Stenotrophomonas maltophilia is slightly smaller (0.7–1.8 × 0.4–0.7 μm) than other members of the genus. They are motile due topolarflagella, and grow well onMacConkey agar producing pigmented colonies.S. maltophilia iscatalase-positive,oxidase-negative (which distinguishes it from most other members of the genus) and has a positive reaction for extracellularDNase.[citation needed]
Stenotrophomonas maltophilia is ubiquitous in aqueous environments, soil, and plants; it has also been used inbiotechnology applications.[5] Inimmunocompromised patients,S. maltophilia can lead tonosocomial infections. It is also an emergingnosocomial pathogen associated with opportunistic infections in patients withcystic fibrosis,cancer, andHIV/AIDS. Adherence of this organism to abiotic surfaces such as medical implants andcatheters represents a major risk for hospitalized patients.[6]
Stenotrophomonas maltophilia frequently colonizes humid surfaces such as the tubes used inmechanical ventilation and indwellingurinary catheters, as well as medical devices such as suction catheters and endoscopes.[2] Infection is usually facilitated by the presence of prosthetic material (plastic or metal), and the most effective treatment is removal of the prosthetic material (usually acentral venous catheter or similar device).S. maltophilia adheres strongly and formsbiofilm on plastic surfaces although these abilities may vary greatly between strains. Hydrophobicity was correlated to successful adhesion and biofilm formation on polystyrene surfaces.[7]S. maltophilia frequently co-occurs and forms multispecies biofilms withPseudomonas aeruginosa.S. maltophilia substantially influences the architecture ofP. aeruginosa structures, causing development of extended filaments. These changes arise due to diffusiblesignalling factor encoded byS. maltophilia.[8][9]
The growth ofS. maltophilia inmicrobiological cultures of respiratory or urinary specimens is difficult to interpret due to its low pathogenicity, and is not proof of infection.[2] If, however, it is grown from sites which would be normally sterile (e.g., blood), then it usually represents true infection.S. maltophilia can be found in the flora of captive snakes.[10]
Deliberate induction of inflammatory responses is the main pathogenic mechanism ofS. maltophilia infection.S. maltophilia secretesouter membrane vesicles (OMVs), that cause an inflammatory response. OMVs fromS. maltophilia ATCC 13637 were found to be cytotoxic to human lung epithelial cells. These OMVs stimulate the expression of proinflammatorycytokine and chemokine genes, including interleukin(IL)-1β,IL-6,IL-8,tumor necrosis factor-α andmonocyte chemoattractant protein-1.[13]
Stenotrophomonas maltophilia is naturally resistant to many broad-spectrumantibiotics (including allcarbapenems) due to the production of two inducible chromosomal metallo-β-lactamases (designated L1 and L2).[3][14] This makes treatment of infected patients very difficult.S. maltophilia is ubiquitously present in the environment and impossible to eradicate, which makes prevention also extremely difficult.
Sensitivity testing requires nonstandard culture techniques (incubation at 30 °C).[15][16] Testing at the wrong temperature results in isolates being incorrectly reported as being susceptible when they are, in fact, resistant. Disc diffusion methods should not be used, as they are unreliable, andagar dilution should be used instead.[17][18]
Stenotrophomonas maltophilia is not a virulent organism and removal of the infected prosthesis is frequently sufficient to cure the infection; antibiotics are only required if the prosthesis cannot be removed. Many strains ofS. maltophilia aresensitive toco-trimoxazole andticarcillin, though resistance has been increasing.[19] It is usually susceptible topiperacillin andceftazidime.[20]Tigecycline is also an effective drug.Polymyxin B may be effective treatment, at leastin vitro, though not without frequent adverse effects.
Stenotrophomonas maltophilia has had multiple different names in the past. It was first found in apleural effusion in 1943 and given the nameBacterium bookeri. It was then renamed toPseudomonas maltophilia in 1961. It was moved to the genusXanthomonas in 1983, and most recently toStenotrophomonas in 1993.[2]
^Hejnar, Petr; Bardoň, Jan; Sauer, Pavel; Kolář, Milan (April 2007). "Stenotrophomonas maltophilia as a part of normal oral bacterial flora in captive snakes and its susceptibility to antibiotics".Veterinary Microbiology.121 (3–4):357–362.doi:10.1016/j.vetmic.2006.12.026.ISSN0378-1135.PMID17276020.
^McGowan JE (June 2006). "Resistance in nonfermenting gram-negative bacteria: multidrug resistance to the maximum".The American Journal of Medicine.119 (6 Suppl 1): S29-36, discussion S62-70.doi:10.1016/j.amjmed.2006.03.014.PMID16735148.
^Bradley, John (2017).Nelson's Pediatric Antimicrobial Therapy, 23rd edition. AAP.
^Kwa AL, Low JG, Lim TP, Leow PC, Kurup A, Tam VH (October 2008). "Independent predictors for mortality in patients with positive Stenotrophomonas maltophilia cultures".Annals of the Academy of Medicine, Singapore.37 (10):826–30.PMID19037515.
^Falagas ME, Kastoris AC, Vouloumanou EK, Rafailidis PI, Kapaskelis AM, Dimopoulos G (November 2009). "Attributable mortality of Stenotrophomonas maltophilia infections: a systematic review of the literature".Future Microbiology.4 (9):1103–9.doi:10.2217/fmb.09.84.PMID19895214.
^Paez JI, Costa SF (October 2008). "Risk factors associated with mortality of infections caused by Stenotrophomonas maltophilia: a systematic review".The Journal of Hospital Infection.70 (2):101–8.doi:10.1016/j.jhin.2008.05.020.PMID18621440.
Betriu, C.; et al. (2002). "Correspondence: Comparativein vitro activities of tigecycline (GAR-936) and other antimicrobial agents againstStenotrophomonas maltophilia".Journal of Antimicrobial Chemotherapy.50 (5):758–759.doi:10.1093/jac/dkf196.
