A Coordinated Effort to Manage Soybean Rust in North America: A Success Story in Soybean Disease Monitoring.

Existing crop monitoring programs determine the incidence and distribution of plant diseases and pathogens and assess the damage caused within a crop production region. These programs have traditionally used observed or predicted disease and pathogen data and environmental information to prescribe management practices that minimize crop loss. Monitoring programs are especially important for crops with broad geographic distribution or for diseases that can cause rapid and great economic losses. Successful monitoring programs have been developed for several plant diseases, including downy mildew of cucurbits, Fusarium head blight of wheat, potato late blight, and rusts of cereal crops. A recent example of a successful disease-monitoring program for an economically important crop is the soybean rust (SBR) monitoring effort within North America. SBR, caused by the fungus Phakopsora pachyrhizi, was first identified in the continental United States in November 2004. SBR causes moderate to severe yield losses globally. The fungus produces foliar lesions on soybean (Glycine max) and other legume hosts. P. pachyrhizi diverts nutrients from the host to its own growth and reproduction. The lesions also reduce photosynthetic area. Uredinia rupture the host epidermis and diminish stomatal regulation of transpiration to cause tissue desiccation and premature defoliation. Severe soybean yield losses can occur if plants defoliate during the mid-reproductive growth stages. The rapid response to the threat of SBR in North America resulted in an unprecedented amount of information dissemination and the development of a real-time, publicly available monitoring and prediction system known as the Soybean Rust-Pest Information Platform for Extension and Education (SBR-PIPE). The objectives of this article are (i) to highlight the successful response effort to SBR in North America, and (ii) to introduce researchers to the quantity and type of data generated by SBR-PIPE. Data from this system may now be used to answer questions about the biology, ecology, and epidemiology of an important pathogen and disease of soybean.

First Report and Confirmed Distribution of Soybean Sudden Death Syndrome Caused by Fusarium virguliforme in Southern Michigan.

Leaf lesions and root rot symptoms typical of soybean sudden death syndrome (SDS) caused by Fusarium virguliforme O'Donnell & T. Aoki were observed in commercial soybeans (Glycine max (L.) Merr.) in southern Michigan. Leaf symptoms ranged from chlorotic spots to severe interveinal chlorosis and necrosis, no foliar pathogens were noted. In 2008, isolates were collected from Berrien and St. Joseph counties. In 2009, isolates were collected from Cass, St. Joseph, Van Buren, Allegan, and Monroe counties. Pieces of roots with root rot symptoms were washed prior to surface disinfestation with 70% ethanol for 30 s and 0.5% NaOCl for 1 min and incubated on water agar (WA) in petri plates amended with 50 µg/ml of chloramphenicol for the production of sporodochia. Alternatively, spores were collected directly from nondisinfested roots expressing blue sporodochia. Single-spore cultures were derived by streaking macroconidia with a bacterial loop onto 3% WA + chloramphenicol and incubated overnight. With a dissecting microscope, single germinated macroconidia were collected with a sterile 0.2-mm-diameter insect pin and transferred to potato dextrose agar (PDA). Cultures on PDA grew slowly and developed blue-to-purple masses of sporodochia typical of F. virguliforme descriptions and similar to a representative isolate, Mont-1, grown alongside (1,2). Size of macroconidia from the six representative isolates, one from each county (including isolates derived from surface-disinfested and nondisinfested roots), and Mont-1 were determined to be within the range for F. virguliforme (42 to 56 × 5 to 6 µm), with an average of four septa per macroconidia. Identity of the representative isolates was confirmed by partial DNA sequencing of both strands of the internal transcribed spacer (ITS) region of the ribosomal RNA gene, translation elongation factor 1-α, and ß-tubulin loci. All six representative isolates were identical in each of the three loci and matched with 100% similarity F. virguliforme accessions in GenBank and Fusarium-ID database searches, except for the ß-tubulin locus in which a single nucleotide insertion was noted (Accession Nos. HM453328-HM453330). Sequences were 98 to 99% similar to other SDS Fusarium spp. not yet recorded in the United States. Koch's postulates were performed in the greenhouse according to Malvick and Bussey (3). Infested sorghum seed (~20 g) was placed 2 cm below soybean seed of susceptible cv. Williams 82 in plastic pots. Noninfested sorghum seed was used as a negative control and sorghum infested with Mont-1 as a positive control. Chlorotic spots developed 2 weeks after establishing the trial, and 3 to 4 weeks postinoculation, severe SDS symptoms of foliar interveinal chlorosis and necrosis and severe root rot developed. Koch's postulates were completed by reisolating F. virguliforme from a subset of infected plants. In addition, an isolate of F. virguliforme collected in 2008 was used to inoculate a 2009 field trial in East Lansing, MI with no history of SDS. Typical SDS symptoms developed in the field trial and F. virguliforme was isolated from a symptomatic plant that was identified as described above. Despite being reported across the majority of soybean-producing states, to our knowledge, this is the first confirmation and distribution report for SDS in Michigan. References: (1) T. Aoki et al. Mycoscience 46:162, 2005. (2) G. L. Hartman et al. Plant Dis. 81:515, 1997. (3) D. K. Malvick and K. E. Bussey. Can. J. Plant Pathol. 30:467, 2008.

Outbreak of Leucostoma Canker Caused by Leucostoma cincta on McIntosh Apple Trees in Wisconsin.

In fall 1996, cankers were observed on branches of 7- to 9-year-old apple trees (Malus domestica cvs. Empire and McIntosh, strains Marshall and Redmax) in a research orchard in Sturgeon Bay, WI. By summer 1997, cankers had developed on scaffold limbs or the central leaders of 48 of 48 Marshall McIntosh trees and 26 of 40 Redmax McIntosh trees, but they rarely were found in an adjacent block of 40 Empire trees. In 1998, new cankers were not observed, but existing cankers expanded. By 1999, the Marshall McIntosh block was so severely affected it was removed; 50% of the Redmax trees and 13% of the Empire trees also were removed. Initially, cankers appeared as orange discolored areas on bark and frequently, but not always, were associated with pruning wounds. Canker expansion was greater during spring and fall than during summer. At later stages of canker development, bark cracked and peeled, and leaves distal to cankers died. These features were consistent with descriptions of Leucostoma canker of apple (2,3), a disease previously reported only in Michigan, Germany, and Iran (1-3). All of 10 cankers sampled in 1997 and several more cankers sampled in 1998 yielded fungal colonies on potato-dextrose agar resembling Leucocytospora spp., which are anamorphs of Leucostoma spp. (2). Colonies initially were white to buff and later turned brown. Conidium morphology was consistent with descriptions of Leucocytospora spp. (2). Alternaria spp. also were isolated frequently; other fungi, which were not identified, were isolated rarely. The presence of abundant pycnidia of Leuco-cytospora, but not perithecia of Leucostoma, on cankers was different from the signs described for Leucostoma canker caused by Leucostoma cincta in Michigan (2,3). However, simple matching coefficient analysis of randomly amplified polymorphic DNA data indicated 74% similarity between a typical isolate from apple in Wisconsin (97-82) and two isolates of L. cincta from apple in Michigan (3; ATCC 64878 and 64879) but only 49 to 54% similarity to L. cincta and L. persoonii isolated from stone fruit trees (Prunus spp.). Inoculation of wounded branches of mature apple trees (cvs. Golden Delicious and Cortland) with isolate 97-82 in July 1998 and 1999 resulted in cankers that resembled young cankers observed on trees in the research orchard. Eight weeks after inoculation, the pathogen was reisolated from these cankers, which fulfilled Koch's Postulates. Therefore, we conclude that Leucostoma canker was responsible for the serious damage to apple trees of different cultivars at the research station, with strains of McIntosh affected most severely. We speculate that low-temperature injury during the unusually cold winter of 1995-1996 might have created infection sites and predisposed trees to disease development. This is the first report of Leucostoma canker of apple in Wisconsin. It is rare that this disease causes such significant losses (2). References: (1) M. Ashkan. Iranian J. Plant Pathol. 30:33, 1994. (2) A. L. Jones and H. S. Aldwinckle, eds. 1991. Pages 40-41 in: Compendium of Apple and Pear Diseases. American Phytopathological Society, St. Paul, MN. (3) T. J. Proffer and A. L. Jones. Plant Dis. 73:508, 1989.