“…Stenotrophomonas maltophilia is a Gram-negative bacillus and increasingly being recognized as an important nosocomial pathogen ( Looney et al, 2009 ; Brooke, 2012 ). It can cause serious infections such as bacteremia, pneumonia, endocarditis, meningitis, urinary tract infections, skin and soft tissue infections in immunocompromised patients ( Falagas et al, 2009 ; Sood et al, 2013 ; Hotta et al, 2014 ; Trignano et al, 2014 ; Guzoglu et al, 2015 ). The available therapeutic option for invasive S. maltophilia infection is limited, as this pathogen shows high levels of resistance to commonly used antibiotics ( Sánchez, 2015 ).…”
Maltocin P28 is a phage-tail like bacteriocin produced by Stenotrophomonas maltophilia P28. The ORF8 of maltocin P28 gene cluster is predicted to encode an endolysin and we name it endolysin P28. Sequence analysis revealed that it contains the lysozyme_like superfamily conserved domain. Endolysin P28 has the four consensus motifs as that of Escherichia coli phage lambda gpR. In this study, endolysin P28 was expressed in E. coli BL21 (DE3) and purified with a C-terminal oligo-histidine tag. The antibacterial activity of endolysin P28 increased as the temperature rose from 25 to 45°C. Thermostability assays showed that endolysin P28 was stable up to 50°C, while its residual activity was reduced by 55% after treatment at 70°C for 30 min. Acidity and high salinity could enhance its antibacterial activity. Endolysin P28 exhibited a broad antibacterial activity against 14 out of 16 tested Gram-positive and Gram-negative bacteria besides S. maltophilia. Moreover, it could effectively lyse intact Gram-negative bacteria in the absence of ethylenediaminetetraacetic acid as an outer membrane permeabilizer. Therefore, the characteristics of endolysin P28 make it a potential therapeutic agent against multi-drug-resistant pathogens.
“…Stenotrophomonas maltophilia is a Gram-negative bacillus and increasingly being recognized as an important nosocomial pathogen ( Looney et al, 2009 ; Brooke, 2012 ). It can cause serious infections such as bacteremia, pneumonia, endocarditis, meningitis, urinary tract infections, skin and soft tissue infections in immunocompromised patients ( Falagas et al, 2009 ; Sood et al, 2013 ; Hotta et al, 2014 ; Trignano et al, 2014 ; Guzoglu et al, 2015 ). The available therapeutic option for invasive S. maltophilia infection is limited, as this pathogen shows high levels of resistance to commonly used antibiotics ( Sánchez, 2015 ).…”
Maltocin P28 is a phage-tail like bacteriocin produced by Stenotrophomonas maltophilia P28. The ORF8 of maltocin P28 gene cluster is predicted to encode an endolysin and we name it endolysin P28. Sequence analysis revealed that it contains the lysozyme_like superfamily conserved domain. Endolysin P28 has the four consensus motifs as that of Escherichia coli phage lambda gpR. In this study, endolysin P28 was expressed in E. coli BL21 (DE3) and purified with a C-terminal oligo-histidine tag. The antibacterial activity of endolysin P28 increased as the temperature rose from 25 to 45°C. Thermostability assays showed that endolysin P28 was stable up to 50°C, while its residual activity was reduced by 55% after treatment at 70°C for 30 min. Acidity and high salinity could enhance its antibacterial activity. Endolysin P28 exhibited a broad antibacterial activity against 14 out of 16 tested Gram-positive and Gram-negative bacteria besides S. maltophilia. Moreover, it could effectively lyse intact Gram-negative bacteria in the absence of ethylenediaminetetraacetic acid as an outer membrane permeabilizer. Therefore, the characteristics of endolysin P28 make it a potential therapeutic agent against multi-drug-resistant pathogens.
“…Biliary tract infections caused by obstruction due to hepatobiliary neoplasms (Papadakis et al, 1995 ; Chang et al, 2014 ) or post-operative anastomotic strictures of the gastrointestinal tract (Perez et al, 2014 ) have been reported in patients with biliary S. maltophilia sepsis. Pleural infections caused by post-surgical/tube thoracostomy or fistula (broncho-/esophageal-/bilio-) (Lee et al, 2014 ), post-neurosurgical meningitis (Sood et al, 2013 ; Lai et al, 2014b ), complicated urinary tract infections (Vartivarian et al, 1996 ), and obstructive lung cancer (Fujita et al, 1996 ; Vartivarian et al, 2000 ) have all been reported to create a milieu for S. maltophilia infection. In addition, although commonly perceived as nosocomial pathogens, community-acquired infections appear to be on the rise (Falagas et al, 2009a ; Chang et al, 2014 ).…”
Stenotrophomonas maltophilia is a Gram-negative, biofilm-forming bacterium. Although generally regarded as an organism of low virulence, S. maltophilia is an emerging multi-drug resistant opportunistic pathogen in hospital and community settings, especially among immunocompromised hosts. Risk factors associated with S. maltophilia infection include underlying malignancy, cystic fibrosis, corticosteroid or immunosuppressant therapy, the presence of an indwelling central venous catheter and exposure to broad spectrum antibiotics. In this review, we provide a synthesis of information on current global trends in S. maltophilia pathogenicity as well as updated information on the molecular mechanisms contributing to its resistance to an array of antimicrobial agents. The prevalence of S. maltophilia infection in the general population increased from 0.8–1.4% during 1997–2003 to 1.3–1.68% during 2007–2012. The most important molecular mechanisms contributing to its resistance to antibiotics include β-lactamase production, the expression of Qnr genes, and the presence of class 1 integrons and efflux pumps. Trimethoprim/sulfamethoxazole (TMP/SMX) is the antimicrobial drug of choice. Although a few studies have reported increased resistance to TMP/SMX, the majority of studies worldwide show that S. maltophilia continues to be highly susceptible. Drugs with historically good susceptibility results include ceftazidime, ticarcillin-clavulanate, and fluoroquinolones; however, a number of studies show an alarming trend in resistance to those agents. Tetracyclines such as tigecycline, minocycline, and doxycycline are also effective agents and consistently display good activity against S. maltophilia in various geographic regions and across different time periods. Combination therapies, novel agents, and aerosolized forms of antimicrobial drugs are currently being tested for their ability to treat infections caused by this multi-drug resistant organism.
“…S. maltophilia is associated with various systemic infections including cystic fibrosis, bacteremia, endocarditis, meningitis, and respiratory/urinary tract and skin/soft tissue infections in immune-compromised individuals. [7][8][9][10] S. maltophilia infection has a high mortality rate, 11 probably due to its poor response to antibiotic therapy. Ocular infections caused by S. maltophilia have been reported, including conjunctivitis, 12 keratitis, [13][14][15][16][17] and endophthalmitis.…”
The Australian ocular isolates of S. maltophilia remain susceptible to trimethoprim-sulfamethozole, tigecycline, and most fluoroquinolones. However, the isolates showed resistance to certain multipurpose disinfecting solutions.
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