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Risk factors and clinical characteristics for Stenotrophomonas maltophilia infection in an acute care hospital in Japan: a single-center retrospective study

Journal of Pharmaceutical Health Care and Sciences volume 11, Article number: 24 (2025) Cite this article

Abstract

Background

Stenotrophomonas maltophilia (S. maltophilia) is a Gram-negative pathogen that causes opportunistic infections. Although the mortality rate among patients with nosocomial infections caused by S. maltophilia is high, the risk factors for infection vary among studies. Moreover, S. maltophilia is highly resistant to several classes of antimicrobial agents. To date, few studies on S. maltophilia have been conducted in Japan, and the details remain unclear. Therefore, the objective of this study was to investigate the risk factors associated with S. maltophilia infection and the antimicrobial susceptibility of S. maltophilia isolates identified in our hospital.

Methods

In this study, we investigated the risk factors associated with S. maltophilia infection and clinical characteristics isolated from patients at the NTT Medical Center Tokyo (Tokyo, Japan). We retrospectively examined the S. maltophilia isolates and the corresponding patients between March 2022 and August 2023.

Results

Fifty-eight patients with S. maltophilia isolated (median age, 80.5 years; age range, 49–100 years; 70.7% male) were enrolled in this study. Twelve cases (20.7%) were placed in the S. maltophilia infection group and 46 cases were placed in the S. maltophilia colonization group. Central venous (CV) catheterization and higher Sequential Organ Failure Assessment (SOFA) scores were identified as risk factors for S. maltophilia infection. In addition, the 30-day mortality rate was significantly higher, and the survival rate was significantly lower in patients with S. maltophilia infection. The antimicrobial susceptibility rates of S. maltophilia were as follows: 28.6% for ceftazidime, 2.4% for cefozopran, 96.6% for levofloxacin, 100% for minocycline, and 98.3% for trimethoprim-sulfamethoxazole.

Conclusions

In actual clinical practice, S. maltophilia was more frequently isolated from sputum. However, most of the cases were colonization, and cases of infection were rare. Early treatment initiation should be considered for S. maltophilia infection in cases where the pathogen is detected from sterile sites, such as blood cultures and pleural fluid or from sputum in cases with a high SOFA score and CV catheter insertion.

Background

Stenotrophomonas maltophilia (S. maltophilia) is a Gram-negative pathogen that causes a variety of infections, primarily pneumonia and bloodstream infections. In the hospital environment, it is isolated from sources such as tap water, nebulizers, ventilator circuits, and contaminated disinfectants, making it an important opportunistic pathogen causing healthcare-associated infections [1]. Nosocomial infections caused by S. maltophilia have a high mortality rate, ranging between 12.5–41% for bacteremia, 40–50% for pneumonia, and 39% for endocarditis [1, 2]. Risk factors for S. maltophilia infection, including malignancy, intravenous device placement, chronic respiratory disease, immunodeficiency, prolonged antimicrobial use, and prolonged hospitalization or intensive care unit (ICU) admission, vary among reports [3,4,5,6,7]. In addition, in a real clinical setting, it is difficult to determine whether a patient is eligible for treatment if S. maltophilia is isolated in a non-sterile specimen.

Fluoroquinolones, tetracyclines, and trimethoprim-sulfamethoxazole (TMP-SMX) are commonly used to treat S. maltophilia infections [8,9,10]. However, the resistance rates of S. maltophilia to these drugs vary based on region [11]. S. maltophilia is highly resistant to several antimicrobial agents and is reported to acquire resistance genes and genetic mutations that limit antimicrobial therapy [12, 13]. Recently, increased resistance of S. maltophilia to fluoroquinolones and TMP-SMX has been reported in several countries [14,15,16]. The emergence of fluoroquinolone- and TMP-SMX-resistant strains limits the choice of antimicrobial agents to treat S. maltophilia infections, potentially posing a public health concern in the future. Understanding regional antimicrobial susceptibility is important when using antimicrobial agents. However, there are few reports on the resistance of S. maltophilia in Japan, and the characteristics remain unknown. Therefore, in this study, we aimed to investigate the antimicrobial susceptibility of S. maltophilia isolates in our hospital and the risk factors for S. maltophilia infection.

Methods

Study design, setting, and patients

This retrospective study was conducted at the NTT Medical Center in Tokyo, Japan, an acute care hospital with 594 inpatient beds. The monthly antimicrobial use in our hospital during the study period is presented in terms of antimicrobial use density (AUD) and days of therapy (DOT). The mean (standard deviation) values for various antimicrobials were as follows: fluoroquinolones, 0.43 (0.19) AUD, 0.47 (0.17) DOT; tetracyclines, 0.21 (0.07) AUD, 0.20 (0.07) DOT; TMP-SMX, 0.03 (0.04) AUD, 0.02 (0.03) DOT; 3rd-generation cephalosporins, 4.10 (0.72) AUD, 4.75 (1.05) DOT; 4th-generation cephalosporins, 1.27 (0.43) AUD, 1.57 (0.47) DOT; and carbapenems, 2.99 (0.61) AUD, 4.43 (0.86) DOT. The definitions of AUD and DOT were as follows: AUD = [total usage / defined daily dose; DDD × total patient days] × 100 and DOT = [total days of used / total patient days] × 100.

S. maltophilia isolates and the patients from whom S. maltophilia was isolated were retrospectively examined between March 2022 and August 2023. If multiple strains were isolated from the same patient, the first strain detected was included in this study. There were no cases in which S. maltophilia was detected in culture samples from different sites in the same patient. This study was approved by the Ethics Committee of NTT Medical Center Tokyo prior to the study (Approval number: 22–66). Owing to the retrospective and non-invasive nature of the study, the requirement for individual informed consent was waived. Disclosures about the study and an opt-out option were available for the patients on the hospital website. The study was conducted with full consideration of protecting patients’ personal information according to the privacy policy guidelines.

Investigation of antimicrobial use history and susceptibility testing

A total of 58 S. maltophilia clinical isolates and the corresponding patients were enrolled in this study. We evaluated the antimicrobial susceptibility of S. maltophilia isolates, antimicrobial use history within 30 days prior to isolation of S. maltophilia. In this study, antimicrobials used for more than 3 days were counted as “use” cases. All bacterial species were identified using conventional methods and/or a MALDI Biotyper (Bruker Daltonics, Billerica, MA, USA). Antimicrobial susceptibility tests were conducted using MicroScan Neg MIC3J (Beckman Coulter, Inc., CA, USA) and Microscan WalkAway plus System (Beckman Coulter, Inc., CA, USA). The results were interpreted based on the Clinical and Laboratory Standards Institute guidelines M100-S30.

Comparison of the S. maltophilia infection and colonization groups

S. maltophilia infection was defined as a positive microbiological culture from one or more collected sterile specimens. In cases with positive urine cultures, gram stain evidence of phagocytosis, fever, and abdominal symptoms were considered in the determination of infection or colonization. Cases in which S. maltophilia was detected in sputum were defined as infection (S. maltophilia-associated pneumonia) based on the criteria of previous studies [17]. Briefly, S. maltophilia-associated pneumonia was diagnosed via a positive microbiological culture accompanied by radiographic signs on chest X-ray or a computed tomography scan of pulmonary infection (presence of new or increasing infiltrates on chest radiograph) along with one or more of the following symptoms: fever (≥ 38 °C) or hypothermia (< 35 °C); new cough with or without sputum production, pleurisy chest pain, dyspnea, and altered breathing sounds on auscultation.

S. maltophilia colonization was defined as a positive microbiological culture for S. maltophilia without the above clinical signs of infection. In this study, the SM group included patients with S. maltophilia infection, and the colonization group included patients with S. maltophilia colonization. The following factors associated with S. maltophilia infection were obtained from clinical data: Sequential Organ Failure Assessment (SOFA) score at the time of S. maltophilia isolation; history of ICU admission, history of surgery, presence of tracheal intubation, presence of central venous (CV) catheter insertion within 30 days prior to S. maltophilia isolation; neutropenia (neutrophil count < 500/μL) within 14 days prior to S. maltophilia isolation; and length of hospital stay up to the time of S. maltophilia isolation were recorded. In addition, a history of chronic obstructive pulmonary disease, diabetes, cerebrovascular disease, cardiovascular disease, and chronic kidney disease was analyzed. History of drug administration within 30 days prior to S. maltophilia isolation, including steroid, chemical, antimicrobial, or immunosuppressive therapy, was also investigated. Mortality was defined as death within 7–30 days of S. maltophilia isolation. The results obtained were compared between the SM and colonization groups.

Statistical analysis

Statistics analyses to determine the risk factors between the two groups were conducted using the χ2 test or Fisher's exact test for univariate comparisons and the Mann‒Whitney test for continuous variable comparisons. Survival rates were estimated using Kaplan‒Meier curves and compared between groups using the log-rank test. Statistical significance was set at p < 0.05. All analyses were performed using SPSS version 24 software (SPSS Inc., Chicago, IL, USA).

Results

Patient characteristics

A total of 58 patients with S. maltophilia isolates (median age, 80.5 years; age range, 49–100 years; 70.7% male) were enrolled in this study. The basic demographic data and characteristics of patients are listed in Table 1. Antimicrobial use in the 30 days prior to the isolation of S. maltophilia was observed in 55/58 (94.8%) patients, with 43.1, 31.0, 27.6, 25.9, 5.2, 3.4, and 0% of patients receiving meropenem, sulbactam/ampicillin, tazobactam/piperacillin, vancomycin, levofloxacin (LVFX), TMP-SMX, and minocycline (MINO), respectively.

Table 1 Demographic data and patients’ characteristics
Full size table

Bacterial strains detected along with S. maltophilia

In 40/58 patients (69.0%), strains other than S. maltophilia were simultaneously isolated; 27.7% were Candida spp. and 23.1% were Corynebacterium spp. (Table 2).

Table 2 Bacterial strains detected along with Stenotrophomonas maltophilia
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Antimicrobial susceptibility of S. maltophilia isolates

Owing to missing data, only 42 of the 58 samples could be analyzed for antimicrobial susceptibility of ceftazidime (CAZ) and cefozopran (CZOP). The susceptibility rates of S. maltophilia were as follows: 28.6% to CAZ, 2.4% to CZOP, 100% to MINO, 96.6% to LVFX, and 98.3% to TMP-SMX (Table 3). There was no significant correlation between the history of antimicrobial use prior to S. maltophilia infection and antimicrobial resistance.

Table 3 Antimicrobial susceptibility of Stenotrophomonas maltophilia
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Case analysis of the S. maltophilia infection group

The SM group included 12/58 patients (20.7%), with 58.3% of the specimens from sputum, 25.0% blood, 8.3% pleural fluid, and 8.3% bile (Table 4). Invasive medical procedures were performed in 10/12 (83.3%) patients: 75.0% had CV catheter insertion, 25.0% underwent a surgical procedure, and 16.7% had tracheal intubation. Notably, all the patients from whom S. maltophilia was isolated from sterile sites had undergone CV insertion. Comorbidities included cerebrovascular disease (0.0%) and cardiac disease (41.7%). Concomitant medications included steroids (33.3%) and immunosuppressants (0.0%). In the SM group, all patients had a history of antimicrobial use prior to isolation of S. maltophilia. Eleven patients were treated, excluding one who was receiving end-of-life palliative care. The most commonly used antimicrobial agents included MINO (41.7%), LVFX (33.3%), and TMP-SMX (16.7%). Death within 30 days was observed in 4/5 (80.0%) of cases of S. maltophilia isolated from sterile sites in blood, pleural fluid or bile. Among the cases where S. maltophilia was detected in sputum, 1 out of 7 (14.3%) resulted in death within 30 days.

Table 4 Clinical features of patients with Stenotrophomonas maltophilia infection
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Analysis of risk factors for S. maltophilia infection

Antimicrobial susceptibilities in the SM and colonization groups were as follows: CAZ, 25.0 and 29.4%; CZOP, 0 and 2.9%, MINO, 100 and 100%; LVFX, 100 and 95.7%; and TMP-SMX, 100 and 97.8%, respectively. Comparative data for the SM and colonization groups are shown in Table 1. SOFA score (median, 5; range, 0–9 vs. median, 3; range, 0–11; p = 0.01) and CV catheterization (75.0%, 37.0%; p = 0.03) were identified as risk factors for S. maltophilia infection. The SM group also had a significantly higher 30-day mortality rate than that of the colonization group (41.7%, 6.5%; p = 0.01). ANeutropenia within 14 days (16.7%, 4.3%; p = 0.19) was higher in the SM group than in the colonization group, but the difference was not significant. In contrast, cerebrovascular disease history was significantly higher in the S. maltophilia colonization group (0.0%, 37.0%; p = 0.01). Carbapenems were the most commonly used antimicrobial agents (58.3%, 45.7%). In contrast, fluoroquinolones were used by 8.3 and 4.3% of individuals in the SM and colonization groups, respectively. Non-antimicrobial concomitant medications included steroids (33.3%, 13.0%), antineoplastics (25.0%, 8.7%), and immunosuppressants (0%, 2.2%). Furthermore, the Kaplan‒Meier curve-estimated 30-day survival rate was significantly lower in the SM group (58.3%) than in the colonization group (93.5%) (p < 0.01; Fig. 1).

Fig. 1
figure 1

Kaplan–Meier survival curve for patients with Stenotrophomonas maltophilia infection (solid line) and colonization (dotted line); p < 0.01

Full size image

Discussion

This study is one of the few reports investigating risk factors for S. maltophilia infection in acute care hospitals in Japan. High SOFA score and CV catheterization were risk factors for S. maltophilia infection. History of cerebrovascular disease was significantly higher in the S. maltophilia colonization group.

In our hospital, S. maltophilia was more frequently isolated from sputum. However, most of the cases were colonization, and infections were rare. Although there are other strategies to assess the severity of pneumonia, such as the Pneumonia Severity Index [18], CURB-65 [19], A-DROP [20], and I-ROAD [21], the SOFA score was used in this study because these scores overlap with certain assessment factors.

The present study identified elevated SOFA scores and the presence of CV catheters as risk factors for S. maltophilia infection. However, due to the limited number of cases of S. maltophilia infection, multivariate analysis of risk factors and outcomes was not feasible. The SOFA score and CV catheterization have been reported as risk factors for S. maltophilia infection in several previous studies [22,23,24,25].

In our study, a high rate of CV catheterization was observed in cases of S. maltophilia pneumonia, consistent with previous findings identifying CV catheterization as a risk factor for pneumonia in studies investigating S. maltophilia pneumonia among COVID-19 patients [26]. S. maltophilia produces biofilm and other virulence factors that enable colonization or infection in vulnerable hosts. The development of a biofilm is likely to be an important virulence factor associated with S. maltophilia infection [27, 28].

The results of this study suggest that S. maltophilia infection is strongly associated with disease severity and may be due to a combination of host and medical factors, including a history of antimicrobial use, high SOFA scores, and CV catheterization. Patients with S. maltophilia infection generally exhibit more severe symptoms compared to carriers and may play a role as a causative agent of opportunistic infections for other patients. Consequently, the implementation of enhanced monitoring procedures for patients exhibiting risk factors associated with S. maltophilia infection, in conjunction with the implementation of infection prevention measures, has the potential to result in a reduction of infection rates and the associated mortality rate. Previous studies have reported mortality rates of 12–49% for S. maltophilia infection [25, 29,30,31]. Consistent with previous literature, the mortality rate in our study was 36.4%. The 30-day mortality rate was found to be higher in cases where S. maltophilia was detected in the blood culture. The occurrence of fatalities was exclusively associated with cases involving CV catheterization. These findings underscore the necessity of meticulous monitoring of vascular access devices in patients with S. maltophilia detected from sterile sites and the implementation of an evaluation process to discern early indications of infection. In cases with high SOFA scores and CV catheterization, clinicians should give serious consideration to the possibility of S. maltophilia infection and initiate antimicrobial therapy even in cases where S. maltophilia is detected in sputum.

Antimicrobial susceptibility testing revealed that all isolates from the infected group demonstrated susceptibility to the antibiotics utilized in the treatment. Eleven patients were treated with MINO, LVFX, or TMP-SMX, with the exception of one patient who was terminally ill. Despite the administration of treatment, five patients died within 30 days. TMP-SMX is widely acknowledged as the preferred initial treatment for S. maltophilia infections. Despite the longstanding clinical experience with the use of TMP-SMX for S. maltophilia infections, several pharmacokinetic/pharmacodynamics (PK/PD) studies have emerged indicating that TMP-SMX is not bactericidal against S. maltophilia, even those with low TMP minimum inhibitory concentrations (MICs), regardless of the TMP-SMX dosage [32,33,34]. Similar limitations have been observed with other treatment options such as LVX and MINO [35,36,37]. Recent PK/PD studies call into question the current clinical breakpoints for TMP-SXT, LVFX, and MINO. In light of these findings, the 2024 guidance issued by the Infectious Diseases Society of America (IDSA) recommends the utilization of these agents exclusively as part of combination therapy. Studies have indicated that the combination of agents, such as cefiderocol, MINO, TMP-SMX, and fluoroquinolones, exhibits enhanced in vitro activity against S. maltophilia when compared to monotherapy [38]. In this study, the utilization of monotherapy may have contributed to unfavorable outcomes. However, given the high SOFA scores and the presence of CV catheterization, it is possible that the S. maltophilia infection was influenced by an unstable condition with a poor prognosis rather than a strong toxicity. Unfortunately, further analysis of the extant data was not possible.

The antimicrobial resistance rates of S. maltophilia in our hospital were 71.4% for CAZ, 3.4% for LVFX, 1.7% for TMP-SMX, and 0% for MINO. A previous study in Japan reported resistance rates of 67.4% for CAZ, 6.1% for LVFX, 17.7% for TMP-SMX, and 0% for MINO [39]; the TMP-SMX resistance rate was higher than that reported in our study, whereas other drug resistance rates were similar. A recent study has reported increasing resistance rates to LVFX, TMP-SMX, and MINO, and the emergence of strains resistant to two of these drugs [40]; therefore, future trends in antimicrobial resistance should be closely monitored. The mechanisms of resistance of S. maltophilia to fluoroquinolones involve multiple processes, including antimicrobial exposure [41], mutations in target sites of DNA gyrase and topoisomerase IV [42, 43], mechanisms such as drug efflux pumps [44, 45], and plasmid- or chromosome-mediated mutations in drug resistance genes [44,45,46]. In particular, among these drug-resistance genes, Qnr has the potential to transfer and confer quinolone resistance to other bacteria [47, 48].

According to data reported by the Japan Surveillance for Infection Prevention and Healthcare Epidemiology System (J-SIPHE) in Japan in 2023, the LVFX susceptibility rate for S. maltophilia was found to be 92.2% [49]. In the present study, the LVFX susceptibility rate was found to be 96.6%, a figure that similar with the data reported by J-SIPHE. The median AUD and DOT for fluoroquinolone use in 2023 were 2.1 and 2.4, respectively, whereas the AUD and DOT in our hospital were 7.0 and 7.9. This finding indicates that quinolone resistance in S. maltophilia may be influenced by factors other than antimicrobial exposure. In the present study, an investigation into resistance induced by antimicrobial exposure showed no significant differences in antimicrobial usage within 30 days prior to S. maltophilia isolation. A survey by the World Health Organization reported fluoroquinolone use (DDD/1000 inhabitation/day) in 2015 in Asia (Japan, 2.74; South Korea, 2.47), Europe (Italy, 3.8; France, 1.83), North America (Canada, 1.99), and Latin America (Brazil, 2.83) [50]. Farrell et al. investigated the susceptibility of S. maltophilia clinical isolates collected worldwide from 2003 to 2008 and reported that LVFX susceptibility rate was 78.0% in the Asia–Pacific region, 82.5% in North America, 83.7% in Europe, and 91.3% in Latin America [10]. Fluoroquinolone resistance does not necessarily correlate with usage or resistance rates. This finding suggests that factors other than antimicrobial exposure may be strongly involved and that the mechanism of acquiring resistance may differ among regions. Therefore, it is necessary to screen for fluoroquinolone resistance genes to obtain further data on antimicrobial resistance in S. maltophilia.

In addition, our investigation of bacteria isolated concurrently with S. maltophilia revealed that 31.0% were Candida spp. and 25.9% were Corynebacterium spp. Both species were isolated primarily in cases of compromised host defenses or microbial substitution due to the use of broad-spectrum antimicrobial agents. A few patients in this study had neutropenia. However, there was a high use of broad-spectrum antimicrobial agents, such as carbapenems and tazobactam/piperacillin, which may have contributed to the presence of Candida and Corynebacterium spp.

This study had several limitations. First, the sample size was small, and many risk factors were not statistically significant. Moreover, in severe cases where S. maltophilia was isolated, many strains were isolated simultaneously. However, the influence of concurrent strains on mortality risk remains unclear. Second, an accurate diagnosis of S. maltophilia pneumonia is difficult, and the definitions of S. maltophilia pneumonia vary among studies. Colonization may not have been completely excluded in this study. Finally, this was a single-center study, and the antimicrobial susceptibility of S. maltophilia was limited to strains detected in our hospital. In addition, no study was performed at the genetic level, and detailed data on antimicrobial resistance remain unclear. Regional differences in antimicrobial susceptibility have been reported, and further studies are warranted to evaluate the susceptibility of S. maltophilia in Japan.

Conclusions

We investigated the risk factors for S. maltophilia infection and antimicrobial resistance in an acute care hospital in Japan. High SOFA score and CV catheterization were identified as risk factors for S. maltophilia infection. The 30-day mortality rate was significantly higher, and the survival rate was significantly lower in patients with S. maltophilia infection. The results of this study suggest that when S. maltophilia is isolated from severe cases or cases of CV insertion, early treatment with consideration of S. maltophilia infection is recommended. Therefore, a multicenter prospective cohort study is needed to identify the risk factors associated with mortality in S. maltophilia infection.

Data availability

The datasets generated and/or analyzed during the current study are available from the corresponding author upon reasonable request.

Abbreviations

AUD:

Antimicrobial use density

CAZ:

Ceftazidime

CV:

Central venous

CZOP:

Cefozopran

DOT:

Days of therapy

ICU:

Intensive care unit

LVFX:

Levofloxacin

MINO:

Minocycline

SOFA:

Sequential Organ Failure Assessment

TMP-SMX:

Trimethoprim-sulfamethoxazole

References

  1. Senol E. Stenotrophomonas maltophilia: the significance and role as a nosocomial pathogen. J Hosp Infect. 2004;57:1–7.

    Article  CAS  PubMed  Google Scholar 

  2. Looney WJ, Narita M, Mühlemann K. Stenotrophomonas maltophilia: an emerging opportunist human pathogen. Lancet Infect Dis. 2009;9:312–23.

    Article  CAS  PubMed  Google Scholar 

  3. Chang Y-T, Lin C-Y, Chen Y-H, Hsueh P-R. Update on infections caused by Stenotrophomonas maltophilia with particular attention to resistance mechanisms and therapeutic options. Front Microbiol. 2015;6:893.

    Article  PubMed  PubMed Central  Google Scholar 

  4. Nseir S, Di Pompeo C, Brisson H, Dewavrin F, Tissier S, Diarra M, et al. Intensive care unit-acquired Stenotrophomonas maltophilia: incidence, risk factors, and outcome. Crit Care. 2006;10:R143.

    Article  PubMed  PubMed Central  Google Scholar 

  5. Jeon YD, Jeong WY, Kim MH, Jung IY, Ahn MY, Ann HW, et al. Risk factors for mortality in patients with Stenotrophomonas maltophilia bacteremia. Medicine (Baltimore). 2016;95:e4375.

    Article  PubMed  Google Scholar 

  6. Wu RX, Yu CM, Hsu ST, Wang CH. Emergence of concurrent levofloxacin- and trimethoprim/sulfamethoxazole-resistant Stenotrophomonas maltophilia: Risk factors and antimicrobial sensitivity pattern analysis from a single medical center in Taiwan. J Microbiol Immunol Infect. 2022;55:107–13.

    Article  CAS  PubMed  Google Scholar 

  7. Gopalakrishnan R, Hawley HB, Czachor JS, Markert RJ, Bernstein JM. Stenotrophomonas maltophilia infection and colonization in the intensive care units of two community hospitals: A study of 143 patients. Heart Lung J Crit Care. 1999;28:134–41.

    Article  CAS  Google Scholar 

  8. Falagas ME, Valkimadi P-E, Huang Y-T, Matthaiou DK, Hsueh P-R. Therapeutic options for Stenotrophomonas maltophilia infections beyond co-trimoxazole: a systematic review. J Antimicrob Chemother. 2008;62:889–94.

    Article  CAS  PubMed  Google Scholar 

  9. Nicodemo AC, Paez JIG. Antimicrobial therapy for Stenotrophomonas maltophilia infections. Eur J Clin Microbiol Infect Dis Off Publ Eur Soc Clin Microbiol. 2007;26:229–37.

    Article  CAS  Google Scholar 

  10. Farrell DJ, Sader HS, Jones RN. Antimicrobial Susceptibilities of a Worldwide Collection of Stenotrophomonas maltophilia Isolates Tested against Tigecycline and Agents Commonly Used for S. maltophilia Infections. Antimicrob Agents Chemother. 2010;54:2735–7.

  11. Banar M, Sattari-Maraji A, Bayatinejad G, Ebrahimi E, Jabalameli L, Beigverdi R, et al. Global prevalence and antibiotic resistance in clinical isolates of Stenotrophomonas maltophilia: a systematic review and meta-analysis. Front Med. 2023;10:1163439.

    Article  Google Scholar 

  12. Sanchez MB, Hernandez A, Martinez JL. Stenotrophomonas maltophilia drug resistance. Future Microbiol. 2009;4:655–60.

    Article  CAS  PubMed  Google Scholar 

  13. Insuwanno W, Kiratisin P, Jitmuang A. Stenotrophomonas maltophilia Infections: Clinical Characteristics and Factors Associated with Mortality of Hospitalized Patients. Infect Drug Resist. 2020;13:1559–66.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  14. Herrera-Heredia SA, Pezina-Cantú C, Garza-González E, Bocanegra-Ibarias P, Mendoza-Olazarán S, Morfín-Otero R, et al. Risk factors and molecular mechanisms associated with trimethoprim–sulfamethoxazole resistance in Stenotrophomonas maltophilia in Mexico. J Med Microbiol. 2017;66:1102–9.

    Article  CAS  PubMed  Google Scholar 

  15. Hu L-F, Chen G-S, Kong Q-X, Gao L-P, Chen X, Ye Y, et al. Increase in the Prevalence of Resistance Determinants to Trimethoprim/Sulfamethoxazole in Clinical Stenotrophomonas maltophilia Isolates in China. PLoS ONE. 2016;11:e0157693.

    Article  PubMed  PubMed Central  Google Scholar 

  16. Neela V, Rankouhi SZR, van Belkum A, Goering RV, Awang R. Stenotrophomonas maltophilia in Malaysia: molecular epidemiology and trimethoprim–sulfamethoxazole resistance. Int J Infect Dis. 2012;16:e603–7.

    Article  CAS  PubMed  Google Scholar 

  17. Stenotrophomonas maltophilia bacteremia and pneumonia at a tertiary-care oncology center: a review of 16 years | Supportive Care in Cancer. [cited 2024 Jul 3]. Available from: https://link.springer.com/article/https://doiorg.publicaciones.saludcastillayleon.es/10.1007/s00520-017-4032-x

  18. Fine MJ, Auble TE, Yealy DM, Hanusa BH, Weissfeld LA, Singer DE, et al. A prediction rule to identify low-risk patients with community-acquired pneumonia. N Engl J Med. 1997;336:243–50.

    Article  CAS  PubMed  Google Scholar 

  19. Lim WS, van der Eerden MM, Laing R, Boersma WG, Karalus N, Town GI, et al. Defining community acquired pneumonia severity on presentation to hospital: an international derivation and validation study. Thorax. 2003;58:377–82.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  20. Miyashita N, Matsushima T, Oka M. The JRS Guidelines for the Management of Community-acquired Pneumonia in Adults: An Update and New Recommendations. Intern Med. 2006;45:419–28.

    Article  PubMed  Google Scholar 

  21. Seki M, Watanabe A, Mikasa K, Kadota J, Kohno S. Revision of the severity rating and classification of hospital-acquired pneumonia in the Japanese Respiratory Society guidelines. Respirol Carlton Vic. 2008;13:880–5.

    Article  Google Scholar 

  22. Saugel B, Eschermann K, Hoffmann R, Hapfelmeier A, Schultheiss C, Phillip V, et al. Stenotrophomonas maltophilia in the respiratory tract of medical intensive care unit patients. Eur J Clin Microbiol Infect Dis. 2012;31:1419–28.

    Article  CAS  PubMed  Google Scholar 

  23. Alsuhaibani M, Aljarbou A, Althawadi S, Alsweed A, Al-Hajjar S. Stenotrophomonas maltophilia bacteremia in children: risk factors and mortality rate. Antimicrob Resist Infect Control. 2021;10:19.

    Article  PubMed  PubMed Central  Google Scholar 

  24. Wang N, Tang C, Wang L. Risk Factors for Acquired Stenotrophomonas maltophilia Pneumonia in Intensive Care Unit: A Systematic Review and Meta-Analysis. Front Med. 2021;8:808391.

    Article  Google Scholar 

  25. Araoka H, Baba M, Yoneyama A. Risk factors for mortality among patients with Stenotrophomonas maltophilia bacteremia in Tokyo, Japan, 1996–2009. Eur J Clin Microbiol Infect Dis Off Publ Eur Soc Clin Microbiol. 2010;29:605–8.

    Article  CAS  Google Scholar 

  26. Raad M, Abou Haidar M, Ibrahim R, Rahal R, Abou Jaoude J, Harmouche C, et al. Stenotrophomonas maltophilia pneumonia in critical COVID-19 patients. Sci Rep. 2023;13:3392.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  27. Falagas ME, Kastoris AC, Vouloumanou EK, Rafailidis PI, Kapaskelis AM, Dimopoulos G. Attributable mortality of Stenotrophomonas maltophilia infections: a systematic review of the literature. Future Microbiol. 2009;4:1103–9.

    Article  PubMed  Google Scholar 

  28. Flores-Treviño S, Bocanegra-Ibarias P, Camacho-Ortiz A, Morfín-Otero R, Salazar-Sesatty HA, Garza-González E. Stenotrophomonas maltophilia biofilm: its role in infectious diseases. Expert Rev Anti Infect Ther. 2019;17:877–93.

    Article  PubMed  Google Scholar 

  29. Wu H, Wang J-T, Shiau Y-R, Wang H-Y, Lauderdale T-LY, Chang S-C, et al. A multicenter surveillance of antimicrobial resistance on Stenotrophomonas maltophilia in Taiwan. J Microbiol Immunol Infect Wei Mian Yu Gan Ran Za Zhi. 2012;45:120–6.

  30. Xun M, Zhang Y, Li B-L, Wu M, Zong Y, Yin Y-M. Clinical characteristics and risk factors of infections caused by Stenotrophomonas maltophilia in a hospital in northwest China. J Infect Dev Ctries. 2014;8:1000–5.

    Article  PubMed  Google Scholar 

  31. Ince N, Yekenkurul D, Danış A, Çalışkan E, Akkaş İ. An evaluation of six-year Stenotrophomonas maltophilia infections in a university hospital. Afr Health Sci. 2020;20:1118–23.

    Article  PubMed  PubMed Central  Google Scholar 

  32. Wei C, Ni W, Cai X, Zhao J, Cui J. Evaluation of Trimethoprim/Sulfamethoxazole (SXT), Minocycline, Tigecycline, Moxifloxacin, and Ceftazidime Alone and in Combinations for SXT-Susceptible and SXT-Resistant Stenotrophomonas maltophilia by In Vitro Time-Kill Experiments. PLoS ONE. 2016;11:e0152132.

    Article  PubMed  PubMed Central  Google Scholar 

  33. Araoka H, Baba M, Okada C, Abe M, Kimura M, Yoneyama A. Evaluation of trimethoprim-sulfamethoxazole based combination therapy against Stenotrophomonas maltophilia: in vitro effects and clinical efficacy in cancer patients. Int J Infect Dis IJID Off Publ Int Soc Infect Dis. 2017;58:18–21.

    CAS  Google Scholar 

  34. Muder RR, Harris AP, Muller S, Edmond M, Chow JW, Papadakis K, et al. Bacteremia due to Stenotrophomonas (Xanthomonas) maltophilia: a prospective, multicenter study of 91 episodes. Clin Infect Dis Off Publ Infect Dis Soc Am. 1996;22:508–12.

    Article  CAS  Google Scholar 

  35. Toleman MA, Bennett PM, Bennett DMC, Jones RN, Walsh TR. Global emergence of trimethoprim/sulfamethoxazole resistance in Stenotrophomonas maltophilia mediated by acquisition of sul genes. Emerg Infect Dis. 2007;13:559–65.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  36. Hevia EC, Wooten L, Carr AL. Trimethoprim/Sulfamethoxazole vs Minocycline for the Treatment of Nonurinary Monomicrobial Stenotrophomonas maltophilia Infections in Hospitalized Patients. Ann Pharmacother. 2024;58:698–704.

    Article  CAS  PubMed  Google Scholar 

  37. Jacobson S, Junco Noa L, Wallace MR, Bowman MC. Clinical outcomes using minocycline for Stenotrophomonas maltophilia infections. J Antimicrob Chemother. 2016;71:3620.

    Article  CAS  PubMed  Google Scholar 

  38. Tamma PD, Heil EL, Justo JA, Mathers AJ, Satlin MJ, Bonomo RA. Infectious Diseases Society of America 2024 Guidance on the Treatment of Antimicrobial-Resistant Gram-Negative Infections. Clin Infect Dis Off Publ Infect Dis Soc Am. 2024;ciae403.

  39. Kanamori H, Yano H, Tanouchi A, Kakuta R, Endo S, Ichimura S, et al. Prevalence of Smqnr and plasmid-mediated quinolone resistance determinants in clinical isolates of Stenotrophomonas maltophilia from Japan: Novel variants of Smqnr. New Microbes New Infect. 2015;7:8–14.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  40. Kumwenda GP, Kasambara W, Phiri A, Chizani K, Banda A, Choonara F, et al. A multidrug-resistant Stenotrophomonas maltophilia clinical isolate from Kamuzu Central Hospital. Malawi Malawi Med J. 2021;33:82–4.

    Article  PubMed  Google Scholar 

  41. Chatree Y, Charoenlap N, Vanitshavit V, Ruangrassamee P, Mongkolsuk S, Vattanaviboon P. Induction of Antimicrobial Resistance of Stenotrophomonas maltophilia by Exposure to Nonlethal Levels of Antibiotics. Microb Drug Resist. 2023;29:115–26.

    Article  CAS  PubMed  Google Scholar 

  42. Vranakis I, Sandalakis V, Chochlakis D, Tselentis Y, Psaroulaki A. DNA Gyrase and Topoisomerase IV Mutations in an In Vitro Fluoroquinolone-Resistant Coxiella burnetii Strain. Microb Drug Resist. 2010;16:111–7.

    Article  CAS  PubMed  Google Scholar 

  43. Weigel LM, Anderson GJ, Tenover FC. DNA Gyrase and Topoisomerase IV Mutations Associated with Fluoroquinolone Resistance in Proteus mirabilis. Antimicrob Agents Chemother. 2002;46:2582–7.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  44. Poole K. Multidrug efflux pumps and antimicrobial resistance in Pseudomonas aeruginosa and related organisms. J Mol Microbiol Biotechnol. 2001;3:255–64.

    CAS  PubMed  Google Scholar 

  45. Soto SM. Role of efflux pumps in the antibiotic resistance of bacteria embedded in a biofilm. Virulence. 2013;4:223–9.

    Article  PubMed  PubMed Central  Google Scholar 

  46. Gordon NC, Wareham DW. Novel variants of the Smqnr family of quinolone resistance genes in clinical isolates of Stenotrophomonas maltophilia. J Antimicrob Chemother. 2010;65:483–9.

    Article  CAS  PubMed  Google Scholar 

  47. Sánchez MB, Hernández A, Rodríguez-Martínez JM, Martínez-Martínez L, Martínez JL. Predictive analysis of transmissible quinolone resistance indicates Stenotrophomonas maltophilia as a potential source of a novel family of Qnr determinants. BMC Microbiol. 2008;8:148.

    Article  PubMed  PubMed Central  Google Scholar 

  48. Shimizu K, Kikuchi K, Sasaki T, Takahashi N, Ohtsuka M, Ono Y, et al. Smqnr, a New Chromosome-Carried Quinolone Resistance Gene in Stenotrophomonas maltophilia. Antimicrob Agents Chemother. 2008;52:3823–5.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  49. National Center for Global Health and Medicine. Jpn. Surveill. Infect. Prev. Healthc. Epidemiol. 2024. [cited 2024 Dec 26]. Available from: https://j-siphe.ncgm.go.jp/

  50. WHO report on surveillance of antibiotic consumption: 2016–2018 early implementation. https://www.who.int/publications/i/item/9789241514880. 2023.

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Acknowledgements

We would like to thank Editage (www.editage.com) for providing writing support.

Funding

This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

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Authors and Affiliations

  1. Department of Pharmacy, NTT Medical Center Tokyo, 5-9-22 Higashi-Gotanda, Shinagawa-Ku, Tokyo, 141-8625, Japan

    Michiya Tanuma & Masayo Tanaka

  2. Department of Clinical Microbiology, School of Pharmacy, Tokyo University of Pharmacy and Life Sciences, 1432-1 Horinouchi, Hachioji, Tokyo, 192-0392, Japan

    Michiya Tanuma & Hidemasa Nakaminami

  3. Department of Infectious Diseases, NTT Medical Center Tokyo, 5-9-22 Higashi-Gotanda, Shinagawa-Ku, Tokyo, 141-8625, Japan

    Takayuki Sakurai

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  1. Michiya Tanuma
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  4. Masayo Tanaka
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Contributions

MT and HN conceived and designed the study. MT and TS collected the clinical data. HN and MT reviewed the data. MT, TS, HN, and MT conducted data analysis and interpretation. MT drafted the manuscript. HN assisted with the drafting of the manuscript. All authors have read and approved the final version of this manuscript. All authors agree to be accountable for all aspects of the work involved and ensure that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

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Correspondence to Michiya Tanuma.

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Ethics approval and consent to participate

This study was approved by the Ethics Committee of NTT Medical Center Tokyo prior to the study (Approval number: 22–66). Owing to the retrospective and non-invasive nature of the study, the requirement for individual informed consent was waived. The study was conducted with full consideration for protecting patients’ personal information according to the privacy policy guidelines.

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Not applicable.

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Tanuma, M., Sakurai, T., Nakaminami, H. et al. Risk factors and clinical characteristics for Stenotrophomonas maltophilia infection in an acute care hospital in Japan: a single-center retrospective study. J Pharm Health Care Sci 11, 24 (2025). https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s40780-025-00429-2

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Keywords

Journal of Pharmaceutical Health Care and Sciences

ISSN: 2055-0294

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