|Goodwin, Stephen - Steve|
Submitted to: Phytopathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/17/1996
Publication Date: N/A
Citation: N/A Interpretive Summary: Severe epidemics of late blight disease have occurred on potatoes and tomatoes in the United States and Canada since 1990. The 1993 and 1994 epidemics were particularly severe in the northeast, causing millions of dollars of damage. Many farmers were ruined economically by this disease and went out of business in 1995. Analyses with molecular markers including gDNA fingerprinting revealed the primary cause of these epidemics to be new genotypes of the fungus that were recently introduced, most likely from northwestern Mexico. Prior to these introductions, late blight was controlled by the fungicide metalaxyl. However resistance to this fungicide was detected at about the same time as the migrations occurred. The purpose of this study was to test the hypothesis that resistance to metalaxyl in populations of the late blight pathogen in the United States and Canada was introduced in the new genotypes from Mexico. Analyses of 251 isolates of the fungus collected from 1987 thru 1993 revealed that metalaxyl resistanc only occurred in genotypes that were recently introduced. The new genotypes were 100% resistant, regardless of whether they came from sprayed or unsprayed fields. Field experiments confirmed that metalaxyl alone had no effect on epidemics caused by the new, resistant genotypes. Thus resistance to metalaxyl was almost certainly introduced and there was nothing U.S. potato growers could have done to prevent its occurrence. Alerting growers about this problem will save the potato industry time & money, & hopefully avoid repetition of the devastating epidemics of 1993 and 1994. Seed potatoes should be monitored for the new genotypes to limit their migration, and fields containing them should not be sprayed with metalaxyl.
Technical Abstract: The sensitivity of 251 isolates of Phytophthora infestans to phenylamide fungicide metalaxyl was assessed using an in vitro radial growth assay on agar media. Isolates were obtained from 15 states and one Canadian province from 1987 through 1993. Isolates that grew at less than 40% of the control on 5 mg/ml metalaxyl were considered sensitive; all other isolates were scored as resistant. Isolates collected from 1987 through 1989 were sensitive. Metalaxyl-resistant isolates were detected in 13 states and in British Columbia in 1992 and 1993. With one exception, metalaxyl sensitivity was absolutely correlated with clonal lineage as determined by mating type, allozyme genotype & DNA fingerprint analysis. All isolates in the US-1 clonal lineage were sensitive. In contrast, isolates with the US-7 and US-8 clonal genotypes (probable recent immigrants from northwestern Mexico) were resistant, even those that had been isolated from fields with no history of metalaxyl application. All US-6 isolates collected since 199 have been resistant, but one sensitive US-6 isolate was detected in California in 1989. The cause of this polymorphism within US-6 could not be determined. Metalaxyl alone had no effect on epidemics caused by US-6 and US-8 in two independent field experiments; isolates scored as resistant in vitro were also resistant in vivo. These data strongly support the hypothesis that resistance to metalaxyl in P infestans in the United States and Canada originated by migration from northwestern Mexico, and thus there was probably nothing that U.S. potato growers could have done to prevent the development of resistance.