|Crop Knowledge Master||Fungi|
|papaya collar rot (Plant Disease Pathogen)|
Wayne Nishijima, Extension Plant Pathologist
Department of Plant Pathology
University of Hawaii at Hilo
Collar rot of papaya has only been reported from Hawaii. The causal organism has a very wide host range and is an important pathogen of many other economically important crops such as peanuts, alfalfa, grape, ivy, anthurium, eucalyptus, and koa.
Warm-temperate and tropical regions.
Common symptoms of the disease are chlorosis, stunting, root and collar rot and eventually death of young seedlings. In the early stage of the disease, the stem at or near the ground line (collar) of the plant is usually affected. In the advanced stages, the collar and the entire root system becomes affected and numerous orange-red perithecia are produced in the collar area. Leaves become chlorotic and petioles droop and the plant eventually dies. It is not unusual for one plant in a planting hole to remain healthy while the other become infected.
Papaya collar rot produces scattered orange to red perithecia that are 320-570 Ám diameter x 265-530 Ám in length. Asci are hyaline, clavate and 11-21 Ám diameter at its widest point and 107-160 Ám in length. Ascospores are hyaline, curved, fusoid with mostly rounded ends, one to three septate and 4.3-7.1 Ám in diameter and 31-59 Ám in length. Cylindrocladium crotalariae is its imperfect stage. It produces hyaline, cylindrical, 1-3 septate conidia that measure 4.1-7.6 Ám in diameter and 46-89 Ám in length. Vesicles are globose with primary vesicles measuring 6.7-17.2 Ám in diameter x 11.4-28.6 Ám in length. The pathogen produces numerous thick-walled, brown pigmented microsclerotia that are important for long term survival in the soil.
The disease was first noticed in the Puna district of Hawaii island in 1970. This disease has been primarily observed on papaya seedlings planted in fields newly cleared of native ohia (Metrosideros collina) forests. The disease usually occurs during or following prolonged heavy rains in areas where drainage is poor.
The fungus produces abundant conidia, ascospores and microsclerotia. Conidia and ascospores are responsible for long distance spread and microsclerotia for long term survival. The fungus is capable of surviving for more than three years in the absence of host plants. Microsclerotia are more effective in killing seedlings than conidia or ascospores. Despite these attributes this disease has not been a major problem in replant fields.
The clearing of ohia forests for papaya orchards is no longer practiced and the disease incidence, therefore, is erratic. The disease does appear periodically when weather conditions (i.e. frequent and heavy rains) are favorable.
The susceptibility of four commercial lines of papaya in increasing susceptibility are Kapoho Solo, Line 8, Waimanalo and Sunrise Solo.
The fungus is sensitive to most of the broad spectrum fungicides used in papaya culture but fungicide application has usually not been necessary because of the scattered and sporadic occurrence. Spot treating of the planting sites where the disease occurs with fungicide or fumigant and replanting with containerized seedling have been successful.
Hwang, S.C., and Ko, W.H. 1976. Biology of conidia, ascospores, and microsclerotia of Calonectria crotalariae in soil. Phytopathology 66:51-54.
Laemmlen, F.F., and Aragaki, M. 1971. Collar rot of papaya caused by Calonectria sp. Plant Dis. Rep. 55:743-745.
Nishijima, W.T., and Aragaki, M. 1973. Pathogenicity and further characterization of Calonectria crotalariae causing collar rot of papaya. Phytopathology 73:553-558.
JANUARY 1993, revised APRIL 1994.