Anthropogenic activities, such as the movement of plant material, have contributed to non-native pathogen and pest introductions worldwide. As invasive plant pathogens often impact “naïve” host populations with few coevolved defenses, they may act as novel biotic disturbances, generating community shifts. In the coastal forests of California, the introduced pathogen, Phytophthora ramorum causes an emerging plant disease, sudden oak death (SOD). This pathogen displays a wide host range, but exhibits differential virulence and sporulation among hosts, generating apparent competition within these communities and selectively removing several common tree species. However, many susceptible species are prolific resprouters, capable of asexual regeneration following death of aboveground stems, and in these fire-prone forests, wildfire can disrupt disease dynamics. Thus, the long-term impacts of SOD on regeneration trajectories remain unclear. We examined the impacts of SOD on patterns of forest regeneration and possible compositional shifts across a gradient of disease impacts and fire history. We conducted this study in a network of long-term forest monitoring plots established in 2006 in the coastal forests of Big Sur, CA. In this network, we surveyed stand structure, disease progression, and recruitment for over a decade, including the impacts of the 2008 Basin Complex fires.
Results/Conclusions
We constructed a series of multilevel generalized linear mixed models, utilizing a Bayesian approach, to assess the impacts of disease occurrence and susceptible host mortality caused by SOD on patterns of seedling and sprout regeneration in unburned and recently burned forests. Our results suggest that non-susceptible host species (including California bay laurel, a primary driver of disease dynamics and apparent competition) did not exhibit measurable shifts related to SOD impacts, in terms of tree growth or seedling regeneration. Instead, understory shrubs exhibited the strongest positive responses to gaps generated by disease mortality. Though vegetative reproduction of tanoak, a susceptible host, was hindered by disease pressure, tanoak seedlings responded positively (in terms of occurrence and growth responses) to gaps formed by disease-related mortality. This result suggests that pulses in tanoak seed dispersal, likely due to stress in overstory trees, and advanced regeneration may play an important role in prolonging the persistence of susceptible host populations. Wildfire altered regeneration outcomes in areas previously impacted by disease, leading to increased relative dominance of many non-susceptible species. These results have implications for future predictions of the long-term impacts of a non-native disease on forest structure and composition.