Fusiform Rust

Fusiform Rust

Fusiform rust continues to be recognized as the most damaging disease of southern pine forests and plantations. The causal agent, Cronartium quercuum (Berk.) Miyabe ex Shirai f. sp. fusiforme (Hedge. & N. Hunt) Burdsall & G. Snow, occurs in a broad band across the Southern States and is prevalent in the most productive high-quality loblolly and slash pine sites in this region (Anderson and others 1986). Fusiform rust incidence has increased dramatically within the last 30 years, especially in intensively cultured stands and in afforestation areas, where 47.9 million acres of former agricultural lands have been converted into pine stands and plantations (Starkey and others 1997). Annual losses to the disease have been estimated at $35 million in five Southeastern States (Schmidt 1998). Forest managers throughout the South are concerned about this disease because it affects stocking, product quantity, and product quality. Fusiform rust management in many areas is highly integrated into land management activities. For example, pine fertilization is frequently delayed by managers until after the trees are 5 years of age to reduce infection during the most vulnerable years (Blakeslee 1997).

Extensive planting of susceptible slash and loblolly pines since the 1930s has resulted in an epidemic of fusiform rust. Infected trees can be found throughout the southern pine region (see figure below), but losses are most serious on Coastal Plain sites from Louisiana to southeastern South Carolina. Several variables including weather, amount of inoculum, abundance of oaks (the alternate host), and susceptibility of the pine species govern incidence of the disease. Nonindustrial private and industrial forest landowners own a majority of the pine host type in the South. Over 13.4 million acres southwide have at least 10 percent of the slash and/or loblolly pines infected (Starkey and others 1997).

Incidence of Fusiform Rust

The development of genetic resistance in planting stock has been the major disease management strategy used to reduce the incidence and severity of fusiform rust. The efforts of many forest pathologists over the past 40 years have brought genetic resistance to the forefront as an effective routine tool for managing this disease. The absence of a genetic linkage between rust resistance and tree growth rate has allowed the simultaneous development of genetically superior fast-growing trees with enhanced fusiform rust resistance. The genetic resistance approach generally has reduced pine mortality and disease severity in many sites, but some problems have been encountered as a consequence of the wide geographical variation in the genetics of the fungus, which has apparently given rise to strain-specific resistance, variations in pathogen virulence, and perhaps pathogen adaptations to host-resistance genes (Powers and Matthews 1979). Consequently, fungal strains in some areas eventually overcome resistance. Previously, pine breeders have attempted to stay ahead of the rust fungus by constantly producing and rotating new resistant pine growing stock to avoid genetic changes in the fungus that occur when pine selections are grown for too many rotations in the field. However, a new strategy involves the production of breeding lines that minimize rust damage, not prevent infection entirely, to avoid putting selection pressure on the fungus to produce new virulent strains, but maintain low-virulence strains to which pines are tolerant (Walkinshaw and Barnett 1995). Nevertheless, development of fusiform rust resistance has translated directly to increased economic value because the disease affects both the quantity and quality of timber produced (Cubbage and Wagner 2000).

Alternative approaches to fusiform rust suppression have been helpful in shaping efforts to develop integrated programs to manage this disease. The development of predictive models has been useful for identifying the relative hazard or susceptibility of sites to rust damage based on site and stand characteristics (Anderson and others 1986, Borders and Bailey 1986, Froelich and Snow 1986, Starkey and others 1997); and for predicting preharvest rust-associated mortality (Devine and Clutter 1985, Geron and Hafley 1988). Other models have emphasized the importance of preventing rust during stand establishment (during the first 5 years) when the potential impact of rust infection is the greatest (Nance and others 1985). Triadimefon (Bayleton) seed treatments followed by protective foliar sprays have helped reduce the incidence of rust in the early stages of stand development (Hare and Snow 1983). The selective thinning of trees with moderate-to-severe stem girdling caused by rust galls is an effective means of reducing losses to fusiform rust and greatly improves the quality of trees in residual stands (Belanger and others 2000).

Recent research has utilized molecular techniques to study population structure, cellular, and biological aspects of the pathogen to determine genetic variation, identify the genetic mechanism of fungus-induced gall formation in pine hosts, locate rust-resistance genes in pine host genomes, and define cellular resistance responses (Covert and others 1977, Roberds and others 1997, Wilcox and others 1996). This information will ultimately be useful in developing new genetic engineering strategies for creating more resistant pines by taking advantage of new knowledge of host-pathogen interactions at the molecular level.