Stenotrophomonas Maltophilia

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Background

Stenotrophomonas maltophilia, previously classified as Xanthomonas maltophilia, is an aerobic gram-negative bacillus prevalent in various aquatic environments. Although it is considered an uncommon pathogen in humans, there has been a notable rise in the recognition of S maltophilia infections, particularly in nosocomial settings (hospital-acquired infections). This organism is categorized as a nonfermentative gram-negative bacillus, distinct from the Enterobacterales family. Its increasing prevalence in clinical infections highlights the need for awareness and understanding of its role in healthcare-associated infections.[1]

S maltophilia is an organism of low virulence and frequently colonizes fluids used in the hospital setting (eg, hospital tap water,[2]  irrigation solutions, intravenous fluids) and patient secretions (eg, respiratory secretions, urine, wound exudates). S maltophilia usually must bypass normal host defenses to cause human infection. For example, if an irrigation solution becomes colonized with this organism, irrigating an open wound can cause colonization or infection of the wound. S maltophilia usually is incapable of causing disease in healthy hosts without the assistance of invasive medical devices that bypass normal host defenses.[3]

Risk factors associated with S maltophilia infection may include underlying malignancy, immunosuppressant therapy, cystic  fibrosis, COPD, HIV, neutropenia, mechanical ventilation, prior colonization with stenotrophomonas, central venous catheter, genitourinary catheter, continuous ambulatory peritoneal dialysis (CAPD), recent surgery, trauma, prolonged hospitalization, ICU admission, and exposure to broad-spectrum antibiotics, third or fourth generation cephalosporins and carbapenems, and hyperalimentation.[4, 5, 6, 7, 8]

 

 

Pathophysiology

S maltophilia has few pathogenic mechanisms and, for this reason, predominantly results in colonization rather than infection. The main virulence factors that lend to disease pathogenesis include production of a variety of extracellular enzymes, evasion of host immune response, and triggering intense tissue inflammation.

When infections do occur, invasive medical devices often serve as the means by which the organism evades the body's normal defenses. Factors that facilitate the colonization of the respiratory tract or prosthetic devices—such as intravascular catheters, surgical catheters, and endotracheal tubes—include a cationic surface charge, flagella, and fimbriae, which aid in adhesion and biofilm formation.[43]

Epidemiology

Frequency

United States

S maltophilia is a noninvasive organism that has low virulence. It frequently colonizes body fluids but rarely causes infection (eg, intravenous line infections).

International

S maltophilia frequently colonizes the respiratory tract in patients with cystic fibrosis.[9, 10, 11, 12, 13]

The global pooled prevalence of S maltophilia is 5.3%, with a higher prevalence of 10.5% in the Western Pacific Region and a lower prevalence of 4.3% in the Americas. A meta-analysis indicated that the highest antibiotic resistance rate was against cefuroxime at 99.1%, whereas the lowest resistance was associated with minocycline at 4.8%.[14]

The prevalence of S maltophilia continues to rise; it has increased from 7% during 2004 - 2007 to 15% during 2020-2022.[44]

Mortality/Morbidity

Mortality and morbidity relate to the inoculum of S maltophilia that is able to bypass normal host defense mechanisms.

If an intravenous infusion contains large numbers of S maltophilia, then direct injection into the bloodstream may result in the signs and symptoms associated with gram-negative bacteremia.

Likewise, in the urinary tract, the use of urologic irrigation fluids containing high levels of S maltophilia during invasive procedures, such as cystoscopy, can lead to gram-negative bacteremia. The associated mortality and morbidity from this condition are influenced by various host factors.

A meta-analysis identified key risk factors for mortality in patients with S maltophilia bacteremia. Out of 1248 patients analyzed, 506 (40.5%) died. Significant risk factors for mortality included ICU admission, septic shock, the need for mechanical ventilation, indwelling central venous catheters, neutropenia, comorbid hematological malignancies, chronic kidney disease, inappropriate antimicrobial therapy, and prior antibiotic use.[15]

The analysis concluded that appropriate antimicrobial therapy had a protective effect against mortality. Additionally, the presence of indwelling central venous catheters, neutropenia, hematological malignancies, and chronic kidney disease were associated with increased mortality risk.

S maltophilia bacteremia should be considered in patients with recent use of broad-spectrum antibiotics or recent isolation from any other site. The 30-day all-cause mortality rate associated with S maltophilia bacteremia (33.3%) is reported to be more than that of bacteremia caused by Pseudomonas aeruginosa (21.5%) and Acinetobacter species (17.3%). The independent factor associated with 30-day mortality was the SOFA score.[16]

Prognosis

The course of S maltophilia infection depends on the site of the infection, severity, response to antibiotics, and existence of other comorbidities. S maltophilia infections may be life-threatening, especially in immunocompromised patients.[17]

 

History

Because Stenotrophomonas maltophilia infections are extremely uncommon, no specific patient history suggests its presence other than contact with other colonized individuals.

Obtaining a history of the use of irrigant solutions that potentially could contain S maltophilia is important in an epidemiologic setting rather than in a clinical setting.

Patients often have a history of indwelling catheters, use of immunosuppressant therapy or broad-spectrum antibiotics, or cystic fibrosis.

Physical

Signs and symptoms of S maltophilia infections are related to the organ system involved and are indistinguishable from infections with other pathogens.

Causes

S maltophilia is a nonfermentative aerobic gram-negative bacillus formerly classified in the genus Pseudomonas. Unlike Pseudomonas aeruginosa, S maltophilia is an organism of low virulence, with limited ability to cause infection in humans.

S maltophilia is a water organism, and it survives and multiplies in aqueous environments, particularly respiratory secretions, urine, intravenous fluids, and irrigant solutions.

S maltophilia may persist in an aquatic environment for extended periods.

Sources of S maltophilia colonization include the following:

Personnel

Respiratory equipment and/or fluids

Intravenous lines and/or fluids

Pressure monitoring devices - Pressure transducer fluids

Dialysis machines[18]

Urine and/or fluids

Laboratory Studies

Culture of the organism from body fluids and proper identification from the microbiology laboratory confirms the presence of Stenotrophomonas maltophilia. Usually, the presence of S maltophilia represents colonization. A potential pathogenic role must be evaluated by an infectious disease specialist. The mere recovery of a potential pathogen from any body fluid does not indicate a pathogenic role for the organism.

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, DNase 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.[27]

Histologic Findings

The histology of S maltophilia in the rare situations when it causes infection is indistinguishable from the histology of infections caused by other aerobic gram-negative bacilli.

Approach Considerations

Antimicrobial Resistance

The overall CFDC-NS prevalence is low; however, it is significantly higher for specific carbapenem-resistant phenotypes in certain regions, underscoring the need for ongoing surveillance as cefiderocol is increasingly used in clinical practice.[28]

A systematic review found an overall low prevalence of CFDC-NS (EUCAST breakpoints) that varied by species: Stenotrophomonas maltophilia at 0.4%, Enterobacterales at 3.0%, P aeruginosa at 1.4%, and A baumannii at 8.8%. Higher rates were noted in carbapenem-resistant (CR) Enterobacterales (12.4%) and A baumannii (13.2%), whereas CR P aeruginosa was lower at 3.5%. Alarmingly high rates were found in New Delhi metallo-β-lactamase-producing Enterobacterales (38.8%) and A baumannii (44.7%).

 

Medical Care

Colonization of body fluids in hospitalized patients should be minimized if possible. Foley catheters should be used only as long as necessary and should be avoided if at all possible in immunocompromised hosts predisposed to urinary tract infections, eg, patients with diabetes, SLE, or multiple myeloma.

Colonization of respiratory secretions in intubated patients in ICUs is the rule and is difficult to prevent.

Patient-to-patient spread of organisms may be minimized or prevented by effective infection-control measures.

Consultations

Consultation with an infectious disease specialist is essential for differentiating colonization from infection in patients with S maltophilia isolated from various body fluids.

Prevention

Because S maltophilia is a common nosocomial colonizer in patients and medical fluids, the recovery of S maltophilia should be considered nonpathogenic unless proven otherwise.

If S maltophilia is recovered from several patients in the same area, sections of an ICU or ward can become the focus of further spread within the hospital setting.

Effective infection control measures can minimize or limit the spread of this and other organisms in the ICU.

Appropriate isolation procedures, rather than antimicrobial therapy, should be used to control the spread of S maltophilia.

Medical personnel, including medical students, housekeeping staff, attending physicians, nursing personnel, and respiratory therapists, are potential carriers of the organism from patient to patient.

 

Medication Summary

Because Stenotrophomonas maltophilia is predominantly a colonizer, antimicrobial treatment may be unnecessary and may be potentially harmful. Thus, determination of whether the organism is truly the cause of an infection is necessary to determine the need for antibiotic therapy.

As a general principle, colonization should not be treated with antimicrobial therapy.

S maltophilia is intrinsically resistant to aminoglycosides, antipseudomonal penicillins, cephalosporins and carbapenems. S maltophilia is consistently susceptible to trimethoprim-sulfamethoxazole (TMP-SMX) and is a drug of choice.[29, 30] If TMP-SMX cannot be used, the organism usually is sensitive to minocycline, levofloxacin, or cefiderocol.[31, 32, 45]  IDSA guidelines 2024 recommend use of combination of any two of the following agents: TMP/SMX, minocycline, levofloxacin and cefiderocol, OR a combination of  ceftazidime/avibactam with aztreonam for treatment of S maltophilia infections.[47]

A recent metaanalysis suggested resistant rate to ceftazidime was 50%, lowest resistance rates were reported for minocycline (3%) cefiderocol (4%), and TMP-SMX (14.7%).[45]  IDSA guidelines do not recommend use of ceftazidime for S maltophilia due to ineffectivity despite of being senisitive in vitro.[46]

Due to suboptimal results with monotherapy and resistance during treatment, IDSA panel has suggested levofloxacin in combination therapy with some other active agent.[47]  

Minocycline has been recommended to be used in high doses 200mg every 12hrly in combination therapy as per IDSA guidelines.[47]  In 2023, susceptibility breakpoints for minocycline has been reduced from < 4 ug/mL to < 1ug/mL in CLSI for S maltophilia which will result in more resistant strains.[49]

Tigecycline may potentially be helpful, but clinical investigation is needed, it can be used in situations where alternative therapy is not suitable.[29, 33, 34]  Polymyxin B/Colistin may be effective, at least in vitro, though not without frequent adverse effects. [35, 36]

Studies have demonstrated activity of eravacycline and omadacycline in vitro but further studies are required to ascertain the clinical efficacy and potential therapeutic option for multidrug-resistant S maltophilia infections.[37, 38, 39, 40, 41]  IDSA panel does not suggests use of eravacycline or omadacycline for S maltophilia.[47]

Cefiderocol demonstrated activity in vitro against S.maltophilia however it was found to be resistant in clinical isolates. Given the limited clinical experience, IDSA panel has suggested use of cefiderocol as a component of combination therapy until clinical improvement is seen.[47]

The combination of aztreonam with ceftazidime/avibactam has been successfully used for the treatment of a persistent S maltophilia bacteremia in a renal transplant patient.[42]  This synergistic combination suggests a potential therapeutic option for multidrug resistant S maltophilia infections and is now recommended by IDSA panel.[47]

 

 

Sulfamethoxazole/trimethoprim (Bactrim, Bactrim DS, Septra, Septra DS)

Clinical Context:  Inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid. Antibacterial activity includes common urinary tract pathogens, except P aeruginosa.

Cefepime (Maxipime)

Clinical Context:  Fourth-generation cephalosporin with good gram-negative coverage, similar to ceftazidime, but better gram-positive coverage.

Minocycline (Dynacin, Minocin)

Clinical Context:  Treats infections caused by susceptible gram-negative and gram-positive organisms, in addition to infections caused by susceptible Chlamydia, Rickettsia, and Mycoplasma.

Tigecycline (Tygacil)

Clinical Context:  A glycylcycline antibiotic that is structurally similar to tetracycline antibiotics. Inhibits bacterial protein translation by binding to 30S ribosomal subunit, and blocks entry of amino-acyl tRNA molecules in ribosome A site. Indicated for complicated skin and skin structure infections caused by E coli, E faecalis (vancomycin-susceptible isolates only), S aureus (methicillin-susceptible and -resistant isolates), S agalactiae, S anginosus group (includes S anginosus, S intermedius, and S constellatus), S pyogenes, and B fragilis.

Class Summary

Therapy should be selective to avoid covering multiple isolates from a body site in the context of the clinical setting.

What is Stenotrophomonas maltophilia?What is the pathophysiology of Stenotrophomonas maltophilia?What is the prevalence of Stenotrophomonas maltophilia in the US?What is the prevalence of Stenotrophomonas maltophilia in cystic fibrosis?What is the mortality and morbidity associated with Stenotrophomonas maltophilia?What is the prognosis of Stenotrophomonas maltophilia?Which clinical history findings are characteristic of Stenotrophomonas maltophilia infection?Which physical findings are characteristic of Stenotrophomonas maltophilia?What are the characteristics of Stenotrophomonas maltophilia?What are sources of Stenotrophomonas maltophilia colonization?When should Stenotrophomonas maltophilia infection be considered?What is the role of lab testing in the workup of Stenotrophomonas maltophilia infection?Which histologic findings are characteristic of Stenotrophomonas maltophilia?How are Stenotrophomonas maltophilia infections treated?Which specialist consultations are beneficial to patients with Stenotrophomonas maltophilia infections?How are Stenotrophomonas maltophilia infections prevented?What is the role of medications in the treatment of Stenotrophomonas maltophilia?Which medications in the drug class Antibiotics are used in the treatment of Stenotrophomonas Maltophilia?

Author

Sara Ahmed, MBBS, MRCP(UK), FCPS, Faculty, Infectious Diseases, Aga Khan University Hospital , Pakistan

Disclosure: Nothing to disclose.

Coauthor(s)

Syed Faisal Mahmood, MBBS, Associate Professor of Infectious Diseases, Program Director, Infectious Diseases Fellowship Program, Department of Medicine, Aga Khan University Hospital, Pakistan

Disclosure: Nothing to disclose.

Specialty Editors

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Michael Stuart Bronze, MD, David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America; Fellow of the Royal College of Physicians, London

Disclosure: Nothing to disclose.

Additional Contributors

Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital

Disclosure: Nothing to disclose.

Charles S Levy, MD, Associate Professor, Department of Medicine, Section of Infectious Disease, George Washington University School of Medicine

Disclosure: Nothing to disclose.

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Infection Predisposing Factor
Catheter-associated bacteriuriaIndwelling urinary catheters
Intravenous line infectionsCentral intravenous catheters
UrosepsisUrinary tract instrumentation
Primary bacteremiaArterial monitoring devices
PseudobacteremiaContamination of blood during collection/processing of blood cultures