Gradients of primary and secondary infection by Monilinia vaccinii-corymbosi from point sources of ascospores and conidia

Authors
Citation
Kd. Cox et H. Scherm, Gradients of primary and secondary infection by Monilinia vaccinii-corymbosi from point sources of ascospores and conidia, PLANT DIS, 85(9), 2001, pp. 955-959
Citations number
33
Categorie Soggetti
Plant Sciences
Journal title
PLANT DISEASE
ISSN journal
01912917 → ACNP
Volume
85
Issue
9
Year of publication
2001
Pages
955 - 959
Database
ISI
SICI code
0191-2917(200109)85:9<955:GOPASI>2.0.ZU;2-Y
Abstract
Spread of mummy berry disease of blueberry, caused by Monilinia vaccinii-co rymbosi, occurs in two discrete monocycles; primary infection by ascospores results in shoot blight, while secondary infection of open flowers by coni dia leads to fruit mummification. Gradients of primary and secondary infect ion from point sources of ascospores and conidia placed in separate plant r ows were recorded in each of 2 years at two sites with no history of the di sease. Primary infection gradients were longer downwind than upwind, with 9 5% of blighted shoots occurring within 30 in of the ascospore point source. This observation, along with a positive correlation (r = 0.852, P = 0.0072 , n = 8) between the distance over which shoot blight occurred and wind spe ed parallel to the row, supports the role of wind as a key factor in ascosp ore dispersal. By contrast, secondary infection gradients were shorter down wind and longer upwind, with 95% of infected fruit occurring within 20 in o f the conidial point source. The shorter downwind spread of secondary infec tion, along with a nonsignificant correlation (r = -0.649, P = 0.0812, n = 8) between the distance over which infected fruit occurred and wind speed, suggests that factors other than wind are important in the transfer of coni dia to open flowers; this could include conidial dispersal by bee pollinato rs, which have been shown previously to forage primarily upwind. Exponentia l and Pareto cumulative distribution functions were fitted to cumulative co unts of blighted shoots and infected fruit to model spread of primary and s econdary infection. The Pareto, model, which is characterized by a longer t ail and predicts more infection farther from the inoculum source, better fi ts the observed disease gradients in most cases.