Stenotrophomonas maltophilia

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Stenotrophomonas maltophilia clinical isolates on MacConkey agar

Stenotrophomonas maltophilia
Scientific classification
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Class:
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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. It is also an emerging nosocomial pathogen associated with opportunistic infections in patients with cystic fibrosis, cancer, and HIV. Adherence of this organism to abiotic surfaces such as medical implants and catheters represents a major risk for hospitalized patients.[6]

Pathogenesis[edit]

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.[7] 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.[8][9]

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.[10] S. maltophilia colonization rates in individuals with cystic fibrosis have been increasing.[11]

Deliberate induction of inflammatory responses is the main pathogenic mechanisms of S. maltophilia infection. S. maltophilia secretes outer membrane vesicles (OMVs), that cause an 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.[12]

Treatment[edit]

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).[13] 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).[14][15] 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.[16][17]

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.[18] It is usually susceptible to piperacillin, and ceftazidime.[19] Tigecycline is also an effective drug. Polymyxin B may be effective treatment, at least in vitro, though not without frequent adverse effects.

Epidemiology[edit]

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][20][21][22]

History[edit]

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[edit]

  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 YT, Lin CY, Chen YH, Hsueh PR (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 KG (January 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.
  4. ^ Palleroni NJ, Bradbury JF (July 1993). "Stenotrophomonas, a new bacterial genus for Xanthomonas maltophilia (Hugh 1980) Swings et al. 1983". International Journal of Systematic Bacteriology. 43 (3): 606–9. doi:10.1099/00207713-43-3-606. PMID 8347518.
  5. ^ Berg G, Roskot N, Smalla K (November 1999). "Genotypic and phenotypic relationships between clinical and environmental isolates of Stenotrophomonas maltophilia". Journal of Clinical Microbiology. 37 (11): 3594–600. doi:10.1128/JCM.37.11.3594-3600.1999. PMC 85701. PMID 10523559.
  6. ^ de Oliveira-Garcia D, Dall'Agnol M, Rosales M, Azzuz AC, Martinez MB, Girón JA (September 2002). "Characterization of flagella produced by clinical strains of Stenotrophomonas maltophilia". Emerging Infectious Diseases. 8 (9): 918–23. doi:10.3201/eid0809.010535. PMC 2732543. PMID 12194767.
  7. ^ Pompilio A, Piccolomini R, Picciani C, D'Antonio D, Savini V, Di Bonaventura G (October 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): 41–7. doi:10.1111/j.1574-6968.2008.01292.x. PMID 18681866.
  8. ^ Ryan RP, Fouhy Y, Garcia BF, Watt SA, Niehaus K, Yang L, et al. (April 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. PMID 18312265.
  9. ^ Dufour N, Rao RP (January 2011). "Secondary metabolites and other small molecules as intercellular pathogenic signals". FEMS Microbiology Letters. 314 (1): 10–7. doi:10.1111/j.1574-6968.2010.02154.x. PMID 21114519.
  10. ^ 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. PMID 16735148.
  11. ^ Waters VJ, Gómez MI, Soong G, Amin S, Ernst RK, Prince A (April 2007). "Immunostimulatory properties of the emerging pathogen Stenotrophomonas maltophilia". Infection and Immunity. 75 (4): 1698–703. doi:10.1128/IAI.01469-06. PMC 1865680. PMID 17220304.
  12. ^ Kim YJ, Jeon H, Na SH, Kwon HI, Selasi GN, Nicholas A, et al. (November 2016). Carbonetti N (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. PMID 27756813.
  13. ^ Denton M, Kerr KG (January 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.
  14. ^ Wheat PF, Winstanley TG, Spencer RC (September 1985). "Effect of temperature on antimicrobial susceptibilities of Pseudomonas maltophilia". Journal of Clinical Pathology. 38 (9): 1055–8. doi:10.1136/jcp.38.9.1055. PMC 499358. PMID 4044874.
  15. ^ Wilcox MH, Winstanley TG, Spencer RC (March 1994). "Outer membrane protein profiles of Xanthomonas maltophilia isolates displaying temperature-dependent susceptibility to gentamicin". The Journal of Antimicrobial Chemotherapy. 33 (3): 663–6. doi:10.1093/jac/33.3.663. PMID 8040133.
  16. ^ Pankuch GA, Jacobs MR, Appelbaum PC (February 1994). "Susceptibilities of 123 Xanthomonas maltophilia strains to clinafloxacin, PD 131628, PD 138312, PD 140248, ciprofloxacin, and ofloxacin". Antimicrobial Agents and Chemotherapy. 38 (2): 369–70. doi:10.1128/AAC.38.2.369. PMC 284459. PMID 8192468.
  17. ^ Pankuch GA, Jacobs MR, Rittenhouse SF, Appelbaum PC (October 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". Antimicrobial Agents and Chemotherapy. 38 (10): 2317–22. doi:10.1128/AAC.38.10.2317. PMC 284737. PMID 7840563.
  18. ^ Al-Jasser AM (September 2006). "Stenotrophomonas maltophilia resistant to trimethoprim-sulfamethoxazole: an increasing problem". Annals of Clinical Microbiology and Antimicrobials. 5: 23. doi:10.1186/1476-0711-5-23. PMC 1578578. PMID 16978420.
  19. ^ Bradley, John (2017). Nelson's Pediatric Antimicrobial Therapy, 23rd edition. AAP.
  20. ^ 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. PMID 19037515.
  21. ^ 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. PMID 19895214.
  22. ^ 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. PMID 18621440.

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