Relevant bibliographies by topics / Drug resistance mutation

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Drug resistance mutation'

Author: Grafiati
Published: 4 June 2021
Last updated: 24 April 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Drug resistance mutation.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Drug resistance mutation"

1

Chen, Lamei, Alla Perlina, and Christopher J. Lee. "Positive Selection Detection in 40,000 HumanImmunodeficiency Virus (HIV) Type 1 Sequences Automatically IdentifiesDrug Resistance and Positive Fitness Mutations in HIV Proteaseand ReverseTranscriptase." Journal of Virology 78, no. 7 (2004): 3722–32. http://dx.doi.org/10.1128/jvi.78.7.3722-3732.2004.

Full text
Abstract:
ABSTRACT Drug resistance is a major problem in the treatment of AIDS, due to the very high mutation rate of human immunodeficiency virus (HIV) and subsequent rapid development of resistance to new drugs. Identification of mutations associated with drug resistance is critical for both individualized treatment selection and new drug design. We have performed an automated mutation analysis of HIV Type 1 (HIV-1) protease and reverse transcriptase (RT) from approximately 40,000 AIDS patient plasma samples sequenced by Specialty Laboratories Inc. from 1999 to mid-2002. This data set provides a nearly complete mutagenesis of HIV protease and enables the calculation of statistically significant Ka /Ks values for each individual amino acid mutation in protease and RT. Positive selection (i.e., a Ka /Ks ratio of> 1, indicating increased reproductive fitness) detected 19 of 23 known drug-resistant mutation positions in protease and 20 of 34 such positions in RT. We also discovered 163 new amino acid mutations in HIV protease and RT that are strong candidates for drug resistance or fitness. Our results match available independent data on protease mutations associated with specific drug treatments and mutations with positive reproductive fitness, with high statistical significance (the P values for the observed matches to occur by random chance are 10−5.2 and 10−16.6, respectively). Our mutation analysis provides a valuable resource for AIDS research and will be available to academic researchers upon publication at http://www.bioinformatics.ucla.edu/HIV . Our data indicate that positive selection mapping is an analysis that can yield powerful insights from high-throughput sequencing of rapidly mutating pathogens.
APA, Harvard, Vancouver, ISO, and other styles
2

Hu, Yi, Sven Hoffner, Linlin Wu, Qi Zhao, Weili Jiang, and Biao Xu. "Prevalence and Genetic Characterization of Second-Line Drug-Resistant and Extensively Drug-Resistant Mycobacterium tuberculosis in Rural China." Antimicrobial Agents and Chemotherapy 57, no. 8 (2013): 3857–63. http://dx.doi.org/10.1128/aac.00102-13.

Full text
Abstract:
ABSTRACTThis study aimed to investigate the prevalence of resistance to second-line antituberculosis (anti-TB) drugs and its association with resistance-related mutations inMycobacterium tuberculosisisolated in China. In the present study, we collected 380 isolates from a population-based study in China and tested the drug susceptibility to first- and selected second-line drugs. These results were compared with polymorphisms in the DNA sequences of genes associated with drug resistance and MIC values of the studied second-line drugs. Of 43 multidrug-resistantM. tuberculosisisolates, 13 showed resistance to fluoroquinolones or injectable second-line drugs (preextensively drug-resistant TB [pre-XDR-TB]), and 4 were resistant to both and thus defined as extensively drug-resistant TB (XDR-TB). Age and previous TB therapy, including use of second-line drugs, were two independent factors associated with increased resistance to both first- and second-line drugs. Molecular analysis identified the most frequent mutations in the resistance-associated genes: D94G ingyrA(29.1%) and A1401G inrrs(30.8%). Meanwhile, all 4 XDR-TB isolates had a mutation ingyrA, and 3 of them carried the A1401G mutation inrrs. Mutations ingyrAandrrswere associated with high-level resistance to fluoroquinolones and the second-line injectable drugs. In addition to the identification of resistance-associated mutations and development of a rapid molecular test to diagnose the second-line drug resistance, it should be a priority to strictly regulate the administration of second-line drugs to maintain their efficacy to treat multidrug-resistant TB.
APA, Harvard, Vancouver, ISO, and other styles
3

Click, Eleanor S., Ekaterina V. Kurbatova, Heather Alexander, et al. "Isoniazid and Rifampin-Resistance Mutations Associated With Resistance to Second-Line Drugs and With Sputum Culture Conversion." Journal of Infectious Diseases 221, no. 12 (2020): 2072–82. http://dx.doi.org/10.1093/infdis/jiaa042.

Full text
Abstract:
Abstract Background Mutations in the genes inhA, katG, and rpoB confer resistance to anti-tuberculosis (TB) drugs isoniazid and rifampin. We questioned whether specific mutations in these genes were associated with different clinical and microbiological characteristics. Methods In a multicountry prospective cohort study of multidrug-resistant TB, we identified inhA, katG, and rpoB mutations in sputum isolates using the Hain MTBDRplus line probe assay. For specific mutations, we performed bivariate analysis to determine relative risk of baseline or acquired resistance to other TB drugs. We compared time to sputum culture conversion (TSCC) using Kaplan-Meier curves and stratified Cox regression. Results In total, 447 participants enrolled from January 2005 to December 2008 from 7 countries were included. Relative to rpoB S531L, isolates with rpoB D516V had less cross-resistance to rifabutin, increased baseline resistance to other drugs, and increased acquired fluoroquinolone resistance. Relative to mutation of katG only, mutation of inhA promoter and katG was associated with baseline extensively drug resistant (XDR) TB, increased acquired fluoroquinolone resistance, and slower TSCC (125.5 vs 89.0 days). Conclusions Specific mutations in inhA and katG are associated with differences in resistance to other drugs and TSCC. Molecular testing may make it possible to tailor treatment and assess additional drug resistance risk according to specific mutation profile.
APA, Harvard, Vancouver, ISO, and other styles
4

Sandgren, Andreas, Michael Strong, Preetika Muthukrishnan, Brian K. Weiner, George M. Church, and Megan B. Murray. "Tuberculosis Drug Resistance Mutation Database." PLoS Medicine 6, no. 2 (2009): e1000002. http://dx.doi.org/10.1371/journal.pmed.1000002.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Yerly, Sabine, Catherine Fagard, Huldrych F. Günthard, Bernard Hirschel, and Luc Perrin. "Drug Resistance Mutations during Structured Treatment Interruptions." Antiviral Therapy 8, no. 5 (2002): 411–15. http://dx.doi.org/10.1177/135965350300800508.

Full text
Abstract:
Background We assessed whether treatment interruptions induce selection of mutations associated with drug resistance in the Swiss–Spanish Intermittent Treatment Trial (SSITT). Patients had been on HAART without previous failure and had undetectable viraemia for at least 6 months. Their HAART was interrupted for 2 weeks and restarted for 8 weeks. After four of these cycles, treatment was definitively interrupted at week 40. Methods Genotypic resistance testing was performed in 87/97 Swiss patients: in those failing treatment before week 40, at the time of first viral rebound >500 copies/ml off treatment and preceding failure to reach RNA <50 copies/ml after 8 weeks of re-treatment; for patients without virological failure, on the first sample with HIV-1 RNA >1000 copies/ml after week 40. Results Mutations associated with drug resistance were detected in 9/25 (36%) patients with virological failure during the first 40 weeks and in 6/59 (10%) patients after week 40. Overall, drug resistance mutations were detected in 17% of patients, all but two with the 184V/I mutation. Among the 74 patients receiving lamivudine, the M184V/I mutation was detected in 13/74 (17.6%) patients. A wild-type codon at position 184 was detected in previous samples in all b'ut two. The relative risk for virological failure was 2.55-fold higher in patients with the M184V/I mutation than in patients without detectable mutation ( P=0.007). Conclusions The M184V/I mutation is frequently selected during repeated treatment interruptions.
APA, Harvard, Vancouver, ISO, and other styles
6

Hachem, Ahmad A., Essa H. Hariri, Anthony Mansour, and Jacques Mokhbat. "Human Immunodeficiency Virus type 1 Drug Resistance Mutations in Patients Failing Antiretroviral Therapy in Lebanon from 2009 to 2013." International Journal of Clinical Research 1, no. 1 (2021): 113–23. http://dx.doi.org/10.38179/ijcr.v1i1.20.

Full text
Abstract:
Background: Antiretroviral drug resistance remains a significant problem in the clinical management of patients infected with the Human Immunodeficiency Virus type-1. Aim: This study investigates and reports data on the molecular characterization of HIV-1 isolates from patients who are in a state of therapy failure. Methods: This is a retrospective study conducted on 65 patients in therapy failure. Inclusion criteria included patients diagnosed as being in therapy failure between the years 2009 and 2013. We defined ART failure as either a failure to achieve viral suppression or a failure to detect viral loads below 500 copies/mL after virological suppression in at least two plasma samples. We used the published WHO list for surveillance of transmitted resistance and the Stanford HIV Drug Resistance Database to identify drug resistance mutations. Results: 65% of the participants had at least one drug resistance mutation (DRM). 12% of the population sampled had resistance to only one ART class, 32% presented with resistance to two classes of antiretroviral drugs, and 20% had resistance to all three classes of drugs. The prevalence of nucleoside transcriptase inhibitor (NRTI) mutations was 55%, the most common DRM being M184V. The prevalence of non-nucleoside reverse transcriptase inhibitor (NNRTI) mutations was 58%, with the most common mutation being the K103N mutation. The prevalence of protease inhibitors drug resistance mutations was 23%, with mutations V82A and I47V being present in 10% of the study population. Conclusion: Our study is the first molecular characterization of DRM emergence in HIV-1 strains from patients failing antiretroviral therapy in Lebanon. Continuous monitoring of resistance patterns for HIV in the country is necessary to tackle the emergent drug resistance.
APA, Harvard, Vancouver, ISO, and other styles
7

Tsubata, Yukari, Ryosuke Tanino, and Takeshi Isobe. "Current Therapeutic Strategies and Prospects for EGFR Mutation-Positive Lung Cancer Based on the Mechanisms Underlying Drug Resistance." Cells 10, no. 11 (2021): 3192. http://dx.doi.org/10.3390/cells10113192.

Full text
Abstract:
The discovery of activating mutations in the epidermal growth factor receptor (EGFR) gene and the development of EGFR tyrosine kinase inhibitors (TKIs) have led to a paradigm shift in the treatment of non-small cell lung cancer (NSCLC). EGFR mutation-positive NSCLC is common in East Asia, and approximately 50% of adenocarcinomas harbor EGFR mutations. Undoubtedly, EGFR-TKIs, with their promising efficacy, are the mainstay of primary therapy. However, even if tumor shrinkage is achieved, most patients become resistant to EGFR-TKIs and relapse; hence, EGFR-TKIs do not achieve a radical cure. The problem of the development of resistance to targeted drugs has been a persistent challenge. After the role of EGFR T790M mutation in acquired drug resistance was reported, osimertinib, a third-generation irreversible EGFR-TKI, was designed to overcome the resistance conferred by T790M mutation. In addition, some studies have reported the mechanism of drug resistance caused by mutations other than the T790M mutation and strategies to overcome them. Elucidating the mechanism underlying drug resistance development and combining therapeutic approaches are expected to further improve NSCLC prognosis.
APA, Harvard, Vancouver, ISO, and other styles
8

Avizienyte, Egle, Richard A. Ward, and Andrew P. Garner. "Comparison of the EGFR resistance mutation profiles generated by EGFR-targeted tyrosine kinase inhibitors and the impact of drug combinations." Biochemical Journal 415, no. 2 (2008): 197–206. http://dx.doi.org/10.1042/bj20080728.

Full text
Abstract:
Recent clinical data indicates that the emergence of mutant drug-resistant kinase alleles may be particularly relevant for targeted kinase inhibitors. In order to explore how different classes of targeted therapies impact upon resistance mutations, we performed EGFR (epidermal-growth-factor receptor) resistance mutation screens with erlotinib, lapatinib and CI-1033. Distinct mutation spectra were generated with each inhibitor and were reflective of their respective mechanisms of action. Lapatinib yielded the widest variety of mutations, whereas mutational variability was lower in the erlotinib and CI-1033 screens. Lapatinib was uniquely sensitive to mutations of residues located deep within the selectivity pocket, whereas mutation of either Gly796 or Cys797 resulted in a dramatic loss of CI-1033 potency. The clinically observed T790M mutation was common to all inhibitors, but occurred with varying frequencies. Importantly, the presence of C797S with T790M in the same EGFR allele conferred complete resistance to erlotinib, lapatinib and CI-1033. The combination of erlotinib and CI-1033 effectively reduced the number of drug-resistant clones, suggesting a possible clinical strategy to overcome drug resistance. Interestingly, our results also indicate that co-expression of ErbB2 (v-erb-b2 erythroblastic leukaemia viral oncogene homologue 2) has an impact upon the EGFR resistance mutations obtained, suggesting that ErbB2 may play an active role in the acquisition of drug-resistant mutations.
APA, Harvard, Vancouver, ISO, and other styles
9

Pauly, Matthew D., and Adam S. Lauring. "Effective Lethal Mutagenesis of Influenza Virus by Three Nucleoside Analogs." Journal of Virology 89, no. 7 (2015): 3584–97. http://dx.doi.org/10.1128/jvi.03483-14.

Full text
Abstract:
ABSTRACTLethal mutagenesis is a broad-spectrum antiviral strategy that exploits the high mutation rate and low mutational tolerance of many RNA viruses. This approach uses mutagenic drugs to increase viral mutation rates and burden viral populations with mutations that reduce the number of infectious progeny. We investigated the effectiveness of lethal mutagenesis as a strategy against influenza virus using three nucleoside analogs, ribavirin, 5-azacytidine, and 5-fluorouracil. All three drugs were active against a panel of seasonal H3N2 and laboratory-adapted H1N1 strains. We found that each drug increased the frequency of mutations in influenza virus populations and decreased the virus' specific infectivity, indicating a mutagenic mode of action. We were able to drive viral populations to extinction by passaging influenza virus in the presence of each drug, indicating that complete lethal mutagenesis of influenza virus populations can be achieved when a sufficient mutational burden is applied. Population-wide resistance to these mutagenic agents did not arise after serial passage of influenza virus populations in sublethal concentrations of drug. Sequencing of these drug-passaged viral populations revealed genome-wide accumulation of mutations at low frequency. The replicative capacity of drug-passaged populations was reduced at higher multiplicities of infection, suggesting the presence of defective interfering particles and a possible barrier to the evolution of resistance. Together, our data suggest that lethal mutagenesis may be a particularly effective therapeutic approach with a high genetic barrier to resistance for influenza virus.IMPORTANCEInfluenza virus is an RNA virus that causes significant morbidity and mortality during annual epidemics. Novel therapies for RNA viruses are needed due to the ease with which these viruses evolve resistance to existing therapeutics. Lethal mutagenesis is a broad-spectrum strategy that exploits the high mutation rate and the low mutational tolerance of most RNA viruses. It is thought to possess a higher barrier to resistance than conventional antiviral strategies. We investigated the effectiveness of lethal mutagenesis against influenza virus using three different drugs. We showed that influenza virus was sensitive to lethal mutagenesis by demonstrating that all three drugs induced mutations and led to an increase in the generation of defective viral particles. We also found that it may be difficult for resistance to these drugs to arise at a population-wide level. Our data suggest that lethal mutagenesis may be an attractive anti-influenza strategy that warrants further investigation.
APA, Harvard, Vancouver, ISO, and other styles
10

Xu, Hao, Zekuan Xu, Jianghao Xu, and Yang Shao. "Exploration of drug resistance in advanced gastrointestinal stromal tumor." Journal of Clinical Oncology 40, no. 4_suppl (2022): 662. http://dx.doi.org/10.1200/jco.2022.40.4_suppl.662.

Full text
Abstract:
662 Background: Gastrointestinal stromal tumors (GISTs) are prone to multi-drug resistance after drug treatment, but tissue samples from advanced patients with drug resistance are hard to obtain, impeding the study of the mechanism of drug resistance. In this study, plasma samples from TKI-resistant GIST patients were collected for next generation sequencing (NGS) to detect circulating tumor DNA (ctDNA), which were then used to generate mutation profiles leading to TKI resistance. Methods: A total of 82 GIST patients who acquired TKI resistance were enrolled from Apr. 2016 to Jun. 2021. Plasma ctDNA samples after drug resistance were collected for NGS analysis of 425 genes. Results: Among 82 patients, 54 received monotherapy with imatinib, 24 with 2 TKIs (21 with imatinib and subsequent sunitinib, 2 with imatinib subsequent regorafenib, and 1 with imatinib subsequent anlotinib), and 4 with 3 TKIs (imatinib subsequent sunitinib and regorafenib). Fifty patients (61%) were ctDNA-positive and their mutation profiles were further analyzed. Detection rate of ctDNA in imatinib-resistant patients was 57% (31/54). Among these 31 patients, 12 (39%) showed KIT gene mutation (8 with the known drug-resistant KIT mutations, 6 of these patients exhibited single-drug resistance while 2 showed multi-drug resistance due to KIT mutations mainly in Exon 13 V654A, Exons 17 Y823D, D820Y, N822Y, and N822K). The remaining 19/31 cases (61%) could be attributed to other gene mutations, with 47% due to cancer-associated mutations or other downstream signaling pathways (such as, cell cycle, TP53, RAS and PI3K). Among patients resistant to imatinib followed by other TKIs, ctDNA detection rate was 68% (19/28). Among these 19 patients, 10 (53%) showed KIT gene mutation (including 5 with the known drug-resistant KIT mutations, 4 of these patients exhibited single-drug resistance, while 1 showed multi-drug resistance due to mutations mainly in Exon 13 V654A, Exons 17 D820A, and D820G). The remaining 9/19 cases (47%) could be attributed to other gene mutations, with 44% due to cancer-associated mutations or other in downstream signaling pathways (such as Wnt, cell cycle, TP53, RAS and PI3K). Results indicated a growing trend of mutations leading to resistance among GIST patients treated with multiple TKIs (baseline vs. imatinib resistance vs. multiple TKIs resistance, 3.95% vs. 25.81% vs. 26.32%). Conclusions: Advanced GIST patients who received one or more TKI(s) may be resistant to single or multiple drugs due to complex mutations. NGS can be used to detect ctDNA without the need to obtain tumor tissue samples. This approach facilitates the monitoring of drug resistance in patients with advanced tumors, especially those with multiple metastases. NGS allows detection of mutations at multiple secondary sites and helps to overcome tumor heterogeneity, ctDNA-based NGS analysis will play an increasingly important role in assessment of drug resistance in GIST patients.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Drug resistance mutation"

1

Liu, Fengling. "Kinetic and Crystallographic Studies of Drug-Resistant Mutants of HIV-1 Protease: Insights into the Drug Resistance Mechanisms." Digital Archive @ GSU, 2007. http://digitalarchive.gsu.edu/biology_diss/19.

Full text
Abstract:
HIV-1 protease (PR) inhibitors (PIs) are important anti-HIV drugs for the treatment of AIDS and have shown great success in reducing mortality and prolonging the life of HIV-infected individuals. However, the rapid development of drug resistance is one of the major factors causing the reduced effectiveness of PIs. Consequently, various drug resistant mutants of HIV-1 PR have been extensively studied to gain insight into the mechanisms of drug resistance. In this study, the crystal structures, dimer stabilities, and kinetics data have been analyzed for wild type PR and over 10 resistant mutants including PRL24I, PRI32V, PRM46L, PRG48V, PRI50V, PRF53L, PRI54V, PRI54M, PRG73S and PRL90M. These mutations lie in varied structural regions of PR: adjacent to the active site, in the inhibitor binding site, the flap or at protein surface. The enzymatic activity and inhibition were altered in mutant PR to various degrees. Crystal structures of the mutants complexed with a substrate analog inhibitor or drugs indinavir, saquinavir and darunavir were determined at resolutions of 0.84 – 1.50 Å. Each mutant revealed distinct structural changes, which are usually located at the mutated residue, the flap and inhibitor binding sites. Moreover, darunavir was shown to bind to PR at a new site on the flap surface in PRI32V and PRM46L. The existence of this additional inhibitor binding site may explain the high effectiveness of darunavir on drug resistant mutants. Moreover, the unliganded structure PRF53L had a wider separation at the tips of the flaps than in unliganded wild type PR. The absence of flap interactions in PRF53L suggests a novel mechanism for drug resistance. Therefore, this study enhanced our understanding of the role of individual residues in the development of drug resistance and the structural basis of drug resistance mechanisms. Atomic resolution crystal structures are valuable for the design of more potent protease inhibitors to overcome the drug resistance problem.
APA, Harvard, Vancouver, ISO, and other styles
2

Hayes, Cindy. "Prevalence and resistance gene mutations of multi-drug resistant and extensively drug resistant mycobacterium tuberculosis in the Eastern Cape." Thesis, Nelson Mandela Metropolitan University, 2014. http://hdl.handle.net/10948/d1020374.

Full text
Abstract:
The emergence and spread of multi-drug resistant (MDR-TB) and extensively drugresistant tuberculosis (XDR-TB) are a major medical and public problem threatening the global health. The objectives of this study were to (i) determine the prevalence of MDR-TB and XDR-TB in the Eastern Cape; (ii) analyze patterns of gene mutations in MDR-TB and (iii) identify gene mutations associated with resistance to second line injectable drugs in XDR-TB isolates. A total of 1520 routine sputum specimens sequentially received within a period of 12 months i.e. February 2012 to February 2013 from all MDR-TB and XDR-TB patients treated by Hospitals and clinics in the Eastern Cape were included in this study, of which 1004 had interpretable results. Samples were analyzed with the Genotype MTBDRplus VER 2.0 assay kit (Hain Lifescience) for detection of resistance to Rifampicin and Isoniazid while solid and liquid culture drug susceptibility tests were used for ethambutol, streptomycin, ethionamide, ofloxacin, capreomycin and amikacin. PCR and sequence analysis of short regions of target genes gyrA, (encode subunit of DNA topoisomerase gyrase), rrs (16S rRNA) and tlyA (encodes a 2’-O-methyltransferase) were performed on 20 XDR-TB isolates. MTBDRplus kit results and drug susceptibility tests identified 462 MDR-TB, 284 pre-XDR and 258 XDR-TB isolates from 267 clinics and 25 hospitals in the Eastern Cape. There was a high frequency of resistance to streptomycin, ethionamide, amikacin, ofloxacin and capreomycin. Mutation patterns indicated differences between the health districts as well as differences between the facilities within the health districts. The most common mutation patterns observed were: (i) ΔWT3, ΔWT4, MUT1 [D516V+del515] (rpoB), ΔWT, MUT1 [S315T1] (katG), ΔWT1 [C15T] (inhA) [39 MDR, 204 XDR-TB and 214 pre XDR-TB isolates], (ii) ΔWT8, MUT3 [L533P+S531L] (rpoB), ΔWT, MUT1 [S315T1] [145 MDR, 18 pre-XDR and 3 XDR-TB solates] and (iii) ΔWT3, WT4 [D516Y+del515] (rpoB), ΔWT, MUT1 [S315T1] (katG) [75 MDR, 1 pre-XDR and 7 XDR-TB isolates]. Mutations in inhA promoter regions were strongly associated with XDR-TB isolates. Two thirds (66.6 percent (669/1004) of the isolates had inhA mutations present with 25.4 percent (170/669) found among the MDR isolates, 39.2 percent (262/669) among the pre-XDR isolates and 35.4 percent (237/669) among the XDR-TB isolates, which implies that these resistant isolates are being spread by transmission within the community and circulating in the province. There was good correlation between XDR-TB drug susceptibility test results and sequence analyses of the gyrA and rrs genes. The majority of XDR-TB isolates contained mutations at positions C269T (6/20) and 1401G (18/20) in gyrA and rrs genes respectively. Sequence analysis of short regions of gyrA and rrs genes may be useful for detection of fluoroquinolone and amikacin/ kanamycin resistance in XDR-TB isolates but the tlyA gene is not a sensitive genetic marker for capreomycin resistance. This study highlighted the urgent need for the development of rapid diagnostics for XDR-TB and raised serious concerns regarding ineffective patientmanagement resulting in ongoing transmission of extremely resistant strains of XDRTB in the Eastern Cape suggesting that the Eastern Cape could be fast becoming the epicenter for the development of Totally Drug-resistant Tuberculosis (TDR-TB) in South Africa.
APA, Harvard, Vancouver, ISO, and other styles
3

Chan, Kin Tak. "Investigations of p53 mutations and effects on drug resistance /." View abstract or full-text, 2003. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202003%20CHAN.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Svedhem, Johansson Veronica. "Kinetics of HIV-1 drug resistance mutations in vivo /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-671-9/.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Fearon, Abbie Elizabeth. "Dissection of drug resistance mechanisms in FGFR2 mutant endometrial cancer." Thesis, Queen Mary, University of London, 2015. http://qmro.qmul.ac.uk/xmlui/handle/123456789/9027.

Full text
Abstract:
Mutations in FGFR2 are common in a subset of endometrial carcinomas. Given the emergence of small molecule inhibitors specific to this receptor tyrosine kinase, FGFR2 is an attractive therapeutic target. However, compensatory and adaptation mechanisms limit the clinical utility of compounds that target nodes in the receptor tyrosine kinase network. Here, we analysed the impact of FGFR inhibition in endometrial cancer cells and observed the emergence of a resistant population in an FGFR2-mutant cell line. To understand the mechanisms underlying this adaptation response, we used a phosphoproteomics approach to measure the kinase network in an unbiased manner. These experiments led to the identification of an AKT-related compensatory mechanism underpinning this resistance. Further dissection of this resistance mechanism utilising gene expression analysis showed PHLDA1, a negative regulator of AKT, was significantly down-regulated in resistant cells. This was further confirmed at the protein level. siRNA knockdown of PHLDA1 conferred immediate drug resistance in the FGFR2-mutant endometrial cancer cell line. Therefore, we identified PHLDA1 down-regulation as a mediator of drug resistance in FGFR2 mutant cancer cells, the first demonstration of the role of PHLDA1 in the acquisition and maintenance of drug resistance. Using a 3D physiomimetic model, we demonstrated that AKT inhibition alone also led to generation of a drug-resistant population. Most importantly, dual-drug therapy inhibited proliferation and induced cell death. Our data highlight how mass spectrometry and microarray gene expression analysis can complement each other in the identification of novel resistance mechanisms in cancer cells. These data suggest that combination treatment of FGFR2-mutant endometrial cancers, targeting both FGFR2 and AKT, represents a promising therapeutic approach.
APA, Harvard, Vancouver, ISO, and other styles
6

Zelnikar, Mojca. "Evolution of drug resistance in influenza A viruses." Thesis, University of Edinburgh, 2015. http://hdl.handle.net/1842/16203.

Full text
Abstract:
Influenza A viruses are important pathogens of humans, other mammals and birds. Swine are considered to be the ‘mixing vessel’ for influenza viruses because of their susceptibility to infection with not only swine influenza viruses but also human and avian influenza viruses. After infection of pigs with different influenza viruses, reassortment events between genomic RNA segments and point mutations can take place which can result in novel influenza virus strains capable of causing human pandemics. To combat infections, vaccination is available in many countries for humans, but not typically used in pigs. However, anti-influenza drugs have been used to treat livestock, and mutations conferring drug resistance occur in circulating strains. The mechanisms responsible for the emergence and spread of drug resistant mutations against amantadine and oseltamivir have been studied previously but often gave conflicting results. Therefore, this PhD thesis focused on resolving the mechanisms responsible for this rapid drug resistance spread. In chapter one I examine the extent of reassortment events in swine influenza A viruses by analysing within subtype reassortment and extrapolating the results for the between subtype reassortment. Reassortment is one of the mechanisms that can be responsible for mutations, conferring resistance to drugs, to spread between strains, and thus spread in the host population. The findings of this chapter show that the genomic segments most prone to reassortment code for a polymerase (PB1) and both glycoproteins, within all three subtypes studied. Since particular mutations in the matrix protein (MP) segment cause resistance to amantadine, my study focused on MP compared to other segments and revealed moderate level of reassortment. MP reassorts well with polymerases, both within and between subtype, while nonstructural (NS) is least likely to reassort. Chapter two of this thesis aimed at resolving the origin and spread of the most common drug resistance conferring mutation in swine influenza viruses which causes amantadine resistance. I show first that this mutation occurred in swine influenza viruses and was therefore not transmitted from the recently ancestral avian influenza strains, and second that the prevalence of resistance in swine influenza viruses is due to functional linkage of mutations at other sites and not by direct drug pressure. In chapter three I examine the mechanisms responsible for the rapid rise and spread of oseltamivir resistance in human influenza H1N1 viruses which arose in the absence of drug use. The primary mutation lies in the neuraminidase glycoprotein but because of the close functional interaction I focus on changes in haemagglutinin that occurred in association with resistance. The results showed several mutations in haemagglutinin were associated with resistance suggesting selection acting on haemagglutinin in order to balance the activity of both glycoproteins. Overall these results show the importance of functional linkage between segments as a mechanism for the occurrence of drug resistance conferring mutations, and reassortment as a means of spreading these mutations into newly emerging strains.
APA, Harvard, Vancouver, ISO, and other styles
7

Cousin, Sydney Louis. "Macrolide resistance in Neisseria gonorrhoeae /." Thesis, Connect to this title online; UW restricted, 2003. http://hdl.handle.net/1773/5078.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Hales, Jason J. "Development of antibiotic resistance due to chromosomal mutation caused by AH26 endodontic sealer." Morgantown, W. Va. : [West Virginia University Libraries], 2002. http://etd.wvu.edu/templates/showETD.cfm?recnum=2304.

Full text
Abstract:
Thesis (M.S.)--West Virginia University, 2002.
AH26 is a registered trademark. Title from document title page. Document formatted into pages; contains vii, 55 p. : ill. (some col.). Includes a video file in the AVI format. Vita. Includes abstract. Includes bibliographical references (p. 48-53).
APA, Harvard, Vancouver, ISO, and other styles
9

Werngren, Jim. "Rapid assessment of drug susceptibility and mutation to resistance in mycobacterium tuberculosis Beijing type /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7357-024-9/.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Paulander, Wilhelm. "Mechanisms of adaptation to the fitness cost of antibiotic resistance /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-149-4/.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Drug resistance mutation"

1

Shamputa, Isdore Chola. Report on the detection of mutations in mycobacterium tuberculosis genes associated with drug resistance: From 21 January to 20 April, 1998. Tropical Diseases Research Centre, 1998.

APA, Harvard, Vancouver, ISO, and other styles
2

Larry, Jameson J., ed. Hormone resistance syndromes. Humana Press, 1999.

APA, Harvard, Vancouver, ISO, and other styles
3

Jameson, J. Larry. Hormone Resistance Syndromes. Humana, 2013.

APA, Harvard, Vancouver, ISO, and other styles
4

(Editor), Ulf Dieckmann, Johan A. J. Metz (Editor), Maurice W. Sabelis (Editor), and Karl Sigmund (Editor), eds. Adaptive Dynamics of Infectious Diseases: In Pursuit of Virulence Management (Cambridge Studies in Adaptive Dynamics). Cambridge University Press, 2005.

APA, Harvard, Vancouver, ISO, and other styles
5

Adaptive Speciation (Cambridge Studies in Adaptive Dynamics). Cambridge University Press, 2004.

APA, Harvard, Vancouver, ISO, and other styles
6

Adaptive Dynamics of Infectious Diseases: In Pursuit of Virulence Management. Cambridge University Press, 2002.

APA, Harvard, Vancouver, ISO, and other styles
7

1966-, Dieckmann Ulf, ed. Adaptive speciation. Cambridge University Press, 2004.

APA, Harvard, Vancouver, ISO, and other styles
8

Thursfield, Rebecca, Chris Orchard, Rosanna Featherstone, and Jane C. Davies. Future treatments. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198702948.003.0013.

Full text
Abstract:
There are only a relatively limited armoury of drugs, the majority of which are aimed at downstream symptoms of cystic fibrosis. Therapies targeting the basic defect in CF as well as continued availability of more conventional drugs are required. Progress in gene therapy has been limited by the significant barriers to gene transfer of the CF lung, but the UK is hosting a large repeated dose trial of nebulized non-viral gene therapy designed around clinically meaningful outcomes. The UK CF Gene Therapy Consortium is also seeking to develop a promising modified lentiviral approach, although this is some years off. Perhaps the exciting development of recent decades has come from small molecule CFTR modulators, driven by an understanding of basic pathophysiological mechanisms. Ivacaftor is the first drug to be licensed, having proved itself highly clinically efficacious in patients with the class-3 gating mutation G551D. The trial pipeline seeks to expand indications for this and to explore the potential of Phe508del correctors. Finally, a number of anti-inflammatory and anti-infective strategies are being pursued. The emerging global problem of antibiotic resistance is leading to exciting alternatives such as biofilm disruption and bacteriophage to be explored.
APA, Harvard, Vancouver, ISO, and other styles
9

Ben-Tal, Nir, Daisuke Kihara, and Arun Prasad Pandurangan, eds. Computational Approaches to Study the Impact of Mutations on Disease and Drug Resistance. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88974-212-7.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "Drug resistance mutation"

1

Rund, Deborah, Idit Azar, and Olga Shperling. "A Mutation in the Promoter of the Multidrug Resistance Gene (MDR1) in Human Hematological Malignancies may Contribute to the Pathogenesis of Resistant Disease." In Drug Resistance in Leukemia and Lymphoma III. Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4811-9_9.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Gelmann, Edward P. "Androgen Receptor Mutations in Prostate Cancer." In Drug Resistance. Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-1267-3_12.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Bonomo, Robert A. "Mutations as a Basis of Antimicrobial Resistance." In Antimicrobial Drug Resistance. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-46718-4_6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Babic, Maja, and Robert A. Bonomo. "Mutations as a Basis of Antimicrobial Resistance." In Antimicrobial Drug Resistance. Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-180-2_6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Lao, Thuan Duc, Hung Chi Lieu, Thuy Thanh Thi Ho, and Thuy Ai Huyen Le. "Evaluation of the HBV Genotype, Viral Load and Antivirus Drug Resistance Mutation in Tay Ninh Hospital, Vietnam by Real-Time PCR." In IFMBE Proceedings. Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-5859-3_103.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Bikker, Jack Andrew. "Chapter 5. Kinase Mutations and Resistance in Cancer." In Drug Discovery. Royal Society of Chemistry, 2011. http://dx.doi.org/10.1039/9781849733557-00126.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Louw, Gail E., and Samantha L. Sampson. "Implications of Chromosomal Mutations for Mycobacterial Drug Resistance." In Drug Resistance in Bacteria, Fungi, Malaria, and Cancer. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-48683-3_10.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Dhillon, Kiranjit K., and Toshiyasu Taniguchi. "Resistance to PARP Inhibitors Mediated by Secondary BRCA1/2 Mutations." In Cancer Drug Discovery and Development. Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-14151-0_18.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Martis, Elvis A. F., and Evans C. Coutinho. "Free Energy-Based Methods to Understand Drug Resistance Mutations." In Challenges and Advances in Computational Chemistry and Physics. Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-05282-9_1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Kozyryev, Ivan, and Jing Zhang. "Bayesian Analysis of Complex Interacting Mutations in HIV Drug Resistance and Cross-Resistance." In Advances in Experimental Medicine and Biology. Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-017-9245-5_22.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Drug resistance mutation"

1

"Detecting Interacting Mutation Clusters in HIV-1 Drug Resistance." In International Conference on Bioinformatics Models, Methods and Algorithms. SciTePress - Science and and Technology Publications, 2013. http://dx.doi.org/10.5220/0004238800340043.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Duan, Baobin, Bin Zou, Debby D. Wang, Hong Yan, and Lixin Han. "Computational Evaluation of EGFR Dynamic Characteristics in Mutation-Induced Drug Resistance Prediction." In 2015 IEEE International Conference on Systems, Man, and Cybernetics (SMC). IEEE, 2015. http://dx.doi.org/10.1109/smc.2015.402.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Fang, Yueh-Fu, Chun-Yu Lin, and Peichih Lee. "Abstract 2940: The p53 mutation R273H contributed to drug resistance of EGFR tyrosine kinase inhibitors." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2940.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Tan, Jian Jun, Ting Guang Sun, Wei Zu Chen, and Cun Xin Wang. "Molecular Dynamics Simulation of HIV-1 gp41 and the N554D/S649A Double Mutation for Drug Resistance to Enfuvirtide." In 2009 3rd International Conference on Bioinformatics and Biomedical Engineering (iCBBE). IEEE, 2009. http://dx.doi.org/10.1109/icbbe.2009.5163084.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Chen, W., H. Luo, Z. Mai, et al. "P132 A novel PCR-CRISPR based diagnosis for Treponema pallidum detection, genotyping, and drug-resistance mutation identification in real-time." In Abstracts for the STI & HIV World Congress, July 14–17 2021. BMJ Publishing Group Ltd, 2021. http://dx.doi.org/10.1136/sextrans-2021-sti.246.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Tokarsky, Jack P., Jesse Crow, Lillian Guenther, Emily Theisen, Kimberly Stegmaier, and Stephen Lessnick. "Abstract PO-041: Genome-wide CRISPR/Cas9 screen reveals mitochondrial gene mutation as a driver for drug resistance in Ewing sarcoma." In Abstracts: AACR Special Virtual Conference on Epigenetics and Metabolism; October 15-16, 2020. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.epimetab20-po-041.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Kakiuchi, Soji, Seiji Yano, Wei Wang, et al. "Abstract A178: Role of tumor and host‐derived HGF in drug resistance to EGFR inhibitors in EGFR activating mutation‐positive lung cancer." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-a178.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Schaefer, Gabriele, Emily J. Hanan, Emily Chan, et al. "Abstract 1735: Discovery of novel and selective reversible inhibitors of EGFR containing the T790M drug resistance mutation with activity in vitro and in vivo." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-1735.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Pierro, Joanna, Jason Saliba, Sonali Narang, et al. "Abstract 5399: The NSD2 p.E1099K mutation is enriched at relapse and confers drug resistance in a cell context dependent manner in pediatric acute lymphoblastic leukemia." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-5399.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Cheng, Betty Y., and Jaime G. Carbonell. "Automatic Detection of HIV Drug Resistance-Associated Mutations." In 2010 International Conference on Machine Learning and Applications (ICMLA). IEEE, 2010. http://dx.doi.org/10.1109/icmla.2010.83.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Drug resistance mutation"

1

Perelson, A. S., B. Goldstein, and B. T. Korber. Emerging pathogens: Dynamics, mutation and drug resistance. Office of Scientific and Technical Information (OSTI), 1997. http://dx.doi.org/10.2172/534529.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

McKenzie, Gregory. Role of the SOS Response in Stationary-Phase Hypermutation: A Model for Mutation in Oncogenesis and Chemotherapeutic Drug-Resistance. Defense Technical Information Center, 2002. http://dx.doi.org/10.21236/ada408280.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

McKenzie, Gregory. Role of the SOS Response in Stationary-Phase Hypermutation: A Model for Mutation in Oncogenesis and Chemotherapeutic Drug-Resistance. Defense Technical Information Center, 2000. http://dx.doi.org/10.21236/ada390995.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Yusim, Karina, Bette T. M. Korber, Shihai Feng, and Chang-Shung Tung. Compensatory mutation in RpoC restores fitness to rifampicin-resistant multi-drug resistant Mycobacterium tuberculosis. Office of Scientific and Technical Information (OSTI), 2012. http://dx.doi.org/10.2172/1049993.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Jorgensen, Frieda, Andre Charlett, Craig Swift, Anais Painset, and Nicolae Corcionivoschi. A survey of the levels of Campylobacter spp. contamination and prevalence of selected antimicrobial resistance determinants in fresh whole UK-produced chilled chickens at retail sale (non-major retailers). Food Standards Agency, 2021. http://dx.doi.org/10.46756/sci.fsa.xls618.

Full text
Abstract:
Campylobacter spp. are the most common bacterial cause of foodborne illness in the UK, with chicken considered to be the most important vehicle for this organism. The UK Food Standards Agency (FSA) agreed with industry to reduce Campylobacter spp. contamination in raw chicken and issued a target to reduce the prevalence of the most contaminated chickens (those with more than 1000 cfu per g chicken neck skin) to below 10 % at the end of the slaughter process, initially by 2016. To help monitor progress, a series of UK-wide surveys were undertaken to determine the levels of Campylobacter spp. on whole UK-produced, fresh chicken at retail sale in the UK. The data obtained for the first four years was reported in FSA projects FS241044 (2014/15) and FS102121 (2015 to 2018). The FSA has indicated that the retail proxy target for the percentage of highly contaminated raw whole retail chickens should be less than 7% and while continued monitoring has demonstrated a sustained decline for chickens from major retailer stores, chicken on sale in other stores have yet to meet this target. This report presents results from testing chickens from non-major retailer stores (only) in a fifth survey year from 2018 to 2019. In line with previous practise, samples were collected from stores distributed throughout the UK (in proportion to the population size of each country). Testing was performed by two laboratories - a Public Health England (PHE) laboratory or the Agri-Food & Biosciences Institute (AFBI), Belfast. Enumeration of Campylobacter spp. was performed using the ISO 10272-2 standard enumeration method applied with a detection limit of 10 colony forming units (cfu) per gram (g) of neck skin. Antimicrobial resistance (AMR) to selected antimicrobials in accordance with those advised in the EU harmonised monitoring protocol was predicted from genome sequence data in Campylobacter jejuni and Campylobacter coli isolates The percentage (10.8%) of fresh, whole chicken at retail sale in stores of smaller chains (for example, Iceland, McColl’s, Budgens, Nisa, Costcutter, One Stop), independents and butchers (collectively referred to as non-major retailer stores in this report) in the UK that are highly contaminated (at more than 1000 cfu per g) with Campylobacter spp. has decreased since the previous survey year but is still higher than that found in samples from major retailers. 8 whole fresh raw chickens from non-major retailer stores were collected from August 2018 to July 2019 (n = 1009). Campylobacter spp. were detected in 55.8% of the chicken skin samples obtained from non-major retailer shops, and 10.8% of the samples had counts above 1000 cfu per g chicken skin. Comparison among production plant approval codes showed significant differences of the percentages of chicken samples with more than 1000 cfu per g, ranging from 0% to 28.1%. The percentage of samples with more than 1000 cfu of Campylobacter spp. per g was significantly higher in the period May, June and July than in the period November to April. The percentage of highly contaminated samples was significantly higher for samples taken from larger compared to smaller chickens. There was no statistical difference in the percentage of highly contaminated samples between those obtained from chicken reared with access to range (for example, free-range and organic birds) and those reared under standard regime (for example, no access to range) but the small sample size for organic and to a lesser extent free-range chickens, may have limited the ability to detect important differences should they exist. Campylobacter species was determined for isolates from 93.4% of the positive samples. C. jejuni was isolated from the majority (72.6%) of samples while C. coli was identified in 22.1% of samples. A combination of both species was found in 5.3% of samples. C. coli was more frequently isolated from samples obtained from chicken reared with access to range in comparison to those reared as standard birds. C. jejuni was less prevalent during the summer months of June, July and August compared to the remaining months of the year. Resistance to ciprofloxacin (fluoroquinolone), erythromycin (macrolide), tetracycline, (tetracyclines), gentamicin and streptomycin (aminoglycosides) was predicted from WGS data by the detection of known antimicrobial resistance determinants. Resistance to ciprofloxacin was detected in 185 (51.7%) isolates of C. jejuni and 49 (42.1%) isolates of C. coli; while 220 (61.1%) isolates of C. jejuni and 73 (62.9%) isolates of C. coli isolates were resistant to tetracycline. Three C. coli (2.6%) but none of the C. jejuni isolates harboured 23S mutations predicting reduced susceptibility to erythromycin. Multidrug resistance (MDR), defined as harbouring genetic determinants for resistance to at least three unrelated antimicrobial classes, was found in 10 (8.6%) C. coli isolates but not in any C. jejuni isolates. Co-resistance to ciprofloxacin and erythromycin was predicted in 1.7% of C. coli isolates. 9 Overall, the percentages of isolates with genetic AMR determinants found in this study were similar to those reported in the previous survey year (August 2016 to July 2017) where testing was based on phenotypic break-point testing. Multi-drug resistance was similar to that found in the previous survey years. It is recommended that trends in AMR in Campylobacter spp. isolates from retail chickens continue to be monitored to realise any increasing resistance of concern, particulary to erythromycin (macrolide). Considering that the percentage of fresh, whole chicken from non-major retailer stores in the UK that are highly contaminated (at more than 1000 cfu per g) with Campylobacter spp. continues to be above that in samples from major retailers more action including consideration of interventions such as improved biosecurity and slaughterhouse measures is needed to achieve better control of Campylobacter spp. for this section of the industry. The FSA has indicated that the retail proxy target for the percentage of highly contaminated retail chickens should be less than 7% and while continued monitoring has demonstrated a sustained decline for chickens from major retailer stores, chicken on sale in other stores have yet to meet this target.
APA, Harvard, Vancouver, ISO, and other styles
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography