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EXOTIC RACES OF COLLETOTRICHUM GLOEOSPORIOIDES POSE POTENTIAL THREAT TO AUSTRALIAN STYLOSANTHES CULTIVARS

S. Chakraborty1, C.D. Fernandes2, M.d'A. Charchar3 and S. Kelemu4

1CSIRO Tropical Agriculture, CRC for Tropical Plant Pathology, 2EMBRAPA-CNPGC, 3EMBRAPA-CPAC and 4Tropical Forages Program, CIAT

Abstract

Extensive pathogenic variation in the South American anthracnose pathogen Colletotrichum gloeosporioides was detected from screenings of Australian host differentials and other selections of Stylosanthes guianensis, S. scabra, S. macrocephala and S. capitata in Brazil. Pathogen diversity in South America is more extensive than what is present in Australia. Some pathogen isolates caused severe anthracnose on accessions and cultivars, which are highly resistant to all Australian races. If accidentally introduced, these can potentially devastate Australian cultivars.

Key words: Tropical pasture, pathogen diversity, centre of origin, risk assessment.

Species of the tropical pasture legume, Stylosanthes spp., introduced from south and central America, provide nutritive forage for animals and improve soil fertility. Inadvertently, strains of the anthracnose pathogen, Colletotrichum gloeosporioides, have been introduced with Stylosanthes germplasm into many countr- ies, including Australia. Worldwide, anthracnose restricts the utilisation, productivity and spread of Stylosanthes. In Australia, 4 races in each of 2 biotypes have devastated previously resistant cultivars following their release. Pathogenic specialisation exists in Colombia and Brazil, and South America is considered the centre of host-pathogen diversity.

Building on a preliminary study (1), this paper reports two further studies on a more extensive characterisation of pathogenic variation in South American isolates of C. gloeosporioides. In the first study, 66 isolates were screened in glasshouse trials in Brazil using 4 Australian biotype A differentials, S. scabra cultivars Seca and Fitzroy and accessions Q10042 and 93116. Seedlings were inoculated with 106 conidia/ml suspension of a single isolate, maintained in a saturated atmosphere for 48 hr and assessed for anthracnose severity using a 0-9 point scale (2). Disease severity data were loge (severity+1) transformed and isolates were classified into races using linear discriminant functions, developed using 182 Australian isolates of known racial grouping (2).

In the second study 23 isolates from South America were screened in Brazil using 24 lines of S. guianensis, S. scabra, S. macrocephala and S. capitata using methods described above. Analysis of variance was used to summarise and to draw inferences.

Results and discussion

The training data set of 182 Australian isolates was clustered into three groups following Ward's method to develop linear discriminant functions (2). South American isolates, within the 95th percentile of the distance from a cluster centre, were classified as a member of that cluster and labelled with the cluster number, while isolates lying outside these limits were unclassified and were represented by a zero (Fig. 1). Fourty four of the 66 Brazilian isolates could not be classified into any known Australian biotype A race cluster. Two were classified as race 2 (virulent on Fitzroy and Q10042) and 20 were classified as race 3 (virulent on Seca) but none fitted the race 1 (virulent only on Fitzroy) virulence pattern. This shows that the wide range of pathogenic diversity in South America can not be adequately classified using the Australian differential set.

Accessions of S. guianensis were most susceptible, followed by S. capitata, and S. scabra, and accessions of S. macrocephala were the most resistant (Table 1). Of the 4 discernible groups, isolates (CG39R, CG56R, CG64 and CG65), avirulent (disease rating ) on all 4 species, constitutes group 1. Isolates (CG03, CG15, CG22R, CG25, CG26, CG27, CG28, CG30, CG31 and CG 39), virulent (disease rating 1) only on S. guianensis, represent group 2. Isolates CG13, CG22, CG29, and CG50, virulent on 2-3 species represent group 3. The remaining 5 isolates, CG20, CG41, CG42, CG57R and CG58R, representing group 4, are virulent on all 4 species (Table 1). All group 2 isolates originate from S. guianensis and isolates in groups 3 and 4 were mainly from S. capitata with one isolate in each group from S. scabra. Group 2 appears similar to the Australian biotype B with pathogenicity towards S. guianensis only. Groups 3 and 4 represent complex races not present in Australia. S. guianensis can be infected with Australian biotype A isolates producing biotype A like symptoms (Chakraborty, unpublished) and a putative inter- biotype recombinant has been detected in Australia (3), but isolates causing serious anthracnose to both biotype A and B hosts have not been detected in Australia. In common with earlier studies (1), this study has revealed extensive pathogenic variation in C. gloeosporioides population in South America.

Conclusion

Pathogenic diversity is more extensive in South America than what is present in Australia. Isolates that cause severe anthracnose on Australian lines otherwise highly resistant to all Australian races can potentially devastate current and future cultivars, if accidentally introduced.

References

1. Chakraborty, S., Perrott, R., Charchar, M.J., Fernandes, C.D. and Kelemu, S. 1997. Trop. Grassl. 31, 393-401.

2. Chakraborty, S., Thomas, M.R., and Ellis, N. 1996. Phytopathology 86, 283-289.

3. Masel, A., He, C., Poplawski, A.M., Irwin, J.A.G. and Manners, J.M. 1996. Mol. Pl-Micro. Int. 9, 339-348.

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