Stenotrophomonas maltophilia

Authors: W.J. Looney, CSci FIBMSMasashi Narita, M.D.Prof. Kathrin Mühlemann, MD PhDAmjad Shidyak, M.D.


Stenotrophomonas maltophilia is a motile non-fermentative, gram negative bacillus that is readily isolated from environmental sources and water. It is an obligate aerobe, and is capable of growth between 5o and 40oC (18). S. maltophilia isolates from environmental and clinical sources represent a number of genomic groups, which may possibly be of clinical significance, although this remains to be established (133537).


S. maltophilia is widely distributed in natural and man-made environments, and can survive in chlorinated water distribution networks (38). Infection presumably results from human acquisition of environmental organisms, although in most instances the source of the organisms is not precisely known. Contamination of wounds with soil may lead to soft tissue infection (1). In developed countries, most recognized infections are nosocomial. The source and mode of transmission of the organism is often uncertain. In a number of hospitals with endemic or epidemic S. maltophiliainfection, multiple genetically distinct strains have been isolated from patients (687). However, common source nosocomial outbreaks have resulted from contamination of medical equipment or hospital water systems (2696).

Clinical Manifestations

Most human isolates represent colonization rather than infection; it is, however, an opportunistic pathogen in highly debilitated patients (9425292103). Patients at highest risk include those with underlying malignancy, neutropenia, chemotherapy, presence of an indwelling central catheter, and prior antimicrobial therapy. The major clinical syndromes are pneumonia and bacteremia; in bacteremia the portal of entry is typically a vascular catheter, or is unknown (221283244576397103). Other reported clinical syndromes include urinary tract infection (89), soft tissue infection (190), ocular infection (1041), endocarditis (3658), and meningitis (586166).

Laboratory Diagnosis

Culture from normally sterile body sites is straightforward, and bacteremia and septicemia can be detected using standard blood-culture techniques (51). Selective media can improve culture sensitivity for specimens from non-sterile body sites, such as respiratory secretion from patients with cystic fibrosis (CF) (27). Isolation of the organism from normally sterile sites such as blood, pleural fluid or cerebrospinal fluid is indicative of infection. Isolation from non sterile sites such as sputum or wounds often represents colonization rather than infection. Differentiation of infection from colonization based on clinical criteria may be problematic.

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S. maltophilia is not highly virulent, nevertheless several factors may promote its ability to colonize the respiratory tract and plastic surfaces, such as catheters and endotracheal tubes. These include a positively charged surface as well as flagella and fimbrial adhesion, the latter have been associated with biofilm formation (161740, 95). The outer membrane lipopolysaccharide (LPS) plays a role in colonization and resistance to complement-mediated cell killing, and its lipid A moiety can stimulate peripheral blood monocytes and alveolar macrophages to produce TNFα, which plays a role in the pathogenesis of airway inflammation (539195). S. maltophilia produces a number of extracellular enzymes, (18) whose contribution to virulence is currently uncertain (99).


In Vitro and In Vivo

In vitro susceptibility testing of S. maltophilia poses numerous technical problems, however, the Clinical Laboratory Standards Institute (CLSI) and the British Society for Antimicrobial Chemotherapy (BSAC) have each published standard methods for the susceptibility testing of S. maltophilia (412). The methods cover a limited range of antibiotics and are not interchangeable as they vary in numerous details. In-vitro synergy testing, sometimes used for particularly problematic cases, has indicated synergy between certain antibiotic combinations when tested against S. maltophilia (7578). The different kinds of synergy tests may either give the same or differing results when testing the same strain-antibiotic combinations, and this should be taken into consideration when interpreting the results (1569,  93).

Table 1 shows the in vitro susceptibility of S. maltophilia to selected antibiotics, the data being drawn from published studies.

In most reports, over 90% of strains are susceptible to trimethoprim-sulfamethoxazole (72429, 57). A recent report from a major oncology centre found that only 75% of strains were susceptible (88). In two series reporting episodes of bacteremia from Taiwan, 60%-76% of strains were susceptible to trimethoprim-sulfamethoxazole (4694). The highest rate of trimethoprim-sulfamethoxazole resistance, 84% occurred in a study of S. maltophilia isolated from the sputum of patients with cystic fibrosis (78). Thus, susceptibility to trimethoprim sulfamethoxazole should not be assumed. Most isolates are susceptible in vitro to minocycline.

The majority of clinical isolates of S. maltophilia infections are resistant to multiple agents used to treat gram-negative infections. Resistance to beta-lactam antibiotics is mediated by two unique, inducible beta-lactamases, a zinc-containing penicillinase (77) and a cephalosporinase (76). Some isolates appear to produce additional beta-lactamases as well (67). A TEM-2 beta lactamase has been identified within a transposon in the genome of a clinical isolate of S. maltophilia (5). As a consequence, many strains are resistant to extended spectrum penicillins and third generation cephalosporins; nearly all strains are resistant to imipenem and meropenem (436065). The majority of strains are susceptible to the combination of ticarcillin and the beta-lactamase inhibitor clavulanic acid in vitro; however, the degree of growth inhibition is dependent on testing conditions (6065). In a murine model of S. maltophilia pneumonia, the efficacy of ticarcillin/clavulanate acid was similar to that of trimethoprim-sulfamethoxazole (71). Piperacillin/tazobactam is less active in vitro; the majority of strains are resistant (2285). Ampicillin/sulbactam is generally inactive. Most strains are resistant to aztreonam (7).

The majority of strains are resistant to aminoglycosides. Three different mechanisms have been described so far: aminoglycoside-modifying enzymes, efflux pumps and outer-membrane permeability changes (48505364). S. maltophilia strains are variably susceptible to fluoroquinolones such as ciprofloxacin and ofloxacin. Newer quinolones, such as moxifloxacin, clinafloxacin and gatifloxacin are significantly more active in vitro than the previously available members of the class (708598). Emergence of resistance during quinolone therapy by an initially susceptible strain has been reported (11). Spontaneous mutants that are resistant to multiple quinolones occur at a frequency of 10-5 to 10-7 (49); exposure to a quinolone may result in selection of the resistant clone.

Combinations of Antimicrobials

The use of two or three antimicrobials to treat S. maltophilia infection has become established practice, although there are no clinical trials to support this approach. This strategy is, however, supported by in vitro synergy testing (101). Given the lack of clinical trials, caution must be exercised when attempting to extrapolate in vitro synergy testing into clinical practice. Synergistic bacterial killing occurs in vitro with ticarcillin/clavulanate plus trimethoprim/ sulfamethoxazole whether or not the isolates are susceptible to either of the two combination agents (69). In vitro synergy has also been reported for trimethoprim/sulfamethoxazole combined with ceftazidime, ciprofloxacin, gentamicin, and tobramycin (101) when the strain tested was susceptible to trimethoprim/sulfamethoxazole and susceptible or intermediately susceptible to the second agent. Synergy may also occur with either ticarcillin/clavulanate or ceftazidime plus ciprofloxacin for strains with a ciprofloxacin MIC < 32 ug/ml (69). Although most strains are resistant to aztreonam, the combination of aztreonam and clavulanate in a fixed 2:1 ratio shows synergistic activity (33). The addition of aztrenonam to ticarcillin/clavulanate reportedly increases the activity of the latter combination up to 128-fold, with synergy demonstrated by time-kill curves for the majority of isolates tested (45). These reports of synergy are based on a limited number of strains.

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Drug of Choice

There are no controlled trials of therapy of S. maltophilia infection in humans. Therapy should be guided by the results of in vitro susceptibility testing (see above section). Trimethoprim-sulfamethoxazole should be considered the primary therapeutic agent for susceptible strains (57).

Combination therapy is warranted in life-threatening infections including bacteremia and pneumonia (see below). In a large case series (57) bacteraemic patients who received at least two agents including trimethoprim-sulfamethoxazole, an extended spectrum penicillin or a third generation cephalosporin had a significantly lower mortality (11%) than patients who received only one of these agents (31%) or other therapies (55%).

Neutropenic patients, and those with bacteremia or pneumonia should be treated with combination antimicrobial therapy. The combination of trimethoprim/sulfamethoxazole (10 mg/kg/day) and ticarcillin/clavulanate may have synergistic bactericidal activity even if the isolate is resistant to one or both agents. Other potential combinations include trimethoprim/sulfamethoxozole and ceftazidime if the isolate is susceptible to ceftazidime. For patients allergic to trimethoprim/ sulfamethoxazole, a newer quinolone such as moxifloxacin or gatifloxacin combined with one of the aforementioned beta-lactam agents is a reasonable alternative.

Recommended dosages for specific agents are given in Table 2.

Specific Infections


Most bacteremic patients have serious underlying conditions including malignancy, immunosuppression, or neutropenia. Bacteremic patients should be treated with combination antimicrobial therapy (see above). Most bacteremias are associated with indwelling central venous catheters; removal of an infected catheter is a key component of successful treatment (2179). Bacteremia was polymicrobial in a variable proportion of cases in reported series; antimicrobial therapy should also be directed at concomitant blood isolates.

Respiratory Infection

Pulmonary infection occurs primarily in patients with malignancy or in those receiving mechanical ventilation. Patients rendered profoundly neutropenic after intensive chemotherapy for leukemia may develop fulminant pneumonia culminating in fatal pulmonary hemorrhage (2072). Combination antimicrobial therapy is warranted.


S. maltophilia meningitis may occur in infants, or as a complication of neurosurgical procedures (6166).Trimethoprim-sulfamethoxazole penetrates well into the cerebrospinal fluid; a limited number of cases have been treated with bacteriologic cure (586166). One case of post-operative meningitis was cured following a three week course of ciprofloxacin (34). Intraventricular drains associated with infection should be removed if possible.


S. maltophilia endocarditis occurs in the setting of intravenous drug abuse or following valve replacement surgery (3639545859). Complications such as valve ring abscesses and emboli are frequent; therefore; in addition to combination antimicrobial therapy, early valve replacement is often indicated.

Ocular Infections

External infections such as keratitis and conjunctivitis predominate, although orbital cellulitis and endopthalmitis may occur (68). Most infections are preceded by surgery, corneal inflammation, or prosthetic devices including soft contact lenses. Treatment is limited by the organism's resistance to available ophthalmic antimicrobial preparations including aminoglycosides and quinolones. Keratitis may result from wearing of contact lenses or from corneal surgery. Topical therapy with an agent to which the isolate is susceptible is indicated. Topical quinolones have been effective (25); ciprofloxacin and ofloxacin are readily available as ophthalmic preparations. Treatment with alternative agents, for example, ceftazidime, may require compounding of an ophthalmic preparation from an intravenous preparation by the pharmacy.

Endopthalmitis following cataract extraction was successfully treated by vitrectomy, intravitreal injection of ceftazidime and gentimicin, topical application of polymixin, trimethoprim, and ciprofloxacin, and oral administration of Trimethoprim-sulfamethoxazole and ciprofloxacin (41). Endopthalmitis after implantation of a sustained-release ganciclovir failed to respond to vitrectomy, removal of the capsule, intravitreal injection of amikacin, ciprofloxacin, and ceftazidime, along with systemic administration of ceftazidime (10). It would appear from the limited number of reports that vitrectomy coupled with intravitreal and systemic administration of 2 or more agents with activity against the infecting isolate may result in bacteriologic cure and salvage of vision in cases of S. maltophilia endophthalmitis.

Skin and Soft Tissue Infection

S. maltophilia is an occasional pathogen in wounds contaminated with soil or occurring due to farm machinery related accidents (114). Reported cases have responded to debridement and administration of Trimethoprim-sulfamethoxazole

Soft tissue infection may occur in the course of systemic S. maltophilia infection in neutropenic patients. Reported syndromes include cellulitis, multiple subcutaneous nodules, ecthyma gangrenosa, mucous membrane ulcerations, necrotizing gingivitis, and myositis (19555690). Treatment appropriate for infection in neutropenic patients with combination therapy is indicated.

Peritonitis (Dialysis-Related)

S. maltophilia is an occasional cause of peritonitis complicating chronic peritoneal dialysis (380). Combination antimicrobial therapy and removal of the dialysis catheter are usually necessary for cure. Immediate replacement of the catheter has resulted in therapeutic failure in the majority of the reported cases. Catheter removal with a temporary period of hemodialysis and completion of a course of antimicrobial therapy was required before re-insertion of a peritoneal catheter and resumption of peritoneal dialysis. There are reports of successful treatment of peritonitis without catheter removal (83). In these cases, there was no clinical evidence of inflammation at the catheter site. Patient initially received a 15 day course of intravenous trimethoprim/sulfamethoxazole with or without additional antimicrobial agents, which included intravenous ciprofloxacin, intraperitoneal ceftazidime, or intraperitoneal amikacin. This was followed by one month of therapy with oral trimethoprim/sulfamethoxazole.

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Underlying Diseases


Any clinical infection in a neutropenic patient should be treated with combination antimicrobial therapy.

Cystic Fibrosis

Approximately 10% of patients with cystic fibrosis have sputum colonized with S. maltophilia (8). These patients may be transiently or persistently colonized with S. maltophilia; persistent colonization is more likely among older patients aged 16 and older (86). The relationship between colonization and clinical deterioration in cystic brosis patients is unclear; there is no evidence that treating asymptomatic colonization is beneficial. S. maltophiliapneumonia in a cystic fibrosis patient should be treated with combination antimicrobial therapy.

Alternative Agents

Some authors recommend the addition of rifampin (100) or minocycline (88) as to the combination of trimethoprim/sulfamethoxazole and a beta-lactam agent. Fluoroquinolones are variably active against S. maltophilia, and may be an appropriate alternative to trimethoprim/sulfametholxazole in a combination regimen with a beta-lactam agent. Although there is little information regarding synergy between the newer quinolones, such as moxifloxacin, and gatifloxacin, and beta-lacatams against S. maltophilia, these agents are substantially more active against most strains than is ciprofloxacin, and may be preferable as one component of combination therapy. Fluoroquinolones should not be used as single agent therapy. Although the frequency of this phenomenon is uncertain, emergence of quinolone resistance during therapy has been reported (11). Synergy between ciprofloxacin and beta-lactam agents appears to be unlikely if the isolate has a ciprofloxacin MIC > 32 ug/ml. It is not clear if this is the case with the newer quinolones, but MIC’s to these agents are typically < 4 ug/ml. The combination of chloramphenicol and ciprofloxacin was clinically effective in a case of prosthetic valve endocarditis, with sterilization of blood cultures after 1 week of therapy (54). The combination of aztreonam and ticarcillin/clavulanate is highly active in an animal model; clinical experience is extremely limited.

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Removal of foreign bodies associated with infection, including intravascular catheters, peritoneal dialysis catheters and intraventricular drains is usually necessary. Early valve replacement should be a consideration in prosthetic valve endocarditis.


In bacteremic patients, failure to clear the bacteremia should prompt consideration of an intravascular focus of infection, including an infected vascular catheter, septic thrombophlebitis, or endocarditis. Neutropenic patients may not clear bacteremia until the neutrophil count recovers.


No vaccine is available.


The ultimate source of the infecting strains is often uncertain.  S. maltophilia is a common environmental contaminant. As noted, however, multiple strains are often in circulation at any one time in a hospital unit; these strains may not match those isolated from recognized environmental sources, including tap water. Surveillance of potable water or other environmental sources, with subsequent decontamination remains to be studied.  If an environmental source, such as a contaminated medical device, can be identified, then this source should be removed. Prior broad spectrum antimicrobial therapy is a major risk factor for S. maltophilia infection. Reduction in unnecessary antimicrobial therapy should lead to a reduction in the incidence of S. maltophilia infection.


There are no controlled trials of therapy for this bacterium. All of the recommendations contained herein are based on the results of in vitro susceptibility and synergy studies, animal studies, case series, and anecdotal reports.

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1. Agger WA, Cogbill TH, Busch H, Landercasper J, Callister SM. Wounds caused by corn-harvesting machines: an unusual source of infection due to gram-negative bacilli. Rev Infect Dis 1986; 8:927-931. [PubMed]

2. Aisenberg G, Rolston KV, Dickey BF, Kontoyiannis DP, Raad II, Safdar A.  Stenotrophomonas maltophilia pneumonia in cancer patients without traditional risk factors for infection, 1997-2004 Eur J Clin Microbiol Infect Dis 2007;26:13-20 [PubMed] 

3. Al-Hilali N, Nampoory MR, Johny KV, Chugh TD. Xanthomonas maltophilia infection in chronic peritoneal dialysis. Scand J Urol Nephrol 2000; 34:67-69. [PubMed]

4. Andrews JM for the BSAC Working Party on Susceptibility Testing. BSAC standardized disc susceptibility testing method (version 7). J Antimicrob Chemother. 2008 Advanced Access published May 12. doi:10.1093/jac/dkn194

5. Avison MB, von Heldreich CJ, Higgins CS, Bennett PM, Walsh TR. A TEM-2 β-lactamase encoded on an active TN1-like transposon in the genome of a clinical isolate of Stenotrophomonas maltophilia. J Antimicrob Chemother 2000; 46:879-884. [PubMed]

6.  Barbier-Frebour N, Boutiba-Boubake I, Nouvello M, Lemelan J. Molecular investigation of Stenotrophomonas maltophilia isolates exhibiting rapid emergence of ticarcillin-clavulanate resistance. J Hosp Infect 2000; 45:35-41.[PubMed] 

7. Betriu C, Sanchez A, Palau ML, Gomez M, Picazo JJ. Antibiotic resistance surveillance of Stenotrophomonas maltophilia, 1993-1999. J Antimicrob Chemother 2001;48:152-154. [PubMed]

8. Burns JL, Emerson J, Stapp JR, Yim DL, Krzewinski J, Louden L, Ramsey BW, Clausen CR. Microbiology of sputum from patients at cystic fibrosis centers in the United States. Clin Infect Dis 1998;27:158-163. [PubMed] 

9. Calza L, Manfredi R, Chiodo F. Stenotrophomonas (Xanthomonas) maltophilia as an emerging opportunistic pathogen in association with HIV infection: a 10-year surveillance study. Infection 2003;31: 55–61. [PubMed] 

10.  Chen S, Stroh EM, Wald K, Jalkh A. Xanthomonas maltophilia endopthalmitis after implantation of sustained release ganciclovir. Am J Opthalmol 1992;114:772-773. [PubMed]

11. Cheng AF, Li MK, Ling TK, French GL. Emergence of ofloxacin-resistant Citrobacter freundii and Pseudomonas maltophilia after ofloxacin therapy. J Antimicrob Chemother 1987;20:283-285. [PubMed] 

12. CLINICAL AND LABORATORY STANDARDS INSTITUTE 2008 Performance Standards for Antimicrobial Susceptibility Testing; Eighteenth Informational Supplement M100-S18 Vol. 28 No. 1. Clinical and Laboratory Standards Iinstitute Wayne, Pa.,USA

13. Coenye T, Vanlaere E, LiPuma JJ, Vandamme P. Identification of genomic groups in the genus Stenotrophomonas using gyrB RFLP analysis. FEMS Immunol Med Microbiol. 2004;40:181-5 [PubMed] 

14. Daley AJ, McIntyre PB. Stenotrophomonas maltophila and lawn mower injuries in children. J Trauma 2000; 48:536-539. [PubMed] 

15.  Dawis MA, Isenberg HD, France KA, Jenkins SG. In vitro activity of gatifloxacin alone and in combination with cefepime, meropenem, piperacillin and gentamicin against multidrug-resistant organisms J Antimicrob Chemoth 2003;51:1203-1211 [PubMed] 

16. de Oliveira-Garcia D, Dall'Agnol M, Rosales M, et al. Fimbriae and adherence of Stenotrophomonas maltophilia to epithelial cells and to abiotic surfaces. Cell Microbiol 2003;5:625–36. [PubMed] 

17. de Oliveira-Garcia D, Dall'Agnol M, Rosales M, Azzuz ACGS, Martinez MB, Girón JA. Characterization of flagella produced by clinical strains of Stenotrophomonas maltophilia Emerg Infect Diseases 2002;8:918-923 [PubMed] 

18. Denton M, Kerr KG. Microbiologic and clinical aspects of infection associated with Stenotrophomonas maltophilia. Clin Microbiol Rev 1998; 11:57-80. [PubMed] 

19. Downhour NP, Petersen EA, Krueger TS, Tangella KV, Nix DE. Severe cellulitis/myositis caused by Stenotrophomonas maltophilia. Ann Pharmacother 2002; 36:63-66. [PubMed]

20. Elsner HA, Duhrsen U, Hollwitz B, Kaulfers PM, Hossfeld DK. Fatal pulmonary hemorrhage in patients with acute leukemia and fulminant pneumonia caused by Stenotrophomonas maltophilia. Ann Hematol 1997;155-161. [PubMed]

21. Elting LS, Bodey GP. Septicemia due to Xanthomonas species and non-aeruginosa Pseudomonas species: increasing incidence of catheter related infections. Medicine 1990;69:296-306. [PubMed]

22.  Fass RJ, Barnishan J, Solomon MC, Ayers LW. In vitro activities of quinolones, β-lactams, tobramycin, and trimethoprim-sulfamethoxazole agarinst non-fermentative gram-negative bacilli. Antimicrob Agents Chemother 1996; 40:1412-1418. [PubMed]

23. Fedler KA, Biedenbach DJ, Jones RN. Assessment of pathogen frequency and resistance patterns among pediatric patient isolates: report from the 2004 SENTRY Antimicrobial Surveillance Program on 3 continents. Diagn Microbiol Infect Dis. 2006;56:427-36.[PubMed]

24. Felegie TP, Yu VL, Rumans LW, Yee RB. Susceptibility of Pseudomonas maltophilia to antimicrobial agents, singly and in combination. Antimicrob Agents Chemother 1979; 16:833-837. [PubMed]

25. Fernandes M, Gangopadhyay N, Sharma S. Stenotrophomonas maltophilia keratitis after penetrating keratoplasty. Eye 2005 Mar 11 [epub ahead of print].   [PubMed]

26. Fisher MC, Long SS, Roberts EM, Dunn JM, Balsera RK. Pseumodomonas maltophilia bacteremia in children undergoing open heart surgery. JAMA 1981;246:1571-1574. [PubMed]

27. Foster NF, et al., Evaluation of a modified selective differential medium for the isolation of Stenotrophomonas maltophilia, J. Microbiol. Methods (2008), doi:10.1016/j.mimet.2008.05.003.  [PubMed]

28. Gales AC, Jones RN, Forward KR, Liñares J, Sader HS, Verhoef J. 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). Clin Infect Dis 2001; 32(Suppl 2): 104–13. [PubMed]

29. Gales AC, Jones RN, Foward KR, Linares J, Sader HS, Verhoef J. Emerging importance of multidrug-resistant Acinetobacter species and Stenotrophomonas maltophilia as pathogens in seriously ill patients: geographic patterns, epidemiologic features, and trends in the SENTRY antimicrobial surveillance program (1997-1999). Clin Infect Dis 2001; 32(Suppl 2);104-113. [PubMed]

30. Gales AC, Jones RN, Sader HS. Antimicrobial susceptibility profile of contemporary clinical strains of Stenotrophomonas maltophilia isolates: can moxifloxacin activity be predicted by levofloxacin mic results? J Chemoth 2008;20:38-42.  [PubMed] 

31. Gales AC, Jones RN, Sader HS. Global assessment of the antimicrobial activity of polymyxin B against 54 731 clinical isolates of Gram-negative bacilli: report from the SENTRY antimicrobial surveillance programme (2001-2004). Clin Microbiol Infect. 2006;12:315-21. [PubMed]

32. Garcia Paez JI, Tengan FM, Barone AA, Levin AS, Costa SF. Factors associated with mortality in patients with bloodstream infection and pneumonia due to Stenotrophomonas maltophilia. Eur J Clin Microbiol Infect Dis. 2008 DOI 10.1007/s10096-008-0518-2. [PubMed] 

33. Garcia-Rodriguez JA, Garcia Sanchez JE, Munoz Bellido JL, Garcia Garcia MI, Garcia Sanchez E. Kinetics of antimicrobial activity of aztreonam/clavulanic acid (2:1) against Xanthomonas maltophilia. J Antimicrob Chemother 1991; 27:552-554. [PubMed]

34. Girijaratnakumari T, Raja A, Ramani R, Antony B, Shivananda PG. Meningitis due to Xanthomonas maltophilia. J Postgrad Med 1993; 39:153-155. [PubMed]

35. Gould VC, Okazaki A, Avison MB. Beta-lactam resistance and beta-lactamase expression in clinical Stenotrophomonas maltophilia isolates having defined phylogenetic relationships. J Antimicrob Chemother. 2006;57:199-203. [PubMed]

36.  Gutierrez Rodero F, del Mar Masia M, Cortes J, Ortiz de la Tabla V, Mainar V, Vilar A. Endocarditis caused by Stenotrophomonas maltophilia: case report and review. Clin Infect Dis 1996; 23:1261-1265. [PubMed]

37.  Hauben L, Vauterin L, Moore ERB, Hoste B, Swings J. Genomic diversity of the genus Stenotrophomonas Int J Systematic Bacteriol 1999;49:1749-1760. [PubMed]

38. Hoefel D, Monis PT, Grooby WL, Andrews S, Saint CP. Profiling bacterial survival through a water treatment process and subsequent distribution system. J Appl Microbiol. 2005;99:175-86. [PubMed]

39. Jang TN, Wang FD, Wang LS, Liu CY, Liu IM. Xanthomonas maltophilia bacteremia: an analysis of 32 cases. J Formosan Med Assoc 1992; 91:1170-1176. [PubMed]

40. Jucker BA, Harms H, Zehnder AJB. Adhesion of the positively charged bacterium Stenotrophomonas (Xanthomonas) maltophilia 70401 to glass and teflon J Bact 1996;178:5472-5479.  [PubMed]

41. Kaiser GM, Tso PC, Morris R, McCurdy D. Xanthomonas maltophilia endopthalmitis after cataract extraction. Am J Opthalmol 1997; 123:410-411. [PubMed]

42. Khardori N, Elting L, Wong E, Schable B, Bodey GP. Nosocomial infections due to Xanthomonas maltophilia (Pseudomonas maltophilia) in patients with cancer. Rev Infect Dis 1990; 12:997-1003. [PubMed]

43. Khardori N, Reuben A, Rosenbaum B, Rolston K, Bodey GP. In vitro susceptibility of Xanthomonas (Pseudomonas) maltophilia to newer antimicrobial agents. Antimicrob Agents Chemother 1990; 34:1609-1610. [PubMed]

44 Krcmery V, Pichna P, Oracova E, Lacka J, Kukuckova E, Studenda M, Grausova S, Stopkova K, Krupova I. Stenotrophomonas maltophilia bacteremia in cancer patients; report on 31 cases. J Hosp Infect 1996; 34:75-55. [PubMed]

45. Krueger TS, Clark EA, Nix DE. In vitro susceptibility of Stenotrophomonas maltophilia to various antimicrobial combinations. Diagn Micrbiol Infect Dis 2001;41:71-78. [PubMed]

46. Lai C-H, Chi C-Y, Chen H-P, et al. Clinical characteristics and prognostic factors of patients with Stenotrophomonas maltophilia bacteremia. J Microbiol Immunol Infect 2004;37:350-358. [PubMed]

47. Laing FPY, Ramotar K, Read RR et al. Molecular epidemiology of Xanthomonas maltophilia colonization and infection in the hospital environment. J Clin Microbiol 1995; 33: 513–8.[PubMed]

48. Lambert T, Ploy MC, Denis F, Courvalin P Characterization of the chromosomal aac(6′)-Iz gene of Stenotrophomonas maltophilia. Antimicrob Agents Chemother 1999;43:2366–2371. [PubMed]

49. Lecso-Bornet M, Pierre J, Sarkis-Karam D, Lubera S, Bergogne-Berezin E. Susceptibility of Xanthomonas maltophilia to six quinolones and study of outer membreane proteins in resistant mutants selected in vitro. Antimicrob Agents Chemother 1992; 36:669-671. [PubMed]

50.  Li XZ, Zhang L, McKay GA, Poole K. Role of the acetyltransferase AAC(6')-Iz modifying enzyme in aminoglycoside resistance in Stenotrophomonas maltophilia. J Antibicrob Chemother 2003; 51: 803–11.  [PubMed]

51. LiPuma JJ, Currie BJ, Lum GD, Vandamme PAR. Burkholderia, Stenotrophomonas, Ralstonia, Cupriavidus, Pandoraea, Brevundimonas, Comamonas, Delftia and Acidovorax. In: Manual of clinical microbiology (9th edn). Washington: ASM Press, 2007:749–769.

52. Marshall WF, Keating MR, Anhalt JP, Steckelberg JM. Xanthomonas maltophilia: an emerging nosocomial pathogen. Mayo Clin Proc 1989; 64:1097-1104. [PubMed]

53. McKay GA, Woods DE, MacDonald KL, Poole K. Role of phosphoglucomutase of Stenotrophomonas maltophilia in lipopolysaccharide biosynthesis, virulence and antibiotic resistance. Infect Immun 2003;71: 3068–75. [PubMed]

54. Mehta NJ, Khan IA, Mehta RN, Gulati A. Stenotrophomonas maltophilia endocarditis of prosthetic aortic valve: Report of a case and review of literature. Heart Lung 2000;29:251-355. [PubMed]

55. Micozzi A, Venditti M, Monaco M, Friedrich A, Taglietti F, Santilli S, Martino P. Bacteremia due to Stenotrophomonas maltophilia in patients with hematologic malignancies. Clin Infect Dis 2000; 31:705-711. [PubMed]

56. Miyari I, Franlin JA, Andreansky M, Knapp KM, Hayden RT. Acute necrotizing ulcerative gingivitis and bacteremia caused by Stenotrophomonas maltophilia in an immunocompromised host. Peditr Infect Dis J 2005:24:181-183. [PubMed]

57. Muder RR, Harris AP, Muller S, Edmund M, Chow JW, Papadakis K, Wagener MW, Bodey GP, Steckelberg JM. Bacteremia due to Stenotrophomonas maltophilia: a prospective, multicenter study of 91 episodes. Clin Infect Dis 1996; 22:508-512. [PubMed]

58.  Muder RR, Yu VL, Dummer JS, Vinson C, Lumish RM. Infections caused by Pseudomonas maltophilia: expanding clinical spectrum. Arch Intern Med 1987; 147:1672-1674. [PubMed]

59.  Munter RG, Yinnon AM, Schlesinger Y, Hershko C. Infective endocarditis due to Stenotrophomonas (Xanthomonas) maltophilia. Eur J Clin Microbiol Infect Dis 1998; 17:353-356. [PubMed]

60. Neu HC, Saha G, Chin NX. Resistance of Xanthomonas maltophilia to antibiotics and the effect of beta-lactamase inhibitors. Diagn Microbiol Infect Dis 1989; 12:283-285. [PubMed]

61. Nguyen MH, Muder RR. Xanthomonas maltophilia meningitis: case report and review of the literature. Clin Infect Dis 1994; 19:325-326. [PubMed]

62. Nicodemo AC, Araujo MRE, Ruiz AS, Gales AC. In vitro susceptibility of Stenotrophomonas maltophilia isolates: comparison of disc diffusion, Etest and agar dilution methods J Antimicrob Chemoth 2004;53:604-608. [PubMed]

63. Noskin GA, Grohmann SM. Xanthomonas maltophilia bactermia: an analysis offactors influencing outcome. Infect Dis Clin Pract 1992; 1:230-236.

64. Okazaki A, Avison MB. Aph(3')-IIc, an aminoglycoside resistance determinant from Stenotrophomonas maltophilia. Antimicrob Agents Chemother. 2007;51:359-60.  [PubMed]

65.  Pankuch GA, Jacobs MR, Rittenhouse SF, Appelbaum PC. Susceptibilities of 123 strains of Xanthomonas maltophilia to eight b-lactams (including b-lactam - b-lactamase inhibitor combinations) and ciprofloxacin tested by five methods. Antimicrob Agents Chemother 1994; 38:2317-2322. [PubMed]

66. Papadakis KA, Varivarian SE, Vassilaki ME, Anaissie EJ. Stenotrophomonas maltophilia meningitis: report of two cases and review of the literature. J Neurosurg 1997; 87:106-108. [PubMed]

67. Paton R, Miles RS, Amyes SG. Biochemical profiles of inducible beta-lactamases produced from Xanthomonas maltophilia. Antimicrob Ag Chemother 1994; 38:2143-2149. [PubMed]

68. Penland RL, Wilhelmus KR. Stenotrophomonas maltophilia ocular infections. Arch Opthalmol 1996; 114:433-436.[PubMed]

69.  Poulos CD, Matsumura SO, Willey BM, Low DE, McGeer A. In vitro activities of antimicrobial combinations against Stenotrophomonas (Xanthomonas) maltophilia. Antimicrob Agents Chemother 1995;39:2220-2223. [PubMed]

70. Rolston KVI, Kontoyiannis DP, Yadegarynia D, Raad II. Non-fermentative gram-negative bacilli in cancer patients: increasing frequency of infection and antimicrobial susceptibility of clinical isolates to fluorquinolones. Diagn Microbiol Infect Dis 2005;51:215-218. [PubMed]

71. Rouse MS, Tallan BM, Henry NK, Steckelberg JM, Wilson WR. Treatment of Xanthomonas maltophilia experimental pneumonia in mice. Chest 1991; 100(2suppl); 147S.

72.  Rousseau A, Morcos M, Amrouche L, et al. Lethal pulmonary hemorrhage caused by a fulminant Stenotrophomonas maltophilia respiratory infection in an acute myeloid leukemia patient. Leukemia Lymphoma 2004;45:1293-1296.[PubMed]

73. Sader HS, Jones RN, Dowzicky MJ, Fritsche TR. Antimicrobial activity of tigecycline tested against nosocomial bacterial pathogens from patients hospitalized in the intensive care unit. Diagn Microbiol Infect Dis. 2005;52:203-8.[PubMed]

74. Sader HS, Jones RN. Antimicrobial susceptibility of uncommonly isolated non-enteric Gram-negative bacilli. Int J Antimicrob Agents. 2005 Feb;25:95-109. [PubMed]

75. Saiman L, Chen Y, San Gabriel P, Knirsch C. Synergistic activities of macrolide antibiotics against Pseudomonas aeruginosa, Burkholderia cepacia, Stenotrophomonas maltophilia, and Alkaligenes xylosoxidans isolated from patients with cystic fibrosis. Antimicrob Agents Chemoth 2002;46:1105-1107. [PubMed]

76. Saino Y, Inoue M, Mitsuhashi S. Purification of an inducible cephalosporinase from Pseudomonas maltophilia GN12873. Antimicrob Agents Chemother 1984: 25:362-365. [PubMed]

77.  Saino Y, Kobayashi M, Inoue M, Mitsuhashi S. Purification and properties of inducible penicillin b-lactamase isolated from Pseudomonas maltophilia. Antimicrob Agents Chemother 1982; 22:564-570.

78. San Gabriel P, Zhou J, Tabibi S, Chen Y, Trauzzi M, Saiman L. Antimicrobial susceptibility and synergy studies of Stenotrophomonas maltophilia isolates from patients with cystic fibrosis. Antimicrob Ag Chemother 2004;48:168-171.[PubMed]

79. Sattler CA, Mason EO, Kaplan SL. Nonrespiratory Stenotrophomonas maltophilia infection at a children’s hospital. Clin Infect Dis 2000; 31:1321-1330. [PubMed]

80.  Szeto CC, Li PK, Leung CB, Yu AW, Lui SF, Lai KN. Xanthomonas maltophilia peritonitis in uremic patients receiving continuous ambulatory peritoneal dialysis. Am J Kidney Dis 1997; 29:91-95. [PubMed]

81. Talmaciu I, Varlotta L, Mortensen J, Schidlow DV. Risk factors for emergence of Stenotrophomonas maltophilia in cystic fibrosis Pediatr Pulmonol 2000; 30: 10–5 [PubMed]

82. Travassos LH, Pinheiro MN, Coelho FS, Sampaio JLM, Merquior VLC, Marques EA. Phenotypic properties, drug susceptibility and genetic relatedness of Stenotrophomonas maltophilia clinical strains from seven hospitals in Rio de Janeiro, Brazil. J Appl Microbiol 2004; 96: 1143–50. [PubMed]

83. Tzanetou K, Triantiphillis T, Tsoutsos D et al. Stenotrophomonas maltophilia peritonitis in CAPD patients: susceptibility to antibiotics and treatment outcome: a report of five cases. Perit Dial Int 2004;24:401-404. [PubMed]

84. Valdezate S, Vindel A, Baquero F, Canton R. Comparative in vitro activity of quinolones against Stenotrophomonas maltophilia. Eur J Clin Microbiol Infect Dis 1999;18:908–11. [PubMed]

85. Valdezate S, Vindel A, Loza E, Baquero F, Canton R. Antimicrobial suscptibilities of unique Stenotrophomonas maltophilia clinical strains. Antimicrob Agents Chemother 2001; 45:1581-1584. [PubMed]

86. Valdezate S, Vindel A, Maiz L, Baquero F, Escobar H, Canton R. Persistence and variability of Stenotrophomonas maltophilia in cystic fibrosis patients, Madrid, 1991-1998. Emerg Infect Dis 2001; 7:113-122.  [PubMed]

87. VanCouwenberghe CJ, Cohen SH, Tang YJ, Gumerlock PH, Silva J. Genomic fingerprinting of epidemic and endemic strains of Stentrophomonas maltophilia (formerly Xanthomonas maltophilia) by arbitrarily primed PCR. J Clin Microbiol 1995; 1289-1291. [PubMed]

88. Vartivarian S, Anaissie E, Bodey G, Sprigg H, Rolston K. A changing pattern of susceptibility of Xanthomonas maltophilia to antimicrobial agents: implications for therapy. Antimicrob Agents Chemother 1994; 38:624-627.  [PubMed]

89 Vartivarian SE, Papadakis KA, Anaissie EJ. Stenotrophomonas (Xanthomonas) maltophilia urinary tract infection: a disease that is unusually severe and complicated. Arch Intern Med 1996; 156:433-435. [PubMed]

90. Vartivarian SE, Papadakis KA, Palacios JA, Manning JT, Anaissie EJ. Mucocutaneous and soft tissue infections caused by Xanthomoans maltophilia: a new spectrum. Ann Intern Med 1994; 121:969-973. [PubMed]

91. Vickers IE, Smikle MF. The immunomodulatory effect of antibiotics on the secretion of tumour necrosis factor alpha by peripheral blood mononuclear cells in response to Stenotrophomonas maltophilia stimulation. West Indian Med J. 2006;55:138-41. [PubMed]

92. Victor MA, Arpi M, Bruun B, Jonsson V, Hansen MM. Xanthomonas maltophilia bacteremia in immunocompromised hematological patients. Scand J Infect Dis 1994; 26:163-170. [PubMed]

93. Visalli MA, Jacobs MR, Appelbaum PC. Activities of three quinolones, alone and in combination with extended-spectrum cephalosporins or gentamicin, against Stenotrophomonas maltophilia Antimicrob Agents Chemother 1998;42:2002-2005. [PubMed]

94. Wang W-S, Liu C-P, Lee, C-M, Huang F-Y. Stenotrophomonas maltophilia bacteremia in adults: four years’ experience in a medical center in northern Taiwan. J Micrbiol Immunol Infect 2004;37:359-365. [PubMed]

95. Waters VJ, Gómez MI, Soong G, Amin S, Ernst RK, Prince A. Immunostimulatory Properties of the emerging pathogen Stenotrophomonas maltophilia Infect Immun 2007;75:1698-1703. [PubMed]

96.  Weber DJ, Rutala WA, Blanchet CN, Jordan M, Gergen MF. Faucet aerators: a source of patient colonization with Stenotrophomonas maltophilia. Am J Infect Control 1999; 27:59-63. [PubMed]

97. Weber DJ, Rutala WA, Sickbert-Bennett EE, Samsa GP, Brown V, Niederman MS. Microbiology of ventilator-associated pneumonia compared with that of hospital-acquired pneumonia. Infect Control Hosp Epidemiol. 2007;28:825-31.  [PubMed]

98. Weiss K, Restieri C, De Carolis E, Laverdiere M, Guay H. Comparative activity of new quinolones against 326 clinical isolates of Stenotrophomonas maltophilia. J Antimicrob Chemother 2000; 45:363-365. [PubMed]

99.  Windhorst S, Frank E, Georgieva DN, Genov N, Buck F, Borowski P, Weber W. The major extracellular protease of the nosocomial pathogen Stenotrophomonas maltophilia J Biological Chem 2002;277:11042-11049. [PubMed]

100.  Yu VL, Felegie TP, Yee RB, Pasculle AW, Taylor RH. Synergistic interactions in vitro with use of three antibiotics simultaneously against Pseudomonas maltophilia. J Infect Dis 1980; 38:624-627. [PubMed]

101. Zelenitsky SA, Iacovides H, Ariano RE, Harding GKM. Antibiotic combinations significantly more active than montherapy in an in vitro infection model of Stenotrophomonas maltophilia. Diag Microbiol Infect Dis 2005;51:39-43.[PubMed]

102. Zhanel GG, DeCorby M, Nichol KA, Wierzbowski A, Baudry PJ, Karlowsky JA, Lagacé-Wiens P, Walkty A, Mulvey MR, Hoban DJ. Antimicrobial susceptibility of 3931 organisms isolated from intensive care units in Canada: Canadian national Intensive Care Unit Study, 2005/2006 Diag Micro Infect Dis 2008;62:67-80. [PubMed]

103. Zuravleff JJ, Yu VL. Infections caused by Pseudomonas maltophilia: case reports and review of the literature. Rev Infect Dis 1982; 4:1236-1246. [PubMed]

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Table 1: In vitro Susceptibility of S. maltophilia to Selected Antibiotics

Antibiotic MIC50 mg/ml


MIC90 mg/ml


% of strains susceptible* % of strains resistant* No. of strains tested† References


TMP-SMZ 0·25 to >64‡ 0·25 to >64 0 to 100§ 4 to 100 3872 82, 23, 47, 94, 78, 75, 7, 98, 74, 88, 102, 85, 62
Ticarcillin 16 to 512 64 to >1024 29 to 69 32 to 74 329 47, 7, 85
TIM 2 to 128 32 to >1024 27 to 95 14 to 50 3764 82, 23, 47, 94, 78, 75, 7, 81, 74, 88, 85, 62
Cefepime 16 to 64 >16 to ≥128 0 to 30 45 to 100 2508 23, 94, 7, 74, 102, 85
Cefotaxime 60 to ≥64 ≥64 to 512 10 62 to 64 249 7, 85
Ceftazidime 8 to 128 >16 to 256 5 to 53 34 to 86 2649 82, 23, 47, 94, 7, 74, 88, 85
Ceftriaxone >32 to 256 >32 to >256 1 to 2 92 to 96 2184 74, 102
Aztreonam >16 to 256 >16 to >1024 0 to 10 85 to 100 2347 94, 7, 74, 85
Norfloxacin 16 to ≥16 ≥16 to 64 20 56 358 7, 85, 84
Ofloxacin 0·5 to 0·5 4 to 4 89 5 208 85, 84
Ciprofloxacin 0·25 to >8 2 to 32 0 to 82 13 to 96 3865 82, 23, 47, 94, 78, 7, 98, 74, 88, 102, 85, 84
Gatifloxacin 0·1 to 4 0·12 to 16 23 to 97 0 to 46 2642 23, 94, 98, 74, 85, 62
Levofloxacin 0·2 to 2 2 to 8 55 to 86 3 to 11 2631 94, 98, 74, 102, 85
Moxifloxacin 0·06 to 0·5 0·5 to 4 85 6 1405 30, 98, 102, 85, 84
Doxycycline 1 to 2 2 to 8 80 to 100 1 to 11 968 47, 78, 75, 85, 62
Minocycline 0·2 to 1 1 to 4 91 to 100 0 to 5 1014 94, 30, 88, 85
Tetracycline >8 to 32 >8 to 64 8 to 9 70 to 86 2325 7, 74, 85
Tigecycline 1 to 1 2 to 4 90 3 239 102, 73
Polymixin B 1 to 2 4 to 8 72 to 77 28 1322 62, 31
Chloramphenicol 4 to 32 16 to 64 1 to 80 35 to 39 395 47, 7, 85, 62
Amikacin >32 to 512 >32 to >512 0 to 31 61 to 100 2535 47, 94, 7, 74, 102, 85
Gentamicin >8 to 64 >8 to >256 14 to 31 58 to 81 2433 7, 74, 102, 85
Tobramycin ≥16 to 64 ≥16 to 512 2 to 25 68 to 78 2405 47, 7, 74, 85
Imipenem >8 to 512 >8 to >1024 0 to 2 97 to 100 3261 23, 47, 78, 7, 74, 88, 85
Meropenem >8 to >64 >8 to 256 0 to 4 88 to 100 2433 7, 74, 102, 85

Table 2.  Antimicrobial Agents Used in Treatment of S. maltophilia Infections.

Drug Dose
  Trimethoprim/sulfamethoxazole   15mg/kg/day divided in 2 to 3 doses
Ticarcillin/clavulanate 3.1 g q6h IV
Ceftazidime 2 gm q8h IV
Ciprofloxacin 400 mg q12h IV
Levofloxacin 500-750 mg q24h IV
Moxifloxacin 1 x 400mg/day
Doxycycline 100 mg q12h IV

Dosages for adults with normal renal function and weight about 70 kg.


Baron EJ.  Flow Diagram for  Gram Neg   Rods on BAP & MacConkey (NOT for stool isolates)

Javey G, Zuravleff J. Retinitis and Endophthalmitis.

Raad, I., Hanna, H. and Maki, D. Intravascular Catheter-related Infections: Advances in Diagnosis, Prevention and Management. The LANCET Infectious Diseases 2007; Vol.7, Issue 10, 645-657.

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