First Report of Ramulispora sorghicola in the United States Causing Oval Leaf Spot on Johnsongrass and Sorghum in Texas.

Oval leaf spot (OLS) caused by Ramulispora sorghicola Harris was observed on grain sorghum, Sorghum bicolor (L.) Moench, and johnsongrass, S. halepense (L.) Pers., near Beeville, TX during August 2002. Symptoms were first observed on several sorghum lines and hybrids in a field nursery including a bulk planting of the line ATx623. Highest incidence of OLS occurred in rows adjacent to johnsongrass with symptoms of OLS. Average lesion size (mm) was 1.3 × 2.8 with a range from 0.5 to 2.5 × 1.5 to 5.0. Lesions had a straw-colored sunken center and on red- and purple-pigmented sorghums, lesion borders were highly pigmented. Cone-shaped conidial masses and superficial sclerotia (subglobose, black, 80 to 190 µm in diameter × 50 to 70 µm high, with spiny setae) were sometimes present or readily produced on lesions within 48 to 72 h after placement in humidity chambers. Conidia were branched, filiform, tapered, and 1.1 to 2.4 × 20 to 75 µm. The pathogen, R. sorghicola, was isolated from conidia and sclerotia. A water suspension of culturally derived conidia of R. sorghicola (3 × 104 conidia per ml) was spray inoculated (5:30 p.m., October 11, 2002) onto four or more upper leaves per plant of six grain sorghum plants (ATx623) and approximately nine johnsongrass plants (three tillers each of three plants) at a Corpus Christi field location where OLS was absent. Three grain sorghum and one johnsongrass plant were sprayed with a water control. Cloudy, wet, and cool conditions after inoculation and increasingly cooler nights probably delayed symptom expression until 3 to 4 weeks after inoculation. Typical lesions were observed simultaneously on both hosts with symptoms restricted to inoculated plants. Lesions from both hosts were placed onto water agar at 25°C for 24 h, and the pathogen was reisolated from field-produced conidia of rehydrated conidial masses. Through 2004, OLS was observed on sorghum hosts in 29 counties from central Texas to the Lower Rio Grande Valley. During the growing season, OLS was predominantly absent in grain and forage sorghum fields and absent or often difficult to detect in johnsongrass. In all 3 years, OLS was most common after the normal growing season from August through December with occurrence primarily on johnsongrass but also on late-planted and feral S. bicolor hosts, especially when proximal to symptomatic johnsongrass. Presence and incidence of OLS was highly variable between and within stands of johnsongrass with incidence ranging from a few to most plants. Incidence in forage or grain sorghum fields was highest at field borders adjacent to johnsongrass with OLS. Disease severity was low except on johnsongrass at a few locations. The pathogen appears to pose low economic risk to any sorghum host in Texas at any time of the year although highly susceptible lines and hybrids should be identified and possibly avoided. The previous most proximal report of R. sorghicola in the Western Hemisphere was in Honduras (1). The widespread distribution of OLS across southern Texas and its pattern of occurrence in johnsongrass suggest that the pathogen may have been unobserved in Texas for several years. Presence of OLS near the Rio Grande indicates probable occurrence in johnsongrass at least in some areas along this river in northeastern Mexico. Reference: (1) G. C. Wall et al. Trop. Pest Manag. 35:57, 1989.

First Report and Epidemics of Buffelgrass Blight Caused by Pyricularia grisea in South Texas.

A blight on buffelgrass, Cenchrus ciliaris L., has been observed for several years in south Texas and Mexico. The disease did not reach epidemic proportions until 1996. The causal agent, identified as Pyricularia grisea (Cooke) Sacc., is a common pathogen of grasses and other cultivated crops. Several Pennisetum spp. have been reported as hosts of Pyricularia spp.; this is the first report of buffelgrass as a host of this pathogen (1,2). Pathogenicity of P. grisea on buffelgrass was confirmed by greenhouse inoculations of 2-month-old buffelgrass plants with conidia washed with distilled water from monoconidial isolations of the pathogen, grown on potato dextrose agar, from infected leaves collected in several locations in south Texas and Mexico. Plants were placed for 8 h every night inside a plastic enclosure with a humidifier, simulating the high relative humidity conditions prevalent during the epidemic. Typical lesions developed after 7 days. The pathogen was re-isolated from the lesions after 10 days, fulfilling Koch's postulates. Conidia harvested from the sporulating samples were hyaline, transversely septate, with one to three septa, most of them having two. Conidia were obpyriform, with hylum often protuberant, measuring 20.6 to 26.3 µm in length and 8.5 to 10.1 µm wide. These measurements are consistent with those given for Pyricularia spp. by Ellis (1). Conidiophores were hyaline, single, slender, and unbranched. Initial symptoms were dark, discolored spots on the leaf that developed into tan, round to elliptical, necrotic lesions with a dark red border and a yellow, chlorotic halo. With increasing severity, lesions can coalesce, killing the entire leaf blade. Under heat and moisture stress, leaves with few lesions and yellow discoloration will wilt completely. Except for the presence of distinct lesions, wilted plants appear to be suffering from severe drought stress or herbicide injury. Losses vary from a few lesions to wilted whole plants and entire pastures. The pathogen also reduces the quantity and quality of seed by infecting involucres of the head. In the absence of the disease, even under severe moisture or drought stress, buffelgrass is able to thrive. Common T-4464 buffelgrass, which is highly susceptible to P. grisea, was introduced into south Texas in the late 1940s and is currently grown on 8 to 10 million acres in south Texas and Mexico. Buffelgrass reproduces by obligate apomixis, in which seeds are formed without sexual fertilization. Consequently, the progeny are genetically identical to the maternal parent. The monoculture of this grass with its unique type of reproduction encompasses millions of acres with genetically identical plants. Interaction of inoculum with weather conditions (nights with 8 to 10 h of more than 75% relative humidity) in 1996, 1997, and the late summer of 1998 produced epidemics of buffelgrass blight throughout south Texas and northern Mexico. P. grisea was also isolated from lesions on grassburr Cenchrus incertus M. A. Curtis collected throughout the area. References: (1) M. B. Ellis 1971. Dematiaceous hyphomycetes. Commonwealth Mycological Institute, Kew, Surrey, England. (2) D. F. Farr et al. 1989. Fungi of Plants and Plant Products in the United States. American Phytopathological Society, St. Paul, MN.

Spread of Ergot of Sorghum (Claviceps africana) in Central Mexico.

By late August 1997, sorghum ergot (Claviceps africana Frederickson, Mantle & De Milliano) had not been detected in the Bajio area in central Mexico, the second-largest sorghum (Sorghum bicolor (L.) Moench) producing area in the country, despite earlier 1997 reports of the disease in the adjacent states of San Luis Potosi, Michoacan, and Jalisco. A mid-September survey was conducted in el Bajio, primarily in the state of Guanajuato, and adjacent areas in the states of Michoacan and Jalisco. Infected sorghum heads showing ergot symptoms of honeydew and white secondary sporulation were observed in commercial grain and hybrid seed fields in all three states. Environmental conditions, late summer rains and early low temperatures promoting abundant dew, as well as extended periods of sorghum blooming, contributed to a low and delayed incidence of ergot in Guanajuato. In Michoacan and Jalisco the higher relative humidity and rainfall (around 750 ml) probably contributed to the observed epidemic of ergot. Johnsongrass (Sorghum halepense (L.) Pers.) florets also showed ergot symptoms. Macroconidia in honeydew were hyaline, oblong to oval, slightly constricted at the center, with an average size of 15 × 7 µm, agreeing with the given description of Sphacelia sorghi McRae (2), the anamorph stage of C. africana. No sclerotia were found on any host. Ergot control in this region of Mexico is being attempted by chemical means and burning of heads, even in commercial fields with minimal incidence of ergot. This report of ergot spread complements an earlier note describing the initial detection of the disease in Tamaulipas, the largest sorghum-producing state in Mexico (1). References: (1) J. Aguirre R. et al. Plant Dis. 81:831, 1997. (2) D. E. Frederickson et al. Mycol. Res. 95:1101, 1991.

First Report of Sorghum Ergot Caused by Claviceps africana in the United States.

In March 1997, ergot was found on sorghum (Sorghum bicolor (L.) Moench) regrowth in several abandoned commercial grain sorghum fields in Cameron and Hidalgo counties in the Lower Rio Grande Valley (LRGV) of Texas. White sphacelia in florets produced honeydew containing macrospores (hyaline, oblong to oval, 10 to 25 µm × 5 to 7 µm) and microspores (hyaline, spherical, 3 µm in diameter). Macrospores germinated iteratively to form secondary conidia when placed on water agar and in situ following rain. Secondary conidia were hyaline, pyriform, with a protruding hilum, and measured 10 to 17 µm × 5 to 7 µm. High-pressure liquid chromatography analysis detected the alkaloid di-hydroergosine in sphacelia, which is unique to C. africana (1). The pathogen was also confirmed on adjacent johnsongrass (S. halepense). The spread of ergot across Texas was associated with the progressive maturation of the commercial sorghum crop as follows: LRGV (mid-May), Coastal Bend near Corpus Christi (June), Winter Garden area southwest of San Antonio (July), and the seed production region of the Texas Panhandle (mid-August). Ergot incidence ranged from a trace to 10% of the heads in (self-fertile) grain sorghum fields of the LRGV. Most heads had only a few infected florets, but a few heads had 35 to 50% of the florets infected. Only trace amounts were found in grain sorghum fields in other areas of the state. Incidence and severity of ergot were greatest in fields of male-sterile sorghums grown for forage. Ergot was generally low in primary heads of male-sterile sorghums in hybrid seed production fields but, in the absence of pollen, axillary tillers sometimes developed high levels of ergot. The major impact of sorghum ergot is expected to be in hybrid seed production fields in the High Plains of Texas. Reference: (1) D. E. Frederickson et al. Mycol. Res. 95:1101, 1991.

A Description of Silk Cut, a Stress-Related Loss of Kernel Integrity in Preharvest Maize.

Silk cut is an important recurring problem of many commercial maize (Zea mays) hybrids exposed to late-season drought stress in southern Texas. Silk cut is the preharvest occurrence of one or more lateral splits in the kernel pericarp that expose the kernel tissues and embryo to either pre- or postharvest attack by fungi and insects. It can occur as multiple lateral splits anywhere on the seed surface but its primary and most common occurrence is as a single, lateral split at the kernel edge on either side or both sides of the embryo. Individual splits range from nearly microscopic to those that almost encircle the seed. Silk cut can be initiated at kernel moistures as high as 50% but is more commonly initiated and observed at kernel moistures of 28% and lower. In yearly observations from 1986 to 1994, silk cut was highest in incidence and severity on normal-yield-potential maize crops exposed to rapidly increasing environmental stress (decreasing soil moisture and high soil and air temperatures) during the latter stages of maturity but especially after black-layer formation. Hybrids with open ear tips and loose husks were among those most vulnerable to silk cut but incidence and severity varied widely across years, sites, and stress environments. Incidence also varied widely between adjacent plants. Total silk cut (kernels with silk cut colonized by fungi and noncolonized) on 105 and 110 ears from consecutive plants of two vulnerable hybrids averaged 23 and 31% but ranged from 0 to 94 and 0 to 97%, respectively. Average difference in silk cut incidence between ears of adjacent plants of these hybrids was 28 and 29% and individual differences ranged from 0 to 93 and <1 to 97%, respectively. Kernels on the top one-third of the ear had a higher average incidence of silk cut (44%) than those in the middle (38%) or bottom (shank end) (31%) positions.

A Disease of Pearl Millet in Zimbabwe Caused by Pantoea agglomerans.

Necrosis at the leaf tips and margins of pearl millet (Pennisetum glaucum (L.) R. Br.) was observed in 1995 in a Pseudomonas syringae resistance screening nursery near Bulawayo, Zimbabwe. Straw-colored lesions with a chlorotic edge often extended the leaf length, and were atypical of the round spots, with a brown margin, caused by P. syringae (1). Bacteria were isolated from cut lesions macerated in water by dilution streaking onto King's medium B and nutrient agar. A gram-negative, nonfluorescent, fermentative, rod-shaped bacterium, forming yellow colonies on nutrient agar was consistently observed. Three pots of 10, 2-to 3-week-old seedlings of a susceptible cultivar, 852B, were inoculated with a 108 CFU per ml suspension from cultures by misting or injection into the whorl. In three experiments, the treatment and uninoculated control were incubated at 25°C and 95% relative humidity for 48 h before transfer to the greenhouse. The original symptoms of watersoaking at leaf tips and margins were observed after 4 days. Necrotic lesions surrounded by chlorotic tissue were observed a day later. Fluorescence on King's medium B, and levan, oxidase, potato-rot, arginine dihydrolase, 2-keto gluconate, nitrate reduction, gelatin, phenylalanine deaminase, and acid from starch tests were negative. Tobacco hypersensitivity, acid from sucrose and glycerol, aesculin hydrolysis, lipase, indole production, and growth on tetrazolium chloride were positive. The identification of the pathogen to the species level as Pantoea agglomerans (Ewing and Fife 1972) Gavini et al. 1989, formerly Erwinia herbicola, was by fatty acid analysis by the International Mycological Institute (Egham, Surrey, UK). P. agglomerans was recorded as a pathogen of pearl millet in India in 1958 (2). References: (1) G. N. Odvody and A. K. Vidaver. Sorghum Newsl. 23:134, 1980. (2) C. K. S. Rajagopalan and G. Rangaswami. Curr. Sci. 27:30, 1958.