PS 89-195
Measuring immune development in larval amphibians to understand age-dependent susceptibility to infection by Ribeiroia ondatrae (class Trematoda)

Friday, August 9, 2013
Exhibit Hall B, Minneapolis Convention Center
Johanna Nifosi, Science and Technology, Universidad Metropolitana, San Juan, PR
Pieter T. J. Johnson, Ecology and Evolutionary Biology, University of Colorado at Boulder, CO
Bethany Hoye, Ecology and Evolutionary Biology, University of Colorado at Boulder, Boulder, CO
Background/Question/Methods

Ribeiroia ondatrae, a trematode from the Psilostomatidae family, is one of the major contributors to amphibian malformations. Infection with Ribeiroia during limb development may result in the amphibian developing deformities such as multiple limbs, skin webbing, missing limbs and total suppression of limb development.  Johnson et al. (2011) found that the age and the stage of development of these amphibian hosts influenced the probability of infection and the resulting infection intensity, both decreasing with amphibian development. The objective of our research is to determine if a change in the composition of the innate immune system could be a possible explanation for these age dependent malformations. We hypothesize that the variations in the degree of infection and pathology within different stages of development of larval amphibians may be explained by the relative abundance of certain cells of the immune system. To assess this hypothesis tadpoles were exposed of the species Pseudacris triseriata with Ribeiroia ondatrae cercariae (n=20), extracted from already infected Planorbella snails. Different types of blood cells were counted – lymphocytes, neutrophils, eosinophils, basophils, monocytes and erythrocytes- from blood smears collected from tadpoles at different time points of development (stages). Controls were compared within each stage (n=6 per stage) to Ribeiroia exposed individuals (n=6 per stage) to examine the immune response to infection. 

Results/Conclusions

The results of the success of infection per stage confirmed our hypothesis, as younger tadpoles were more susceptible to infection than older tadpoles. However, leukocytes counts showed unexpected results, as their concentration decrease through the stages. This means that the innate immune system is not developing.  Moreover, a lack of difference in between the infected treatment and uninfected treatment was found. This means that the immune response to parasite exposure is almost null when the tadpole is close to metamorphosis, as there is no difference in leukocytes count if it is infected or not. In conclusion our hypotheses were rejected because the development of the immune system did not explain the stage-dependent pathology and leukocytes did not increase with development.