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© 2008 Plant Management Network.
Accepted for publication 19 February 2008. Published 19 May 2008.

Evaluation of Sorghum Germplasm from China against Claviceps africana, Causal Agent of Sorghum Ergot

Louis K. Prom, USDA-ARS, Southern Plains Agriculture Research Center, College Station, TX 77845; John E. Erpelding, USDA-ARS Tropical Agriculture Research Station, 2200 Pedro Albizu Campos Ave., Mayaguez, PR 00680; and Noe Montes-Garcia, Instituto Nacional de Investigacuones Forestales, Agricolas y Pecuarias, Centro de Investigación Regional del Noreste, Rio Bravo, Tamaulipas, Mexico CP 88900

Corresponding author: Louis K. Prom.

Prom, L. K., Erpelding, J. E., and Montes-Garcia, N. 2008. Evaluation of sorghum germplasm from China against Claviceps africana, causal agent of sorghum [Sorghum bicolor (L.) Moench] ergot. Online. Plant Health Progress doi:10.1094/PHP-2008-0519-01-RS.


Forty Chinese sorghum landraces maintained by the USDA-ARS Plant Genetic Resources Conservation Unit, Griffin, GA were evaluated for ergot resistance at the Texas A&M Research Farm, College Station, Texas, during the 2005 and 2006 growing seasons. The male sterile line, ATx623, was included as a susceptible control and three IS8525 derived lines were included as resistant controls. The disease infection level was low in the susceptible check in 2005 due to unfavorable environmental conditions, but the majority of the Chinese accessions showed a higher level of tolerance than the resistant controls and in contrast, infection severity was high in 2006. The IS8525 resistant controls averaged 25% infection compared to an average infection of 18% for the 40 Chinese accessions. Four Chinese accessions, PI63923, PI511832, PI610749, and PI610688, recorded less than 10% ergot infection and thus, these four accessions may possess genes for ergot resistance. Further research is underway to evaluate these accessions under multi-environments to confirm resistance and to determine if the resistance is associated with pollination characteristics.


Sorghum ergot is a predominant disease in Asia and Africa. In 1996, sorghum ergot was reported in Brazil (4) and Australia (21), with the disease observed in the United States in 1997 (11). Globally, sorghum ergot is caused by three Claviceps species. Claviceps africana Frederickson, Mantle, & de Milliano is the most common and is found in the Americas (11,5), Australia, Asia, and Africa. Claviceps sorghi P. Kulkarni et al. is limited to Asia and C. sorghicola Tsukiboshi, Shimanuki, & Uematsu is reported only in Japan (3,7,15,24,25). Claviceps africana and C. sorghi share the same anamorph, Sphacelia sorghi, which is different from that of C. sorghicola (12). The pathogen infects unfertilized ovaries and therefore poses a serious threat to the hybrid seed production industry. Male-sterile sorghum lines used in hybrid seed production are highly susceptible to the disease, especially when pollination is delayed due to environmental or genetic factors (3,10). Yield losses due to ergot in hybrid seed production fields ranged from 10 to 80% (3,22). In addition, the sugary exudates produced by the pathogen reduce seed quality and make harvesting and seed processing more difficult (3).

Management strategies used to minimize the impact of ergot include fungicide treatment, pollen management, and the use of resistant or tolerant sorghum lines (1,20). The use of fungicides for disease management has been inconsistent and frequent applications are required to reduce disease severity (6,17). For low input sorghum production systems, control with fungicides is not economically feasible and there are environmental and human health concerns associated with chemical control. Pollen management strategies can be successfully used for hybrid seed production, but they cannot eliminate disease outbreaks due to environmental variation (3). Thus, host plant resistance would appear to be the best approach for controlling the disease.

Ergot resistance sources have been reported by a number of researchers (13,14,18,19,23). Most sources of resistance are not stable across environments and, at present no stable source of resistance is available for sorghum improvement. Thus, it is imperative to explore the possibilities of identifying resistance sources from exotic germplasm. The aim of this study was to evaluate potential sources of ergot resistance within the USDA-ARS National Plant Germplasm System (NPGS) sorghum collection.

Chinese Accessions and Ergot Evaluation

A random survey of 2,013 accessions from the NPGS sorghum collection were evaluated at the USDA-ARS Tropical Agriculture Research Station (TARS), Isabela, Puerto Rico in 2001 to identify sources of ergot resistance ( Results of this evaluation showed a low percentage of ergot infection for the Chinese sorghum collection. Therefore, 40 sorghum accessions maintained by the NPGS, Griffin, GA were randomly selected from the Chinese landrace collection for evaluation. Three of 40 Chinese sorghum accessions (Grif627, PI542747, and PI610688) have been evaluated over several growing seasons at the TARS and were included in the study to evaluate ergot response in Texas. IS8525 was included in the evaluation as a resistant control (19) and was obtained from R. G. Henzell (Queensland Department of Primary Industries, Warwick, Australia). IS8525 is a heterogeneous Ethiopian landrace and has two morphological phenotypes based on midrib juiciness, designated as IS8525J (juicy midrib) and IS8525D (dry midrib), and both were included in the study as resistant controls. The male sterile line, ATx623, was included as a susceptible control. IS8525J, IS8525D, and ATx623 were obtained from the sorghum breeding program at Texas A&M University, College Station, TX.

Experiments were conducted in 2005 and 2006 at the Texas A&M Agricultural Research Farm, College Station, TX. Field preparation included fall plowing followed by a fertilizer application of 40-65-90 (NPK) kg/ha before planting. An additional 90 kg of N per ha was applied as top dressing five weeks after planting. A pre-emergent insecticide (Counter 20 CR, BASF Group, Southfield, MI) for seedling insect control and herbicide (Atrazine, Syngenta Crop Protection Inc. Greenboro, NC) for weed control were applied before planting. The experiment in 2005 was planted on April 9 and the 2006 experiment was planted on April 4. The experiments were conducted using a randomized complete block design with three replications. Seeds were planted in 6 m rows with 0.31 m row spacing. There were 20 to 30 plants per row, and each row was considered a replication.

The ergot inoculation method was previously described by Prom and Erpelding (16). Briefly, C. africana (Texas isolate) conidia from infected greenhouse-grown sorghum plants were soaked in plastic pans containing a 0.1% solution of Tween 20 in sterile distilled water. The spore suspension was filtered and adjusted to 1 × 106 conidia/ml for inoculation. Five panicles from each replication were tagged and inoculated before or at the start of anthesis. Panicles were sprayed until run-off and then bagged for seven days. Three control panicles per replication were sprayed with sterile distilled water and then bagged for seven days. Due to the differences in developmental stage, panicles from each of the lines were inoculated on different dates. No drastic change in temperature for the 2005 and 2006 evaluations was observed within the three weeks that the plants were inoculated and bagged. Disease evaluation of each inoculated or control panicle was conducted at 10 and 15 days after inoculation (DAI). The total number of florets and the number of infected florets were counted for each panicle to determine the percentage of ergot severity. The percent ergot severity was averaged for the five panicles for statistical analysis. Data for percent ergot infection were subjected to the analysis of variance using the command PROC GLM (SAS version 9.1, SAS Institute Inc., Cary, NC) to determine the effect of sorghum accessions. Accession least-squares means were compared using Tukey-Kramer test at the 5% probability level.

Ergot Infection and Resistance Sources

The treatment main effect of sorghum accession was highly significant at the 1% probability level in both years (Table 1). Disease severity was low in 2005 as compared to 2006. Infection severity at 15 DAI for the susceptible, male-sterile control (ATx623) was less than 42% in 2005 with nearly a two-fold difference in disease severity observed in 2006. The average ergot severity for the resistant controls (IS8525, IS8525J, and IS8525D) was 4% in 2005 compared to an average of 25% in 2006. The infection severity for the 40 Chinese sorghum accessions averaged 3.6% in 2005 and ranged from 0.1 to 19.2% for the evaluation conducted 15 DAI. In contrast, infection severity averaged 18.6% in 2006 for the Chinese accessions and ranged from 4.8 to 48% at 15 DAI. Although infection severity was lower in 2005, a four-fold increase in disease severity was observed from 10 to 15 DAI. In 2006, a two-fold increase in disease severity was observed between 10 to 15 DAI. Only one accession (PI567929) showed a higher disease severity in 2005 as compared to 2006. All the Chinese accessions showed an increase in disease severity from 10 to 15 DAI in 2006. Four accessions (PI563550, PI563960, PI610691, and PI610742) showed no increase in disease severity from 10 to 15 DAI in 2005. Three accessions (PI563905, PI542747, and PI567929) that showed the highest level of disease severity in 2005 also had the largest increase in disease severity from 10 to 15 DAI. No pattern was observed in 2006 for infection severity from 10 to 15 DAI. Only one accession (PI542747) consistently showed a high level of infection severity in 2005 and 2006. In 2006, disease severity for PI542747 was not significantly different from the susceptible control (ATx623). In both years, the majority of the Chinese accessions showed less disease severity than the IS8525 resistant controls, and in 2006 four accessions (PI63923, PI511832, PI610749, and PI610688) exhibited less than 10% infection with ergot as compared the 25% ergot infection observed for the IS8525 controls.

Sorghum ergot caused by C. africana was first detected a decade ago in the United States and is now endemic in most sorghum-producing states. The pathogen is a serious threat to the seed industry where male-sterile sorghum lines are used for hybrid seed production (3,10). Several disease evaluation studies have indicated that a variation in ergot resistance is present in sorghum germplasm (5,8,14,23). In most cases, the expression of resistance was associated with rapid self-pollination characteristics resulting in fertilization reducing the potential for ergot infection (3). Although this type of resistance would be functional in varieties and hybrids, it would be ineffective for hybrid seed production. When these sources of genetic resistance are crossed to A3-cytoplasm male-sterile testers, the sterile hybrid that is developed is highly susceptible to ergot infection, since the pollen-based resistance mechanism is circumvented (16). Reed et al. (18) identified IS14131 and IS14257 as resistance sources for ergot in a field study; however, the inheritance and physiological basis for this resistance has yet to be established. As a whole, the lack of confirmed sources of resistance to sorghum ergot is a serious problem that requires urgent attention. Studies conducted so far clearly indicate that no sorghum genotype provides suitable ergot resistance for the development of male-sterile lines (3,9,12,13).

To identify potential ergot resistance sources with a higher level of resistance as compared to IS8525, 40 Chinese sorghum landraces were evaluated in the present study in 2005 and 2006. As indicated in the earlier study by Dahlberg et al. (5), IS8525 was the only reported germplasm source of physiological resistance to ergot in a male-sterile genetic background. Male-sterile hybrids produced by means of IS8525 were shown to be significantly more resistant to ergot than susceptible checks (19); however, male-sterile hybrids derived from crosses between IS8525 derived lines (IS8525J and IS8525D) with A2Tx623 were found to be susceptible to ergot (16). Hence, to confirm the results from earlier studies and to assess the comparative resistance performance, IS8525, IS8525J, and IS8525D were also included as resistant checks in this study. The present study clearly shows that these lines are not as resistant to C. africana as the majority of the Chinese accessions. This would suggest that potential sources of resistance may be present not only in the Chinese sorghum collection, but in other collections maintained by the NPGS, and further evaluation of the NPGS sorghum collection will be essential.

Weather conditions during the 2005 evaluation were not conducive to ergot development as reflected by the low severity in ergot infection in all the accessions tested. However, ergot severity in susceptible ATx623 was significantly higher than all other accessions evaluated in 2005. In contrast, environmental conditions in 2006 were favorable for ergot infection and high levels of infection were observed for ATx623. From the 40 Chinese accessions evaluated, four accessions (PI63923, PI511832, PI610749, and PI610688) recorded ergot infection less than 10% during the 2006 evaluation. As a result, these four accessions are considered highly tolerant to ergot infection and may possess genes for resistance. However, genotypes that apparently are resistant at one location may be susceptible at another (2). Thus, research is underway to evaluate these accessions under multi-environments to confirm the high level of tolerance observed in this study. Three of the accessions have been evaluated at the TARS, Isabela, Puerto Rico and similar results have been observed (Erpelding and Prom, unpublished results). The highly resistant accession (PI610688) averaged 1.3% ergot infection in Puerto Rico and the two susceptible accessions (Grif627 and PI542747) averaged 36 and 32% infection, respectively. Preliminary evaluation of Grif627 suggests that poor pollen viability may be responsible for the greater ergot susceptibility observed for this germplasm line. Furthermore, these four accessions will be characterized in corresponding male-sterile hybrids to determine whether they possess physiological resistance to ergot infection and not pollen-mediated resistance as was observed for IS8525.


Mention of trade names or commercial products in this article is solely for the purpose of providing specific information and does not imply recommendation or endorsement by the United States Department of Agriculture.

Literature Cited

1. Bandyopadhyay, R. 1999. Role of ICRISAT in sorghum ergot research. Pages 169-177 in: Proc. of the Global Conf. Ergot Sorghum (1-8 June 1997). C. R. Casela and J.A. Dahlberg, eds. EMBRAPA, Sete Lagaos, Brazil.

2. Bandyopadhyay, R., Frederickson, D. E., McLaren, N and Odvody, G. N. 1996. Ergot: A global threat to sorghum. Int. Sorg. Millets Newsl. 37:1-132.

3. Bandyopadhyay, R., Frederickson, D. E., McLaren., N, Odvody, G. N., and Ryley, M. J. 1998. Ergot: A new disease threat to sorghum in the Americas and Australia. Plant Dis. 82:356-367.

4. Casela, R., Ferreira, A. S., and Pinto, N. F. J. A. 1999. Sugary disease of sorghum in Brazil: An Overview. Pages 23-25 in: Proc. Global Conf. Ergot Sorghum (1-8 June 1997). C. R. Casela and J.A. Dahlberg, eds. EMBRAPA, Sete Lagaos, Brazil.

5. Dahlberg, J., Bandyopadhyay, R., Rooney, B., Odvody, G., and Frederickson, D. 1998. Host-plant strategies within the United States. In: Proc. of the Status of Sorghum Ergot in North America (24-26 June 1998). J. A. Dahlberg, ed. Corpus Christi, TX.

6. de Almeida Pinto, N. F. J., da Silva Ferreira, A., and Casela, C. R. 1999. Pages 158-160 in: Proc. of the Global Conf. Ergot Sorghum (1-8 June 1997). C. R. Casela and J.A. Dahlberg, eds. EMBRAPA, Sete Lagaos, Brazil.

7. Frederickson, D., Mantle, P. G., and De Milliano, W. A. J. 1991. Claviceps africana sp. Nov.; the distinctive ergot pathogen of sorghum in Africa. Mycol. Res. 95:1101-1107.

8. Frederickson, D. E., Mantle, P. G., and De Milliano, W. A. J. 1994. Susceptibility to ergot in Zimbabwe of sorghums that remained uninfected in their native climates in Ethiopia and Rwanda. Plant Pathol. 43:27–32.

9. Frederickson, D. E., and McLaren, N. W. 2000. Ergot. Pages 40-42 in: Compendium of Sorghum Diseases. R. A. Frederiksen and G. N. Odvody, Eds. The American Phytopathological Society, St. Paul, MN.

10. Futrell, M. C., and Webster, O. J. 1965. Ergot infection and sterility in grain sorghum. Plant Dis. Rep. 49:680-683.

11. Isakeit, T., Odvody, G. N., and Shelby, R. A. 1998. First report of sorghum ergot caused by Claviceps africana in the United States. Plant Dis. 82:592.

12. Mantle, P. G., and Bogo, A. 2002. Biosynthesis of bioactive honeydew oligosaccharides by sorghum ergot pathogens. Pages 91-94 in: Sorghum and Millet Diseases. J. L. Leslie, ed. Iowa State Press.

13. McLaren, N. W. 1992. Quantifying resistance of sorghum genotypes to the sugary disease pathogen (Claviceps africana). Plant Dis. 76:986-988.

14. Musabyimana, T., Sehene, C., and Bandyopadhyay, R. 1995. Ergot resistance in sorghum in relation to flowering, inoculation technique and disease development. Plant Pathol. 44:109-115.

15. Pažoutová, S., Bandyopadhyay, R., Frederickson, D. E., Mantle, P. G., and Frederiksen, R. A. 2000. Relations among sorghum ergot isolates from the Americas, Africa, India, and Australia. Plant Dis. 84:437-442.

16. Prom, L. K., and Erpelding, J. E. 2006. Ergot response for the sorghum genotype IS8525. Plant Pathol. J. 5:216-220.

17. Prom, L. K., and Isakeit, T. 2003. Laboratory, greenhouse, and field assessment of fourteen fungicides for activity against Claviceps africana, causal agent of sorghum ergot. Plant Dis. 87:252-258.

18. Reed, J. D., Ramundo, B. A., Claflin, L. E., and Tuinstra, M. R. 2002. Analysis of resistance to ergot in sorghum and potential alternate hosts. Crop Sci. 42:1135-1138.

19. Reed, J. D., Tuinstra, M. R., McLaren, N. W., Kofoid, K. D., Ochanda, N. W., and Claflin, L. E. 2002. Analysis of combining ability for ergot resistance in grain sorghum. Crop Sci. 42:1818-1823.

20. Reis, E. M., and Casa Blum, M. M. 1999. Integrated management of sugary disease of sorghum – Practical Aspects. Pages 161-166 in: Proc. Global Conf. Ergot Sorghum (1-8 June 1997). C. R. Casela and J.A. Dahlberg, eds. EMBRAPA, Sete Lagaos, Brazil.

21. Ryley, M. J., and Henzell, B. 1999. Sorghum ergot in Australia.Pages 182-190 in: Proc. Global Conf. Ergot Sorghum (1-8 June 1997). C. R. Casela and J.A. Dahlberg, eds. EMBRAPA, Sete Lagaos, Brazil.

22. Sangitrao, C. S., Indira, S., and Bandyopadhyay, R. 1999. Sorghum ergot in India. Pages 41-54 in: Proc. Global Conf. Ergot Sorghum (1-8 June 1997). C. R. Casela and J.A. Dahlberg, eds. EMBRAPA, Sete Lagaos, Brazil.

23. Tegegne, G., Bandyopadhyay, R., Mulatu, T., and Kebede, Y. 1994. Screening for ergot resistance in sorghum. Plant Dis. 78:873-876.

24. Tooley, P. W., O'Neill, N. R., Goley, E. D., and Carras, M. M. 2000. Assessment of diversity in Claviceps africana and other Claviceps species by RAM and AFLP analyses. Phytopathology 90:1126-1130.

25. Tsukiboshi, T., Shimanuki, T., and Koga, H. 2001. Claviceps sorghicola and C. africana, the ergot pathogens of sorghum, and their cultural control in Japan. JARQ 35:221-226.