Stenotrophomonas maltophilia

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Stenotrophomonas maltophilia
DSC 0701 Steno.jpg
Stenotrophomonas maltophilia clinical isolates on MacConkey agar
Scientific classification
Domain:
Bacteria
Phylum:
Pseudomonadota
Class:
Gammaproteobacteria
Order:
Xanthomonadales
Family:
Xanthomonadaceae
Genus:
Stenotrophomonas
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 hibiscicolaMoniz 1963
Pseudomonas betelicorrig. (Ragunathan 1928) Savulescu 1947

Contents

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/AIDS. Adherence of this organism to abiotic surfaces such as medical implants and catheters represents a major risk for hospitalized patients. [6]

Pathogenesis

Gram-stained S. maltophilia Stenotrophomonas maltophilia.jpg
Gram-stained S. maltophilia

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 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]

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. [11] S. maltophilia colonization rates in individuals with cystic fibrosis have been increasing. [12]

Deliberate induction of inflammatory responses is the main pathogenic mechanism 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. These 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. [13]

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). [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, and agar dilution should be used instead. [17] [18]

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. [19] It is usually susceptible to piperacillin and ceftazidime. [20] 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, extracorporeal membrane oxygenation, central venous catheters, recent surgery, trauma, prolonged hospitalization, intensive care unit admission and broad-spectrum antibiotic use. [2] [21] [22] [23] [24]

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]

Related Research Articles

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A biofilm is an syntrophic community of microorganisms in which cells stick to each other and often also to a surface. These adherent cells become embedded within a slimy extracellular matrix that is composed of extracellular polymeric substances (EPSs). The cells within the biofilm produce the EPS components, which are typically a polymeric combination of extracellular polysaccharides, proteins, lipids and DNA. Because they have three-dimensional structure and represent a community lifestyle for microorganisms, they have been metaphorically described as "cities for microbes".

<i>Staphylococcus aureus</i> Species of Gram-positive bacterium

Staphylococcus aureus is a Gram-positive spherically shaped bacterium, a member of the Bacillota, and is a usual member of the microbiota of the body, frequently found in the upper respiratory tract and on the skin. It is often positive for catalase and nitrate reduction and is a facultative anaerobe that can grow without the need for oxygen. Although S. aureus usually acts as a commensal of the human microbiota, it can also become an opportunistic pathogen, being a common cause of skin infections including abscesses, respiratory infections such as sinusitis, and food poisoning. Pathogenic strains often promote infections by producing virulence factors such as potent protein toxins, and the expression of a cell-surface protein that binds and inactivates antibodies. S. aureus is one of the leading pathogens for deaths associated with antimicrobial resistance and the emergence of antibiotic-resistant strains, such as methicillin-resistant S. aureus (MRSA), is a worldwide problem in clinical medicine. Despite much research and development, no vaccine for S. aureus has been approved.

<span class="mw-page-title-main">Phage therapy</span> Therapeutic use of bacteriophages to treat bacterial infections

Phage therapy, viral phage therapy, or phagotherapy is the therapeutic use of bacteriophages for the treatment of pathogenic bacterial infections. This therapeutic approach emerged at the beginning of the 20th century but was progressively replaced by the use of antibiotics in most parts of the world after the Second World War. Bacteriophages, known as phages, are a form of virus that attach to bacterial cells and inject their genome into the cell. The bacteria's production of the viral genome interferes with its ability to function, halting the bacterial infection. The bacterial cell causing the infection is unable to reproduce and instead produces additional phages. Phages are very selective in the strains of bacteria they are effective against.

<span class="mw-page-title-main">Colistin</span> Antibiotic

Colistin, also known as polymyxin E, is an antibiotic medication used as a last-resort treatment for multidrug-resistant Gram-negative infections including pneumonia. These may involve bacteria such as Pseudomonas aeruginosa, Klebsiella pneumoniae, or Acinetobacter. It comes in two forms: colistimethate sodium can be injected into a vein, injected into a muscle, or inhaled, and colistin sulfate is mainly applied to the skin or taken by mouth. Colistimethate sodium is a prodrug; it is produced by the reaction of colistin with formaldehyde and sodium bisulfite, which leads to the addition of a sulfomethyl group to the primary amines of colistin. Colistimethate sodium is less toxic than colistin when administered parenterally. In aqueous solutions it undergoes hydrolysis to form a complex mixture of partially sulfomethylated derivatives, as well as colistin. Resistance to colistin began to appear as of 2015.

<i>Staphylococcus haemolyticus</i> Species of bacterium

Staphylococcus haemolyticus is a member of the coagulase-negative staphylococci (CoNS). It is part of the skin flora of humans, and its largest populations are usually found at the axillae, perineum, and inguinal areas. S. haemolyticus also colonizes primates and domestic animals. It is a well-known opportunistic pathogen, and is the second-most frequently isolated CoNS. Infections can be localized or systemic, and are often associated with the insertion of medical devices. The highly antibiotic-resistant phenotype and ability to form biofilms make S. haemolyticus a difficult pathogen to treat. Its most closely related species is Staphylococcus borealis.

<span class="mw-page-title-main">Tigecycline</span> Chemical compound

Tigecycline, sold under the brand name Tygacil, is a tetracycline antibiotic medication for a number of bacterial infections. It is a glycylcycline administered intravenously. It was developed in response to the growing rate of antibiotic resistant bacteria such as Staphylococcus aureus, Acinetobacter baumannii, and E. coli. As a tetracycline derivative antibiotic, its structural modifications has expanded its therapeutic activity to include Gram-positive and Gram-negative organisms, including those of multi-drug resistance.

<i>Pseudomonas aeruginosa</i> Species of bacterium

Pseudomonas aeruginosa is a common encapsulated, Gram-negative, aerobic–facultatively anaerobic, rod-shaped bacterium that can cause disease in plants and animals, including humans. A species of considerable medical importance, P. aeruginosa is a multidrug resistant pathogen recognized for its ubiquity, its intrinsically advanced antibiotic resistance mechanisms, and its association with serious illnesses – hospital-acquired infections such as ventilator-associated pneumonia and various sepsis syndromes. P. aeruginosa is able to selectively inhibit various antibiotics from penetrating its outer membrane - and has high resistance to several antibiotics, according to the World Health Organization P. aeruginosa poses one of the greatest threats to humans in terms of antibiotic resistance.

<i>Burkholderia cepacia</i> complex Species of bacterium

Burkholderia cepacia complex (BCC), or simply Burkholderia cepacia, is a group of catalase-producing, lactose-nonfermenting, Gram-negative bacteria composed of at least 20 different species, including B. cepacia, B. multivorans, B. cenocepacia, B. vietnamiensis, B. stabilis, B. ambifaria, B. dolosa, B. anthina, B. pyrrocinia and B. ubonensis. B. cepacia is an opportunistic human pathogen that most often causes pneumonia in immunocompromised individuals with underlying lung disease. Patients with sickle-cell haemoglobinopathies are also at risk. The species complex also attacks young onion and tobacco plants, and displays a remarkable ability to digest oil. Burkholderia cepacia is also found in marine environments and some strains of Burkholderia cepacia can tolerate high salinity. S.I. Paul et al. (2021) isolated and biochemically characterized salt tolerant strains of Burkholderia cepacia from marine sponges of Saint Martin's Island of the Bay of Bengal, Bangladesh.

<i>Alcaligenes</i> Genus of bacteria

Alcaligenes is a genus of Gram-negative, aerobic, rod-shaped bacteria in the order of Burkholderiales.

<i>Burkholderia cenocepacia</i> Species of bacterium

Burkholderia cenocepacia is a Gram-negative, rod-shaped bacterium that is commonly found in soil and water environments and may also be associated with plants and animals, particularly as a human pathogen. It is one of over 20 species in the Burkholderia cepacia complex (Bcc) and is notable due to its virulence factors and inherent antibiotic resistance that render it a prominent opportunistic pathogen responsible for life-threatening, nosocomial infections in immunocompromised patients, such as those with cystic fibrosis or chronic granulomatous disease. The quorum sensing systems CepIR and CciIR regulate the formation of biofilms and the expression of virulence factors such as siderophores and proteases. Burkholderia cenocepacia may also cause disease in plants, such as in onions and bananas. Additionally, some strains serve as plant growth-promoting rhizobacteria.

<i>Acinetobacter baumannii</i> Species of bacterium

Acinetobacter baumannii is a typically short, almost round, rod-shaped (coccobacillus) Gram-negative bacterium. It is named after the bacteriologist Paul Baumann. It can be an opportunistic pathogen in humans, affecting people with compromised immune systems, and is becoming increasingly important as a hospital-derived (nosocomial) infection. While other species of the genus Acinetobacter are often found in soil samples, it is almost exclusively isolated from hospital environments. Although occasionally it has been found in environmental soil and water samples, its natural habitat is still not known.

<i>Stenotrophomonas</i> Genus of bacteria

Stenotrophomonas is a genus of Gram-negative bacteria, comprising at least ten species. The main reservoirs of Stenotrophomonas are soil and plants. Stenotrophomonas species range from common soil organisms to opportunistic human pathogens ; the molecular taxonomy of the genus is still somewhat unclear.

Enterococcus faecium is a Gram-positive, gamma-hemolytic or non-hemolytic bacterium in the genus Enterococcus. It can be commensal in the gastrointestinal tract of humans and animals, but it may also be pathogenic, causing diseases such as neonatal meningitis or endocarditis.

<span class="mw-page-title-main">Etest</span>

Etest is a way of determining antimicrobial sensitivity by placing a strip impregnated with antimicrobials onto an agar plate. A strain of bacterium or fungus will not grow near a concentration of antibiotic or antifungal if it is sensitive. For some microbial and antimicrobial combinations, the results can be used to determine a minimum inhibitory concentration (MIC). Etest is a proprietary system manufactured by bioMérieux. It is a laboratory test used in healthcare settings to help guide physicians by indicating what concentration of antimicrobial could successfully be used to treat patients' infections.

SmeT is a transcriptional repressor protein of 24.6 kDa, found in the pathogenic bacteria Stenotrophomonas maltophilia. SmeT is responsible for the regulation of the Multidrug Resistance (MDR) efflux pump, SmeDEF, that gives the bacteria resistance to several antibiotics including macrolides, TMP/SMX, tetracycline, chloramphenicol, quinolones and erythromycin. SmeT is encoded 223 bp upstream of SmeDEF, with just 56 base pairs between their transcription start sites and an overlapping region between the promoters. The production of the SmeT protein downregulates its own transcription, along with that of the efflux pump by sterically hindering the binding of RNA Polymerase to the DNA. SmeDEF was the first MDR pump discovered in the S. maltophilia species. The pump is named by its different parts: SmeE, the transporter itself that spans the plasma membrane, SmeF, the protein on the outer portion of the membrane, and SmeD, a membrane fusion protein. On general purpose media and no selectors, the genes for MDR pumps are typically not expressed, and the repressor is found bound to the DNA. In fact, mutations in SmeT that lead to overexpression of SmeDEF can pose fitness challenges to the bacteria. However, this overexpression has been identified in the bacterium and may pose a threat to our health.

<i>Achromobacter xylosoxidans</i> Species of bacterium

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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. 1 2 3 4 5 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.
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  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. ↑ 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. ISSN   0378-1135. PMID   17276020.
  11. ↑ 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.
  12. ↑ 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.
  13. ↑ 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.
  14. ↑ Korotetskiy I, Jumagaziyeva A, Kerimzhanova B, Reva O, Kuznetsova T, Shilov S, Ivanova L, Zubenko N, Parenova R, Iskakbayeva Z, Baimakhanov B, Bekmuhamedova A (2022). "Whole genome sequence data of Stenotrophomonas maltophilia SCAID WND1-2022 (370)". Data in Brief. 45: 108694. doi:10.1016/j.dib.2022.108694. PMC   9679662 . PMID   36425995.
  15. ↑ 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.
  16. ↑ 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.
  17. ↑ 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.
  18. ↑ 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.
  19. ↑ 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.
  20. ↑ Bradley, John (2017). Nelson's Pediatric Antimicrobial Therapy, 23rd edition. AAP.
  21. ↑ 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.
  22. ↑ 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.
  23. ↑ 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.
  24. ↑ Mojica MF, Humphries R, Lipuma JJ, Mathers AJ, Rao GG, Shelburne SA, Fouts DE, Van Duin D, Bonomo RA (June 2022). "Clinical challenges treating Stenotrophomonas maltophilia infections: an update". JAC- Antimicrobial Resistance. 4 (3): dlac040. doi:10.1093/jacamr/dlac040. PMC   9071536 . PMID   35529051.
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