<oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
  <dc:creator>Mikaberidze A</dc:creator>
  <dc:creator>Paveley N</dc:creator>
  <dc:creator>Bonhoeffer S</dc:creator>
  <dc:creator>van den Bosch F</dc:creator>
  <dc:date>2017</dc:date>
  <dc:description xmlns:ns0="xml" ns0:lang="en">Resistance to antimicrobial drugs allows pathogens to survive drug treatment. The time taken for a new resistant mutant to reach a population size that is unlikely to die out by chance is called "emergence time." Prolonging emergence time would delay loss of control. We investigate the effect of fungicide dose on the emergence time in fungal plant pathogens. A population dynamical model is combined with dose-response data for Zymoseptoria tritici, an important wheat pathogen. Fungicides suppress sensitive pathogen population. This has two effects. First, the rate of appearance of resistant mutants is reduced, hence the emergence takes longer. Second, more healthy host tissue becomes available for resistant mutants, increasing their chances to invade and accelerates emergence. In theory, the two competing effects may lead to a non-monotonic dependence of the emergence time on fungicide dose that exhibits a minimum. But according to field data, fungicides are unable to reduce the fungicide-sensitive population strongly enough even at high doses. Hence, for full resistance over realistic ranges of pathogen's life history and fungicide dose-response parameters, emergence time decreases monotonically with increasing dose. For partial resistance, there can be cases within a limited parameter range, when emergence decelerates at higher doses.</dc:description>
  <dc:format>application/pdf</dc:format>
  <dc:identifier>https://sonar.ch/global/documents/155265</dc:identifier>
  <dc:language>eng</dc:language>
  <dc:relation>info:eu-repo/semantics/altIdentifier/doi/10.1094/PHYTO-08-16-0297-R</dc:relation>
  <dc:relation>info:eu-repo/semantics/altIdentifier/pmid/28079455</dc:relation>
  <dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
  <dc:source>Phytopathology. - 2017</dc:source>
  <dc:subject xmlns:ns1="xml" ns1:lang="en">disease control</dc:subject>
  <dc:subject xmlns:ns2="xml" ns2:lang="en">epidemiology</dc:subject>
  <dc:subject xmlns:ns3="xml" ns3:lang="en">fungicide resistance</dc:subject>
  <dc:subject xmlns:ns4="xml" ns4:lang="en">host−pathogen interaction</dc:subject>
  <dc:subject xmlns:ns5="xml" ns5:lang="en">infectious disease</dc:subject>
  <dc:subject xmlns:ns6="xml" ns6:lang="en">mathematical model</dc:subject>
  <dc:subject xmlns:ns7="xml" ns7:lang="en">plant pathogens</dc:subject>
  <dc:subject xmlns:ns8="xml" ns8:lang="en">Ascomycota</dc:subject>
  <dc:subject xmlns:ns9="xml" ns9:lang="en">Azoles</dc:subject>
  <dc:subject xmlns:ns10="xml" ns10:lang="en">Drug Resistance, Fungal</dc:subject>
  <dc:subject xmlns:ns11="xml" ns11:lang="en">Fungicides, Industrial</dc:subject>
  <dc:subject xmlns:ns12="xml" ns12:lang="en">Host-Pathogen Interactions</dc:subject>
  <dc:subject xmlns:ns13="xml" ns13:lang="en">Models, Theoretical</dc:subject>
  <dc:subject xmlns:ns14="xml" ns14:lang="en">Mutation</dc:subject>
  <dc:subject xmlns:ns15="xml" ns15:lang="en">Plant Diseases</dc:subject>
  <dc:subject xmlns:ns16="xml" ns16:lang="en">Triticum</dc:subject>
  <dc:title xmlns:ns17="xml" ns17:lang="en">Emergence of Resistance to Fungicides: The Role of Fungicide Dose.</dc:title>
  <dc:type>http://purl.org/coar/resource_type/c_6501</dc:type>
</oai_dc:dc>