Stenotrophomonas maltophilia
| Stenotrophomonas maltophilia | |
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S. maltophilia
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| Binomial name | |
| Stenotrophomonas maltophilia Palleroni & Bradbury 1993
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Pseudomonas maltophilia (ex Hugh and Ryschenkow 1961) Hugh 1981 |
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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 Pseudomonas maltophilia, S. maltophilia was also grouped in the genus Xanthomonas before eventually becoming the type species of the genus Stenotrophomonas in 1993.[2][3]
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.[4] In immunocompromised patients, S. maltophilia can lead to nosocomial infections.
Pathogenesis
S. maltophilia frequently colonizes breathing tubes such as endotracheal or tracheostomy tubes, the respiratory tract and indwelling urinary catheters. 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). The growth of S. maltophilia in microbiological cultures of respiratory or urinary specimens is, therefore, sometimes difficult to interpret and not a proof of infection. 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.[5] S. maltophilia colonization rates in individuals with cystic fibrosis have been increasing.[6]
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).[7] 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).[8][9] 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.[10][11]
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.[12] It is not usually susceptible to piperacillin, and susceptibility to ceftazidime is variable.[citation needed] 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, and broad-spectrum antibiotic use.[13][14][15]
References
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External links
- Stenotrophomonas maltophilia article at eMedicine.
- The genus Stenotrophomonas
- Stenotrophomonas Genome Projects from Genomes OnLine Database
- [1] Relevance to Cystic Fibrosis
- Effect of different antibiotics eg minocycline, Tigecycline; JAC 2002 correspondence
