scholarly journals Complex Phenotypic and Genotypic Responses of Listeria monocytogenes Strains Exposed to the Class IIa Bacteriocin Sakacin P

2009 ◽  
Vol 75 (22) ◽  
pp. 6973-6980 ◽  
Author(s):  
Girum Tadesse Tessema ◽  
Trond M�retr� ◽  
Achim Kohler ◽  
Lars Axelsson ◽  
Kristine Naterstad
Keyword(s):  
Listeria Monocytogenes ◽  
Acquired Resistance ◽  
Resistance Mechanisms ◽  
Gene Encoding ◽  
Genetic Characteristics ◽  
Food Borne ◽  
Resistant Strains ◽  
Resistant Mutants ◽  
Related Stress ◽  
The Stability

ABSTRACT Sakacin P is a class IIa bacteriocin that is active against the food-borne pathogen Listeria monocytogenes, and use of this compound as a biopreservative in foods has been suggested. In the present study, we characterized 30 spontaneous sakacin P-resistant mutants of L. monocytogenes obtained after single exposure to sakacin P. The frequency of development of sakacin P resistance for all strains was in the range from 10−8 to 10−9. Using the 50% inhibitory concentration (IC50) of sakacin P, the strains could be grouped into strains with high levels of resistance (IC50, ≥104 ng ml−1) and strains with low levels of resistance (IC50, <104 ng ml−1). Resistant strains belonging to the same IC50 group also had similar physiological and genetic characteristics. Generally, the resistant strains showed substantial variations in many parameters, such as differences in the stability of the acquired resistance to sakacin P, growth fitness, food-related stress tolerance, and biofilm-forming ability. Fourier transform infrared spectroscopy revealed differences between wild-type and resistant strains in polysaccharide, fatty acid, and, protein regions. A mannose-specific phosphotransferase (PTS) operon has been described for class IIa bacteriocin resistance, and the sakacin P-resistant strains displayed both up- and downregulation of the expression of the mptA gene encoding the PTS system. This is the first comprehensive study of the diversity of a large number of spontaneous resistant mutants obtained after one exposure to a class IIa bacteriocin, particularly to sakacin P. The great diversity among the resistant strains exposed to the same stress conditions suggests that there are different resistance mechanisms.

scholarly journals Two perspectives of Listeria monocytogenes hazards in dairy products: the prevalence and the antibiotic resistance

2019 ◽  
Author(s):  
Beyza H Ulusoy ◽  
Kefyalew Chirkena
Keyword(s):  
Antibiotic Resistance ◽  
Listeria Monocytogenes ◽  
Dairy Products ◽  
Acquired Resistance ◽  
Raw Milk ◽  
Resistance Mechanisms ◽  
Penicillin G ◽  
Conjugative Transposons ◽  
Food Borne ◽  
Veterinary Importance

Abstract Listeria monocytogenes is among the most food-borne pathogens. It has the ability to grow over a range of temperature, including refrigeration temperature. Foods kept in refrigerator more than the prescribed period of time create an opportunity for the occurrence of Listeria monocytogenes. As this review shows, the prevalence of L. monocytogenes has more likely evident in pasteurized milk than other dairy products, such as raw milk. Inadequate temperature and faults in technology during pasteurization can be the disposing factors for the presence of the organism in dairy products. The organism, on the other hand, has been found to be resistant to those commonly known antibiotics that have human and veterinary importance, namely, ampicillin, Tetracycline, and chloramphenicol, streptomycin, erytromycin, penicillin G., and others. Resistance ability of the organism can be mediated by different natural and acquired resistance mechanisms, such as self-transferrable plasmids, mobilizable plasmids, and conjugative transposons. The emergence and spread of antibiotic resistance of L. monocytogenes has serious public health and economic impacts at large. This paper has reviewed the prevalence and the antibiotic resistance of L. monocytogenes isolates of dairy products and the strategic mechanisms of the organism develop resistance against the antibiotics.

scholarly journals Conservation of Genomic Localization and Sequence Content of Sau3AI-Like Restriction-Modification Gene Cassettes among Listeria monocytogenes Epidemic Clone I and Selected Strains of Serotype 1/2a

2010 ◽  
Vol 76 (16) ◽  
pp. 5577-5584 ◽  
Author(s):  
Suleyman Yildirim ◽  
Driss Elhanafi ◽  
Wen Lin ◽  
Anthony D. Hitchins ◽  
Robin M. Siletzky ◽  
...  
Keyword(s):  
Listeria Monocytogenes ◽  
Gene Cassette ◽  
Conclusive Evidence ◽  
Gene Encoding ◽  
Epidemic Clone ◽  
Food Borne ◽  
Serotype 1 ◽  
Serotype 4B ◽  
Clonal Population Structure ◽  
Restriction Modification

ABSTRACTListeria monocytogenesis a food-borne pathogen with a clonal population structure and apparently limited gene flow between strains of different lineages. Strains of epidemic clone I (ECI) have been responsible for numerous outbreaks and invariably have DNA that is resistant to digestion by Sau3AI, suggesting methylation of cytosine at GATC sites. A putative restriction-modification (RM) gene cassette has been identified in the genome of the ECI strain F2365 and all other tested ECI strains but is absent from other strains of the same serotype (4b). Homologous RM cassettes have not been reported amongL. monocytogenesisolates of other serotypes. Furthermore, conclusive evidence for the involvement of this RM cassette in the Sau3AI resistance phenotype of ECI strains has been lacking. In this study, we describe a highly conserved RM cassette in certain strains of serotypes 1/2a and 4a that have Sau3AI-resistant DNA. In these strains the RM cassette was in the same genomic location as in the ECI reference strain F2365. The cassette included a gene encoding a putative recombinase, suggesting insertion via site-specific recombination. Deletion of the RM cassette in the ECI strain F2365 and the serotype 1/2a strain A7 rendered the DNA of both strains susceptible to Sau3AI digestion, providing conclusive evidence that the cassette includes a gene required for methylation of cytosine at GATC sites in both strains. The findings suggest that, in addition to its presence in ECI strains, this RM cassette and the accompanying genomic DNA methylation is also encountered among selected strains of other lineages.

scholarly journals Antimicrobial Resistance of Listeria monocytogenes Strains Isolated from Humans in France

2010 ◽  
Vol 54 (6) ◽  
pp. 2728-2731 ◽  
Author(s):  
A. Morvan ◽  
C. Moubareck ◽  
A. Leclercq ◽  
M. Hervé-Bazin ◽  
S. Bremont ◽  
...  
Keyword(s):  
Listeria Monocytogenes ◽  
Antimicrobial Resistance ◽  
Resistant Strain ◽  
Temporal Evolution ◽  
Acquired Resistance ◽  
Mechanisms Of Resistance ◽  
Resistant Strains ◽  
High Level ◽  
Level Resistance ◽  
Microbiological Surveillance

ABSTRACT Susceptibility to antibiotics of 4,816 clinical L. monocytogenes strains isolated since 1926 was studied, and the temporal evolution of susceptibility to antibiotics was analyzed through several decades. The mechanisms of resistance in each resistant strain were studied. The prevalence of resistant strains was estimated at 1.27% among isolates from humans. Resistance to tetracyclines+ and fluoroquinolones was more common and has recently emerged. Although acquired resistance in clinical L. monocytogenes did not implicate clinically relevant antibiotics, the possibility of resistance gene transfers, the description of the first clinical isolate with high-level resistance to trimethoprim, and the recent increase in penicillin MICs up to 2 μg/ml reinforce the need for microbiological surveillance.

scholarly journals In Vitro Activity of CEM-101 against Streptococcus pneumoniae and Streptococcus pyogenes with Defined Macrolide Resistance Mechanisms

2009 ◽  
Vol 54 (1) ◽  
pp. 230-238 ◽  
Author(s):  
Pamela McGhee ◽  
Catherine Clark ◽  
Klaudia M. Kosowska-Shick ◽  
Kensuke Nagai ◽  
Bonifacio Dewasse ◽  
...  
Keyword(s):  
Streptococcus Pyogenes ◽  
Bacterial Species ◽  
Resistance Mechanisms ◽  
Macrolide Resistance ◽  
23S Rrna ◽  
Resistant Strains ◽  
Resistant Mutants ◽  
The One ◽  
Selection Of

ABSTRACT CEM-101 had MIC ranges of 0.002 to 0.016 μg/ml against macrolide-susceptible pneumococci and 0.004 to 1 μg/ml against macrolide-resistant phenotypes. Only 3 strains with erm(B), with or without mef(A), had CEM-101 MICs of 1 μg/ml, and 218/221 strains had CEM-101 MICs of ≤0.5 μg/ml. CEM-101 MICs were as much as 4-fold lower than telithromycin MICs against all strains. For Streptococcus pyogenes, CEM-101 MICs ranged from 0.008 to 0.03 μg/ml against macrolide-susceptible strains and from 0.015 to 1 μg/ml against macrolide-resistant strains. Against erm(B) strains, erythromycin, azithromycin, and clarithromycin MICs were 32 to >64 μg/ml, while 17/19 strains had telithromycin MICs of 4 to 16 μg/ml; CEM-101 MICs were 0.015 to 1 μg/ml. By comparison, erm(A) and mef(A) strains had CEM-101 MICs of 0.015 to 0.5 μg/ml, clindamycin and telithromycin MICs of ≤1 μg/ml, and erythromycin, azithromycin, and clarithromycin MICs of 0.5 to >64 μg/ml. Pneumococcal multistep resistance studies showed that although CEM-101 yielded clones with higher MICs for all eight strains tested, seven of eight strains had clones with CEM-101 MICs that rose from 0.004 to 0.03 μg/ml (parental strains) to 0.06 to 0.5 μg/ml (resistant clones); for only one erm(B) mef(A) strain with a parental MIC of 1 μg/ml was there a resistant clone with a MIC of 32 μg/ml, with no detectable mutations in the L4, L22, or 23S rRNA sequence. Among two of five S. pyogenes strains tested, CEM-101 MICs rose from 0.03 to 0.25 μg/ml, and only for the one strain with erm(B) did CEM-101 MICs rise from 1 to 8 μg/ml, with no changes occurring in any macrolide resistance determinant. CEM-101 had low MICs as well as low potential for the selection of resistant mutants, independent of bacterial species or resistance phenotypes in pneumococci and S. pyogenes.

scholarly journals Antipneumococcal Activity of DK-507k, a New Quinolone, Compared with the Activities of 10 Other Agents

2003 ◽  
Vol 47 (12) ◽  
pp. 3815-3824 ◽  
Author(s):  
Frederick A. Browne ◽  
Bülent Bozdogan ◽  
Catherine Clark ◽  
Linda M. Kelly ◽  
Lois Ednie ◽  
...  
Keyword(s):  
Resistance Mechanisms ◽  
Quinolone Resistance ◽  
Penicillin G ◽  
Agar Dilution ◽  
Resistant Strains ◽  
Resistant Mutants ◽  
Subinhibitory Concentrations ◽  
Time Kill

ABSTRACT Agar dilution MIC determination was used to compare the activity of DK-507k with those of ciprofloxacin, levofloxacin, gatifloxacin, moxifloxacin, sitafloxacin, amoxicillin, cefuroxime, erythromycin, azithromycin, and clarithromycin against 113 penicillin-susceptible, 81 penicillin-intermediate, and 67 penicillin-resistant pneumococci (all quinolone susceptible). DK-507k and sitafloxacin had the lowest MICs of all quinolones against quinolone-susceptible strains (MIC at which 50% of isolates were inhibited [MIC50] and MIC90 of both, 0.06 and 0.125 μg/ml, respectively), followed by moxifloxacin, gatifloxacin, levofloxacin, and ciprofloxacin. MICs of β-lactams and macrolides rose with those of penicillin G. Against 26 quinolone-resistant pneumococci with known resistance mechanisms, DK-507k and sitafloxacin were also the most active quinolones (MICs, 0.125 to 1.0 μg/ml), followed by moxifloxacin, gatifloxacin, levofloxacin, and ciprofloxacin. Mutations in quinolone resistance-determining regions of quinolone-resistant strains were in the usual regions of the parC and gyrA genes. Time-kill testing showed that both DK-507k and sitafloxacin were bactericidal against all 12 quinolone-susceptible and -resistant strains tested at twice the MIC at 24 h. Serial broth passages in subinhibitory concentrations of 10 strains for a minimum of 14 days showed that development of resistant mutants (fourfold or greater increase in the original MIC) occurred most rapidly for ciprofloxacin, followed by moxifloxacin, DK-507k, gatifloxacin, sitafloxacin, and levofloxacin. All parent strains demonstrated a fourfold or greater increase in initial MIC in<50 days. MICs of DK-507k against resistant mutants were lowest, followed by those of sitafloxacin, moxifloxacin, gatifloxacin, ciprofloxacin, and levofloxacin. Four strains were subcultured in subinhibitory concentrations of each drug for 50 days: MICs of DK-507k against resistant mutants were lowest, followed by those of sitafloxacin, moxifloxacin, gatifloxacin, levofloxacin, and ciprofloxacin. Exposure to DK-507k and sitafloxacin resulted in mutations, mostly in gyrA.

scholarly journals Genetic Characteristics and Clonal Dissemination of β-Lactamase-Negative Ampicillin-Resistant Haemophilus influenzae Strains Isolated from the Upper Respiratory Tract of Patients in Japan

2007 ◽  
Vol 51 (11) ◽  
pp. 3969-3976 ◽  
Author(s):  
Muneki Hotomi ◽  
Keiji Fujihara ◽  
Dewan S. Billal ◽  
Kenji Suzuki ◽  
Tadao Nishimura ◽  
...  
Keyword(s):  
Haemophilus Influenzae ◽  
Upper Respiratory Tract ◽  
Gene Encoding ◽  
Genetic Characteristics ◽  
Group Iii ◽  
Medical Centers ◽  
Group I ◽  
Dna Restriction ◽  
Resistant Strains ◽  
Upper Respiratory

ABSTRACT We evaluated the recent prevalence of antimicrobial-resistant Haemophilus influenzae isolated from the upper respiratory tracts (URT) of patients in Japan. Mutations in the ftsI gene, which encodes penicillin binding protein 3 (PBP3), and the clonal dissemination of the resistant strains were also investigated. A total of 264 H. influenzae isolates were collected from patients with URT infections. According to the criteria of the Clinical and Laboratory Standards Institute for the susceptibility of H. influenzae to ampicillin (AMP), the isolates were distributed as follows: 161 (61.0%) susceptible strains (MIC ≤ 1 μg/ml), 37 (14.0%) intermediately resistant strains (MIC = 2 μg/ml), and 66 (25.0%) resistant strains (MIC ≥ 4 μg/ml). According to PCR-based genotyping, 172 (65.1%) of the isolates had mutations in the ftsI gene and were negative for the β-lactamase (bla) gene. These 172 isolates were thus defined as genetically β-lactamase-negative ampicillin-resistant (gBLNAR) strains. The ftsI mutant group included 98 (37.1%) strains with group I/II mutations in the variable mutated region (group I/II gBLNAR) and 74 (28.0%) strains with group III mutations in the highly mutated region (group III gBLNAR). Eighty-seven (33.0%) of the isolates were genetically β-lactamase-negative ampicillin-susceptible (gBLNAS) strains. The group III gBLNAR strains showed resistance to β-lactams. Only five strains (1.9%) were positive for a bla gene encoding TEM-type β-lactamase. The three clusters consisting of 16 strains found among the 61 BLNAR strains (MIC ≥ 4 μg/ml and without the bla gene) showed identical or closely related DNA restriction fragment patterns. Those isolates were frequently identified among strains with a MIC to AMP of 16 μg/ml. The current study demonstrates the apparent dissemination and spread of a resistant clone of H. influenzae among medical centers in Japan. The gBLNAR strains show a remarkable prevalence among H. influenzae isolates, with the prevalence increasing with time. This fact should be taken into account when treating URT infections.

scholarly journals The Listeria monocytogenes Virulence Factor InlJ Is Specifically Expressed In Vivo and Behaves as an Adhesin

2008 ◽  
Vol 76 (4) ◽  
pp. 1368-1378 ◽  
Author(s):  
Christophe Sabet ◽  
Alejandro Toledo-Arana ◽  
Nicolas Personnic ◽  
Marc Lecuit ◽  
Sarah Dubrac ◽  
...  
Keyword(s):  
Listeria Monocytogenes ◽  
Cultured Cells ◽  
Brain Heart Infusion ◽  
Gene Encoding ◽  
Regulatory Pathways ◽  
Food Borne ◽  
Food Body ◽  
Brain Heart Infusion Medium

ABSTRACT The food-borne pathogen Listeria monocytogenes is adapted to a diversity of environments, such as soil, food, body fluids, and the cytosol of eukaryotic cells. The transition between saprophytic and pathogenic life is mediated through complex regulatory pathways that modulate the expression of virulence factors. Here we examined the expression of inlJ, a recently identified gene encoding a protein of the LPXTG-internalin family and involved in pathogenesis. We show that inlJ expression is controlled neither by the major listerial regulator of virulence genes, PrfA, nor by AxyR, a putative AraC regulator encoded by a gene adjacent to inlJ and divergently transcribed. The InlJ protein is not produced by bacteria grown in vitro in brain heart infusion medium or replicating in the cytosol of tissue-cultured cells. In contrast, it is efficiently produced and localized at the surface of bacteria present in the liver and blood of infected animals. Strikingly, the expression of inlJ by a heterologous promoter in L. monocytogenes or L. innocua promotes bacterial adherence to human cells in vitro. Taken together, these results strongly suggest that InlJ acts as a novel L. monocytogenes sortase-anchored adhesin specifically expressed during infection in vivo.

Overexpression of SmeGH contributes to the acquired MDR of Stenotrophomonas maltophilia

2019 ◽  
Vol 74 (8) ◽  
pp. 2225-2229 ◽  
Author(s):  
Li-Hua Li ◽  
Man-San Zhang ◽  
Chao-Jung Wu ◽  
Yi-Tsung Lin ◽  
Tsuey-Ching Yang
Keyword(s):  
Stenotrophomonas Maltophilia ◽  
Treatment Options ◽  
Acquired Resistance ◽  
Resistance Mechanisms ◽  
Fluoroquinolone Resistance ◽  
Dilution Method ◽  
Agar Dilution Method ◽  
Real Time Quantitative Pcr ◽  
Resistant Mutants ◽  
High Level

Abstract Background Stenotrophomonas maltophilia displays high-level resistance to various antibiotics. Fluoroquinolone is among the few treatment options for S. maltophilia infection. Overexpression of SmeDEF, SmeVWX and SmQnr are the main mechanisms responsible for fluoroquinolone resistance in S. maltophilia. Objectives To reveal the unidentified fluoroquinolone resistance mechanisms in S. maltophilia. Methods Fluoroquinolone-resistant spontaneous mutants were selected by spreading KJΔDEFΔ5, a SmeDEF- and SmeVWX-null double mutant, on ciprofloxacin- or levofloxacin-containing medium. Antibiotic susceptibility was assessed by the agar dilution method. Outer membrane protein profiles of fluoroquinolone-resistant mutants were assayed by SDS-PAGE and significant protein was characterized by LC-MS/MS. The expression of tolCsm, smeH, smeK, smeN, smeP, smeZ and smQnr was investigated by real-time quantitative PCR. The contribution of SmeGH overexpression to antibiotic resistance was verified by ΔsmeH mutant construction and smeGH complementation assay. Results Most fluoroquinolone-resistant mutants displayed MDR. The TolCsm protein and smeH transcript were concomitantly overexpressed in some MDR mutants. smeH deletion increased the susceptibility of the MDR mutants to fluoroquinolone, macrolide, chloramphenicol and tetracycline, and the resistance compromise was partially reversed by complementation with a plasmid containing smeGH. SmeGH overexpression was found in some fluoroquinolone-resistant clinical S. maltophilia isolates whose SmeDEF, SmeVWX and SmQnr proteins were not or were lowly expressed. Conclusions Overexpression of SmeGH contributes to the acquired resistance of S. maltophilia to fluoroquinolone, macrolide, chloramphenicol and tetracycline.

scholarly journals A Putative ABC Transporter Is Involved in Negative Regulation of Biofilm Formation by Listeria monocytogenes

2008 ◽  
Vol 74 (24) ◽  
pp. 7675-7683 ◽  
Author(s):  
Xinna Zhu ◽  
Fei Long ◽  
Yonghui Chen ◽  
Susanne Knøchel ◽  
Qunxin She ◽  
...  
Keyword(s):  
Listeria Monocytogenes ◽  
Abc Transporter ◽  
Biofilm Formation ◽  
Negative Regulation ◽  
Atp Binding ◽  
Coding Region ◽  
Gene Encoding ◽  
Food Borne ◽  
Atp Binding Protein

ABSTRACT Listeria monocytogenes may persist for long periods in food processing environments. In some instances, this may be due to aggregation or biofilm formation. To investigate the mechanism controlling biofilm formation in the food-borne pathogen L. monocytogenes, we characterized LM-49, a mutant with enhanced ability of biofilm formation generated via transposon Tn917 mutagenesis of L. monocytogenes 4b G. In this mutant, a Tn917 insertion has disrupted the coding region of the gene encoding a putative ATP-binding cassette (ABC) transporter permease identical to Lmof2365_1771 (a putative ABC transporter permease) presented in the sequenced strain L. monocytogenes strain 4b F2365. This disrupted gene, denoted lm.G_1771, encoded a protein with 10 transmembrane helixes. The revertant, LM-49RE, was obtained by replacing lm.G_1771::Tn917 with lm.G_1771 via homologous recombination. We found that LM-49RE formed the same amount of biofilm biomass as the wild-type strain. Furthermore, transcription of the downstream lm.G_1770 gene was not influenced by the upstream Tn917 insertion, and the presence of Tn917 has no effect on biofilm formation. These results suggest that lm.G_1771 was solely responsible for the negative regulation of biofilm formation by L. monocytogenes 4b G. The immediate gene upstream of lm.G_1771 encoded an ATP-binding protein. Bioinformatics analysis suggested that these two genes were organized into an operon and that their proteins formed an export ABC transporter. Here, we report the characterization of the mutant and identification of a novel ABC transporter that functions in negative regulation of biofilm formation in L. monocytogenes.

scholarly journals It’s Not Easy Being Green: A Narrative Review on the Microbiology, Virulence and Therapeutic Prospects of Multidrug-Resistant Pseudomonas aeruginosa

Antibiotics ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 42
Author(s):  
Payam Behzadi ◽  
Zoltán Baráth ◽  
Márió Gajdács
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Excess Mortality ◽  
Review Paper ◽  
Acquired Resistance ◽  
Multidrug Resistant ◽  
Resistance Mechanisms ◽  
Gram Negative Bacteria ◽  
Pathogenic Role ◽  
Carbapenem Resistant ◽  
Resistant Strains

Pseudomonas aeruginosa is the most frequent cause of infection among non-fermenting Gram-negative bacteria, predominantly affecting immunocompromised patients, but its pathogenic role should not be disregarded in immunocompetent patients. These pathogens present a concerning therapeutic challenge to clinicians, both in community and in hospital settings, due to their increasing prevalence of resistance, and this may lead to prolonged therapy, sequelae, and excess mortality in the affected patient population. The resistance mechanisms of P. aeruginosa may be classified into intrinsic and acquired resistance mechanisms. These mechanisms lead to occurrence of resistant strains against important antibiotics—relevant in the treatment of P. aeruginosa infections—such as β-lactams, quinolones, aminoglycosides, and colistin. The occurrence of a specific resistotype of P. aeruginosa, namely the emergence of carbapenem-resistant but cephalosporin-susceptible (Car-R/Ceph-S) strains, has received substantial attention from clinical microbiologists and infection control specialists; nevertheless, the available literature on this topic is still scarce. The aim of this present review paper is to provide a concise summary on the adaptability, virulence, and antibiotic resistance of P. aeruginosa to a readership of basic scientists and clinicians.

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