The marine toad Bufo marinus is native to northern South America, parts of Central America and Southern Texas. It was deliberately introduced into Australia's tropical north-east in 1935 in an unsuccessful attempt to control the cane beetle, a damaging insect pest of sugarcane crops. The toads quickly established in the new environment and began to spread. Today, they inhabit most of the Australian tropics and sub-tropics and have reached Western Australia. Models predict that global warming will enable the toads to extend their range further south. They cause severe environmental impacts, as all life stages of B. marinus contain bufadienolides, alkaloid substances toxic to vertebrates, resulting in death of the predators ingesting it. The continental scale of this biological invasion in combination with the remoteness of the areas affected, poses a specific set of challenges to potential control approaches for cane toads. This review covers different biocontrol strategies pursued over the past 8 years, with particular focus on an immunological approach aiming at the disruption of toad metamorphosis. So far, research efforts have failed to produce a tool for large-scale reduction of toad populations. Considerations of future research priorities and efforts are also discussed.

While most authors believe that autoimmunity against the TSH receptor expressed in the orbital connective tissue cells is the main reaction that leads to the development of ophthalmopathy in patients with Graves’ hyperthyroidism, an older hypothesis that deserves fresh consideration is based on the notion that thyroglobulin (Tg) in the thyroid gland passes in a retrograde fashion to the orbit where it is recognized by Tg autoantibodies, leading to inflammation. Here, we review new evidence that supports a role of Tg and propose a new hypothesis based on the notion that Tg is targeted in the orbit leading to a complex cascade of reactions that leads to Graves’ ophthalmopathy.

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BackgroundThe cane toad, Bufo (Chaunus) marinus, is one of the most notorious vertebrate pests introduced into Australia over the last 200 years and, so far, efforts to identify a naturally occurring B. marinus-specific pathogen for use as a biological control agent have been unsuccessful. We explored an alternative approach that entailed genetically modifying a pathogen with broad host specificity so that it no longer caused disease, but carried a gene to disrupt the cane toad life cycle in a species specific manner.Methodology/Principal FindingsThe adult beta globin gene was selected as the model gene for proof of concept of autoimmunity as a biocontrol method for cane toads. A previous report showed injection of bullfrog tadpoles with adult beta globin resulted in an alteration in the form of beta globin expressed in metamorphs as well as reduced survival. In B. marinus we established for the first time that the switch from tadpole to adult globin exists. The effect of injecting B. marinus tadpoles with purified recombinant adult globin protein was then assessed using behavioural (swim speed in tadpoles and jump length in metamorphs), developmental (time to metamorphosis, weight and length at various developmental stages, protein profile of adult globin) and genetic (adult globin mRNA levels) measures. However, we were unable to detect any differences between treated and control animals. Further, globin delivery using Bohle iridovirus, an Australian ranavirus isolate belonging to the Iridovirus family, did not reduce the survival of metamorphs or alter the form of beta globin expressed in metamorphs.Conclusions/SignificanceWhile we were able to show for the first time that the switch from tadpole to adult globin does occur in B. marinus, we were not able to induce autoimmunity and disrupt metamorphosis. The short development time of B. marinus tadpoles may preclude this approach.