Pecan Scab

Pecan scab, caused by the fungus, Fusicladium effusum, has plagued pecan producers in humid regions since 1888. Since 1920, it has been recognized as the most destructive disease of pecan. Without fungicide applications, certain cultivars grown in the Southeastern U.S. and in other humid growing regions would experience yield losses ranging from 50-100% depending on the year. The severity of scab is primarily influenced by rainfall during the growing season and can be especially damaging in wet years.

Symptoms

Pecan scab occurs on leaves, twigs, and nut shucks. All tissues are most susceptible when young and actively growing. They become less easily infected when mature. Leaves are susceptible from bud break until they reach maturity. Nut shucks are susceptible from development until maturity.

Leaflets may drop if they are infected at the petiole base, but leaf infection does not generally result in complete defoliation of the compound leaves of pecan. Instead, leaf scab results in a reduced photosynthetic area, making leaves less efficient.

Current-season twigs are infected in the tender green, rapid growth stage. Highly susceptible cultivars grown under conditions favorable for pecan scab can suffer from stem die-back.

The most significant damage from pecan scab results from the development of scab lesions on the nut shuck between the onset of fruit growth and shell hardening. The probability of fruit death and drop apparently increases greatly if more than 50% of the shuck is covered with lesions. Quality losses are observed when more than 25% of the shuck surface is covered with scab. Severe scab infections can also cause the shuck to adhere to the nut surface causing “stick-tights” or nuts that won’t fall free of the shuck at harvest. Scab infection can dramatically reduce nut size, depending on the timing and severity of infection. Early infections can cause tremendous yield and crop quality reductions. Once the shell hardens, subsequent infection is apparently more cosmetic then damaging.

Disease Development

The scab fungus overwinters on tissue infected the previous season. In 1924, it was proposed that primary inoculum sources remaining in the tree were more important than those falling to the ground. Spores have been detected as early as February, but typically the major release of spores is in April, coinciding with bud break.

The release of spores is brought about by surface drying and decreasing relative humidity. Spore release peaks in the morning as dew dries. Secondary release may occur after daytime rain showers. Spores can be spread by rain or dew onto susceptible tissue. Spread to other trees is facilitated by the wind.

Free moisture is required for spore germination and infection. Infection can occur within a range of 50-95 °F, with an optimum range of 59-77 °F. Twelve hours of wetness is required for significant leaf infection, although infection has been reported to occur within 4-6 hrs under certain conditions.

Rain frequency is more important than total rainfall in determining scab severity. After infection, leaf lesions become visible in 7-8 days and continue to expand for 7-14 days. Spores produced within these lesions serve as secondary inoculum and further spreads the pathogen. This cycle can be repeated many times during a season.

Control

The most common disease control measure for scab control is the application of preventative fungicides. Currently, the scab is controlled by a series of 7 to 10 fungicide sprays applied between bud break (early April) and shell hardening (early to mid-August). Because fungicides for scab protection are preventative in nature, producers must make applications on a fixed schedule of 10-21 days, depending on orchard history and environmental conditions.

Resistant cultivars would be the most economical and practical control measure. Differences among cultivars in regard to susceptibility to scab have long been observed. By 1927, research confirmed that the scab fungus exists as a group of highly cultivar-specific races, complicating the task of screening for resistance. Many of the older cultivars that were once thought to be resistant are now susceptible to scab. This is likely due to the genetic shift with the pathogen population over time. The search for resistant germplasm continues and may be of future value as more is learned about the variability of F. effusum.