Laboratory selection of chlorpyrifos resistance in an Invasive Pest, Phenacoccus solenopsis (Homoptera: Pseudococcidae): Cross-resistance, stability and fitness cost

2017 ◽  
Vol 137 ◽  
pp. 8-14 ◽  
Author(s):  
Masood Ejaz ◽  
Muhammad Babar Shahzad Afzal ◽  
Ghulam Shabbir ◽  
José Eduardo Serrão ◽  
Sarfraz Ali Shad ◽  
...  
2015 ◽  
Vol 18 (4) ◽  
pp. 779-785 ◽  
Author(s):  
Muhammad Babar Shahzad Afzal ◽  
Sarfraz Ali Shad ◽  
Esteban Basoalto ◽  
Masood Ejaz ◽  
Jose Eduardo Serrao

1990 ◽  
Vol 80 (3) ◽  
pp. 245-250 ◽  
Author(s):  
J.A. Bisset ◽  
M.M. Rodriguez ◽  
C. Diaz ◽  
E. Ortiz ◽  
M.C. Marquetti ◽  
...  

AbstractTwo field-collected strains of Culex quinquefasciatus Say, collected 50 km apart in Havana City, Cuba, were both resistant to malathion and propoxur, while one population also showed low level resistance to temephos. Laboratory selection of the latter population with malathion for 22 generations increased the malathion resistance 1050-fold, temephos resistance 24-fold and propoxur resistance 453-fold compared to the standard laboratory susceptible strain. Synergist studies and biochemical tests indicated that two mechanisms, an elevated esterase and an insensitive acetylcholinesterase, were operative in these strains. The esterase mechanism conferred resistance to malathion, but not to temephos or propoxur. The acetylcholinesterase mechanism increased the level of malathion resistance and extended the cross-resistance spectrum to temephos and propoxur.


2020 ◽  
Vol 6 (1) ◽  
Author(s):  
Engy Elekhnawy ◽  
Fatma Sonbol ◽  
Ahmed Abdelaziz ◽  
Tarek Elbanna

Abstract Background Antibiotic resistance in pathogenic bacterial isolates has increased worldwide leading to treatment failures. Main body Many concerns are being raised about the usage of biocidal products (including disinfectants, antiseptics, and preservatives) as a vital factor that contributes to the risk of development of antimicrobial resistance which has many environmental and economic impacts. Conclusion Consequently, it is important to recognize the different types of currently used biocides, their mechanisms of action, and their potential impact to develop cross-resistance and co-resistance to various antibiotics. The use of biocides in medical or industrial purposes should be monitored and regulated. In addition, new agents with biocidal activity should be investigated from new sources like phytochemicals in order to decrease the emergence of resistance among bacterial isolates.


2003 ◽  
Vol 77 (10) ◽  
pp. 5685-5693 ◽  
Author(s):  
J. Gerardo García-Lerma ◽  
Hamish MacInnes ◽  
Diane Bennett ◽  
Patrick Reid ◽  
Soumya Nidtha ◽  
...  

ABSTRACT Stavudine (d4T) and zidovudine (AZT) are thymidine analogs widely used in the treatment of human immunodeficiency virus type 1 (HIV-1)-infected persons. Resistance to d4T is not fully understood, although the selection of AZT resistance mutations in patients treated with d4T suggests that both drugs have similar pathways of resistance. Through the analysis of genotypic changes in nine recombinant viruses cultured with d4T, we identified a new pathway for d4T resistance mediated by K65R, a mutation not selected by AZT. Passaged viruses were derived from treatment-naïve persons or HIV-1HXB2 and had wild-type reverse transcriptase (RT) or T215C/D mutations. K65R was selected in seven viruses and was associated with a high level of enzymatic resistance to d4T-triphosphate (median, 16-fold; range, 5- to 48-fold). The role of K65R in d4T resistance was confirmed in site-directed mutants generated in three different RT backgrounds. Phenotypic assays based on recombinant single-cycle replication or a whole-virus multiple replication cycle were unable to detect d4T resistance in d4T-selected mutants with K65R but detected cross-resistance to other nucleoside RT inhibitors. Four of the six viruses that had 215C/D mutations at baseline acquired the 215Y mutation alone or in association with K65R. Mutants having K65R and T215Y replicated less efficiently than viruses that had T215Y only, suggesting that selection of T215Y in patients treated with d4T may be favored. Our results demonstrate that K65R plays a role in d4T resistance and indicate that resistance pathways for d4T and AZT may not be identical. Biochemical analysis and improved replication assays are both required for a full phenotypic characterization of resistance to d4T. These findings highlight the complexity of the genetic pathways of d4T resistance and its phenotypic expression.


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