• Energy Research

# Data from: Effect of parasite infection and invasion history on feeding, growth and energy allocation of cane toads [https://doi.org/10.5061/dryad.wm37pvmwd](https://doi.org/10.5061/dryad.wm37pvmwd) ## Description of the data and file structure Data are from an experiment where cane toads from different sites were exposed to lungworm parasites from different sites. Toads were then individually housed and maintained in captivity for 4 months. After 4 months toads were euthanized and their level of infection was determined and their gonads, liver, and fat bodies were weighed. 'na' indicates values that were not measured Variables in the dataset are: **Variable explanation** ID Individual toad identifier Treatment Control vs exposed to parasite larvae from 1 of 6 sites Sex sex of each toad, Male or Female Litter family identifier of each toad toad site capture location of parental toads toad state Australian state each toad site is located in Exposed? Exposed to larvae Yes vs No infected? Adult parasites present in the lungs at postmortem Yes vs No worm state Australian state each parasite location is located in.'null' indicates uninfected Controls total gonad wt gonad mass(g) fat wt fat body mass (g) liver wt liver mass (g) Total Rhabdias number of adult parasites in the lungs at postmortem final SVL snout-vent length at end of study (mm) final mass body mass at end of study (g) start SVL snout-vent length at beginning of study (mm) SVL2-SVL1 change in SVL during study (mm) SVL Growth rate daily growth rate in snout-vent length during study (mm/day) Total food eaten amount of food consumed during study (g) Missing data code: na The energy allocation decisions that organisms make can differ between sexes and populations and be influenced by factors such as age and parasite infection. We conducted experimental parasite infections on common-garden reared cane toads originating from sites across the species’ invasive range in Australia to assess how sex, parasite infection and invasion history affected the toad’s food intake, growth rate and organ weights. Female toads had larger fat stores, larger livers and larger gonads than did males, reflecting increased investment into gametes. Growth rate did not differ between the sexes. Lungworm infection increased feeding by male but not female toads and increased fat storage in all toads. Fat body, liver, gonad sizes and feeding rates all differed among toads from different locations within the toad’s invasion transect across Australia, even though our measurements were made under standardized conditions on captive animals. Toads from populations close to the invasion front ate more and had heavier fatbodies, and livers than did toads from long-colonised areas, but they had smaller gonads. This pattern reflects the evolution of a more dispersive phenotype among invasive populations, whereby the rate of dispersal is enhanced by increased energy intake and storage, and delayed reproduction. Data are measures and identifying information for individual cane toads (Rhinella marina) experimentally infected with a lungworm parasite ( Rhabdias pseudosphaerocephala.)

Variation in food resources can result in dramatic fluctuations in the body condition of animals dependent on those resources. Decreases in body mass can disrupt patterns of energy allocation and impose stress, thereby altering immune function. In this study, we investigated links between changes in body mass of captive cane toads ( Rhinella marina ), their circulating white blood cell populations, and their performance in immune assays. Captive toads that lost weight over a three-month period had increased levels of monocytes and heterophils and reduced levels of eosinophils. Basophil and lymphocyte levels were unrelated to changes in mass. Because individuals that lost mass had higher heterophil levels but stable lymphocyte levels, the ratio of these cell types was also higher, partially consistent with a stress response. Phagocytic ability of whole blood was higher in toads that lost mass, owing to increased circulating levels of phagocytic cells. Other measures of immune performance were unrelated to mass change. These results highlight the challenges faced by invasive species as they expand their range into novel environments which may impose substantial seasonal changes in food availability that were not present in the native range. Individuals facing energy restrictions may shift their immune function towards more economical and general avenues of combating pathogens. This article is part of the theme issue ‘Amphibian immunity: stress, disease and ecoimmunology’.

Variation in food resources can result in dramatic fluctuations in the body condition of animals dependent on those resources. Decreases in body mass can disrupt patterns of energy allocation and impose stress, thereby altering immune function. In this study we investigated links between changes in body mass of captive cane toads (Rhinella marina), their circulating white blood cell populations, and their performance in immune assays. Captive toads that lost weight over a 3-month period had increased levels of monocytes and heterophils and reduced levels of eosinophils. Basophil and lymphocyte levels were unrelated to changes in mass. Because individuals that lost mass had higher heterophil levels but stable lymphocyte levels, the ratio of these cell types was also higher, partially consistent with a stress response. Phagocytic ability of whole blood was higher in toads that lost mass, due to increased circulating levels of phagocytic cells. Other measures of immune performance were unrelated to mass change. These results highlight the challenges faced by invasive species as they expand their range into novel environments which may impose substantial seasonal changes in food availability that were not present in the native range. Individuals facing energy restrictions may shift their immune function towards more economical and general avenues of combating pathogens.

Most evolutionary theory does not deal with populations expanding or contracting in space. Invasive species, climate change, epidemics, and the breakdown of dispersal barriers, however, all create populations in this kind of spatial disequilibrium. Importantly, spatial disequilibrium can have important ecological and evolutionary outcomes. During continuous range expansion, for example, populations on the expanding front experience novel evolutionary pressures because frontal populations are assorted by dispersal ability and have a lower density of conspecifics than do core populations. These conditions favor the evolution of traits that increase rates of dispersal and reproduction. Additionally, lowered density on the expanding front eventually frees populations on the expanding edge from specialist, coevolved enemies, permitting higher investment into traits associated with dispersal and reproduction rather than defense against pathogens. As a result, the process of range expansion drives rapid life‐history evolution, and this seems to occur despite ongoing serial founder events that have complex effects on genetic diversity at the expanding front. Traits evolving on the expanding edge are smeared across the landscape as the front moves through, leaving an ephemeral signature of range expansion in the life‐history traits of a species across its newly colonized range. Recent studies suggest that such nonequilibrium processes during recent population history may have contributed to many patterns usually ascribed to evolutionary forces acting in populations at spatial equilibrium.

The process of rapid range expansion (as seen in many invasive species, and in taxa responding to climate change) may substantially disrupt host–parasite dynamics. Parasites and pathogens can have strong regulatory effects on their host population and, in doing so, exert selection pressure on host life history. We construct a simple individual‐based model of host–parasite dynamics during range expansion. This model shows that the parasites and pathogens of a range‐expanding host are likely to be absent from the host's invasion front, because stochastic events (serial founder events) in low‐density frontal populations result in local extinctions or transmission failure of the parasite/pathogen and, hence, a preponderance of uninfected hosts in the invasion vanguard. This pattern is true for both density‐dependent and density‐independent transmission rates, although it is exacerbated in the case of density‐dependent transmission because, in this case, transmission rates also decline on the front. Data from field surveys on the prevalence of lungworms (Rhabdias pseudosphaerocephala) in invasive cane toads (Bufo marinus) support these predictions, in showing that toads in newly invaded areas of tropical Australia lack the parasite, which only arrives 1–3 years after the toads themselves. The resultant “honeymoon phase” immediately post‐invasion, when individuals in the invasion‐front population are virtually pathogen‐free, may lead to altered host population dynamics on the invasion front, causing, for example, high densities in invasion‐front populations, followed by a decline in numbers as parasites and pathogens arrive and begin to reduce host viability. The honeymoon phase may ultimately impact the evolution of life‐history investment strategies in both host and parasite on the invasion vanguard, as hosts are released from immune challenges and parasites continuously expand into a favorable and unoccupied niche.