Performance of Rust-Resistant Western White Pine in Operational Plantations in Northern Idaho: 1995-2006
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Report 12-03 January 2012 Performance of Rust-Resistant Western White Pine in Operational Plantations in Northern Idaho: 1995-2006 Holly S.J. Kearns, Ph.D., Plant Pathologist USDA Forest Service, Pacific Northwest Region, Forest Health Protection Brennan A. Ferguson, Plant Pathologist Ferguson Forest Pathology Consulting, Inc., Missoula, MT John W. Schwandt, Ph.D., Plant Pathologist USDA Forest Service, Northern Region, Forest Health Protection INTRODUCTION The pandemic caused by WPBR decimated western white pine across much of its native Arrival & impact of white pine blister range, altering species composition and rust successional processes such that shade- tolerant species became much more Western white pine (Pinus monticola Dougl. dominant. This resulted in a loss of ex D. Don) was once a dominant species on ecosystem function and diversity, as well as over five million acres of the Inland an increase in losses due to pathogens and Northwest but now represents the cover type insects to which shade-tolerant species are on less than 5% of its historic range often more susceptible (Byler and Hagle (Neuenschwander et al. 1999, Fins et al. 2000, Harvey et al. 2008, Samman et al. 2001, Harvey et al. 2008). This dramatic 2003, Schwandt 2000). reduction resulted from factors such as selective harvest, mortality due to mountain The introduction of C. ribicola to western pine beetle (Dendroctonus ponderosae North America has long thought to have Hopkins), and lack of natural regeneration been a one-time occurrence when a due to fire exclusion. The primary cause, shipment of infected eastern white pine however, was the introduction of (Pinus strobus L.) seedlings were Cronartium ribicola J.C. Fisch., a non- transported in 1910 from a nursery in France native pathogen that causes white pine to Point Grey, British Columbia (Mielke blister rust (WPBR) of five-needled pines. 1943). An argument has recently been United States Forest Northern 200 East Broadway Department of Service Region P.O. Box 7669 Agriculture Missoula, MT 59807 made, however, that historical evidence Attempts at WPBR control began as soon as suggests at least a handful of separate it was realized that the disease would introductions could easily have occurred in inevitably spread across the Inland western North America (Hunt 2010). In Northwest. Eradication of Ribes spp., either case, C. ribicola had been recognized chemical treatment of cankers, and prior to its introduction as a grave threat to biological control efforts using native fungi North American five-needled pines based on were all attempted to various degrees from the severity of damage in nurseries and the 1920s into the 1960s, but were commercial plantations of various species, eventually abandoned as unfeasible particularly eastern white pine, in western (Ketcham et al. 1968). Europe (Spaulding 1922). Unfortunately these concerns did not halt continued White pine breeding program shipments of WPBR-susceptible, five- needled pine species from European As early as the late 1920s, non-infected, or nurseries to both eastern and western North infected but surviving, western white pine America. A quarantine on seedling imports were observed in Idaho and Montana forests to western North America was imposed in originally composed of a high proportion of 1914 but, in addition to evidence that it was western white pine that had otherwise been not strictly observed (Hunt 2010), it was decimated by WPBR (Bingham 1983, already too late. Hartley 1927). This raised hopes there was some level, however low, of natural The presence of WPBR in the region around resistance to WPBR in the native western Vancouver, British Columbia was not white pine population. In 1950, USDA detected until 1921, by which time it had Forest Service (USFS) scientists formalized already spread from infected eastern white the rust-resistance breeding program for pines into horticultural and native Ribes spp. western white pine in the Inland Empire to (alternate hosts for C. ribicola) and from test for natural, heritable resistance to C. there into native stands of western white ribicola. pine (Mielke 1943). Due to efficient, long- distance spread by the aerially-dispersed Surveys were conducted to identify non- aeciospores of C. ribicola from infected infected western white pine in stands long- pines to Ribes spp. each spring, the fungus exposed to WPBR. Controlled pollinations spread to the east and southeast with among all pairs of rust-free selections in the prevailing winds and entered the white pine field enabled selection of the parent trees zone of northern Idaho and western Montana used to establish the first generation (F1) in the early- to mid-1920’s (Lachmund seed orchard at Sandpoint, ID (Bingham et 1926, Mielke 1943, Pennington 1925). The al. 1963). F1 parents with demonstrated damage from WPBR was severe in all age resistance were then used to establish seed classes of western white pine. Small trees orchards where cross-breeding via wind were killed relatively quickly by girdling pollination produced seed of potentially once C. ribicola branch cankers reached the rust-resistant, second generation (F2) stock stem; the crowns of large trees often (Bingham et al. 1953, Bingham 1983). suffered hundreds of individual branch There have been three “phases” in selecting infections that severely impacted vigor apparently resistant parent trees to before overwhelming the tree (Lachmund incorporate into the breeding program (Hoff 1934). 1977, Howe and Smith 1994, Mahalovich 2 2010). Testing of parent trees to determine Schwandt 1993). The objectives were to their rust-resistant status and potential monitor both WPBR infection levels and inclusion in the breeding program is an long-term survival in operational F1 and F2 ongoing process (Mahalovich 2010). plantations. This report details the findings of this monitoring effort for the period from Early, artificial-inoculation tests in a nursery 1995 to 2006. setting found that 66% of F2 seedlings were rust-free after two and a half years (Hoff et METHODS al. 1973). The long-term expectation was for 65% or greater survival of this F2 stock The original study plan specified plantation- when grown under natural stand conditions selection criteria, sampling design, plot (Bingham 1983). However, artificial installation, baseline data collection, and screening only allows detection of resistance methods of monumenting plantations, plots, mechanisms at early ages and cannot and individual trees (Mathiasen and evaluate long-term field effectiveness Schwandt 1993 - Appendix A). A total of (Yanchuk et al. 1994). 15 IDL plantations and seven USFS plantations were selected for monitoring; all As F1 and then F2 stock became available 22 are located in northern Idaho between beginning in the late 1970s, it was Orofino and the Canadian border (Figure 1). outplanted extensively onto private, state, and federal lands in northern Idaho and western Montana (Fins et al. 2001, Muller 2002). There was, however, no systematic, long-term monitoring of performance put in place for these operational plantings (Mathiasen and Schwandt 1993). Data from early test plantations containing various western white pine stock types, ranging from natural seed sources (also known as “wild” or “woodsrun”) to F2, indicated that survival of F2 might be greater than originally expected (Goddard et al. 1985). However, by the early 1990s, anecdotal reports gave rise to concerns that improved stock on sites with high rust hazard may not be performing as well as expected. Subsequently, the USFS and the Idaho Department of Lands (IDL) cooperated in establishing permanent plots in operational western white pine plantations in order to evaluate the field performance of western white pine stock types (Figure 1) (Mathiasen and Figure 1. Locations of western white pine plantations. 3 Young plantations, ranging in age from newly planted to nine years old, were Data collection consisted of careful selected in order that planted seedlings could examination, branch-by-branch and along be more readily distinguished from natural the stem, for evidence of WPBR. As long as regeneration, as well as to accurately tree height was less than approximately monitor and diagnose WPBR infection and eight feet, a tree could be examined mortality from a relatively early age (Figure carefully in its entirety. As trees grew in 2). Only 13 of the IDL plantations are height, however, the upper branches could reported on here as plots were not installed not be examined as closely as lower in two plantations until the fall of 2000 branches, until finally the uppermost (Table 1). branches could not be examined at all. The upper crowns of such trees were still The study plan called for coordinated scanned visually for evidence of WPBR remeasurements of all plots at infection, but early diagnosis of infections approximately three to five year intervals became much more difficult and new (Mathiasen and Schwandt 1993). However, infections might go undetected for several due to changes in personnel, budgeting and years until symptoms such as a dead branch, scheduling problems, as well as other swollen branch canker, or rodent chewing factors, neither the timeline for installing around a canker could be seen. plots nor the desire to perform concurrent remeasurements on all plots within the same The analysis for percent infection within a year could be met. We therefore chose to plantation is based on the presence of at report here only on data from 1995, 2000, least one identifiable canker anywhere on a and 2006, as these were years when data tree. Interactions between F2 stock and C. were collected in all 20 plantations. Data ribicola can make diagnosis of basal from the two IDL plantations where plots deformations of tree stems problematic were installed in 2000 can be included in (Eckert 2007). In our study, basal future analyses of all 22 plantations. deformation was generally attributed to the presence of a WPBR basal canker whose normal growth had been affected by a resistance mechanism, to the effects of root disease, or to physical damage.