CABI Bioscience, U.K. Centre (Egham), Surrey, TW20 9TY, U.K.

Background and objectives
Tracheomycosis or vascular wilt of coffee was first reported on C. exceisa in the Central African Republic in 1946 and the causal agent (Fusarium xylarioides) identified in 1948. Subsequently, many hectares of C. exceisa and C. canephora were destroyed throughout West and Central Africa including Ivory Coast, Cameroon and in the Democratic Republic of Congo (DRC). The pathogen also attacks Coffea arabica and is endemic in all coffee growing areas of Ethiopia. During the 1950s and 1960s, the disease was considered to be the most serious disease of coffee in Africa and millions of trees were destroyed. Systematic elimination of affected plants over vast areas combined with the development of breeding programmes effectively reduced its impact to a minor disease. However, a wilt-like disease of coffee was again reported from near the town of lsiro (DRC) in 1986. The incidence increased dramatically and spread to the neighbouring province and by 1992 was widespread. Similarly from 1993, farmers began to reporting a wilt disease of coffee in western Uganda near to the border with the DRC and later in 1995, in central Uganda. CABI Bioscience was approached by the International Coffee organization (]CO) in 1996 to undertake surveys of the affected areas in order to confirm the nature and extent of the problem.

Results and Conclusions
Disease surveys, conducted by CABI Bioscience in collaboration with Congolese and Ugandan counterparts, demonstrated that the disease was widespread on robusta coffee in the North-East of the DRC and in western Uganda and considerable yield losses have resulted [1]. The disease was also identified in localised outbreaks in several districts in central Uganda where most Ugandan coffee is produced.

In both countries and at all sites visited, symptoms were typical of a vascular wilt with leaves initially becoming flaccid, followed by desiccation and finally, abscission. Dieback of the branches usually appeared at the top of the tree and spread downwards; the branches may blacken and the tree dies. The bark of the tree becomes hypertrophied with numerous cracks and a characteristic blue-black staining of the xylem is observed under the bark. Fusarium xylarioides was consistently isolated from diseased samples. Also, dark-violet perithecia of the teleomorph Gibberelia xylarioides were observed in the cracks in the bark at the base of the trees during the rainy season; ascospores were easily seen in squashes of the perithecia.

This disease is clearly a serious threat to coffee production in Africa and the causes of its reemergence are under investigation. One possibility is that a new, aggressive genotype of the pathogen may have arisen. Molecular analysis of F. xylarioides isolates have been carried out. Isolates from stem lesions of robusta coffee from the epidemic areas in DRC and Uganda have so far given identical banding patterns using RDNA-IGS RFLP'S, P-tubulin RFLP's and genomic fingerprinting with simple-sequence-repeat primers and M13-core primer (Brayford and Flood, unpublished). These results suggest a low level of genetic diversity amongst epidemic strains. Isolates from other species of coffee (C. arabica, C. exceisa) and parts of Africa (Ivory Coast, Ethiopia) gave different band patterns. These results are surprising for a heterothallic fungus which produces its sexual stage in nature and support the hypothesis that a new, more aggressive strain of the pathogen may have arisen within the wider gene pool of the pathogen population in Africa. Molecular differentiation of isolates from robusta coffee and those from C. arabica and C. exceisa may indicate that host specialization occurs in this pathogen and no C. arabica has been affected in DRC or Uganda during the current disease outbreak.

1. Flood, J. & Brayford, D. 1997. Proceedings of the 17th International Conference on Coffee Science. (in press).