Bacteria > Proteobacteria > Gammaproteobacteria > Xanthomonadales > Xanthomonadaceae > Stenotrophomonas > Stenotrophomonas maltophilia
Other Names (8): Pseudomonas maltophilia; Xanthomonas maltophilia; Stenotrophomonas africana
Description and significance
Stenotrophomonas maltophilia is an aerobic, non-fermentative, gram-negative bacillus possessing flagella in a multitrichous formation, and that naturally lives in the rhizosphere (1). However, it also the third most common nosocomial pathogen with multi-drug-resistance that targets immune-compromised patients in hospitals, making it important in medical bacteriology (5). Stenotrophomonas maltophilia has a number of effective MDR mechanisms against various antibiotics, as well as a number of resistance mechanisms to the following toxic metals: Cadmium (Cd), Lead (Pb), Cobalt (Co), Zinc (Zn), Mercury (Hg), and Silver (Ag) in their elemental forms (1). It tends to produce tiny colonies on many agars used for gram-negative bacteria after twenty-four hours of incubation with a positive ONPG reaction (2). While Stenotrophomonas maltophilia is referred to by many names (including those listed above) in the scientific community, the combination of its stable biochemical and morphological characteristics distinguish it from other members of its genus (2).
The genome of Stenotrophomonas maltophilia has been sequenced, and is fairly straightforward; it consists of one large, dsDNA circular chromosome containing approximately 4,851,126 base pairs. Additionally, its genome has a G+C content of 66.7%. (5). The MDR in Stenotrophomonas maltophilia is chromosomally-mediated, and derived from a three-part system: two RND (Resistance, Nodulation, cell Division) efflux pump systems that produce a series of inner-membrane bound proteins that are capable of removing many different types of substrates from the cytoplasm; followed by a tripartite efflux pump that spans the cell envelope, and finally a series of OMPs (outer membrane proteins). (5) All three systems tend to be encoded within the same operon. (5) However, the ability of Stenotrophomonas maltophilia to resists high concentrations of various toxic metals is thought to not to be due to the high concentration of MDR efflux pumps, but instead was found through chemical microanalysis to the reduction and accumulation of oxyanions to their elemental state, thus requiring a completely different set of genes to be active (1). Certain strains of Stenotrophomonas maltophilia are also granted the ability of self-defense from soil protozoa (i.e. Paramecium) through the toxic products of the rebA-C gene clusters. Furthermore, while no plasmids exist in the genome of Stenotrophomonas maltophilia, it is thought to have gained its multi-drug resistance through horizontal gene transfer from similar nosocomial pathogens, possibly in part due to homologous recombination (2).
Cell structure, metabolism & life cycle
Stenotrophomonas maltophilia is a gram-negative, motile, multitrichous flagellated bacillus that is aerobic and non-fermenting (1). While Stenotrophomonas maltophilia is an aerobe, it can still grow using nitrate as a terminal electron acceptor in the absence of oxygen (5). It tends to produce positive reactions for ONPG (o-nitrophenyl-B-D-galactosidease), lysine decarboxylase, DNAse, esculin hydrolyisis, and gelatinase when cultured on most blood agar media, and can be cultured (2). Within the presence of cadmium (Cd), it accumulates cysteine as a reducer in order to undergo chelation, and form CdS, or cadmium sulfide in order to avoid lethal toxicity (1, 7). While this reaction with cysteine exposes Stenotrophomonas maltophilia to oxidative stress, it is much less harmful than the free radicals produced when cadmium reacts with oxygen and nitrogen freely (1). Stenotrophomonas maltophilia is also found associated with plants. In the rhizoshere it accumulates trehalose as a compatible solute and possible carbon source. Trehalose can be produced here through the conversion of maltose through the trehalose synthase pathway, or glucose through the thehalose-6-phosphate phosphatase pathway (encoded by otsA and otsB) (7). However, while it is often isolated from the rhizosphere, they also can be isolated from the vascular tissues of the root and stem of the following plant species: Brassica naptus (oilseed rape), Triticum astivum (wheat), Cucumis sativus (cucumber), Zea mays (maize), Solanum tuberosum (potato) and Populus (poplar) (1,7). The secretion of extracellular enzymes and secondary metabolites important for plant colonization, as well as the production of pili for adhesion and biofilm formation enables Stenotrophomonas maltophilia to compete with other similar microorganisms, as well as intra-hospital transmission (7).
Ecology (including pathogenesis)
As previously stated, Stenotrophomonas maltophilia is an opportunistic nosocomial pathogen that infects in immune-compromised humans (2). However, while Stenotrophomonas maltophilia can form a malignant lesion at the site of infection, it is thought that it should not be specifically treated, except with broad-range antimicrobial therapy; this is primarily due to its extensive intrinsic MDR, though tetracycline and doxycycline are considered to be effective (2).Stenotrophomonas maltophilia infection is found to occur in hospital patients with the following diseases: cystic fibrosis (3,7) bacteremia, septicemia, endocarditis, pneumonia, cholangitis, conjunctivitis, mastoiditis, meningitis, wound infections, and/or urinary tact infections (2). Thus, while it can be isolated from the rhizosphere, Stenotrophomonas maltophilia can exist in nearly any liquid-filled cavity in the human body, including from the circulatory system (2). Surprisingly, while Stenotrophomonas maltophilia is pathogenic to humans, it promotes plant growth, and provides antagonistic properties against pathogens of the plants mentioned above (1).
Stenotrophomonas maltophilia is rather unique in the way that it has both an intrinsic set of multi-drug resistances, as well as a variety of intrinsic methods for handing the influx of metal ions. However, as previously stated, Stenotrophomonas maltophilia also grants certain plant species protection against various plant pathogens, and thus is also being studied for the use of bio-pesticides (1). Furthermore, Stenotrophomonas maltophilia is able to detoxify high molecular weight polycyclic aromatic hydrocarbons, which have been identified as both carcinogenic, and mutagenic (1). Coupled with the ability of Stenotrophomonas maltophilia to live in a variety of extreme environments, there is much potential for future studies on bioremediation, particularly in oil spills and similar crises.
1) Delphine et. Al. “Heavy metal tolerance in Stenotrophomonas maltophilia”. PLoS ONE 3(2): e1539. Doi:10.1371/journal.pone.001539. p. 1-6.
2) Schoch Paul E., Cunha Burke A., “Pseudomonas maltophilia”. Infection Control, 1987. Volume 8(4). p. 169—172.
3) Felegie Terrance P., et. Al. “Susceptibility of Pseudomonas maltophilia to antimicrobial agents, singly and in combination”. Antimicrobial Agents and Chemotherapy, 1979. Volume 16(6). p. 833—837.
4) Bollet Claude, et. Al. “A simple method for selective isolation of Stenotrophomonas maltophilia from environmental samples”. Applied and Environmental Microbiology, 1995. Volume 61(4). p. 1653—1654.
5) Crossman et. Al. “The complete genome, comparative and functional analysis of Stenotrophomonas maltophilia reveals an organism heavily shielded by drug resistance determinants”. Genome Biology, 2008. Volume 9(4). p. R74.1-12.
6) Denton et. Al. “Molecular epidemiology of Stenotrophomonas maltophilia isolated from clinical specimens from patient with cystic fibrosis and associated environmental sample”. Journal of Clinical Microbiology, 1998. Volume 36(7). p. 1953—1958.
7) Ryan, Robert P., et. Al. “The versatility and adaption of bacteria from the genus Stenotrophomonas”. Nature Reviews: Microbiology, 2009. Volume 7. p. 514—525.
8) http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&id=40324&lvl=3&lin=f&keep=1&srchmode=1&unlock Date Accessed: 10/15/2011.
9) Principles of Clinical Bacteriology. Editors: M. M Emmerson, Stephen H. Gillespie, P.M Hawkey. Published June 1997 by Wiley, John & Sons, Incorporated. p.237—239.