Five Reasons to Consider Phytophthora infestans a Reemerging Pathogen.

Phytophthora infestans has been a named pathogen for well over 150 years and yet it continues to "emerge", with thousands of articles published each year on it and the late blight disease that it causes. This review explores five attributes of this oomycete pathogen that maintain this constant attention. First, the historical tragedy associated with this disease (Irish potato famine) causes many people to be fascinated with the pathogen. Current technology now enables investigators to answer some questions of historical significance. Second, the devastation caused by the pathogen continues to appear in surprising new locations or with surprising new intensity. Third, populations of P. infestans worldwide are in flux, with changes that have major implications to disease management. Fourth, the genomics revolution has enabled investigators to make tremendous progress in terms of understanding the molecular biology (especially the pathogenicity) of P. infestans. Fifth, there remain many compelling unanswered questions.

First Report of Late Blight Caused by Phytophthora infestans Clonal Lineage US-23 on Potato in Idaho.

Late blight, caused by Phytophthora infestans (Mont.) de Bary, is a destructive disease of potato (Solanum tuberosum) and tomato (S. lycopersicum) in the United States. Prior to 2007, the US-8 clonal lineage was the predominant genotype in the United States (4). Since 2007, a significant genetic change in the population of P. infestans occurred in the eastern United States with the appearance of new isolates with unique genotypes and epidemiological characteristics (3). These new genotypes US-22, US-23, and US-24 are sensitive to metalaxyl and represent mating types A2, A1, and A1, respectively (1,2). Prior to 2012, only US-8 had been documented in Idaho (5). In 2013, late blight was discovered in late August on potato crops (cv. Russet Norkotah) in Bingham and Madison counties, ID. Infected foliage (four samples from Bingham County and five from Madison) was sent to Michigan State University and the University of Wisconsin for confirmation of P. infestans and characterization of the isolates. Five sections from the leading edge of lesions were excised with a sterilized scalpel and placed on potato tuber slices ('Dark Red Norkotah'). Pathogen sporulation on the excised lesions was enhanced by incubation in plastic boxes lined with moistened paper towels for 5 days at 18°C in the dark. The sporulating lesions were transferred onto pea agar medium (160 g peas, 5 g sucrose, 15 g agar, 700 ml distilled water) amended with 50 mg/ml vancomycin. Ten pure cultures were obtained for each of 4 isolates per county by hyphal tipping. Cellulose acetate electrophoresis was conducted to determine Gpi allozyme genotype of the 4 isolates (4). The allozyme banding patterns were 100/100 at the Gpi locus, consistent with previously reported analyses of the US-23 genotype (1,2). Genomic DNA was extracted from 10 pure cultures using the DNeasy Plant Mini Kit (Qiagen, Germantown, MD), and SSR analyses were performed. Microsatellite markers Pi02, Pi4B, Pi63, PiG11, and D13 were used in SSR analyses. Pi02, Pi4B, and Pi63 had alleles of 162/164, 213/217, and 270/279 bp in size, respectively which is consistent with the reference US-23 genotype (1). However, heterozygosity was detected at locus D13 in the Idaho genotype with allele size of 134/210 bp and an additional allele of 140/155/176 bp at locus PiG11. This is different from the standard US-23 genotype (homozygous alleles 134/134 at locus D13 and two alleles 140/155 at locus PiG11). These allele changes indicate the isolates may be variants of US-23 isolates as all other phenotypic characteristics were similar to those of reference US-23 isolates. The Idaho genotypes were sensitive to metalaxyl both in vitro on rye A agar medium amended with metalaxyl at <0.1 ppm, and in vivo on Ridomil treated foliage tests at <0.1 ppm (1,2). Mating type assays confirmed the pathogen to be the A1 mating type. In the 2009 and 2010 late blight epidemics in the eastern United States, US-23 was the predominant genotype, but to our knowledge this genotype has never been reported previously in Idaho. Thus, this is the first known report of P. infestans genotype US-23 causing late blight on potato in Idaho, indicating a change in the population of P. infestans. In Idaho, the source of this genotype remains unknown, although infected tomatoes have been implicated in the widespread dissemination of this genotype of P. infestans in the eastern United States. References: (1) G. Danies et al. Plant Dis. 97:873, 2013. (2) C. Hu et al. Plant Dis. 96:1323, 2012. (3) K. Deahl. (Abstr.) Phytopathology 100:S161, 2010. (4) S. B. Goodwin et al. Plant Dis. 79:1181, 1995. (5) USAblight. Recent US Genotypes. Online: www.usablight.org/node/52 , retrieved 3 January 2014.

The 2009 Late Blight Pandemic in the Eastern United States - Causes and Results.

The tomato late blight pandemic of 2009 made late blight into a household term in much of the eastern United States. Many home gardeners and many organic producers lost most if not all of their tomato crop, and their experiences were reported in the mainstream press. Some CSAs (Community Supported Agriculture) could not provide tomatoes to their members. In response, many questions emerged: How did it happen? What was unusual about this event compared to previous late blight epidemics? What is the current situation in 2012 and what can be done? It's easiest to answer these questions, and to understand the recent epidemics of late blight, if one knows a bit of the history of the disease and the biology of the causal agent, Phytophthora infestans.

First Report of Late Blight Caused by Phytophthora infestans Clonal Lineage US-22 on Tomato and Potato in Wisconsin.

Tomato (Solanum lycopersicum) and potato (S. tuberosum) crops are grown on over 67,000 acres (27,114 hectares) in the state of Wisconsin each year. Late blight, caused by Phytophthora infestans (Mont.) deBary, is a potentially devastating oomycete pathogen that sporadically affects tomato and potato crops in the state. Prevention of this disease through prophylactic application of oomycete-specific fungicides can cost producers millions of dollars per year in additional chemical, fuel, and labor expenses. In 2009, late blight was observed on tomato and potato in over 25 Wisconsin counties. The epidemic initiated on tomato in southern WI in early August and progressed northward in the state with additional reports on tomato primarily from home gardens and small farms. Potato late blight was also identified but with limited incidence in central WI, likely due to routine fungicide programs in commercial production. Clonal lineages of P. infestans documented in Wisconsin in previous epidemics included US-1 in the 1970s and US-8 in the mid-1990s. Populations of P. infestans in the U.S. have recently undergone significant genetic changes, resulting in isolates with unique clonal lineages and epidemiological characteristics (1). Symptoms of late blight observed on tomato and potato included water-soaked to dark brown circular lesions with pale green haloes accompanied by signs of pathogen sporulation typically on leaf undersides during periods of high humidity. Isolates of P. infestans were generated from field infected tomato and potato foliar tissues. Axenic, single zoospore derived cultures were generated and maintained on Rye A agar for further characterization. Mycelium was coenocytic with hyphal diameter of 5 to 8 µm (n = 50). Sporangia were limoniform or ovoid, semi- to fully papillate, caducous, had short pedicels, and were 29.6 (h) × 16.8 µm (w) (n = 50). The average length/width ratio was 1.76. Allozyme banding patterns at the glucose-6-phosphate isomerase (Gpi) locus indicated a 100/122 profile, consistent with the US-22 clonal lineage (3). Mating type assays confirmed the isolates to be A2 and in vitro mefenoxam sensitivity was observed (4). Restriction fragment length polymorphic analysis of a representative isolate from Wisconsin with the multilocus RG57 sequence and EcoRI produced the DNA pattern indicative of US-22 (2). The P. infestans clonal lineage US-22 was predominant in U.S. epidemics on tomato in 2009. To our knowledge, this is the first report of P. infestans clonal lineage US-22 causing late blight on tomato and potato in Wisconsin, USA. References: (1) K. Deahl. (Abstr.) Phytopathology 100(suppl.):S161, 2010. (2) S. B. Goodwin et al. Curr. Genet. 22:107, 1992. (3) C. H. Hu et al. Plant Dis. 96:1323, 2012. (4) A. C. Seidl et al. Phytopathology 101(suppl.):S246, 2011.

First Report of Late Blight Caused by Phytophthora infestans Clonal Lineage US-23 on Tomato and Potato in Wisconsin, United States.

Tomato (Solanum lycopersicum) and potato (S. tuberosum) crops are grown on over 67,000 acres (27,114 ha) in Wisconsin annually. Late blight, caused by Phytophthora infestans (Mont.) deBary, is a potentially devastating disease that affects tomato and potato crops in Wisconsin every few years when inoculum is introduced and weather conditions favor disease. Incidence and severity of late blight are highly variable in these few years due to differences in pathogen clonal lineages, their timing and means of introduction, and weather conditions. Prevention of this disease through preventative application of fungicides can cost producers millions of dollars per year in additional chemical, fuel, and labor expenses. In 2009, late blight caused by P. infestans clonal lineage US-23 was observed on potato very late in the season in Vernon County, southwestern Wisconsin, in very low incidence and severity. In 2010, US-23 again appeared but on tomato in two southeastern Wisconsin counties, Waukesha and Ozaukee, again in low incidence and severity. Clonal lineages of P. infestans documented in Wisconsin in previous epidemics included US-8 in the mid-1990s and US-1 in the 1970s. Populations of P. infestans in the United States have recently undergone significant genetic change, resulting in isolates with unique clonal lineages and epidemiological characteristics (1). Foliar symptoms included water-soaked to dark brown circular lesions with pale green haloes accompanied by white pathogen sporulation. On tomato fruit, lesions were firm, sunken, and brown. Isolates of P. infestans were generated from field-infected tomato and potato foliar and fruit tissues collected by the authors and professional crop consultants. In initial pathogen confirmation analysis in 2009, three isolates of P. infestans were generated from one potato plant exhibiting multiple lesions from one of eight fields tested by placing infected leaf excisions onto Rye A agar amended with rifampicin and ampicillin. Axenic, single zoospore-derived cultures of isolates were generated from parent cultures and maintained on Rye A agar for further characterization. In 2010, three US-23 isolates were recovered from three locations (two counties), out of 20 fields tested. Mycelium was coenocytic with hyphal diameter of 5 to 8 µm (n = 50). Sporangia were limoniform or ovoid, semi to fully papillate, caducous, had short pedicels, and were 26.16 µm high × 18.17 µm wide (n = 50). The average length/width ratio was 1.42. Allozyme banding patterns at the glucose-6-phosphate isomerase (Gpi) locus indicated a 100/100 profile, consistent with the US-23 clonal lineage (3) Mating type assays confirmed the isolates to be A1 and in vitro intermediate mefenoxam sensitivity was observed (4). Genomic DNA was extracted with a phenol/chloroform/isoamyl alcohol solution and RFLP analysis was performed using the RG-57 probe on a representative isolate and resulted in banding patterns consistent with US-23 (2,3). The P. infestans clonal lineage US-23 was present in epidemics in 2009 and 2010 in the United States. Disease symptoms associated with US-23 were observed exclusively on potato in 2009 and on tomato in 2010 in Wisconsin. To our knowledge, this is the first report of P. infestans clonal lineage US-23 causing late blight on tomato and potato in Wisconsin and represents a change in the composition of the pathogen population from previous epidemic years. References: (1) K. Deahl. (Abstr.) Phytopathology 100:S161, 2010. (2) S. B. Goodwin et al. Curr. Genet. 22:107, 1992. (3) Hu et al. Plant Dis. 96:1323, 2012. (4) A. C. Seidl and A. J. Gevens. (Abstr.) Phytopathology 101(suppl.):S162, 2011.

First Report of Late Blight Caused by Phytophthora infestans Clonal Lineage US-24 on Potato (Solanum tuberosum) in Wisconsin.

Potato (Solanum tuberosum) crops are grown on over 25,090 ha in Wisconsin annually. Late blight, caused by Phytophthora infestans (Mont.) deBary, is a potentially devastating disease that affects tomato and potato crops in Wisconsin every few years when inoculum is introduced and weather conditions favor disease. Incidence and severity of late blight are highly variable in these few years due to differences in pathogen clonal lineages, their timing and means of introduction, and weather conditions. Prevention of this disease through prophylactic fungicide application can cost producers millions of dollars annually in additional chemical, fuel, and labor expenses. Populations of P. infestans in the U.S. have recently undergone significant genetic change, resulting in isolates with unique clonal lineages and epidemiological characteristics (1). In 2010, late blight epidemics were of low severity in discrete portions of a few fields and were seen exclusively on potato in two counties of central Wisconsin. Symptoms included water-soaked to dark brown circular lesions with pale green haloes accompanied by white fuzzy pathogen sporulation typically on leaf undersides in high humidity conditions. Infected plants were collected by professional crop consultants and submitted to the authors at the University of Wisconsin Vegetable Pathology Laboratory in Madison, Wisconsin. Eight isolates of P. infestans were generated from individual leaf samples, representing separate fields, by removing sporangia from sporulating lesions and placing onto Rye A agar amended with rifampicin and ampicillin. Axenic, single zoospore-derived cultures of isolates were generated from parent cultures and maintained on Rye A agar for further characterization. Mycelium was coenocytic with hyphal diameter of 5 to 8 µm (n = 50). Sporangia were limoniform to ovoid, semi- to fully papillate, caducous, had short pedicels, and were 36.22 × 19.11 µm (height × width; n = 50). The average length-width ratio was 1.91. Allozyme banding patterns at the glucose-6-phosphate isomerase (Gpi) locus indicated a 100/100/111 profile, consistent with the US-24 clonal lineage (3,4). Mating type assays confirmed the isolates to be A1 and intermediate insensitivity to mefenoxam was observed in vitro (4). Genomic DNA was extracted with a phenol:chloroform:isoamyl alcohol solution and restriction fragment length polymorphism (RFLP) analysis was performed using the RG-57 probe on a representative isolate and resulted in banding patterns consistent with US-24 (2,3). Clonal lineages of P. infestans documented in Wisconsin in previous epidemics included US-8 in the mid-1990s and US-1 in the 1970s. The US-24 (A1) clonal lineage was very widespread in the U.S. in 2010 and its presence in Wisconsin in the same year as identification of US-22 (A2) posed great concern for potential sexual recombination, oospore production, and soil persistence. Fortunately, the opposite mating types were separated spatiotemporally. To the best of our knowledge, this is the first report of the P. infestans clonal lineage US-24 causing late blight on potato in Wisconsin. References: (1) K. Deahl. (Abstr.) Phytopathology 100:S161, 2010. (2) S. B. Goodwin et al. Curr. Genet. 22:107, 1992. (3) Hu et al. Plant Dis. 96:1323, 2012. (4) A. C. Seidl and A. J. Gevens. (Abstr.) Phytopathology 101:S162, 2011.

Extension plant pathology: strengthening resources to continue serving the public interest.

Extension plant pathologists deliver science-based information that protects the economic value of agricultural and horticultural crops in the United States by educating growers and the general public about plant diseases. Extension plant pathologists diagnose plant diseases and disorders, provide advice, and conduct applied research on local and regional plant disease problems. During the last century, extension plant pathology programs have adjusted to demographic shifts in the U.S. population and to changes in program funding. Extension programs are now more collaborative and more specialized in response to a highly educated clientele. Changes in federal and state budgets and policies have also reduced funding and shifted the source of funding of extension plant pathologists from formula funds towards specialized competitive grants. These competitive grants often favor national over local and regional plant disease issues and typically require a long lead time to secure funding. These changes coupled with a reduction in personnel pose a threat to extension plant pathology programs. Increasing demand for high-quality, unbiased information and the continued reduction in local, state, and federal funds is unsustainable and, if not abated, will lead to a delay in response to emerging diseases, reduce crop yields, increase economic losses, and place U.S. agriculture at a global competitive disadvantage. In this letter, we outline four recommendations to strengthen the role and resources of extension plant pathologists as they guide our nation's food, feed, fuel, fiber, and ornamental producers into an era of increasing technological complexity and global competitiveness.

First Report of Powdery Mildew Caused by Golovinomyces cichoracearum on Crotalaria juncea ('Tropic Sun' Sunn hemp).

Crotalaria juncea L. (Fabaceae), commonly known as sunn hemp, is a subtropical annual legume grown in the United States as a cover crop that improves soil quality, provides nitrogen, suppresses weeds and nematodes, and adds organic matter to soils. In Florida, sunn hemp is a warm- and short-season cover crop that is typically planted in June and cut and incorporated into soil in September. In 2008, powdery mildew was observed on sunn hemp in a research field in Hastings, FL. This disease is important because it has the potential to impact the health and quality of sunn hemp, and this particular powdery mildew can infect cucurbits that are grown in north Florida from late summer to fall. Fungal growth appeared as typical white, powdery mildew colonies initially seen on upper leaf surfaces, especially along the midvein of infected leaves, but moving to undersides as disease progressed; petioles and floral parts were disease free. As disease progressed, colonies enlarged and coalesced to cover the entire leaf surface; heavily infected leaves senesced and abscised. Infection was primarily seen on the lower, more mature leaves of plants and not on the top 0.6 m (2 feet) of the plant. Mycelia produced white accumulations of conidiophores and conidia. Hyphae were superficial with papillate appressoria and produced conidiophores with cylindrical foot cells that measured 48.5 × 10.0 µm (mean of 100 foot cell measurements) and short chains of conidia. Conidia were hyaline, short-cylindrical to ovoid, lacked fibrosin bodies, borne in chains, had sinuate edge lines with other immature conidia, and measured 22.5 to 40.0 (mean = 29.85 µm) × 12.5 to 20.0 µm (mean = 15.55 µm). The teleomorph was not observed. The nuclear rDNA internal transcribed spacer (ITS) regions were amplified by PCR, using universal primers ITS1 and ITS4, and sequenced (GenBank Accession No. FJ479803). On the basis of morphological characteristics of the asexual, imperfect state that are consistent with published reports of Golovinomyces cichoracearum (2) and ITS sequence data that indicated 100% homology with G. cichoracearum from Helianthus annus (GenBank Accession No. AB077679), this powdery mildew was identified as caused by G. cichoracearum of the classification Golovinomyces Clade III (3). Pathogenicity was confirmed by gently pressing disease leaves onto leaves of healthy C. juncea plants. Inoculated plants were placed into plastic bags containing moist paper towels to maintain high humidity. The temperature was maintained at 24°C, and after 2 days, powdery mildew colonies developed in a manner consistent with symptoms observed under field conditions. A powdery mildew on Crotalaria was previously identified as caused by Microsphaera diffusa Cooke & Peck (1). To our knowledge, this is the first report of G. cichoracearum causing powdery mildew on C. juncea. References: (1) D. F. Farr et al. Fungi on Plants and Plant Products in the United States. The American Phytopathological Society, St. Paul, MN, 1989. (2) D. A. Glawe et al. Online publication. doi: 10.1094/PHP-2006-0405-01-BR. Plant Health Progress, 2006. (3) S. Takamatsu et al. Mycol. Res. 110:1093, 2006.

Characterization of Phytophthora capsici Causing Foliar and Pod Blight of Snap Bean in Michigan.

Green and yellow snap bean plants with water-soaked foliar lesions, stem necrosis, pod blight, and overall plant decline were observed in four commercial fields in three Michigan counties during 2003 to 2005. All fields were cropped to cucurbits that exhibited symptoms of Phytophthora capsici infection in recent years. In all, 680 isolates of P. capsici were obtained from bean stems, petioles, leaves, and pods; the pathogen was not recovered from roots. Koch's postulates were completed with representative isolates, confirming P. capsici as the causal organism. Select isolates also were pathogenic on cucumber fruit, causing symptoms consistent with P. capsici infection. The majority of the P. capsici isolates collected were sensitive to the fungicide mefenoxam and were of the A1 mating type. Under laboratory conditions, six P. capsici isolates from snap bean (2003) were pathogenic on 12 different commercial bean cultivars, including soybean. Infected bean plants exhibited water-soaked lesions, foliar necrosis, and wilting. We subjected 131 isolates collected from 2003 and 2004 to amplified fragment length polymorphism analysis to investigate diversity among isolates and geographical populations and to determine whether bean P. capsici isolates were similar to isolates from a cucurbit host. This is the first in-depth study of P. capsici on snap bean in Michigan. Although bean cultivars previously were considered a suitable rotation for crops susceptible to P. capsici, this is no longer a recommended practice.

First Report of Soybean Rust Caused by Phakopsora pachyrhizi on Erythrina herbacea (Coral Bean).

Soybean rust (SBR), caused by the obligate fungus Phakopsora pachyrhizi Syd. & P. Syd., was initially reported on soybean (Glycine max L.) in Louisiana in 2004 and has since been reported on soybean and/or kudzu (Pueraria lobata (Willd.) Ohwi) in 9 states in 2005, 15 states in 2006, and 19 states in 2007 (1). The host range of P. pachyrhizi includes plants that are all in the Fabaceae or legume family. Six plant species in the United States have been reported as hosts of P. pachyrhizi: soybean, kudzu, Florida beggarweed (Desmodium tortuosum (Sw) DC.), dry bean (Phaseolus vulgaris L.), lima bean (P. lunatus L.), and scarlet runner bean (P. coccineus L.) (4). On 17 April 2008, a rust disease was observed on a weedy legume host with red showy flowers that was growing with kudzu in an overgrown vacant lot in the understory of live oak trees (Quercus virginiana Mill.) in Citra, FL. The discovery was made during routine scouting of this Integrated Pest Management Pest Information Platform for Extension and Education (IPM PIPE) mobile sentinel plot (3). The plant was confirmed by University of Florida botanists to be Erythrina herbaceae L., commonly known as coral bean. Coral bean is native to the southeastern United States and also is planted as a perennial ornamental. A sample of leaves exhibiting rust pustules characteristic of P. pachyrhizi uredinia was collected and examined with a microscope. Brown-to-brick red, angular lesions that were 3 to 11 mm in diameter (average 6.75 mm) were observed on the undersides of the leaves of two trifoliates. Within these lesions, there were several uredinia, some exuding hyaline, echinulate urediniospores (20 × 25 µm). The visual diagnosis and the species of the rust fungus were confirmed to be P. pachyrizi by a real-time PCR protocol (2). The diagnosis on this new host was verified by a USDA, APHIS National Mycologist in Beltsville, MD. Coral bean may serve as an additional overwintering host for P. pachyrhizi in the southeast. To our knowledge, this is the first report of soybean rust caused by P. pachyrhizi on E. herbaceae. References: (1) R. S. C. Christiano and H. Scherm, Phytopathology 97:1428, 2007. (2) R. D. Frederick et al. Phytopathology 92:217, 2002. (3) S. A. Isard et al. Online publication. doi:10.1094/PHP-2006-0915-01-RV. Plant Health Progress, 2006. (4) T. L. Slaminko et al. Plant Dis. 92:767, 2008.

Characterization of Phytophthora capsici from Michigan Surface Irrigation Water.

ABSTRACT Phytophthora capsici infects cucurbitaceous and solanaceous crops worldwide. In free water, P. capsici sporangia release zoospores that may be disseminated by moving surface water. Surface irrigation sources (river system, ponds, and ditches) in three Michigan counties with a history of P. capsici-susceptible crop production were monitored for the pathogen during four growing seasons (2002 to 2005). Pear and cucumber baits were suspended in water at monitoring sites for 3- to 7-day intervals and water temperature was recorded. Baits were washed and lesions were excised and cultured on water agar amended with rifampicin and ampicillin. P. capsici was detected at monitoring sites in multiple years, even when non-host crops were planted nearby. Recovered isolates (N = 270) were screened for sensitivity to the fungicide mefenoxam and characterized for mating type (MT). P. capsici isolates resistant to mefenoxam were common in water sources from southwest and southeast Michigan. Most monitoring sites yielded isolates of a 1:1 ratio of A1:A2 MTs. Amplified fragment length polymorphism analysis of select isolates from 2002 to 2004 indicated a lack of similarity groups persisting over time and in specific geographical locations. Data suggest that P. capsici did not overwinter in any of the surface water sources monitored. Water temperatures were correlated to positive P. capsici detection from all monitoring sites. The frequent detection of P. capsici in surface water used for irrigation in the primary vegetable growing regions in Michigan suggests that this is an important means of pathogen dissemination.

A Detached Cucumber Fruit Method to Screen for Resistance to Phytophthora capsici and Effect of Fruit Age on Susceptibility to Infection.

Identification and utilization of resistance to Phytophthora capsici could provide the basis for a viable management strategy against cucumber fruit rot, a persistent threat in cucumber (Cucumis sativus) production. Our objectives were to develop a method for testing detached, nonwounded, cucumber fruit for resistance to P. capsici, and to screen cucumber cultivars and plant introductions (collectively referred to as cultigens) for resistance. Four P. capsici isolates (differing in their sensitivity to the fungicide mefenoxam and compatibility type) were compared for their fruit infection capability in 1999 and 2000. No significant differences were found among isolates, and a single isolate was used for all subsequent screens. From 1999 to 2004, 480 cucumber cultigens were grown according to standard practices at Michigan State University research farms in four fields with no history of P. capsici. Commercially mature fruit were harvested, inoculated with P. capsici, and rated for lesion diameter, pathogen sporulation diameter, and density of pathogen sporulation. Although no fruit exhibited complete resistance to P. capsici, some cultigens exhibited limited pathogen sporulation. In the process of screening, it was observed that younger, smaller fruit were comparatively more susceptible than older, larger fruit. Replicated trials with hand-pollinated fruit showed that the transition from susceptible to more resistant appeared to coincide with the transition from the period of rapid fruit elongation to the period of increased fruit diameter. This is the first report using a nonwounded fruit screen to analyze cucumber resistance to P. capsici.