Population genetics of the frog-killing fungus Batrachochytrium dendrobatidis

Global amphibian decline by chytridiomycosis is a major environmental disaster that has been attributed to either recent fungal spread or environmental change that promotes disease. Here, we present a population genetic comparison of Batrachochytrium dendrobatidis isolates from an intensively studied region of frog decline, the Sierra Nevada of California. In support of a novel pathogen, we find low diversity, no amphibian-host specificity, little correlation between fungal genotype and geography, local frog extirpation by a single fungal genotype, and evidence of human-assisted fungus migration. In support of endemism, at a local scale, we find some diverse, recombining populations. Therefore neither epidemic spread nor endemism alone explains this particular amphibian decline. Recombination raises the possibility of resistant sporangia and a mechanism for rapid spread as well as persistence that could greatly complicate global control of the pathogen.

Rapid Global Expansion of the Fungal Disease Chytridiomycosis into Declining and Healthy Amphibian Populations.

The fungal disease chytridiomycosis, caused by Batrachochytrium dendrobatidis, is enigmatic because it occurs globally in both declining and apparently healthy (non-declining) amphibian populations. This distribution has fueled debate concerning whether, in sites where it has recently been found, the pathogen was introduced or is endemic. In this study, we addressed the molecular population genetics of a global collection of fungal strains from both declining and healthy amphibian populations using DNA sequence variation from 17 nuclear loci and a large fragment from the mitochondrial genome. We found a low rate of DNA polymorphism, with only two sequence alleles detected at each locus, but a high diversity of diploid genotypes. Half of the loci displayed an excess of heterozygous genotypes, consistent with a primarily clonal mode of reproduction. Despite the absence of obvious sex, genotypic diversity was high (44 unique genotypes out of 59 strains). We provide evidence that the observed genotypic variation can be generated by loss of heterozygosity through mitotic recombination. One strain isolated from a bullfrog possessed as much allelic diversity as the entire global sample, suggesting the current epidemic can be traced back to the outbreak of a single clonal lineage. These data are consistent with the current chytridiomycosis epidemic resulting from a novel pathogen undergoing a rapid and recent range expansion. The widespread occurrence of the same lineage in both healthy and declining populations suggests that the outcome of the disease is contingent on environmental factors and host resistance.

Sugarcane smut after three years: a policy retrospective.

The detection of sugarcane smut disease (Ustilago scitaminea) in the Bundaberg-Childers region of eastern Australia in 2006 triggered a comprehensive and united response from BSES Limited, Queensland Government and CANEGROWERS. The response to sugarcane smut in the Bundaberg-Childers area was the first test for the Emergency Plant Pest Response Deed, an agreement between Australian governments and plant industries to facilitate a response to a plant pest incursion. As part of this response and the subsequent inquiry, economic models of the likely pattern of spread and cost of the smut epidemic were prepared. This paper reviews the predictions of those models in the light of the subsequent three years' experience. It examines reasons for divergence from the modelled outcomes, some of which were good approximations of actual experience.

Yield losses in grain sorghum due to rust infection

Although rust (caused by Puccinia purpurea) is a common disease in Australian grain sorghum crops, particularly late in the growing season (April onwards), its potential to reduce yield has not been quantified. Field trials were conducted in Queensland between 2003 and 2005 to evaluate the effect of sorghum rust on grain yield of two susceptible sorghum hybrids (Tx610 and Pride). Rust was managed from 28-35 days after sowing until physiological maturity by applying oxycarboxin (1 kg active ingredient/100 L of water/ha) every 10 days. When data were combined for the hybrids, yield losses ranged from 13.1% in 2005 to 3.2% in 2003 but differences in yield the between sprayed and unsprayed treatments were statistically significant (P a parts per thousand currency signaEuro parts per thousand 0.05) only in 2005. Final area under the disease progress curve (AUDPC) values reflected the yield losses in each year. The higher yield loss in 2005 can be attributed primarily to the early development of the rust epidemic and the higher inoculum levels in spreader plots at the time of planting of the trials.

A field investigation into a suspected outbreak of pyrrolizidine alkaloid toxicosis in horses in western Queensland

A disease outbreak investigation was conducted in western Queensland to investigate a rare suspected outbreak of pyrrolizidine alkaloid (PA) toxicosis in horses. Thirty five of 132 horses depastured on five properties on the Mitchell grass plains of western Queensland died in the first six months of 2010. Clinical–pathological findings were consistent with PA toxicosis. A local variety of Crotalaria medicaginea was the only hepatotoxic plant found growing on affected properties. Pathology reports and departure and arrival dates of two brood mares provided evidence of a pre wet season exposure period. All five affected properties experienced a very dry spring and early summer preceded by a large summer wet season. The outbreak was characterised as a point epidemic with a sudden peak of deaths in March followed by mortalities steadily declining until the end of June. The estimated morbidity (serum IGG > 50 IU/L) rate was 76%. Average crude mortality was 27% but higher in young horses (67%) and brood mares (44%). Logistic regression analysis showed that young horses and brood mares and those grazing denuded pastures in December were most strongly associated with dying whereas those fed hay and/or grain based supplements were less likely to die. This is the first detailed study of an outbreak of PA toxicosis in central western Queensland and the first to provide evidence that environmental determinants were associated with mortality, that the critical exposure period was towards the end of the dry season, that supplementary feeding is protective and that denuded pastures and the horses physiological protein requirement are risk factors.