scholarly journals A genomic epidemiology investigation of yaws re-emergence and bacterial drug resistance selection

Author(s):  
Mathew A Beale ◽  
Marc Noguera-Julian ◽  
Charmie Godornes ◽  
Maria Casadella ◽  
Camila Gonzalez-Beiras ◽  
...  

Background: In a longitudinal study assessing the WHO strategy for yaws eradication using mass azithromycin treatment, we observed resurgence of yaws cases with dominance of a single JG8 sequence type and emergence of azithromycin-resistant Treponema pallidum. Here, we analyse genomic changes in the bacterial population using samples collected during the study. Methods: We performed whole bacterial genome sequencing directly on DNA extracted from 37 lesion swabs collected from patients on Lihir Island, Papua New Guinea, between 2013 and 2016. We produced phylogenies and correlated these with temporo-spatial information to investigate the source of new cases and the emergence of five macrolide-resistant cases. We used deep amplicon sequencing of surveillance samples to assess the presence of minority macrolide resistance populations. Findings: We recovered 20 whole Treponema genomes, and phylogenetic analysis showed that the re-emerging JG8 sequence type was composed of three bacterial sub-lineages characterised by distinct temporo-spatial patterns. Of five patients with resistant Treponema, all epidemiologically linked, we recovered genomes from three and found no variants. Deep sequencing showed that pre-treatment, the index patient harboured fixed macrolide-sensitive Treponema, while the post-treatment sample harboured a fixed resistant genotype, as did three of four contact cases. We also found no evidence of pre-existing minority Treponema drug-resistance variants in the general population. Interpretation: In this study, re-emergence of yaws cases was polyphyletic, indicating multiple epidemiological sources. However, given the genomic and epidemiological linkage of resistant cases and the rarity of resistance alleles in the general population, it is likely that azithromycin resistance evolved only once in this study, followed by onward dissemination.

2017 ◽  
Vol 111 ◽  
pp. 468-471 ◽  
Author(s):  
Vivianne Marcelino de Medeiros ◽  
Yuri Mangueira do Nascimento ◽  
Augusto Lopes Souto ◽  
Sara Alves Lucena Madeiro ◽  
Vicente Carlos de Oliveira Costa ◽  
...  

2020 ◽  
Vol 2 (1) ◽  
pp. 5
Author(s):  
Sung-Won Kim

<p>The proportion of critically ill patients from neurosurgery wards in hospitals is significantly higher than that from other departments. These patients suffer from low immune. At the same time, because of the severe trauma after surgery and the complexity of pathogens in patients, antibiotics are frequently used. However, the of bacterial drug resistance is relatively high because of the particularity of hospitals, which is a major reason for the high infection rate of neurosurgery patients. Therefore, regarding to these risk factors, intervention measures should be actively explored in hospitals, so as to control the infection rate, reduce the possibility of infection in neurosurgery patients, improve the rehabilitation efficiency of patients, and reduce unnecessary suffering of patients caused by infection. This is also an effective means to improve the quality of hospital medical care. </p>


2000 ◽  
Vol 182 (6) ◽  
pp. 1515-1522 ◽  
Author(s):  
Leah E. Cowen ◽  
Dominique Sanglard ◽  
David Calabrese ◽  
Caroline Sirjusingh ◽  
James B. Anderson ◽  
...  

ABSTRACT Adaptation to inhibitory concentrations of the antifungal agent fluconazole was monitored in replicated experimental populations founded from a single, drug-sensitive cell of the yeast Candida albicans and reared over 330 generations. The concentration of fluconazole was maintained at twice the MIC in six populations; no fluconazole was added to another six populations. All six replicate populations grown with fluconazole adapted to the presence of drug as indicated by an increase in MIC; none of the six populations grown without fluconazole showed any change in MIC. In all populations evolved with drug, increased fluconazole resistance was accompanied by increased resistance to ketoconazole and itraconazole; these populations contained ergosterol in their cell membranes and were amphotericin sensitive. The increase in fluconazole MIC in the six populations evolved with drug followed different trajectories, and these populations achieved different levels of resistance, with distinct overexpression patterns of four genes involved in azole resistance: the ATP-binding cassette transporter genes,CDR1 and CDR2; the gene encoding the target enzyme of the azoles in the ergosterol biosynthetic pathway,ERG11; and the major facilitator gene, MDR1. Selective sweeps in these populations were accompanied by additional genomic changes with no known relationship to drug resistance: loss of heterozygosity in two of the five marker genes assayed and alterations in DNA fingerprints and electrophoretic karyotypes. These results show that chance, in the form of mutations that confer an adaptive advantage, is a determinant in the evolution of azole drug resistance in experimental populations of C. albicans.


2018 ◽  
Vol 121 ◽  
pp. 293-302 ◽  
Author(s):  
Shafiul Haque ◽  
Faraz Ahmad ◽  
Sajad A. Dar ◽  
Arshad Jawed ◽  
Raju K. Mandal ◽  
...  

Author(s):  
Yasuhisa Iwao ◽  
Shuichi Mori ◽  
Manabu Ato ◽  
Noboru Nakata

Mycobacterium leprae is the predominant cause of leprosy worldwide, and its genotypes can be classified into four single nucleotide polymorphism (SNP) types and 16 subtypes. Determining M. leprae drug resistance and genotype is typically done by PCR and Sanger DNA sequencing, which require substantial effort. Here we describe a rapid method involving multiplex PCR in combination with nested amplification and next generation sequence analysis that allows simultaneous determination of M. leprae drug resistance and SNP genotype directly from clinical specimens. We used this method to analyze clinical samples from two paucibacillary, nine multibacillary, and six type-undetermined leprosy patients. Regions in folP1 , rpoB , gyrA , and gyrB that determine drug resistance and those for 84 SNP-InDels in the M. leprae genome were amplified from clinical samples and their sequences were determined. The results showed that seven samples were subtype 1A, three were 1D, and seven were 3K. Three samples of the subtype 3K had folp1 mutation. The method may allow more rapid genetic analyses of M. leprae in clinical samples.


PLoS ONE ◽  
2015 ◽  
Vol 10 (5) ◽  
pp. e0126626 ◽  
Author(s):  
Rebecca E. Colman ◽  
James M. Schupp ◽  
Nathan D. Hicks ◽  
David E. Smith ◽  
Jordan L. Buchhagen ◽  
...  

Author(s):  
John W. Wilson ◽  
Lynn L. Estes

This section contains tables covering spectrum of activity, preferred treatment and alternate treatment options various classes of bacteria, fungi, and viruses. Bacterial drug resistance issues are also reviewed.


2019 ◽  
Vol 22 ◽  
pp. S654
Author(s):  
B. Cabieses ◽  
A. Peters ◽  
M.P. Acuña ◽  
N. Uphoff ◽  
S. Astorga ◽  
...  

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