In this review, we provide a current reference on disease resistance in insect societies. We start with the genetics of immunity in the context of behavioral and physiological processes and scale up levels of biological organization until we reach populations. A significant component of this review focuses on Apis mellifera and its role as a model system for studies on social immunity. We additionally review the models that have been applied to disease transmission in social insects and elucidate areas for future study in the field of social immunity.

No abstract

Honeybees, Apis spp., maintain elevated temperatures inside their nests to accelerate brood development and to facilitate defense against predators. We present an additional defensive function of elevating nest temperature: honeybees generate a brood-comb fever in response to colonial infection by the heat-sensitive pathogen Ascosphaera apis. This response occurs before larvae are killed, suggesting that either honeybee workers detect the infection before symptoms are visible, or that larvae communicate the ingestion of the pathogen. This response is a striking example of convergent evolution between this "superorganism" and other fever-producing animals.

Recent evolutionary models of reproductive partitioning within animal societies (known as`optimal skew',`concessions' or`transactional' models) predict that a dominant individual will often yield some fraction of the group's reproduction to a subordinate as an incentive to stay in the group and help rear the dominant's o¡spring. These models quantitatively predict how the magnitude of the subordinate's`staying incentive' will vary with the genetic relatedness between dominant and subordinate, the overall expected group output and the subordinate's expected output if it breeds solitarily. We report that these predictions accord remarkably well with the observed reproductive partitioning between conesting dominant and subordinate queens in the social paper wasp Polistes fuscatus. In particular, the theory correctly predicts that (i) the dominant's share of reproduction, i.e. the skew, increases as the colony cycle progresses and (ii) the skew is positively associated both with the colony's productivity and with the relatedness between dominant and subordinate. Moreover, aggression between foundresses positively correlated with the skew, as predicted by transactional but not alternative tug-of-war models of societal evolution. Thus, our results provide the strongest quantitative support yet for a unifying model of social evolution.

The domestic cat (Felis catus) shows remarkable sensitivity to the adverse effects of phenolic drugs, including acetaminophen and aspirin, as well as structurally-related toxicants found in the diet and environment. This idiosyncrasy results from pseudogenization of the gene encoding UDP-glucuronosyltransferase (UGT) 1A6, the major species-conserved phenol detoxification enzyme. Here, we established the phylogenetic timing of disruptive UGT1A6 mutations and explored the hypothesis that gene inactivation in cats was enabled by minimal exposure to plant-derived toxicants. Fixation of the UGT1A6 pseudogene was estimated to have occurred between 35 and 11 million years ago with all extant Felidae having dysfunctional UGT1A6. Out of 22 additional taxa sampled, representative of most Carnivora families, only brown hyena (Parahyaena brunnea) and northern elephant seal (Mirounga angustirostris) showed inactivating UGT1A6 mutations. A comprehensive literature review of the natural diet of the sampled taxa indicated that all species with defective UGT1A6 were hypercarnivores (>70% dietary animal matter). Furthermore those species with UGT1A6 defects showed evidence for reduced amino acid constraint (increased dN/dS ratios approaching the neutral selection value of 1.0) as compared with species with intact UGT1A6. In contrast, there was no evidence for reduced amino acid constraint for these same species within UGT1A1, the gene encoding the enzyme responsible for detoxification of endogenously generated bilirubin. Our results provide the first evidence suggesting that diet may have played a permissive role in the devolution of a mammalian drug metabolizing enzyme. Further work is needed to establish whether these preliminary findings can be generalized to all Carnivora.