Ancient Host–Pathogen Associations Maintained by Specificity of Chemotaxis and Antibiosis

Switching by parasites to novel hosts has profound effects on ecological and evolutionary disease dynamics. Switching requires that parasites are able to establish contact with novel hosts and to overcome host defenses. For most host–parasite associations, it is unclear as to what specific mechanisms prevent infection of novel hosts. Here, we show that parasitic fungal species in the genus Escovopsis, which attack and consume the fungi cultivated by fungus-growing ants, are attracted to their hosts via chemotaxis. This response is host-specific: Escovopsis spp. grow towards their natural host cultivars more rapidly than towards other closely related fungi. Moreover, the cultivated fungi secrete compounds that can suppress Escovopsis growth. These antibiotic defenses are likewise specific: in most interactions, cultivars can inhibit growth of Escovopsis spp. not known to infect them in nature but cannot inhibit isolates of their naturally infecting pathogens . Cases in which cultivars are susceptible to novel Escovopsis are limited to a narrow set of host–parasite strain combinations. Targeted chemotactic and antibiotic responses therefore explain why Escovopsis pathogens do not readily switch to novel hosts, consequently constraining long-term dynamics of host–parasite coevolution within this ancient association

Resolving confusions about jarrah dieback - don’t forget the plants

The name jarrah dieback has been used for two different disorders, leading to considerable confusion. It was coined in the 1940s to describe the sudden death of groups of jarrah (Eucalyptus marginata) trees in south western Western Australia, which occurred on poorly drained sites, following exceptionally heavy rainfall. In the 1960s these sites were shown to be infested by Phytophthora cinnamomi and jarrah deaths were attributed to it, even though it was only isolated from 5 % of sampled trees. Also the definition of jarrah dieback was expanded to include deaths of many other plants on infested sites, from which P. cinnamomi was more readily isolated. Jarrah trees die from severe water deficiency, indicating problems with water conduction through roots. Xylem vessel diameters vary along roots, being narrow at the root collar, while distally they are larger, providing water storage. Jarrah transpires vigorously during summer, accessing water at depth on sites with deep soil, but being more dependent on internally stored water when root systems are shallower. Following waterlogging, sapwood vessels become blocked with tyloses, reducing both conductivity and potential water storage; such trees may have insufficient water reserves for summer survival. In jarrah P. cinnamomi is unlikely to cause water deficiency because sapwood invasion is rapidly contained in healthy roots. Recent investigations into P. cinnamomi invasion and host responses in other plants show that it can potentially cause a vascular wilt in Banksia spp. and chronic, symptomless infections in herbaceous plants. Susceptibility to waterlogging damage, and/or mortality resulting from infection by P. cinnamomi can only be clarified by detailed knowledge of the hosts and their vulnerabilities. This is essential for making diagnoses, devising management strategies, and avoiding the confusions of the past