scholarly journals Host range of the conjugative 25.2-megadalton tetracycline resistance plasmid from Neisseria gonorrhoeae and related species.

1988 ◽  
Vol 32 (4) ◽  
pp. 488-491 ◽  
Author(s):  
M C Roberts ◽  
J S Knapp
1990 ◽  
Vol 36 (1) ◽  
pp. 64-67 ◽  
Author(s):  
Jo-Anne R. Dillon ◽  
Maria Carballo

Between October 1987 and June 1989, 84 isolates of Neisseria gonorrhoeae carrying the TetM resistance determinant (TRNG) were received at the Laboratory Centre for Disease Control, Ottawa, from six Canadian provinces and were characterized into classes based on auxotype, serovar and plasmid content. One-fifth (17/84) of the TRNG were also penicillinase producing (PPNG). The PPNG–TRNG isolates comprised six classes based on auxotype, serovar, and plasmid content. Most (16/17) PPNG–TRNG carried 3.2-MDa β-lactamase plasmids and the 25.2-MDa TetM-containing plasmid. We report, for the first time, the association of a 4.5-MDa β-lactamase plasmid with the 25.2-MDa plasmid in a clinical TRNG isolate. Non-PPNG TRNG isolates comprised 11 classes based on auxotype, serovar, and plasmid content, including two previously unreported auxotype–serovar classes, P/IB-26 and P/IB-20. Key words: Neisseria gonorrhoeae, tetracycline resistance, plasmid, epidemiology.


mBio ◽  
2011 ◽  
Vol 2 (5) ◽  
Author(s):  
Trudi L. Bannam ◽  
Xu-Xia Yan ◽  
Paul F. Harrison ◽  
Torsten Seemann ◽  
Anthony L. Keyburn ◽  
...  

ABSTRACTThe pathogenesis of avian necrotic enteritis involves NetB, a pore-forming toxin produced by virulent avian isolates ofClostridium perfringenstype A. To determine the location and mobility of thenetBstructural gene, we examined a derivative of the tetracycline-resistant necrotic enteritis strain EHE-NE18, in whichnetBwas insertionally inactivated by the chloramphenicol and thiamphenicol resistance genecatP. Both tetracycline and thiamphenicol resistance could be transferred either together or separately to a recipient strain in plate matings. The separate transconjugants could act as donors in subsequent matings, which demonstrated that the tetracycline resistance determinant and thenetBgene were present on different conjugative elements. Large plasmids were isolated from the transconjugants and analyzed by high-throughput sequencing. Analysis of the resultant data indicated that there were actually three large conjugative plasmids present in the original strain, each with its own toxin or antibiotic resistance locus. Each plasmid contained a highly conserved 40-kb region that included plasmid replication and transfer regions that were closely related to the 47-kb conjugative tetracycline resistance plasmid pCW3 fromC. perfringens. The plasmids were as follows: (i) a conjugative 49-kb tetracycline resistance plasmid that was very similar to pCW3, (ii) a conjugative 82-kb plasmid that contained thenetBgene and other potential virulence genes, and (iii) a 70-kb plasmid that carried thecpb2gene, which encodes a different pore-forming toxin, beta2 toxin.IMPORTANCEThe anaerobic bacteriumClostridium perfringenscan cause an avian gastrointestinal disease known as necrotic enteritis. Disease pathogenesis is not well understood, although the plasmid-encoded pore-forming toxin NetB, is an important virulence factor. In this work, we have shown that the plasmid that carries thenetBgene is conjugative and has a 40-kb region that is very similar to replication and transfer regions found within each of the sequenced conjugative plasmids fromC. perfringens. We also showed that this strain contained two additional large plasmids that were also conjugative and carried a similar 40-kb region. One of these plasmids encoded beta2 toxin, and the other encoded tetracycline resistance. To our knowledge, this is the first report of a bacterial strain that carries three closely related but different independently conjugative plasmids. These results have significant implications for our understanding of the transmission of virulence and antibiotic resistance genes in pathogenic bacteria.


2008 ◽  
Vol 52 (6) ◽  
pp. 2175-2182 ◽  
Author(s):  
Elena N. Ilina ◽  
Vladimir A. Vereshchagin ◽  
Alexandra D. Borovskaya ◽  
Maja V. Malakhova ◽  
Sergei V. Sidorenko ◽  
...  

ABSTRACT The main goal of this work is to clarify the predictive value of known genetic markers of Neisseria gonorrhoeae resistance to penicillin, tetracycline, and fluoroquinolones. The correlation between the presence of certain genetic markers and susceptibility of N. gonorrhoeae isolates to penicillin, tetracycline, and fluoroquinolones has been analyzed by means of statistical methods. Susceptibility testing with penicillin, tetracycline, and fluoroquinolones was performed by the agar dilution method. N. gonorrhoeae genomic DNA was isolated. The presence of bla TEM-1 and tet(M) genes was analyzed by PCR. A novel method of polymorphism discovery based on a minisequencing reaction followed by matrix-assisted laser desorption ionization-time-of-flight mass spectrometry was applied for the analysis of chromosomal N. gonorrhoeae genes involved in antimicrobial resistance development. Clinical N. gonorrhoeae isolates (n = 464) were collected. Susceptibility levels to penicillin, tetracycline, and fluoroquinolones were found to be 25.9%, 35.9%, and 54.1%, respectively. Among the 19 N. gonorrhoeae isolates with penicillin MICs of ≥4 μg/ml, the bla TEM-1 gene was detected in 12. The Tet(M) determinant was found in 4 of 12 N. gonorrhoeae isolates with tetracycline MICs of ≥16 μg/ml. The chromosomal genetic markers of penicillin and tetracycline resistance were detected especially in isolates with penicillin MICs of 0.25 to 2.0 μg/ml and tetracycline MICs of 0.5 to 4 μg/ml. Mutations in GyrA and ParC were found in 208 of 211 quinolone-resistant N. gonorrhoeae isolates. This work is the first representative molecular research of the N. gonorrhoeae population in Russia. Information about the prevalence of antibiotic resistance mechanisms and the positive predictive value of certain genetic determinants is given. The positive predictive values of the analyzed genetic markers were found to be different for fluoroquinolones (90.3%), penicillin (91.1%), and tetracycline (81.9%).


1996 ◽  
Vol 10 (3) ◽  
pp. 625-636 ◽  
Author(s):  
R. Charudattan ◽  
V. J. Prange ◽  
J. T. Devalerio

We are studying the possibility of altering the virulence and host range of a phytopathogen by transferring and expressing certain genes from the soil-dwelling saprophyte,Streptomyces hygroscopicus, in a plant pathogen model,Xanthomonas campestrispv.campestris(XCC). The genes, referred to herein as the “bialaphos genes,” encode the production of bialaphos, a potent glutamine-synthetase-inhibiting herbicide. This cluster of genes was originally isolated from several biosynthetically blocked mutants ofS. hygroscopicusand constructed into a plasmid vector, pBG9. We have transferred a fragment of the gene cluster into pLAFR3, a plasmid that functions in bothEscherichia coliand XCC and contains a tetracycline resistance marker. The resulting plasmid, named pIL-1, was used to transformE. coliand was incorporated into XCC by conjugation. The transfer of the fragment was confirmed by Southern analysis. The genes were maintained in XCC for about 47 generations in the absence of selection for tetracycline, and no changes in cultural phenotypes were seen in the transformed XCC (XCC/pIL-1). The XCC/pIL-1 cells were pathogenic to their natural hosts cabbage and broccoli, but induced an altered hypersensitive response in the nonhosts bean, pepper, sunflower, and tobacco. The pathogenic host-reaction, induced by the parent XCC, XCC/pLAFR3, and XCC/pIL-1, was a typical black rot disease in inoculated leaves of the two hosts. The nonhost reaction on the nonhost leaves was necrotic hypersensitivity, induced by XCC and XCC/pLAFR3, or the inhibition of hypersensitivity accompanied by only chlorosis at sites inoculated with XCC/pIL-1. We hypothesize that the altered hypersensitivity phenotype may be due to the transformed XCC becoming more compatible with the nonhosts, a step toward acquiring nonhost-virulence, or due to disruption of the normal expression of the hypersensitivity and pathogenicity genes in the transformed XCC. More work is needed to confirm that the introduced genes are being expressed in XCC. With further understanding, this approach may provide a useful model to study host range, virulence, and strain improvement of plant pathogens for biological control of weeds.


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