scholarly journals A second gene in the Staphylococcus aureus cadA cadmium resistance determinant of plasmid pI258.

1991 ◽  
Vol 173 (23) ◽  
pp. 7636-7642 ◽  
Author(s):  
K P Yoon ◽  
S Silver
1999 ◽  
Vol 181 (13) ◽  
pp. 4071-4075 ◽  
Author(s):  
Scott S. Crupper ◽  
Veronica Worrell ◽  
George C. Stewart ◽  
John J. Iandolo

ABSTRACT A cadmium resistance gene, designated cadD, has been identified in and cloned from the Staphylococcus aureusplasmid pRW001. The gene is part of a two-component operon which contains the resistance gene cadD and an inactive regulatory gene, cadX*. A high degree of sequence similarity was observed between cadD and thecadB-like gene from S. lugdunensis, but no significant similarity was found with either cadA orcadB from the S. aureus plasmids pI258 and pII147. The positive regulatory gene cadX* is identical tocadX from pLUG10 over a stretch of 78 codons beginning at the N terminus, but it is truncated at this point and inactive. Sequence analysis showed that the cadmium resistance operon resides on a 3,972-bp element that is flanked by direct repeats of IS257. The expression of cadD in S. aureus and Bacillus subtilis resulted in low-level resistance to cadmium; in contrast, cadA andcadB from S. aureus induced higher level resistance. However, when the truncated version ofcadX contained in pRW001 is complemented intrans with cadX from plasmid pLUG10, resistance increased approximately 10-fold suggesting that the cadmium resistance operons from pRW001 and pLUG10 are evolutionarily related. Moreover, the truncated version ofcadX contained in pRW001 is nonfunctional and may have been generated by deletion during recombination to acquire the cadmium resistance element.


1991 ◽  
Vol 37 (8) ◽  
pp. 624-631 ◽  
Author(s):  
Kenneth Babich ◽  
Mike Engle ◽  
Jeffery S. Skinner ◽  
Richard A. Laddaga

Deletion mutant analysis of the mercury-resistant determinant (mer operon) from the Staphylococcus aureus plasmid pI258 was used to verify the location of the merA and merB genes and to show the existence of mercuric ion transport gene(s). ORF5 was confirmed to be a transport gene and has an amino acid product sequence homologous to the merT gene products from several gram-negative bacteria and a Bacillus species. Deletion analysis established that inactivation of merA on a broad-spectrum mer resistance determinant resulted in a mercury-hypersensitive phenotype. Gene dosage had no apparent effect on the level of resistance conferred by the intact mer operon or on the expression of an inducible phenotype, except that when the intact pI258 mer operon was on a high copy number plasmid, uninduced cells possessed a volatilization rate that was at most only 3.5-fold less than that observed for induced cells. There was no need for mercury ion transport proteins for full resistance when the mer operon was expressed in a high copy number plasmid. Key words: mercury resistance, Staphylococcus aureus plasmid.


2010 ◽  
Vol 54 (9) ◽  
pp. 3605-3608 ◽  
Author(s):  
L. M. Cavaco ◽  
H. Hasman ◽  
M. Stegger ◽  
P. S. Andersen ◽  
R. Skov ◽  
...  

ABSTRACT We recently reported a phenotypic association between reduced susceptibility to zinc and methicillin resistance in Staphylococcus aureus CC398 isolates from Danish swine (F. M. Aarestrup, L. M. Cavaco, and H. Hasman, Vet. Microbiol. 142:455-457, 2009). The aim of this study was to identify the genetic determinant causing zinc resistance in CC398 and examine its prevalence in isolates of animal and human origin. Based on the sequence of the staphylococcal cassette chromosome mec (SCCmec) element from methicillin-resistant S. aureus (MRSA) CC398 strain SO385, a putative metal resistance gene was identified in strain 171 and cloned in S. aureus RN4220. Furthermore, 81 MRSA and 48 methicillin-susceptible S. aureus (MSSA) strains, isolated from pigs (31 and 28) and from humans (50 and 20) in Denmark, were tested for susceptibility to zinc chloride and for the presence of a putative resistance determinant, czrC, by PCR. The cloning of czrC confirmed that the zinc chloride and cadmium acetate MICs for isogenic constructs carrying this gene were increased compared to those for S. aureus RN4220. No difference in susceptibility to sodium arsenate, copper sulfate, or silver nitrate was observed. Seventy-four percent (n = 23) of the animal isolates and 48% (n = 24) of the human MRSA isolates of CC398 were resistant to zinc chloride and positive for czrC. All 48 MSSA strains from both human and pig origins were found to be susceptible to zinc chloride and negative for czrC. Our findings showed that czrC is encoding zinc and cadmium resistance in CC398 MRSA isolates, and that it is widespread both in humans and animals. Thus, resistance to heavy metals such as zinc and cadmium may play a role in the coselection of methicillin resistance in S. aureus.


2003 ◽  
Vol 185 (18) ◽  
pp. 5465-5472 ◽  
Author(s):  
Yuki Katayama ◽  
Hong-Zhong Zhang ◽  
Dong Hong ◽  
Henry F. Chambers

ABSTRACT Although the staphylococcal methicillin resistance determinant, mecA, resides on a mobile genetic element, staphylococcus cassette chromosome mec (SCCmec), its distribution in nature is limited to as few as five clusters of related methicillin-resistant Staphylococcus aureus (MRSA) clones. To investigate the potential role of the host chromosome in clonal restriction of the methicillin resistance determinant, we constructed plasmid pYK20, carrying intact mecA, and introduced it into several methicillin-susceptible Staphylococcus aureus strains, five of which were naive hosts (i.e., mecA not previously resident on the host chromosome) and five of which were experienced hosts (i.e., methicillin-susceptible variants of MRSA strains from which SCCmec was excised). We next assessed the effect of the recipient background on the methicillin resistance phenotype by population analysis, by assaying the mecA expression of PBP2a by Western blot analysis, and by screening for mutations affecting mecA. Each experienced host transformed with pYK20 had a resistance phenotype and expressed PBP2a similar to that of the parent with chromosomal SCCmec, but naive hosts transformed with pYK20 selected against its expression, indicative of a host barrier. Either inducible β-lactamase regulatory genes blaR1-blaI or homologous regulatory genes mecR1-mecI, which control mecA expression, acted as compensatory elements, permitting the maintenance and expression of plasmid-carried mecA.


Plasmid ◽  
2004 ◽  
Vol 52 (1) ◽  
pp. 48-56 ◽  
Author(s):  
Pedro D Loeza-Lara ◽  
Morelia Soto-Huipe ◽  
Victor M Baizabal-Aguirre ◽  
Alejandra Ochoa-Zarzosa ◽  
Juan J Valdez-Alarcón ◽  
...  

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