Whilst the identity of any putative aetiological pathogen(s) is unknown, the two ''epidemic'' clusters differed in the nature of the immune responses observed. Members of both clusters expressed high levels of all immunological genes studied, but cluster 1 was characterized by relatively higher expression of TNF-a at the protein and mRNA level and cluster 2 by higher expression of TLR4 and TLR9 and the regulatory T-helper cell-associated transcription factor FoxP3. These differences may be indicative of more than one infectious agent stimulating different immune responses. Alternatively, different immune responses to the same pathogen may have occurred because the animals involved in the respective clusters were themselves different. Cluster 1 individuals were exclusively over-wintered (1 + ) animals, whilst cluster 2 animals were exclusively young-of-the-year (0 + ) individuals. Phenotypic differences might therefore have arisen from ontogenetic stage variation, or from a different history of programming by environmental cues in the respective cohorts. A further possibility is that animals in the second cluster might have had some level of acquired immunity, following the outbreak earlier in the year, and produced more highly regulated responses indicative of a degree of immunological tolerance. This latter possibility is supported by the fact that some atypical individuals occurred in cluster 1 that were either phenotypically intermediate, or, more similar to cluster 2 individuals (Figure 3 ).