Date of Award


Document Type


Degree Name

Doctor of Philosophy (PhD)

First Advisor

Gerard T. Berggren, Jr.

Second Advisor

Johnnie P. Snow


Soybean (Glycine max) seedling natural infection caused by Rhizoctonia solani Kuhn, anastomosis group 1, intraspecific groups IA and IB (AG1-IA and AG1-IB), causal agents of Rhizoctonia foliar blights of soybeans, is first reported. Infections were predicted by experimental inoculum levels with r$\sp2$ = 0.77-0.87 (P $<$ 0.001). Twenty locations surveyed in 2 years in south Louisiana showed that web blight was the major disease type. Culture characteristics indicated that associated isolates were R. solani Kuhn, AG1-IB. Morphogenisis of microsclerotia from web blight isolates showed a lateral growth type different from the traditionally described loose growth type observed for sasakii-type sclerotia, indicating a genetic difference between AG1-IB and AG1-IA in R. solani. Components of Rhizoctonia aerial blight were quantified from 1986 to 1988. Primary infections were high early in the season and significantly correlated with average amount of daily rainfall. The establishment of disease foci was mainly determined by the rainfall events prior to canopy closure. Significant expansion of disease foci occurred only after canopy closure. Development of aerial blight is divided into two phases related to canopy closure. The first consists of primary infection and has a soilborne nature. Variance-to-mean ratios indicated that early infection was aggregated, and different cluster sizes were determined by paired-quadrat variance. The second phase has a leafborne nature and results in disease focus expansion. Factorial experiments under controlled conditions showed a strong influence of free moisture and plant growth stage on disease focus expansion. Disease focus radius was a linear function of accumulated free moisture hours. Diseased plants/focus and disease incidence were best fitted with circle equations. Slopes of equations were proportional to plant growth stage. Under field conditions, disease focus expansion was explained well using accumulated rain days and soybean growth stages at inoculation as predictors. Natural disease incidence late in the season was determined by distribution pattern and amount of early infection. Incorporation of an aggregation factor into a logistic disease model improved prediction.