Faculty Opinions recommendation of Emergence of a new antibiotic resistance mechanism in India, Pakistan, and the UK: a molecular, biological, and epidemiological study.

Author(s):  
Johann Pitout
2010 ◽  
Vol 10 (9) ◽  
pp. 597-602 ◽  
Author(s):  
Karthikeyan K Kumarasamy ◽  
Mark A Toleman ◽  
Timothy R Walsh ◽  
Jay Bagaria ◽  
Fafhana Butt ◽  
...  

2021 ◽  
Vol 14 (5) ◽  
pp. 420
Author(s):  
Tanveer Ali ◽  
Abdul Basit ◽  
Asad Mustafa Karim ◽  
Jung-Hun Lee ◽  
Jeong-Ho Jeon ◽  
...  

β-Lactam antibiotics target penicillin-binding proteins and inhibit the synthesis of peptidoglycan, a crucial step in cell wall biosynthesis. Staphylococcus aureus acquires resistance against β-lactam antibiotics by producing a penicillin-binding protein 2a (PBP2a), encoded by the mecA gene. PBP2a participates in peptidoglycan biosynthesis and exhibits a poor affinity towards β-lactam antibiotics. The current study was performed to determine the diversity and the role of missense mutations of PBP2a in the antibiotic resistance mechanism. The methicillin-resistant Staphylococcus aureus (MRSA) isolates from clinical samples were identified using phenotypic and genotypic techniques. The highest frequency (60%, 18 out of 30) of MRSA was observed in wound specimens. Sequence variation analysis of the mecA gene showed four amino acid substitutions (i.e., E239K, E239R, G246E, and E447K). The E239R mutation was found to be novel. The protein-ligand docking results showed that the E239R mutation in the allosteric site of PBP2a induces conformational changes in the active site and, thus, hinders its interaction with cefoxitin. Therefore, the present report indicates that mutation in the allosteric site of PBP2a provides a more closed active site conformation than wide-type PBP2a and then causes the high-level resistance to cefoxitin.


Author(s):  
Jacopo Monticelli ◽  
Stefano Di Bella ◽  
Daniele Roberto Giacobbe ◽  
Gerardino Amato ◽  
Roberta Maria Antonello ◽  
...  

mSystems ◽  
2018 ◽  
Vol 3 (5) ◽  
Author(s):  
Johannes Cairns ◽  
Katariina Koskinen ◽  
Reetta Penttinen ◽  
Tommi Patinen ◽  
Anna Hartikainen ◽  
...  

ABSTRACTMobile genetic elements such as conjugative plasmids are responsible for antibiotic resistance phenotypes in many bacterial pathogens. The ability to conjugate, the presence of antibiotics, and ecological interactions all have a notable role in the persistence of plasmids in bacterial populations. Here, we set out to investigate the contribution of these factors when the conjugation network was disturbed by a plasmid-dependent bacteriophage. Phage alone effectively caused the population to lose plasmids, thus rendering them susceptible to antibiotics. Leakiness of the antibiotic resistance mechanism allowing Black Queen evolution (i.e. a “race to the bottom”) was a more significant factor than the antibiotic concentration (lethal vs sublethal) in determining plasmid prevalence. Interestingly, plasmid loss was also prevented by protozoan predation. These results show that outcomes of attempts to resensitize bacterial communities by disrupting the conjugation network are highly dependent on ecological factors and resistance mechanisms.IMPORTANCEBacterial antibiotic resistance is often a part of mobile genetic elements that move from one bacterium to another. By interfering with the horizontal movement and the maintenance of these elements, it is possible to remove the resistance from the population. Here, we show that a so-called plasmid-dependent bacteriophage causes the initially resistant bacterial population to become susceptible to antibiotics. However, this effect is efficiently countered when the system also contains a predator that feeds on bacteria. Moreover, when the environment contains antibiotics, the survival of resistance is dependent on the resistance mechanism. When bacteria can help their contemporaries to degrade antibiotics, resistance is maintained by only a fraction of the community. On the other hand, when bacteria cannot help others, then all bacteria remain resistant. The concentration of the antibiotic played a less notable role than the antibiotic used. This report shows that the survival of antibiotic resistance in bacterial communities represents a complex process where many factors present in real-life systems define whether or not resistance is actually lost.


1987 ◽  
Vol 99 (2) ◽  
pp. 283-290 ◽  
Author(s):  
A. Nastasi ◽  
M. R. Villafrate ◽  
C. Mammina ◽  
M. F. Massenti ◽  
D. Oliva ◽  
...  

SUMMARYA molecular epidemiological study was carried out on 60Salmonella dublinisolates identified at the Southern Italy Enterobacteriaceae Center between 1971 and 1985. These included 23 isolates from children with diarrhoea in Palermo obtained during 1984.All isolates from the outbreak of gastroenteritis in children were resistant to chloramphenicol and streptomycin and harboured two plasmids of 50 MDa and 3 MDa molecular weight, whereas the majority of the isolates identified before 1984 were susceptible to these antibiotics and carried only a 50 MDa molecular weight plasmid. FourS. dublinstrains successively identified from cattle (Palermo, Foggia, Portici) and from a child (Palermo) were shown to possess similar antibiotic resistance patterns and plasmid profiles toS. dublinisolates from the outbreak of gastroenteritis in children.The 50 MDa plasmid was shown to be associated with virulence in mice, while it was not possible to assign any genetic function to the 3 MDa plasmid.


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