Summary: Some disturbances can drive ecological systems to abrupt shifts between alternative stages (tipping points) when critical transitions occur. Drought‐induced tree death can be considered as a nonlinear shift in tree vigour and growth. However, at what point do trees become predisposed to drought‐related dieback and which factors determine this (tipping) point? We investigated these questions by characterizing the responses of three tree species, silver fir (Abies alba), Scots pine (Pinus sylvestris) and Aleppo pine (Pinus halepensis), to a severe drought event. We compared basal area increment (BAI) trends and responses to climate and drought in declining (very defoliated and dying) vs. non‐declining (slightly or not defoliated) trees by using generalized additive mixed models. Defoliation, BAI and sapwood production were related to functional proxies of tree vigour measured at the onset and end of the drought (non‐structural carbohydrate concentrations, needle N content and C isotopic discrimination, presence of wood‐inhabiting fungi). We evaluated whether early warning signals (increases in synchronicity among trees or in autocorrelation and standard deviation) could be extracted from the BAI series prior to tree death. Declining silver fir and Scots pine trees showed less growth than non‐declining trees one to three decades, respectively, before the drought event, whereas Aleppo pines showed growth decline irrespective of tree defoliation. At the end of the drought period, all species showed increased defoliation and a related reduction in the concentration of sapwood soluble sugars. Defoliation was constrained by the BAI of the previous 5 years and sapwood production. No specific wood‐inhabiting fungi were found in post‐drought declining trees apart from blue‐stain fungi, which extensively affected damaged Scots pines. Declining silver firs showed increases in BAI autocorrelation and variability prior to tree death. Synthesis. Early warning signals of drought‐triggered mortality seem to be species specific and reflect how different tree species cope with drought stress. Highly correlated declining growth patterns during drought can serve as a signal in silver fir, whereas changes in the content of sapwood soluble sugars are suitable vigour proxies for Scots and Aleppo pines. Longer growth and defoliation series, additional vigour parameters and multi‐species comparisons are required to understand and predict drought‐induced tree death.

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Forest decline induced by climate change is a global phenomenon that affects many tree species, mainly in drought-prone areas as the Mediterranean region. In southern Italy, several oak species have shown decline symptoms and elevated mortality since the 2000s due to drought stress. However, it remains to be answered whether decline occurred alone or whether a pathogen was also involved. To this aim, we compared two coexisting oak species in a forest located in southern Italy which are assumed to be less (Quercus cerris) and more tolerant to drought (Quercus pubescens). We sampled fifteen couples of neighboring declining (D) and non-declining (ND) trees of both species. Wood cores were taken from all trees to perform dendrochronological analyses to detect the decline onset and link it to potential climatic drivers. Carbon isotope ratios (d¹³C) were analyzed in wood of the two vigor classes to compare their water-use efficiency. Phytophthora presence was also assessed in soil samples from ten D-ND couples of trees per species. The oak species most affected by drought-induced decline in terms of leaf shedding and mortality was Q. cerris, i.e., the least tolerant to drought. In both species, the D trees showed a reduced growth rate compared with ND trees from 2000 onward when drought and warming intensified. Q. pubescens showed higher growth sensitivity to precipitation, temperature and drought than Q. cerris. This sensitivity to climate was magnified in D trees whose growth decreased in response to warm and dry conditions during the prior winter and the late summer. The Q. pubescens D trees were more efficient in their water use than ND trees before the growth divergence between D and ND trees amplified. In the studied area, Phytophthora quercina was isolated from 40% of the sampled trees, and tended to be more frequent amongst ND than amongst D trees. Our data suggests that droughts and warm summer conditions triggered oak decline. The high prevalence of P. quercina in the studied area warrants further study as a potential predisposing factor.

New diseases in forest ecosystems have been reported at an increasing rate over the last century. Some reasons for this include the increased disturbance by humans to forest ecosystems, changed climatic conditions and intensified international trade. Although many of the contributing factors to the changed disease scenarios are anthropogenic, there has been a reluctance to control them by legislation, other forms of government authority or through public involvement. Some of the primary obstacles relate to problems in communicating biological understanding of concepts to the political sphere of society. Relevant response to new disease scenarios is very often associated with a proper understanding of intraspecific variation in the challenging pathogen. Other factors could be technical, based on a lack of understanding of possible countermeasures. There are also philosophical reasons, such as the view that forests are part of the natural ecosystems and should not be managed for natural disturbances such as disease outbreaks. Finally, some of the reasons are economic or political, such as a belief in free trade or reluctance to acknowledge supranational intervention control. Our possibilities to act in response to new disease threats are critically dependent on the timing of efforts. A common recognition of the nature of the problem and adapting vocabulary that describe relevant biological entities would help to facilitate timely and adequate responses in society to emerging diseases in forests.

Disease emergence in northern and boreal forests has been mostly due to tree-pathogen encounters lacking a co-evolutionary past. However, outbreaks involving novel interactions of the host or the pathogen with the environment have been less well documented. Following an increase of records in Northern Europe, the first large outbreak of Diplodia sapinea on Pinus sylvestris was discovered in Sweden in 2016. By reconstructing the development of the epidemic, we found that the attacks started approx. 10 years back from several isolated trees in the stand and ended up affecting almost 90% of the trees in 2016. Limited damage was observed in other plantations in the surroundings of the affected stand, pointing to a new introduced pathogen as the cause of the outbreak. Nevertheless, no genetic differences based on SSR markers were found between isolates of the outbreak area and other Swedish isolates predating the outbreak or from other populations in Europe and Asia Minor. On a temporal scale, we saw that warm May and June temperatures were associated with higher damage and low tree growth, while cold and rainy conditions seemed to favor growth and deter disease. At a spatial scale, we saw that spread occurred predominantly in the SW aspect-area of the stand. Within that area and based on tree-ring and isotope (δ¹³C) analyses, we saw that disease occurred on trees that over the years had shown a lower water-use efficiency (WUE). Spore traps showed that highly infected trees were those producing the largest amount of inoculum. D. sapinea impaired latewood growth and reduced C reserves in needles and branches. D. sapinea attacks can cause serious economic damage by killing new shoots, disrupting the crown, and affecting the quality of stems. Our results show that D. sapinea has no limitations in becoming a serious pathogen in Northern Europe. Management should focus on reducing inoculum, especially since climate change may bring more favorable conditions for this pathogen. Seedlings for planting should be carefully inspected as D. sapinea may be present in a latent stage in asymptomatic tissues.