Natural Selection For Resistance Research Articles

Amphibian infection tolerance to chytridiomycosis.

Animal defences against infection involve two distinct but complementary mechanisms: tolerance and resistance. Tolerance measures the animal's ability to limit detrimental effects from a given infection, whereas resistance is the ability to limit the intensity of that infection. Tolerance is a valuable defence for highly prevalent, persistent or endemic infections where mitigation strategies based on traditional resistance mechanisms are less effective or evolutionarily stable. Selective breeding of amphibians for enhanced tolerance to Batrachochytrium spp. has been suggested as a strategy for mitigating the impacts of the fungal disease, chytridiomycosis. Here, we define infection tolerance and resistance in the context of chytridiomycosis, present evidence for variation in tolerance to chytridiomycosis, and explore epidemiological, ecological and evolutionary implications of tolerance to chytridiomycosis. We found that exposure risk and environmental moderation of infection burdens are major confounders of resistance and tolerance, chytridiomycosis is primarily characterized by variation in constitutive rather than adaptive resistance, tolerance is epidemiologically important in driving pathogen spread and maintenance, heterogeneity of tolerance leads to ecological trade-offs, and natural selection for resistance and tolerance is likely to be dilute. Improving our understanding of infection tolerance broadens our capacity for mitigating the ongoing impacts of emerging infectious diseases such as chytridiomycosis. This article is part of the theme issue 'Amphibian immunity: stress, disease and ecoimmunology'.

Evidence of selection for resistance to paralytic shellfish toxins during the early life history of soft‐shell clam, Mya arenaria, populations

This study identifies early, postmetamorphic soft‐shell clams, Mya arenaria, as the life‐history stage most susceptible to effects of blooms of paralytic shellfish poisoning (PSP) toxin–producing Alexandrium spp. Laboratory experiments used progeny from predominantly susceptible (naϊve) or resistant (annually exposed) NW Atlantic populations. Growth and survival of toxified veliger larvae did not differ from those fed nontoxic algae. In contrast, postlarvae (4–12‐mm shell length) from both populations exposed to a highly toxic Alexandrium tamarense isolate (~ 100 cells mL−1, 64–69 pg saxitoxin equivalents [STXeq] cell−1) suffered burrowing incapacitation, toxin accumulation, and mortalities within 1 week of toxin exposure. These effects were greater and occurred sooner in the naϊve population. Short‐term toxification in the laboratory caused a significant shift in the genotypic composition of this population, determined with a molecular marker for sodium‐channel resistance. Clams with the sensitive genotype were selectively eliminated relative to resistant or heterozygote clams. Ingestion of toxic cells (too large for larval capture) is thus required to elicit toxic effects. Exposure to mixed, toxic, and nontoxic algal suspensions demonstrated that adverse effects to fitness (survival and growth) were dose‐dependent, occurring only at ≥ 50 cells mL−1 of the isolate used (PR18b). Paralysis and thus increased predatory risk occurred even at 10 cells mL−1. Postlarvae < 12 mm, which can co‐occur with red tides throughout the Atlantic range of M. arenaria, were more susceptible to PSP than large (> 30 mm) juveniles. Natural selection for resistance in Atlantic populations will thus vary latitudinally with the timing, duration, and intensity of toxic blooms.

Phenotypic variation for disease resistance and virulence within naturalized populations of Stylosanthes humilis and Colletotrichum gloeosporioides

The extent of variation for host disease reaction and pathogen virulence was studied in naturalized populations of Stylosanthes hurnilis and Colletotrichurn gloeosporioides, the causal fungus of an anthracnose disease of Stylosanthes spp. Diseased plants (S0) were collected from the field at three sites (Townsville, Wrotham Park and Niall) in North Queensland, and first generation selfed (S1) progenies (host-lines) and single spore fungal cultures were grown for each of the collections made. Within a site, all host-lines were inoculated with each fungal isolate from that site, and a fourth experiment was conducted with representative host-pathogen combinations from each site. Sufficient seed was obtained to allow testing of 12, 10 and 8 collections from Niall, Wrotham Park and Townsville respectively. Significant variation (P < 0.01) between disease severity values for host-line means, fungal isolate means and host-line/fungal isolate interactions was found in all four experiments. Differences between fungal isolate means were the main source of variation in three of the four experiments. Both the differences in virulence within the pathogen population and the differences in resistance of the hostlines appeared to be quantitatively inherited. One host-line from Wrotham Park was significantly more resistant than the susceptible check, cv. Paterson, in two replicated experiments indicating that selection for some improvement in resistance within the naturalized populations should be possible. However, none of the host-lines from the Townsville and Niall sites were significantly more resistant than Paterson, suggesting that little natural selection for resistance has occurred within the naturalized host populations over the 10 years following the first outbreak of the disease in northern Australia.