Stenotrophomonas maltophilia

Microbiology

• It is an aerobic, gram-negative bacillus. It is a non-lactose fermenter and is oxidase negative, which separates it from Pseudomonas aeruginosa. It has multitrichous flagella and needs methionine to grow.
• Colonies are pale yellow or lavender-green on blood agar, with a mild ammonia-like odor. (Goldman-Cecil Medicine, Ch. 283)
• It is the only potential human pathogen in a genus of soil and plant-rhizosphere organisms. (Harrison's 22e, Ch. 170)

Epidemiology and risk factors

• It is an opportunistic, mainly nosocomial pathogen. It forms biofilms on catheters, ventilator circuits, nebulizers, dialysis machines, and water and ice supplies. (Goldman-Cecil Medicine)
• Risk factors:
  • Prolonged ICU stay
  • Mechanical ventilation or tracheostomy
  • Intravascular catheters
  • Neutropenia or hematologic malignancy
  • Transplantation
  • Cystic fibrosis or COPD
  • Hemodialysis
• The strongest trigger is broad-spectrum antibiotic exposure, especially carbapenems and advanced cephalosporins. Immunocompromise alone is usually not enough. (Harrison's 22e)

Clinical syndromes

• Respiratory tract: this is the most common site of isolation, and it is often hard to tell colonization from infection. Pneumonia can be severe in ventilated and neutropenic patients.
• Bloodstream and central line infection: most often seen in cancer patients.
• Less common: endocarditis, meningitis, UTI, skin and soft tissue infection, and rarely ecthyma gangrenosum in neutropenic patients.
• Cystic fibrosis: found in about 5% of patients, but not considered a major pathogen there. (Harrison's 22e)

Resistance

• It is intrinsically resistant to carbapenems, aminoglycosides, and most β-lactams. The mechanisms are efflux pumps and two chromosomal β-lactamases: L1, a metallo-β-lactamase, and L2, a cephalosporinase.
• Carbapenems therefore select for it, as in the disseminated infection case in Medical Microbiology 9e (Ch. 27).
• Resistance often emerges during therapy, particularly in high-inoculum infections.
• In-vitro susceptibility testing can be unreliable. (Quick Compendium of Clinical Pathology)

Treatment

• First decide whether it is colonization or infection. Many clinicians do not treat a respiratory isolate in a non-neutropenic patient who has no clear infection.
• For true infection, give combination therapy pending susceptibilities: TMP-SMX plus either levofloxacin, high-dose minocycline, or ticarcillin-clavulanate.
• Remove infected catheters early.
• Ceftazidime is no longer recommended.
• Goldman-Cecil also lists TMP-SMX as the treatment of choice.

• The 2024 IDSA guidance favored combination therapy for moderate to severe disease. It suggested two of cefiderocol, minocycline, TMP-SMX, or levofloxacin, or ceftazidime-avibactam plus aztreonam. For mild disease it allowed monotherapy, with TMP-SMX or minocycline preferred. It advised against levofloxacin alone because resistance emerges. (IDSA 2024 PDF)
• A newer IDSA update appears to have changed this, based on the Guideline Central summary. It now names cefiderocol monotherapy as preferred for invasive infection. It lists aztreonam-avibactam, ideally with a second agent, as an alternative.
• The update says the cefiderocol preference rests largely on susceptibility data and neutropenic animal models, with very little clinical outcome data.
• I only saw a summary of this update, so check the full IDSA document before applying it. It also differs from the textbooks above.
• CLSI removed its ceftazidime breakpoints and added comments against TMP-SMX or levofloxacin monotherapy. (CLSI)

Recent evidence