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Stenotrophomonas maltophilia

Stenotrophomonas maltophilia clinical isolates on McConkey agar

Stenotrophomonas maltophilia
Scientific classification
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Genus:
Species:
S. maltophilia
Binomial name
Stenotrophomonas maltophilia
Palleroni & Bradbury 1993
Synonyms

Pseudomonas maltophilia (ex Hugh and Ryschenkow 1961) Hugh 1981
Xanthomonas maltophilia (Hugh 1981) Swings et al. 1983
Pseudomonas hibiscicola Moniz 1963
Pseudomonas beteli corrig. (Ragunathan 1928) Savulescu 1947

Stenotrophomonas maltophilia is an aerobic, nonfermentative, Gram-negative bacterium. It is an uncommon bacterium and human infection is difficult to treat.[1] Initially classified as Bacterium bookeri,[2] then renamed Pseudomonas maltophilia, S. maltophilia was also grouped in the genus Xanthomonas before eventually becoming the type species of the genus Stenotrophomonas in 1993.[3][4]

S. maltophilia is slightly smaller (0.7–1.8 × 0.4–0.7 μm) than other members of the genus. They are motile due to polar flagella, and grow well on MacConkey agar producing pigmented colonies. S. maltophilia is catalase-positive, oxidase-negative (which distinguishes it from most other members of the genus) and has a positive reaction for extracellular DNase.[citation needed]

S. maltophilia is ubiquitous in aqueous environments, soil, and plants; it has also been used in biotechnology applications.[5] In immunocompromised patients, S. maltophilia can lead to nosocomial infections.

Pathogenesis

S. maltophilia frequently colonizes humid surfaces such as the tubes used in mechanical ventilation and indwelling urinary 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 a central venous catheter or similar device). S. maltophilia adheres strongly and forms biofilm on plastic surfaces although these abilities may vary greatly between strains. Hydrophobicity was correlated to successful adhesion and biofilm formation on polystyrene surfaces.[6] S. maltophilia frequently co-occurs and forms multispecies biofilms with Pseudomonas aeruginosa. S. maltophilia substantially influences the architecture of P. aeruginosa structures, causing development of extended filaments. These changes arise due to diffusible signalling factor encoded by S. maltophilia.[7][8]

The growth of S. maltophilia in microbiological cultures of respiratory or urinary specimens is difficult to interpret due to its low pathogenicity and not a 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.

In immunocompetent individuals, S. maltophilia is a relatively unusual cause of pneumonia, urinary tract infection, or bloodstream infection; in immunocompromised patients, however, S. maltophilia is a growing source of latent pulmonary infections.[9] S. maltophilia colonization rates in individuals with cystic fibrosis have been increasing.[10]

Inflammatory responses against bacteria or bacterial products are the main pathogenic mechanisms of S. maltophilia infection. S. maltophilia secretes outer membrane vesicles (OMVs), that cause inflammatory response. OMVs from S. maltophilia ATCC 13637 were found to be cytotoxic to human lung epithelial cells. There OMVs stimulate the expression of proinflammatory cytokine and chemokine genes, including interleukin (IL)-1β, IL-6, IL-8, tumor necrosis factor-α and monocyte chemoattractant protein-1.[11]

Treatment

S. maltophilia is naturally resistant to many broad-spectrum antibiotics (including all carbapenems) due to the production of two inducible chromosomal metallo-β-lactamases (designated L1 and L2).[12] 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).[13][14] 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, and agar dilution should be used instead.[15][16]

S. 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 of S. maltophilia are sensitive to co-trimoxazole and ticarcillin, though resistance has been increasing.[17] It is usually susceptible to piperacillin, and ceftazidime.[18] Tigecycline is also an effective drug. Polymyxin B may be effective treatment, at least in vitro, though not without frequent adverse effects.

Epidemiology

Stenotrophomonas infections have been associated with high morbidity and mortality in severely immunocompromised and debilitated individuals. Risk factors associated with Stenotrophomonas infection include HIV infection, malignancy, cystic fibrosis, neutropenia, mechanical ventilation, central venous catheters, recent surgery, trauma, prolonged hospitalization, intensive care unit admission and broad-spectrum antibiotic use.[2][19][20][21]

History

Stenotrophomonas maltophilia has had multiple different names in the past. It was first found in a pleural effusion in 1943 and given the name Bacterium bookeri. It was then renamed to Pseudomonas maltophilia in 1961. It was moved to the genus Xanthomonas in 1983, and most recently to Stenotrophomonas in 1993.[2]

References

  1. ^ Gilligan PH, Lum G, VanDamme PAR, Whittier S (2003). Murray PR, Baron EJ, Jorgensen JH, et al. (eds.). Burkholderia, Stenotrophomonas, Ralstonia, Brevundimonas, Comamonas, Delftia, Pandoraea, and Acidivorax. In: Manual of Clinical Microbiology (8th ed.). ASM Press, Washington, DC. pp. 729–748. ISBN 978-1-55581-255-3.
  2. ^ a b c d e Chang, Ya Ting; Lin, Chun Yu; Chen, Yen Hsu; Hsueh, Po-Ren (2015-01-01). "Update on infections caused by Stenotrophomonas maltophilia with particular attention to resistance mechanisms and therapeutic options". Frontiers in Microbiology. 6: 893. doi:10.3389/fmicb.2015.00893. PMC 4557615. PMID 26388847.
  3. ^ Denton M, Kerr K (1 January 1998). "Microbiological and clinical aspects of infection associated with Stenotrophomonas maltophilia". Clin Microbiol Rev. 11 (1): 57–80. doi:10.1128/CMR.11.1.57. PMC 121376. PMID 9457429.
  4. ^ Palleroni N, Bradbury J (1993). "Stenotrophomonas, a new bacterial genus for Xanthomonas maltophilia (Hugh 1980) Swings et al. 1983". Int J Syst Bacteriol. 43 (3): 606–9. doi:10.1099/00207713-43-3-606. PMID 8347518.
  5. ^ Berg G, Roskot N, Smalla K (1999). "Genotypic and phenotypic relationships between clinical and environmental isolates of Stenotrophomonas maltophilia". J Clin Microbiol. 37 (11): 3594–600. PMC 85701. PMID 10523559.
  6. ^ Pompilio, Arianna; Piccolomini, Raffaele; Picciani, Carla; D'Antonio, Domenico; Savini, Vincenzo; Di Bonaventura, Giovanni (2008). "Factors associated with adherence to and biofilm formation on polystyrene by Stenotrophomonas maltophilia : the role of cell surface hydrophobicity and motility". FEMS Microbiology Letters. 287 (1): 41–47. doi:10.1111/j.1574-6968.2008.01292.x. PMID 18681866.
  7. ^ Ryan, Robert P.; Fouhy, Yvonne; Garcia, Belen Fernandez; Watt, Steven A.; Niehaus, Karsten; Yang, Liang; Tolker-Nielsen, Tim; Dow, J. Maxwell (2008). "Interspecies signalling via the Stenotrophomonas maltophilia diffusible signal factor influences biofilm formation and polymyxin tolerance in Pseudomonas aeruginosa". Molecular Microbiology. 68 (1): 75–86. doi:10.1111/j.1365-2958.2008.06132.x. ISSN 0950-382X. PMID 18312265.
  8. ^ Dufour, Nicholas; Rao, Reeta Prusty (2011). "Secondary metabolites and other small molecules as intercellular pathogenic signals: Small-molecule signaling". FEMS Microbiology Letters. 314 (1): 10–17. doi:10.1111/j.1574-6968.2010.02154.x. PMID 21114519.
  9. ^ McGowan J (2006). "Resistance in nonfermenting gram-negative bacteria: multidrug resistance to the maximum". Am J Med. 119 (6 Suppl 1): S29–36, discussion S62–70. doi:10.1016/j.amjmed.2006.03.014. PMID 16735148.
  10. ^ Waters V, Gómez M, Soong G, Amin S, Ernst R, Prince A (2007). "Immunostimulatory properties of the emerging pathogen Stenotrophomonas maltophilia". Infect Immun. 75 (4): 1698–703. doi:10.1128/IAI.01469-06. PMC 1865680. PMID 17220304.
  11. ^ Kim, Yoo Jeong; Jeon, Hyejin; Na, Seok Hyeon; Kwon, Hyo Il; Selasi, Gati Noble; Nicholas, Asiimwe; Park, Tae In; Lee, Sang Hwa; Lee, Je Chul (2016). Carbonetti, Nicholas (ed.). "Stenotrophomonas maltophilia outer membrane vesicles elicit a potent inflammatory response in vitro and in vivo". Pathogens and Disease. 74 (8): ftw104. doi:10.1093/femspd/ftw104. ISSN 2049-632X. PMID 27756813.
  12. ^ Denton, M; Kerr, KG (1998). "Microbiological and Clinical Aspects of Infection Associated with Stenotrophomonas maltophilia". Clinical Microbiology Reviews. 11 (1): 57–80. doi:10.1128/CMR.11.1.57. PMC 121376. PMID 9457429.
  13. ^ Wheat PF, Winstanley TG, Spencer RC (1985). "Effect of temperature of antimicrobial susceptibilities of Pseudomonas maltophilia". J Clin Pathol. 38 (9): 1055–8. doi:10.1136/jcp.38.9.1055. PMC 499358. PMID 4044874.
  14. ^ Wilcox MH, Winstanley TG, Spencer RC (1994). "Outer membrane protein profiles of Xanthomonas maltophilia isolates displaying temperature-dependant susceptibility to gentamicin". J Antimicrob Chemother. 33 (3): 633–666. doi:10.1093/jac/33.3.663. PMID 8040133.
  15. ^ Pankuch GA, Jacobs MR, Applebaum PC (1994). "Susceptibilities of 123 Xanthomonas maltophilia strains to clinafloxacin, PD131628, PD138312, PD140248, ciprofloxacin, and ofloxacin". Antimicrob Agents Chemother. 38 (2): 369–370. doi:10.1128/AAC.38.2.369. PMC 284459. PMID 8192468.
  16. ^ Pankuch GA, Jacobs MR, Rittenhouse SF, Appelbaum PC (1994). "Susceptibilities of 123 strains of Xanthomonas maltophilia to eight beta-lactams (including beta-lactam-beta-lactamase inhibitor combinations) and ciprofloxacin tested by five methods". Antimicrob Agents Chemother. 38 (10): 2317–22. doi:10.1128/AAC.38.10.2317. PMC 284737. PMID 7840563.
  17. ^ Al-Jasser A (2006). "Stenotrophomonas maltophilia resistant to trimethoprim-sulfamethoxazole: an increasing problem". Ann Clin Microbiol Antimicrob. 5: 23. doi:10.1186/1476-0711-5-23. PMC 1578578. PMID 16978420.
  18. ^ Bradley, John (2017). Nelson's Pediatric Antimicrobial Therapy, 23rd edition. AAP.
  19. ^ Kwa AL, Low JG, Lim TP, Leow PC, Kurup A, Tam VH (2008). "Independent predictors for mortality in patients with positive Stenotrophomonas maltophilia cultures". Ann Acad Med Singap. 37 (10): 826–30. PMID 19037515.
  20. ^ Falagas ME, Kastoris AC, Vouloumanou EK, Rafailidis PI, Kapaskelis AM, Dimopoulos G (2009). "Attributable mortality of Stenotrophomonas maltophilia infections: a systematic review of the literature". Future Microbiol. 4 (9): 1103–9. doi:10.2217/fmb.09.84. PMID 19895214.
  21. ^ Paez JI, Costa SF (2008). "Risk factors associated with mortality of infections caused by Stenotrophomonas maltophilia: a systematic review". J Hosp Infect. 70 (2): 101–8. doi:10.1016/j.jhin.2008.05.020. PMID 18621440.

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