ASCOCHYTA SPP - REVIEW OF THE LITERATURE AND SYNTHESIS

Three related Sphaeropsidales (Ascochyta pisi, Ascochyta pinodes (teleomorph Mycosphaerella pinodes, Phoma medicaginis var pinodella) induce spot-like necrosis on pea organs and cause yield and seed quality losses. Diagnosis of the 3 agents based on symptoms remains partly speculative: symptoms are fairly similar in the 3 species and may be mixed on the same host plant However, a diagnostic key is provided by field observation associated with laboratory investigation. Among the 3 seed-borne pathogens, A pisi is the most frequently observed in the seeds. Nevertheless, because of the agressiveness of each fungus, Neegard (1979) estimates that the acceptable disease tolerance level for A pisi is 4-fold that for M pinodes. The majority of seeds contaminated by A pisi are attacked without typical symptoms on pods. Primary epicotyl infections are not generally visually detectable. In contrast with M pinodes and P medicaginis, A pisi produces neither microsclerotia nor chlamydospores. The chlamydospores of P medicaginis are most frequently isolated from the soil, their agressiveness towards roots (footrot) increases with continuous pea cropping. Ten percent of primary M pinodes infections appear during the 4th and 5th week on embryonary bracts. The bulk of infections are observed on the epicotyl after the 6th week. Weak contamination is able to provoke a high level of agressivity towards the plumule. Dispersal of several generations of pycnospores in the field occurs only through rainfall (splashing) and remains limited. Nevertheless, wind-borne ascospores provided from the homothallic phase of M pinodes provide higher potentialities for transmission and secondary spread of the disease. Heath and Wood (1969) showed the formation of leafspots induced by M pinodes. They discriminated limited necroses from spreading lesions. Limited necroses are brown, have a slow growth rate and thickened cell walls. They are almost sterile. Spreading lesions are light green with degraded wails and bear numerous pycnidia. Their frequency increases with inoculum concentration, spore deposit, ageing and turgidity of organs. According to these authors, the major factor in hindering the development of limited lesions is not the resistance of plant cell wall to maceration. This suggests the role of de novo biosynthesis of one (or more) growth inhibitor(s) rather than the inhibition of macerating enzymes by polyphenols. The development of spreading lesions is associated with M pinodes' ability to inactivate the phytoalexin in pea (pisatin) by enzymes (inducible demethylation). The variability in virulence of A pisi and M pinodes has been recently described for 2 separate sets of pea lines. Two strains, showing a good resistance of the epicotyl to isolates and pathotypes of M pinodes, may become useful sources of resistance. A pisi resistance exists in a line selected towards the more frequently isolated pathotypes in Europe. Nevertheless, this resistance does not ensure incompatibility towards all European pathotypes. Currently, the methods of control consist of fungicide treatment of seeds. A long-term strategy for Ascochyta disease must be based on the breeding for resistant cultivars and the production of disease-free seeds.