Diplodia pinea causes tip blight, cankers on branches and stem, branch dieback, and occasionally tree death of weakened two- and three-needle pines and several other conifers.
Diplodia blight commonly afflicts Austrian (Pinus nigra), Scotch (P. sylvestris), red (P. resinosa), ponderosa (P. ponderosa) and mugo (P. mugo) pines. In addition, Sphaeropsis sapinea is known to colonize other conifers growing under unfavorable environmental conditions including Douglasfir (Pseudotsuga menziesii) as well as Colorado (Picea pungens), Norway (P. abies), and white spruces (P. glauca).
The most conspicuous symptom of Diplodia blight is brown, stunted new shoots with short, brown needles.
New shoots throughout the crown may be infected, although damage is generally first evident in the lower crown. Vigorous trees confine infections to the new shoots. Severely weakened trees can have entire branches dieback. Repeated infection reduces growth, deforms trees, and ultimately kills them.
Although Diplodia pinea infects undamaged new shoots, it can infect both current-year and older tissues through wounds. Wounds caused by hail, insect feeding, pruning or shearing operations, and wind damage are typical infection sites.
Diplodia pinea spores develop in small, black fruiting structures that form on needles, fascicle sheaths, scales of second-year seed cones, and bark. Fruiting structures disperse spores when rainfall is frequent via wind and water splash from March to October. New shoots of Austrian, mugo, ponderosa, red, and Scotch pines are most susceptible when buds begin to open until needles are fully elongated. Spores require wet conditions to germinate and penetrate needles and shoots. Once the fungus penetrates needles, tissues are rapidly destroyed resulting in stunted shoots and needles. Diplodia pinea survives the winter in fruiting structures that develop on infected second-year cones, blighted needles, shoots, and cankers.
Written by: Dan Gillman
Photos: G. Stanosz and M. Daughtrey, Diseases of Woody Ornamentals and Trees. APS Press.