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The Roles of Three Fungicides in the Epidemiology of Potato Late Blight H. Mayton, G. A. Forbes, E. S. G. Mizubuti, and W. E. Fry, Department of Plant Pathology, Cornell University, Ithaca, NY 14853

ABSTRACT Mayton, H., Forbes, G. A., Mizubuti, E. S. G., and Fry, W. E. 2001. The roles of three fungicides in the epidemiology of potato late blight. Plant Dis. 85:1006-1012. Three fungicides were tested in the field for efficacy on late blight caused by Phytophthora infestans. The effects of these fungicides on epidemic development, lesion growth rate and sporulation were measured. No fungicide completely arrested epidemic development under the environmental conditions of these experiments. However, the fungicide mixture, propamocarb hydrochloride plus chlorothalonil, had the most suppressive effect of the fungicides tested. The mechanism of effect included suppression of disease progress and lesion expansion. Growth chamber studies demonstrated that 24ºC compared to 10 or 16ºC limited cymoxanil efficacy.

The widespread occurrence of metalaxyl-resistant strains of Phytophthora infestans in the United States and Canada (14) reduced or eliminated the “postinfection” efficacy of metalaxyl as a strategic management tool to suppress late blight infections. Metalaxyl is very effective against sensitive strains and when applied early could suppress an epidemic (10). The immediate effect on epidemic progress was achieved through suppression of lesion expansion (2) and possibly by prevention of latent infections. Effects that also contributed to suppression of established epidemics were reduced sporulation from lesions, and prevention of sporangium germination and subsequent infection (2). However, against resistant strains of P. infestans, metalaxyl alone has little or no detectable effect on epidemic development (14). Metalaxyl-resistant strains were first reported in the United States by Deahl et al. (8) in 1992. They indicated that resistance was present in the western United States in 1989 and that strains were members of the US-6 clonal lineage (14). Since the late 1980s, several other metalaxyl-resistant strains including US-8, the predominant lineage found on potatoes during the late 1990s, were introduced into the United States. In addition to their metalaxyl resisCorresponding author: H. Mayton E-mail: [email protected] Current address of G. A. Forbes: International Potato Center (CIP) P.O. 17-21-1977, Quito, Ecuador. Current address of E. S. G. Mizubuti: Departamento de Fitopatologia, Universidade Federal de Vicosa, 36571-000 Vicosa, MG, Brazil. Accepted for publication 6 June 2001. Publication no. D-2001-0723-01R © 2001 The American Phytopathological Society

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tance, the introduced strains are also more aggressive than the previously dominant US-1 lineage (17,20). Furthermore, some lineages, most likely generated in the United States via sexual recombination (such as the US-11 clonal lineage), are also metalaxyl-resistant (11). In 1994, severe epidemics caused by exotic, metalaxyl-resistant strains of P. infestans throughout the eastern half of the United States and Canada created an urgent need for systemic fungicides that had postinfection efficacy. Except for metalaxyl, no fungicide labeled for late blight suppression in the United States in 1994 had useful postinfection efficacy. Compounds with some systemic activity and presumed postinfection efficacy had been used in Europe, and three of these fungicides were granted emergency temporary registrations by the Environmental Protection Agency (section 18). These registrations were granted individually to potatogrowing states in 1995 and for several subsequent years. These fungicides were: Tattoo C (31% propamocarb hydrochloride plus 31% chlorothalonil), Curzate M8 (8% cymoxanil plus 64% mancozeb), and Acrobat MZ (9% dimethomorph plus 60% mancozeb). The systemic components of Tattoo C, Curzate M8, and Acrobat MZ are propamocarb hydrochloride, cymoxanil, and dimethomorph, respectively. The mixing partners in the formulated products chlorothalonil and mancozeb have been registered for late blight control for years. In research trials throughout the United States, each of these fungicides effectively controlled late blight when applied preventively, but were not necessarily more effective than some of the currently registered fungicides, such as mancozeb or chlorothalonil. The efficacy of the three compounds varied among regions (15,19). Postinfection efficacy of some of these compounds has been demonstrated in greenhouse and growth chamber evaluations (16).

The initial objective of this paper was to test the hypothesis that propamocarb hydrochloride mixed with chlorothalonil and cymoxanil mixed with chlorothalonil would have some suppressive effect on foliar infections in the field. Our initial approach was to evaluate the effect of these fungicides on epidemics in small plots of potatoes in field tests. We further hypothesized that if these fungicides did suppress late blight epidemics, this inhibition would be achieved at least partially by suppression of lesion expansion and sporulation. Therefore we also measured these parameters in the field plots. Another objective emerged during these investigations, which was to examine the role of temperature on the efficacy of cymoxanil. MATERIALS AND METHODS Isolate and inoculum preparation. An isolate (US940480) of the US-8 clonal lineage of P. infestans originally obtained from potato leaves in New York in 1994, and subsequently stored at Cornell and deposited at the American Type Culture Collection (208834), was used for all experiments. Isolate US940480 is A2 mating type, highly pathogenic to potatoes and resistant to metalaxyl (13). Cultures were maintained on Rye B agar (4) at 18ºC. Sporangia used for inoculations were harvested from sporulating lesions on detached leaflets of the susceptible potato cultivar Norchip or Superior by rinsing the lesions with distilled water. The resulting sporangial suspension was chilled at 4ºC for 2 to 4 h to induce zoospore formation prior to each inoculation. Field plots. All field experiments were done at a site adjacent to the Homer C. Thompson Research Farm of Cornell University in Freeville, NY. In 1997 and 1998, the cultivar Superior was used, and in 1999, the cultivar Atlantic was used. Potato seed pieces were planted 23 cm apart within the row on 20 June (1997), 29 June (1998), and 19 June (1999). Each year at planting, a 13-13-13 blend of nitrogen, phosphorus, and potassium (N-P-K) fertilizer was applied at the rate of 167 kg/ha of each element. In 1998, additional nitrogen as calcium nitrate was added on 28 August and 4 September, at the rate of 6 kg/ha. In 1999, additional N-P-K (20-10-10) was added to the plots on 23 July at a rate of 45 kg/ha. Weeds were controlled by preemergent applications of Lorox (Linuron) (DuPont, Wilmington, DE) and postemergent applications of Dual II (Metalochlor, Syngenta, Greensboro, NC), both applied at

labeled rates. Plots consisted of a single row of five plants in 1997, and two rows of six plants in 1998 and 1999. A randomized complete block design with either four replicates (1997 and 1999) or three replicates (1998) was used. Plots were separated by fallow ground of at least 1 m in each direction to minimize treatment interference due to fungicide spray drift. Epidemics. Each year all plots were inoculated with 4 ml of a sporangial/ zoospore suspension, containing 150 sporangia per ml. The goal was to establish only a few lesions in each plot so that most disease resulted from secondary disease spread. Immediately prior to inoculation, plots were irrigated with an overhead sprinkler system. Experimental plots were inoculated at dusk on 14 August (1997), 14 August (1998), and 13 August (1999). After inoculation and periodically during epidemic development, plots were irrigated with the sprinkler system in the early evening for 1 to 2 h at the rate of 0.2 cm of water per hour 3 to 5 times a week. Disease assessments were made visually every 2 to 4 days using a scale derived from that developed by the Commonwealth Mycological Institute (1), as modified by Fry (9). The area under the disease progress curve (AUDPC) was calculated for each fungicide treatment using the method described by Shaner (22). The fungicides used in field experiments were either commercial formulations or tank mixtures of systemic and protectant fungicide. To limit the number of variables in our experiments, the systemic fungicides were applied with chlorothalonil as the protectant mixing partner. In 1997, we applied Tattoo C (31%) propamocarb hydrochloride plus (31%) chlorothalonil (Aventis, Bridgewater, NJ). However, in 1998 and 1999, we also used a mixture of cymoxanil (as Curzate 60 DF, Dupont, Wilmington, DE) with chlorothalonil (Bravo WS, Syngenta) in the spray tank. Fungicide applications were initiated when disease severity in the plots was estimated to be within the range of 1 to 5%. Fungicides were applied in a volume equivalent to the rate of 200 liters/ha with a hand-held CO2 pressurized (275 kPa) sprayer consisting of a boom with two XR11003VS flat fan nozzles spaced 51 cm apart. In 1997 and 1999, fungicides were applied every 3 days, and in 1998 fungicides were applied every 4 days. These intervals were more frequent than allowed in practice; however, we used them to increase the probability of observing an effect. The amounts of fungicides used were chlorothalonil (Bravo WS at 1.3 kg a.i./ha), cymoxanil mixed with chlorothalonil (Curzate 60 DF at 139 g a.i./ha and Bravo WS 1.3 kg a.i./ha), and propamocarb hydrochloride plus chlorothalonil (Tattoo C at 2.0 kg a.i./ha). The cymoxanil-plus-chlorothalonil treatment was not applied in 1997.

Expansion and sporulation of lesions in field plots. We investigated the effects of these fungicides on the expansion of established lesions in the field as a probable mechanism for suppression of an established epidemic. Experiments measuring lesion expansion were conducted in both 1998 and 1999. Lesion sizes were recorded beginning on 29 August 1998 and continued until 8 September. Initially, five randomly selected lesions ranging in size from 0.03 to 0.44 cm2 in each plot were identified and labeled with a 3.5 by 2.5 cm

paper tag. Approximately 1 h before the first fungicide application, the image of each lesion was recorded with a digital camera (Olympus Model D500L). Subsequently, images were obtained on a neardaily basis, and were recorded for four or sometimes for five days. Additional small lesions in each plot were selected periodically and measured daily until later in the epidemic when coalescence of lesions precluded the measurement of single lesions. Lesion areas were measured using UTHSCA ImageTool (University of Texas,

Fig. 1. Disease progress curves of potato late blight in small field plots as influenced by diverse fungicides. Fungicide applications were initiated at 1 to 5% disease (indicated by the arrow). Data are for A, 1997, B, 1998, and C, 1999. Fungicides were applied every 3 days in 1997 and 1999 and every 4 days in 1998. Error bars represent the standard deviation of the mean of either three (1998) or four replicates (1997, 1999) of percent foliar disease at each date. Plant Disease / September 2001 1007

San Antonio), and expansion of lesions over time was calculated. To account for variation in the distance between the leaflet and the camera, each digital image was calibrated with a 3.5 × 2.5 cm labeling tag included in each picture. In 1999, the effects of fungicides on sporulation as well as on lesion expansion were assessed. The experimental evaluation was initiated on 23 August 10 days following inoculation. Three to five lesions in each plot were tagged and lesion expansion was measured from digital pictures taken every 24 to 48 h for 4 days. After 4 days, the tagged leaflets were removed in

the morning while still wet, and placed directly into 45 ml centrifuge tubes containing 25 ml of water. Sporangia were removed by agitating the lesions in the tubes and were counted using a hemacytometer (21). The number of sporangia per unit area of infected leaf tissue was calculated. A new set of lesions was tagged on 26 August and lesion growth and sporulation were again measured as described previously. Effect of temperature on duration of the efficacy of cymoxanil. Since there was no effect of the cymoxanil-plus-chlorothalonil treatment in 1998 and little in 1999

Fig. 2. Maximum and minimum air temperatures measured during the experimental period for A, 1997, B, 1998, and C, 1999. 1008


(Fig. 1B and C), and because higher temperatures occurred in our field plots during the experimental period in both 1998 and 1999 (Fig. 2B and C), we investigated the effect of temperature on the efficacy of cymoxanil. Detached leaflets of Frito-Lay cultivar 1607 were placed at 10, 16, and 24ºC with 14 h photoperiod in growth chambers, and cymoxanil was applied at 96, 48, 24, or 12 h before inoculation or at 8, 24, 48, or 96 h after inoculation. Cymoxanil (Curzate 50 WP) was applied with an H-5 airbrush (Paasche, Harwood Heights, IL) at 112 g a.i./ha, the equivalent of the recommended application rate. Curzate 50 WP was not available for some of our field tests, so for these we used Curzate 60 DF. A fresh suspension of cymoxanil was made for each application. Two leaflets were placed, abaxial side up, in the lids of inverted petri plates containing solidified water agar (1.5%) in the base. Five petri plates, with a total of 10 leaflets, were used as replicates for each temperature-by-treatment combination. For inoculated treatments, a 10-µl drop of inoculum, containing approximately 200 zoospores, was applied to the center of each leaflet with a pipette. The petri plates were maintained in their respective incubators except when the leaflets were inoculated, sprayed with fungicide, or evaluated. Lesion area was measured on digitized images of the individual leaflets and the areas were calculated with the UTHSCSA ImageTool program as previously described. The experiment was conducted twice with similar results, and the data presented here are from one of the two trials. Statistical analyses. Statistical analyses of experimental data were performed using Statistical Analysis System 6.12 (SAS Institute, Cary, NC). Analysis of variance and Fisher’s protected least significant difference test (LSD) were conducted on treatment means of epidemic development (AUDPC), lesion expansion rates, lesion appearance in the growth chamber, and production of sporangia per unit area of infected leaf tissue in the field and growth chamber. Orthogonal contrasts were performed on treatment means for epidemic development (AUDPC). RESULTS Epidemics in small field plots. The initial experiment in 1997 indicated that propamocarb hydrochloride plus chlorothalonil (Tattoo C) had a suppressive effect on established epidemics (Fig. 1A, Table 1). Moderate temperatures favored late blight development (Fig. 2A) (7). Orthogonal contrasts indicated that when both fungicide treatments were combined in the analysis, their effect on epidemic development was not significantly different from that in the unsprayed plots (Table 2). However, when the epidemics in plots sprayed with propamocarb hydrochloride plus

chlorothalonil were compared to those in the unsprayed plots, a significant suppressive effect of propamocarb hydrochloride plus chlorothalonil was detected (Table 1). Thus, the initial experiment supported our first hypothesis that this systemic fungicide would have a suppressive effect on established epidemics. The experiment was expanded in 1998 and 1999 to include cymoxanil mixed with chlorothalonil, as well as propamocarb hydrochloride plus chlorothalonil and chlorothalonil alone. Epidemics developed very rapidly in the field plots in both 1998 and 1999, but were particularly rapid in 1999 (Fig. 1B and C). These epidemics progressed rapidly despite high temperatures during the test period in each year (Fig. 2B and C). Again, no treatment completely controlled disease development (Fig. 1B and C, Table 1). In 1998 there were no significant differences (Table 1). For example, when the effects of all fungicide treatments were combined and compared to the epidemics in unsprayed plots in 1998, orthogonal contrasts identified no significant differences (Table 3). However, epidemics in plots treated with propamocarb hydrochloride were suppressed slightly (P = 0.0525) compared to those in plots treated with cymoxanil (Fig. 1B, Table 3). In 1999, the plots treated with the systemic fungicides had a small but significant (P = 0.0213) suppressive effect on the development of established epidemics when compared to plots that were untreated or treated with chlorothalonil alone (Fig. 1C, Table 3). Effect of fungicide on lesion expansion and sporulation in field plots. Under the conditions of our field experiments, only propamocarb hydrochloride plus chlorothalonil had a consistent and significant effect on lesion expansion in the field. Untreated lesions (controls) expanded at an average rate of 1.6 cm2/day over all the trials (Table 4). Over both years, the lesion expansion rates in plots treated with chlorothalonil, or the cymoxanil plus chlorothalonil mixture, averaged 1.4 cm2/day, and these were not significantly different from the mean expansion rate of untreated lesions (1.6 cm2/day) (Table 4). However, lesions in plots treated with propamocarb hydrochloride plus chlorothalonil had a mean expansion rate of 0.9 cm2/day in 1998 and 1.0 cm2/day in 1999, each of which was significantly slower than that for any other treatment in that year. Lesions treated with chlorothalonil, those treated with cymoxanil plus chlorothalonil, and those not treated, expanded at rates that were not significantly different (Table 4). As was the case with fungicide effect on epidemic development, the fungicides had no effect on sporulation from established lesions in the field. Average sporulation among treatments ranged from 2.1 × 104 to 3.9 × 104 sporangia per cm2 of infected

tence in leaf tissue, the effect of temperature on the duration of efficacy of cymoxanil was tested. At 10 and 16ºC, applications of cymoxanil up to 96 h before inoculation prevented the appearance of most lesions, and therefore also prevented sporulation (Fig. 3A and B). How-

tissue with a high variance (LSD = 1.4 × 104) (Table 4). Effect of temperature on the duration of the efficacy of cymoxanil. No effect from cymoxanil plus chlorothalonil was observed in the field experiments, and because cymoxanil has a very short persis-

Table 1. Effects of fungicides on mean (AUDPC)w epidemic development in inoculated potato field plots in 1997, 1998, and 1999 Year Treatment Chlorx Cymox/chlory Prop/chlorz Unsprayed control LSD P value

1997

1998

1999

1677 ab – 1003 b 1840 a 741 0.0570

349 a 394 a 261 a 311 a 132 0.2011

431 a 371 b 387 ab 431 a 49 0.0428

w Area

under disease progress curve. Chlorothalonil (Bravo WS) applied at 1.3 kg a.i./ha. y Cymoxanil (Curzate 60 DF) applied at 139 g a.i./ha plus chlorothalonil (Bravo WS) applied at 1.3 kg a.i./ha. z Propamocarb hydrochloride plus chlorothalonil (Tattoo C) applied at 2.0 kg a.i./ha. x

Table 2. Orthogonal contrasts of mean (AUDPC)x epidemic development in inoculated potato field plots treated with two fungicides in 1997 Orthogonal contrast Fungicidesy vs. unsprayed Prop/chlorz vs. unsprayed x y z

MS

F value

P>F

538704.1 1400301.1

3.60 9.36

0.1162 0.0281

Area under disease progress curve. Chlorothalonil (Bravo WS) applied at 1.3 kg a.i./ha; propamocarb hydrochloride plus chlorothalonil (Tattoo C) applied at 2.0 kg a.i./ha. Propamocarb hydrochloride plus chlorothalonil (Tattoo C) applied at 2.0 kg a.i./ha.

Table 3. Orthogonal contrasts of mean (AUDPC)v epidemic development in inoculated potato field plots treated with three fungicides in 1998 and 1999 1998 Orthogonal contrast Fungicidesw vs. unsprayed Systemicsx vs. unsprayed Cymox/chlory vs. prop/chlorz

MS

F value

1320.1 578.0 26400.7

0.29 0.13 5.82

1999 P>F 0.6091 0.7334 0.0525

MS

F value

3510.6 7124.3 536.3

3.81 7.74 0.58

P>F 0.0826 0.0213 0.4649

v

Area under the disease progress curve. (Bravo WS) applied at 1.3 kg a.i./ha; cymoxanil (Curzate 60 DF) applied at 139 g a.i./ha plus chlorothalonil (Bravo WS) applied at 1.3 kg a.i./ha; propamocarb hydrochloride plus chlorothalonil (Tattoo C) applied at 2.0 kg a.i./ha. x Cymoxanil (Curzate 60 DF) applied at 139 g a.i./ha plus chlorothalonil (Bravo WS) applied at 1.3 kg a.i./ha; propamocarb hydrochloride plus chlorothalonil (Tattoo C) applied at 2.0 kg a.i./ha. y Cymoxanil (Curzate 60 DF) applied at 139 g a.i./ha plus chlorothalonil (Bravo WS) applied at 1.3 kg a.i./ha. z Propamocarb hydrochloride plus chlorothalonil (Tattoo C) applied at 2.0 kg a.i./ha. w Chlorothalonil

Table 4. Effects of fungicides on expansion rates of late blight lesions and sporulation from those lesions determined in inoculated field plots Lesion expansion rates cm2/day Treatment

1998

1999

Chlorx Cymox/chlory Prop/chlorz Unsprayed control LSD P value

1.4 a 1.4 a 0.9 b 1.6 a 0.4 0.0029

1.4 a 1.4 a 1.0 b 1.6 a 0.4 0.0055

x y z

# Sporangia/cm2 1999 3.3 × 104 a 3.9 × 104 a 2.1 × 104 a 3.1 × 104 a 1.4 × 104 0.09

Chlorothalonil (Bravo WS) applied at 1.3 kg a.i./ha. Cymoxanil (Curzate 60 DF) applied at 139 g a.i./ha plus chlorothalonil (Bravo WS) applied at 1.3 kg a.i./ha. Propamocarb hydrochloride plus chlorothalonil (Tattoo C) applied at 2.0 kg a.i./ha. Plant Disease / September 2001 1009

ever, at 24ºC the effect of cymoxanil was very short. When cymoxanil was applied just 12 h before inoculation, many lesions with profuse sporulation appeared (Fig. 3A and B). The length of time after inoculation during which application of cymoxanil delayed lesion appearance was longer at continuous low temperatures than at constant high temperatures. At 10ºC, cymoxanil effectively prevented lesion appearance when the compound was applied up to 48 h after inoculation (Fig. 4A), while at 96 h after inoculation some small lesions appeared. At 16ºC, when cymoxanil was applied up to 24 h after inoculation, cymoxanil prevented lesion appearance (Fig. 4A). However, when applied at 48 h after inoculation the suppressive effect of cymoxanil on lesion appearance was reduced, and there was almost no detectable suppressive effect at 96 h postinoculation (Fig. 4A). At 24ºC, cymoxanil prevented lesion

appearance only when applied within 8 h after inoculation. There was a slight effect for the 24-h treatment, but no suppressive effect at 48 or 96 h after inoculation (Fig. 4A). When applied after inoculation, cymoxanil suppressed sporulation from lesions, but this effect was again reduced at 24ºC compared to 16ºC and 10ºC (Fig. 4B). Some cymoxanil treatments prevented lesion appearance; therefore, sporulation could be assessed in only a subset of the treatments (those that resulted in lesions). At 10ºC cymoxanil almost completely suppressed sporulation. At 16ºC, there was very limited sporulation. However, at 24ºC, sporulation was typically about half as abundant as that from untreated lesions (Fig. 4B). DISCUSSION In general, the results partially support our first hypothesis that propamocarb hy-

Fig. 3. Effect of temperature on the efficacy of cymoxanil A, to suppress lesion appearance and B, to suppress sporulation per unit area of infected tissue when applied 12 to 96 h before inoculation. Error bars represent the standard error of the mean of five replicates. 1010


drochloride and cymoxanil can reduce disease development in established epidemics. However, it is clear that not all systemic fungicides have equal effects. It is also clear that the dynamics of an epidemic and the environmental conditions in which the epidemic occurs can influence the efficacy of a particular fungicide in suppressing an epidemic. First, we found that in each of the three years of investigation, propamocarb hydrochloride plus chlorothalonil (Tattoo C) had a detectable (if small) suppressive effect on established epidemics. The effect was most easily detected in 1997, when disease development was slower than in 1998 and 1999. In general, the two systemic fungicides we used provided slightly better efficacy on established epidemics than did the protectant fungicide. The protectant fungicide, chlorothalonil, was also the mixing partner for both systemic fungicide treatments. We had further hypothesized that the suppressive effect of these systemic fungicides on established epidemics would be conditioned by the rate of lesion expansion and sporulation levels. We tested the hypothesis by measuring lesion expansion rates and production of sporangia per unit area of infected tissue in the field. Propamocarb hydrochloride plus chlorothalonil consistently suppressed expansion rates of lesions in the field plots. There was no suppression of lesion expansion by cymoxanil plus chlorothalonil in the field. We also did not detect suppression of lesion expansion rates by chlorothalonil, consistent with previous results (3). None of the fungicides tested had a significant effect on suppression of sporulation from established lesions. Although propamocarb hydrochloride plus chlorothalonil inhibited the rate of lesion expansion, it did not reduce the amount of sporangia per unit area of infected tissue compared to the unsprayed control. Systemic fungicides may also prevent the development of latent infections into macroscopic lesions. This mechanism may have contributed to the suppressive effect of these systemic fungicides on development of established epidemics. However, we did not evaluate this aspect of the potential effect of these systemic fungicides in our field experiments. The small effects of cymoxanil plus chlorothalonil on established epidemics, lesion expansion rates, and sporulation were unexpected. In 1998 and 1999, field experiments were conducted under very warm conditions. Thus, we investigated temperature as a factor mitigating the efficacy of cymoxanil. Clearly, temperature can dramatically limit the duration of efficacy of cymoxanil. In growth chamber experiments at 24ºC, the length of time during which cymoxanil prevented lesion appearance and suppressed sporulation was very short. When applied at 8 h after inoculation, cymoxanil prevented lesion

appearance, but when applied at 24 h, many lesions appeared. At 16ºC, the suppressive effect of cymoxanil persisted longer, and at 10ºC, the effect was more persistent. Daytime temperatures in our field plots were regularly above 24ºC, even reaching above 30ºC on some occasions. Thus, we believe that high temperatures limited the efficacy of cymoxanil in our field experiments. Chlorothalonil had no detectable effect on lesion expansion. Cymoxanil is known to degrade rapidly (18), and high temperatures may have accelerated the degradation. Johnson et al. (16) found that propamocarb hydrochloride plus chlorothalonil reduced lesion development and sporulation when applied 48 h after inoculation in growth chamber studies. They reported that cymoxanil (applied as Manex C-8 and

Curzate 60 DF plus Manzate 200 DF) was effective in controlling lesion development and sporulation. Their results diverge slightly from ours in that they found a greater effect for cymoxanil than did we. We believe that differences in method can explain most of the divergences. Johnson et al. (16) used formulations of cymoxanil different from those used in our study, and they used a mist chamber for inoculation and subsequently maintained plants in the greenhouse. Our growth chamber results may help explain why cymoxanil is so popular in the highland tropics. For example, in the highlands of Ecuador, cymoxanil is the most popular systemic compound used to control potato blight (6). Temperatures in this part of the Andean highlands rarely rise above 22ºC, and overnight tempera-

tures generally fall below 10ºC. Under these temperature conditions, cymoxanil is very effective (G. Forbes, unpublished results). The motivation for our study was not to identify a fungicide that could be used routinely as a “curative” fungicide, but rather to identify a strategy that might be helpful if infections are known to have occurred in a crop. The primary strategy still is to use all fungicides in a protectant manner and to prevent infection. When these fungicides were applied prior to the establishment of infections, all were very effective in suppressing disease (5). However, if a grower suspects that infections have been initiated in a field, then it is important to know which compounds might be most effective in controlling an established epidemic. None of the compounds we investigated was effective at suppressing an established epidemic. Nonetheless, the results of our experiments indicate that propamocarb hydrochloride plus chlorothalonil might have some useful postinfection efficacy in the field in environmental conditions similar to those common in upstate New York during the potato production season. Cymoxanil would probably have greater efficacy in temperatures cooler than those in our field experiments in 1998 and 1999. None of the fungicides we investigated was as effective against the US-8 clonal lineage as was metalaxyl against the metalaxyl-sensitive US-1 clonal lineage investigated in earlier experiments (10). At least two factors probably contribute to this difference. First, metalaxyl is inherently more effective against sensitive strains in infected tissue than is propamocarb hydrochloride, which is the systemic component in Tattoo C. Second, the US-8 clonal lineage is more aggressive than the US-1 clonal lineage in the United States and Canada (12,21), so most current fungicides would appear to be less active against isolates in the US-8 clonal lineage than against isolates in the US-1 clonal lineage. ACKNOWLEDGMENTS This work was supported by the Cornell Agriculture Experiment Station, the ARS USDA, and The Empire State Growers.

Fig. 4. Effect of temperature on the efficacy of cymoxanil A, to suppress lesion appearance and B, to suppress sporulation per unit area of infected tissue when applied 8 to 96 h postinoculation. Error bars represent the standard error of the mean of five replicates.

LITERATURE CITED 1. Anonymous. 1947. The measurement of potato late blight. Trans. Br. Mycol. Soc. 31:140-141. 2. Bruck, R. I., Fry, W. E., and Apple, A. E. 1980. Effect of metalaxyl, an acylalanine fungicide, on developmental stages of Phytophthora infestans. Phytopathology 70:597-601. 3. Bruck, R. I., Fry, W. E., Apple, A. E., and Mundt, C. C. 1980. Effect of protectant fungicides on the developmental stages of Phytophthora infestans in potato foliage. Phytopathology 71:164-166. 4. Caten, C. E., and Jinks, J. L. 1968. Spontaneous variability of single isolates of Phytophthora infestans. I. Cultural variation. Can. J. Bot. 46:329-348. 5. Cianchetti, J., Mayton, H., Jamie-Garcia, R.,

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