White pine blister rust pathology is initially manifest in whitebark pine through the appearance of a yellow-orange swelling on the tree's bark (Van Arsdel et al. 1956a, Hunt 1983, Tomback et al. 1995). Cankers, which burst through the bark 2 to 4 years after initial infection, grow incrementally both longitudinally and radially over the course of several years (Lachmund 1926, Mielke 1943). Tree mortality arises through girdling of the bole, or after the loss of branches from multiple cankers (Hoff and Hagle 1989). Depending on the size of the tree and the distance of the blister rust canker from the bole, tree mortality can take many years to occur. In seedlings and saplings, however, the interval between initial infection and death is generally much more rapid. Most seedlings die within 3 years of infection (Tomback et al. 1993). Mortality of all trees due to blister rust is often hastened by cumulative factors. The rate at which trees die is accelerated by the impacts of mountain pine beetle, root diseases, and other pathogens, to which whitebark pine exhibits a heightened susceptibility once infected by C. ribicola (Krebill and Hoff 1994).
Natural resistance of albicaulis to blister rust infection is very low, and may be conditioned by environmental as well as genotypic factors of both albicaulis and the blister rust fungus (McDonald 1992, Krebill and Hoff 1994). Cankers that originate in stems or branches more than 24 inches from the bole are rarely lethal. Girdling of the bole is prevented through natural canker inactivation, natural branch death from inadequate light, or branch death as stems are girdled by the blister rust canker (Hagle et al. 1989). Consequently, trees younger than 20 or 30 years of age are more vulnerable to death by blister rust infection because cankers rarely occur far from the bole, given their smaller size (Mielke 1943, Hagle et al. 1989).
Whitebark pine cone production and thus seed availability for wildlife consumption often ceases long before tree mortality when blister rust infects the top of the tree first, where the tree's cones are concentrated. In the GYE where most inoculum probably blows up to whitebark pine from lower elevations, this pattern of fungal infection is the primary mode by which mortality occurs (J. Smith, pers. comm. 1998).
White pine blister rust development and the epidemiology of pine infestation encompasses five spore stages (Table 8.1). Three stages occur on pine where C. ribicola is perennial, and two on the pathogen's primary or telial host, Ribes spp. (shrubs of currants and gooseberries), where it is an annual (Lachmund 1926, Lloyd et al. 1959). For pine infection to occur, it is necessary that susceptible Ribes species are located relatively near to pine trees. R. petiolare/ hudsonianum (western black currant), R. lacustre (prickly currant), R. viscosissimum (sticky currant), R. cereum (squaw currant), and R. inerme (white-stemmed currant) all inhabit the GYE, mainly lining riparian zones and mesic valley bottoms. R. lacustre and R. viscosissi-mum, however, can also be found growing on hillsides (Hagle et al. 1989). Mountain gooseberry (R. montigenum), a sixth local species, is commonly found growing in areas of whitebark pine. Although extensive studies have not been conducted on all GYE Ribes species, most investigations rank their susceptibility as ranging from low to high (Lachmund 1926, 1934, Mielke et al. 1937, Kim-mey 1935, 1938, Kimmey and Mielke 1944, Maloy 1997, J. Smith, pers. comm. 1998).
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