During the last 3 years Xylella fastidiosa has been reported in four European countries: Italy, France, Germany, and Spain. The initial and continuing emphasis on the outbreak of a devastating epidemic in olives in the southeastern tip of Italy is understandable, but the genetic diversity of the newly discovered X. fastidiosa is evidence that these introductions are independent from each other. Different genotypes of X. fastidiosa will differ in the range of plant species that they can colonize and in what plants they cause disease. The recent discoveries also imply that the recent number of X. fastidiosa introductions into the EU has been larger than originally assumed. Why is this happening in Europe now instead of over the past 100+ years? These new discoveries lead to the expectation that further outbreaks will be identified, as well as novel genotypes of the pathogen. However, not all X. fastidiosa are made equal, and there are two misconceptions we have been frequently hearing from news coming from the Old Continent.
First, the concept that an introduced genotype of X. fastidiosa is ‘avirulent’ has been a common component of current discourse. We strongly disagree with this assessment. The fact that there is no disease epidemic associated with a specific genotype does not mean it is avirulent. It only means that the specific ecological conditions in which it was observed have not been supportive of an epidemic. It also does not mean that the genotype will not have economic or environmental impacts. Under suitable ecological contexts, which would include vector and host plant species, and abiotic factors such as temperature, a genotype considered ‘avirulent’ may become epidemic if conditions are modified.
Associated with this observation, although the EU now has representatives of multiple X. fastidiosa subspecies, the supposition that they are basically the same pathogen is dangerous. There is ample indirect evidence that recombination is associated with the emergence of new X. fastidiosa diseases – at ecological and not evolutionary time scales. Regions where different genotypes of this bacterium would co-occur in the EU could become hotspots for the emergence of new genotypes resulting from genetic recombinations among different genotypes, and consequently new diseases.
Second, there has been confusion about host specificity of X. fastidiosa, specifically as to how specific is a pathogen genotype to a host plant. Here, genotypes are usually described as an ST (sequence type) followed by a number. For example, the genotype associated with the epidemic in Italy is ST53. We note that although there is evidence supporting the concept of one ST – one disease, there is also evidence supporting the opposite. Diseases in citrus and coffee in Brazil are caused by different groups of STs, while also in Brazil olive and coffee can be infected by the same ST. In California, genotypes from subspecies fastidiosa infecting grapevines also cause disease in almonds, while those from subspecies multiplex infecting almonds do not cause disease in grapevines. Moreover, there is large variability in plant virulence for isolates in phylogenetically closely-related STs when compared among each other (e.g. grapevine genotypes in California, or citrus genotypes in Brazil). Therefore, in the case of the EU where X. fastidiosa is encountering new host plant species in a novel environment with different vector communities, it is very difficult to successfully extrapolate data generated in the Americas to novel outbreaks.
We emphasize the need for careful biological experimentation, aligned with extensive field surveys, before any conclusions are made in regards to ‘avirulence/virulence’ of a genotype, as well as its host range. Genetic analysis alone cannot reliably predict their ecological and epidemiological consequences.
by RPPA and AHP
Misconceptions about Xylella fastidiosa that are relevant to emerging epidemics