial infection caused by Xanthomonas maltophilia: a case-control study of predisposing factors.
21 : Attributable mortality of Stenotrophomonas maltophilia infections: a systematic review of the literature.
22 : Pseudomonas maltophilia exoenzyme activity as correlate in pathogenesis of ecthyma gangrenosum.
23 : Adhesion of the positively charged bacterium Stenotrophomonas (Xanthomonas) maltophilia 70401 to glass and Teflon.
24 : Fimbriae and adherence of Stenotrophomonas maltophilia to epithelial cells and to abiotic surfaces.
25 : Biofilm formation by Stenotrophomonas maltophilia: modulation by quinolones, trimethoprim-sulfamethoxazole, and ceftazidime.
26 : Interactions among strategies associated with bacterial infection: pathogenicity, epidemicity, and antibiotic resistance.
27 : Characterization of flagella produced by clinical strains of Stenotrophomonas maltophilia.
28 : Immunostimulatory properties of the emerging pathogen Stenotrophomonas maltophilia.
29 : Plasmid location and molecular heterogeneity of the L1 and L2 beta-lactamase genes of Stenotrophomonas maltophilia.
30 : Overexpression, purification, and characterization of the cloned metallo-beta-lactamase L1 from Stenotrophomonas maltophilia.
31 : Purification and properties of an inducible cephalosporinase from Pseudomonas maltophilia GN12873.
32 : Sequence analysis and enzyme kinetics of the L2 serine beta-lactamase from Stenotrophomonas maltophilia.
33 : The emergence of epidemic, multiple-antibiotic-resistant Stenotrophomonas (Xanthomonas) maltophilia and Burkholderia (Pseudomonas) cepacia.
34 : Resistance mechanisms in Pseudomonas aeruginosa and other nonfermentative gram-negative bacteria.
35 : Characterization of the chromosomal aac(6')-Iz gene of Stenotrophomonas maltophilia.
36 : Role of the acetyltransferase AAC(6')-Iz modifying enzyme in aminoglycoside resistance in Stenotrophomonas maltophilia.
37 : Outer membranes and efflux: the path to multidrug resistance in Gram-negative bacteria.
38 : Stenotrophomonas maltophilia: changing spectrum of a serious bacterial pathogen in patients with cancer.
39 : Therapeutic options for Stenotrophomonas maltophilia infections beyond co-trimoxazole: a systematic review.
40 : Effect of temperature on antimicrobial susceptibilities of Pseudomonas maltophilia.
41 : Growth temperature-dependent variation of cell envelope lipids and antibiotic susceptibility in Stenotrophomonas (Xanthomonas) maltophilia.
42 : Temperature-dependent aminoglycoside resistance in Stenotrophomonas (Xanthomonas) maltophilia; alterations in protein and lipopolysaccharide with growth temperature.
43 : Effect of temperature on aminoglycoside binding sites in Stenotrophomonas maltophilia.
44 : Cloning and characterization of SmeDEF, a novel multidrug efflux pump from Stenotrophomonas maltophilia.
45 : Expression of multidrug efflux pump SmeDEF by clinical isolates of Stenotrophomonas maltophilia.
46 : Fluoroquinolone susceptibilities of efflux-mediated multidrug-resistant Pseudomonas aeruginosa, Stenotrophomonas maltophilia and Burkholderia cepacia.
47 : Stenotrophomonas maltophilia D457R contains a cluster of genes from gram-positive bacteria involved in antibiotic and heavy metal resistance.
48 : Clinical epidemiology of Stenotrophomonas maltophilia colonization and infection: a multicenter study.
49 : Stenotrophomonas maltophilia resistant to trimethoprim-sulfamethoxazole: an increasing problem.
50 : Stenotrophomonas maltophilia as a nosocomial pathogen.
51 : Susceptibilities of 123 strains of Xanthomonas maltophilia to eight beta-lactams (including beta-lactam-beta-lactamase inhibitor combinations) and ciprofloxacin tested by five methods.
52 : In vitro killing effect of moxifloxacin on clinical isolates of Stenotrophomonas maltophilia resistant to trimethoprim-sulfamethoxazole.
53 : In vitro killing effect of moxifloxacin on clinical isolates of Stenotrophomonas maltophilia resistant to trimethoprim-sulfamethoxazole.
54 : Antimicrobial susceptibilities of a worldwide collection of Stenotrophomonas maltophilia isolates tested against tigecycline and agents commonly used for S. maltophilia infections.
55 : Antimicrobial susceptibilities of a worldwide collection of Stenotrophomonas maltophilia isolates tested against tigecycline and agents commonly used for S. maltophilia infections.
56 : Associated mortality and clinical characteristics of nosocomial Pseudomonas maltophilia in a university hospital.
57 : Bacteremia due to Stenotrophomonas (Xanthomonas) maltophilia: a prospective, multicenter study of 91 episodes.
58 : Risk factors associated with mortality of infections caused by Stenotrophomonas maltophilia: a systematic review.
59 : Xanthomonas maltophilia bacteremia in immunocompromised hematological patients.
60 : Comparison of treatment with imipenem vs. ceftazidime as a predisposing factor for nosocomial acquisition of Stenotrophomonas maltophilia: a historical cohort study.
61 : Community-acquired Stenotrophomonas maltophilia infections: a systematic review.
62 : Outbreak of Stenotrophomonas maltophilia on an intensive care unit.
63 : Two consecutive outbreaks of Stenotrophomonas maltophilia (Xanthomonas maltophilia) in an intensive-care unit defined by restriction fragment-length polymorphism typing.
64 : Faucet aerators: A source of patient colonization with Stenotrophomonas maltophilia.
65 : Outbreak of Stenotrophomonas maltophilia bacteremia in allogenic bone marrow transplant patients: role of severe neutropenia and mucositis.
66 : Fulminant Stenotrophomonas maltophilia soft tissue infection in immunocompromised patients: an outbreak transmitted via tap water.
67 : Outbreak of Stenotrophomonas maltophilia bloodstream infections in an outpatient dialysis center
68 : Nosocomial outbreak of colonization and infection with Stenotrophomonas maltophilia in preterm infants associated with contaminated tap water.
69 : Stenotrophomonas maltophilia outbreak in neonatal intensive care unit and outbreak management
70 : An outbreak of trimethoprim/sulfamethoxazole-resistant Stenotrophomonas maltophilia meningitis associated with neuroendoscopy
71 : Outbreak of pulmonary Pseudomonas aeruginosa and Stenotrophomonas maltophilia infections related to contaminated bronchoscope suction valves, Lyon, France, 2014.
72 : Stenotrophomonas maltophilia Pseudo-outbreak at a University Hospital Bronchoscopy Unit in Turkey.
73 : Pseudo-outbreaks of Stenotrophomonas maltophilia on an intensive care unit in England.
74 : A Pseudo-Outbreak of Pseudomonas putida and Stenotrophomonas maltophilia in a Bronchoscopy Unit.
75 : Emerging importance of multidrug-resistant Acinetobacter species and Stenotrophomonas maltophilia as pathogens in seriously ill patients: geographic patterns, epidemiological features, and trends in the SENTRY Antimicrobial Surveillance Program (1997-1999).
76 : Bacteremia due to Stenotrophomonas maltophilia in patients with hematologic malignancies.
77 : Stenotrophomonas maltophilia keratitis and scleritis.
78 : Stenotrophomonas maltophilia ocular infections.
79 : Stenotrophomonas maltophilia in the respiratory tract of medical intensive care unit patients.
80 : Rapidly progressive fatal hemorrhagic pneumonia caused by Stenotrophomonas maltophilia in hematologic malignancy.
81 : Stenotrophomonas maltophilia infection in hematopoietic SCT recipients: high mortality due to pulmonary hemorrhage.
82 : Changing Epidemiology of the Respiratory Bacteriology of Patients With Cystic Fibrosis.
83 : Factors influencing the acquisition of Stenotrophomonas maltophilia infection in cystic fibrosis patients.
84 : Risk factors for lung function decline in a large cohort of young cystic fibrosis patients.
85 : Central venous catheter and Stenotrophomonas maltophilia bacteremia in cancer patients.
86 : Stenotrophomonas maltophilia bacteremia and pneumonia at a tertiary-care oncology center: a review of 16 years.
87 : Central venous catheter-related Stenotrophomonas maltophilia bacteraemia and associated relapsing bacteraemia in haematology and oncology patients.
88 : Risk factors for Stenotrophomonas maltophilia bacteremia in oncology patients: a case-control study.
89 : Clinical Characteristics of Stenotrophomonas maltophilia Keratitis.
90 : Skin manifestation of Stenotrophomonas maltophilia infection--a case report and review article.
91 : Ecthyma Gangrenosum: A Rare Cutaneous Manifestation Caused by Stenotrophomonas maltophilia in a Leukemic Patient.
92 : Significance of positive Stenotrophomonas maltophilia culture in acute respiratory tract infection.
93 : Antimicrobial susceptibility of Gram-negative organisms isolated from patients hospitalised with pneumonia in US and European hospitals: results from the SENTRY Antimicrobial Surveillance Program, 2009-2012.
94 : Update on infections caused by Stenotrophomonas maltophilia with particular attention to resistance mechanisms and therapeutic options.
95 : Stenotrophomonas maltophilia bloodstream infection in patients with hematologic malignancies: a retrospective study and in vitro activities of antimicrobial combinations.
96 : Monotherapy with fluoroquinolone or trimethoprim-sulfamethoxazole for treatment of Stenotrophomonas maltophilia infections.
97 : Clinical implications of stenotrophomonas maltophilia resistant to trimethoprim-sulfamethoxazole: a study of 69 patients at 2 university hospitals.
98 : Comparisons between patients with trimethoprim-sulfamethoxazole-susceptible and trimethoprim-sulfamethoxazole-resistant Stenotrophomonas maltophilia monomicrobial bacteremia: A 10-year retrospective study.
99 : Can levofloxacin be a useful alternative to trimethoprim-sulfamethoxazole for treating Stenotrophomonas maltophilia bacteremia?
100 : Activities of ciprofloxacin and moxifloxacin against Stenotrophomonas maltophilia and emergence of resistant mutants in an in vitro pharmacokinetic-pharmacodynamic model.
101 : Stenotrophomonas maltophilia: emergence of multidrug-resistant strains during therapy and in an in vitro pharmacodynamic chamber model.
102 : Antimicrobial susceptibility profile of contemporary clinical strains of Stenotrophomonas maltophilia isolates: can moxifloxacin activity be predicted by levofloxacin MIC results?
103 : Minocycline Activity against Unusual Clinically Significant Gram-Negative Pathogens.
104 : Tigecycline as a therapeutic option in Stenotrophomonas maltophilia infections.
105 : Monotherapy with minocycline or trimethoprim/sulfamethoxazole for treatment of Stenotrophomonas maltophilia infections.
106 : Activity of Cefiderocol Alone and in Combination with Levofloxacin, Minocycline, Polymyxin B, or Trimethoprim-Sulfamethoxazole against Multidrug-Resistant Stenotrophomonas maltophilia.
107 : Activity of cefiderocol against high-risk clones of multidrug-resistant Enterobacterales, Acinetobacter baumannii, Pseudomonas aeruginosa and Stenotrophomonas maltophilia.
108 : Designing A Pathogen-Focused Study To Address The High Unmet Medical Need Represented By Carbapenem-Resistant Gram-Negative Pathogens - The International, Multicenter, Randomized, Open-Label, Phase 3 CREDIBLE-CR Study.
109 : Designing A Pathogen-Focused Study To Address The High Unmet Medical Need Represented By Carbapenem-Resistant Gram-Negative Pathogens - The International, Multicenter, Randomized, Open-Label, Phase 3 CREDIBLE-CR Study.
110 : Antimicrobial susceptibility of uncommonly isolated non-enteric Gram-negative bacilli.
111 : Activity of Potential Alternative Treatment Agents for Stenotrophomonas maltophilia Isolates Nonsusceptible to Levofloxacin and/or Trimethoprim-Sulfamethoxazole.
112 : Comparison of different antimicrobial susceptibility testing methods for Stenotrophomonas maltophilia and results of synergy testing.
113 : In vitro activities of antimicrobial combinations against clinical isolates of Stenotrophomonas maltophilia.
114 : In vitro activities of antimicrobial combinations against Stenotrophomonas (Xanthomonas) maltophilia.
115 : Successfully treated nosocomial Stenotrophomonas maltophilia bacteremia following desensitization to trimethoprim-sulfamethoxazole.
116 : Attributable mortality of Stenotrophomonas maltophilia bacteremia.
117 : Stenotrophomonas maltophilia bacteremia in adults: four years' experience in a medical center in northern Taiwan.
118 : Risk factors for 30-day mortality among patients with Stenotrophomonas maltophilia bacteraemia.
119 : Acquisition and spread of Acinetobacter baumannii and Stenotrophomonas maltophilia in intensive care patients.
