Leaf curl disease of celery was first reported in 1981, but the etiology of the disease has never previously been unequivocally determined. The work reported in this thesis clearly showed that Colletotrichum acutatum is the causal agent of the disease in the field, although isolates of C. orbiculare also produced the same syndrome following artificial inoculation. These two pathogens had been previously shown to cause leaf-spotting and anthracnose of celery respectively. In my studies however, leaf spot and anthracnose were never observed in the field nor could their symptoms be induced in artificial inoculation with these taxa.
In comparative studies, it was possible to readily distinguish both C. acutatum and C. orbiculare on the basis of cultural and morphological differences. In addition, isolates of C. acutatum readily produced phialoconidia upon germination in vivo and in vitro\ however, isolates of C. orbiculare lacked this ability. Among the isolates of C. acutatum, the predominance of fiisoid-shaped conidia varied and was influenced by the growth medium used. Conidium size ranges for both pathogens were also extended beyond those previously published.
The disease syndrome was initially characterised by epinastic plant growth which occurred within 2-3d of inoculation. Although a spectacular symptom and the one which gives the disease its name, this leaf curling was of minor significance compared to the rapid hydrosis and then often complete necrosis of the emerging crown leaves. Apart from this symptom, celery appeared to be a poor host of both pathogens since no histological evidence was found of fungal invasion beyond production of infection vesicles which were confined to epidermal cells of distorted leaves. Disease appeared to initiate in the field from inoculum of saprophytically produced phialoconidia of C. acutatum which had developed epiphytically on the leaves. Celery plant structure enabled these conidia to subsequently be carried in water droplets down to the crown tissue.
Alternative hosts were not believed to be involved in the disease cycle of celery leaf curl, although several new hosts of C. acutatum (coriander, chervil, celpar and watermelon) were identified. The fungus was not recovered from soil and celery crop debris buried in the soil. The disease was recorded in nursery plants for the first time during this study and although symptoms were often less obvious in these young plants, it was speculated that infected nursery plants might be the primary source of inoculum for field infections.
Field disease incidence was not correlated with rainfall in 1991. Appressorium formation and leaf distortion were enhanced at temperatures from 16-22°C, and while very few appressoria formed above 28°C, hydrosis and necrosis were most severe at and above this temperature. Field and laboratory studies both showed that infection was most severe in rapidly growing plants between 5-9w of age.
It was speculated that leaf curl disease epinasty may be linked to a disruption in the level of IAA in the host. When a paste containing this auxin was externally applied to healthy plants, similar distortion symptoms occurred.
Some celery cultivars were more susceptible than others although none were resistant following artificial inoculations with the pathogen. The studies showed that the more susceptible but agronomically desirable cultivars, Tendercrisp and Bishop, should be restricted to cooler, less disease-conducive periods, while during warm months, moderately resistant cultivars such as Hercules and Summit would be more reliable. Some experimental celery lines were also less susceptible than currently used cultivars, however no useful levels of resistance were identified in 5 wild Apium spp. examined.