Patricia C. Lopes

When is it socially acceptable to feel sick

Disease is a ubiquitous and powerful evolutionary force. Hosts have evolved behavioural and physiological responses to disease that are associated with increased survival. Behavioural modifications, known as ‘sickness behaviours’, frequently involve symptoms such as lethargy, somnolence and anorexia. Current research has demonstrated that the social environment is a potent modulator of these behaviours: when conflicting social opportunities arise, animals can decrease or entirely forgo experiencing sickness symptoms. Here, I review how different social contexts, such as the presence of mates, caring for offspring, competing for territories or maintaining social status, affect the expression of sickness behaviours. Exploiting the circumstances that promote this behavioural plasticity will provide new insights into the evolutionary ecology of social behaviours. A deeper understanding of when and how this modulation takes place may lead to better tools to treat symptoms of infection and be relevant for the development of more efficient disease control programmes.

Infection-induced behavioural changes reduce connectivity and the potential for disease spread in wild mice contact networks.

Infection may modify the behaviour of the host and of its conspecifics in a group, potentially altering social connectivity. Because many infectious diseases are transmitted through social contact, social connectivity changes can impact transmission dynamics. Previous approaches to understanding disease transmission dynamics in wild populations were limited in their ability to disentangle different factors that determine the outcome of disease outbreaks. Here we ask how social connectivity is affected by infection and how this relationship impacts disease transmission dynamics. We experimentally manipulated disease status of wild house mice using an immune challenge and monitored social interactions within this free-living population before and after manipulation using automated tracking. The immune-challenged animals showed reduced connectivity to their social groups, which happened as a function of their own behaviour, rather than through conspecific avoidance. We incorporated these disease-induced changes of social connectivity among individuals into models of disease outbreaks over the empirically-derived networks. The models revealed that changes in host behaviour frequently resulted in the disease being contained to very few animals, as opposed to becoming widespread. Our results highlight the importance of considering the role that behavioural alterations during infection can have on social dynamics when evaluating the potential for disease outbreaks.

The impact of exposure to a novel female on symptoms of infection and on the reproductive axis.

Background/Aim: Sickness behaviors are the behavioral alterations animals exhibit during the course of an infection, often accompanied by reduced reproductive activity. Adopting sickness behaviors may aid in overcoming the infection, by diverting energy from routine activities towards enhancement of the immune system. Nonetheless, sickness behaviors are plastic, being influenced by specific environmental and social circumstances. Here, we tested whether the presentation of a novel female to males suffering from a simulated infection could impact the behavioral effects of sickness, the reproductive axis, or both. Methods: Male zebra finches were housed in isolation and injected intramuscularly with lipopolysaccharide or saline. Behaviors were recorded before (3 h before injection) and after (3.5 h after injection) addition of a novel female to the cage for 30 min. Four hours after injection, we collected the brain and testis for the analysis of important reproductive axis modulators, gonadotropin-releasing hormone, and gonadotropin-inhibitory hormone, and to quantify gene expression of a proinflammatory cytokine involved in the regulation of sickness behaviors [interleukin (IL)-1β]. Testosterone was quantified in the plasma. Results: The presence of a novel female diminished sickness behaviors and induced alterations in the reproductive axis within 30 min, with no associated changes in brain gene expression of IL-1β. Social environment itself altered brain gene expression of IL-1β. Conclusions: Male zebra finches prioritize the opportunity to mate versus investment in recovery from an infection, as determined by reduced expression of sickness behaviors when a potential mate was present. The behavioral effects of IL-1β appear to be context dependent in this species.

Why are behavioral and immune traits linked

Abstract Through behavior, animals interact with a world where parasites abound. It is easy to understand how behavioral traits can thus have a differential effect on pathogen exposure. Harder to understand is why we observe behavioral traits to be linked to immune defense traits. Is variation in immune traits a consequence of behavior‐induced variation in immunological experiences? Or is variation in behavioral traits a function of immune capabilities? Is our immune system a much bigger driver of personality than anticipated? In this review, I provide examples of how behavioral and immune traits co‐vary. I then explore the different routes linking behavioral and immune traits, emphasizing on the physiological/hormonal mechanisms that could lead to immune control of behavior. Finally, I discuss why we should aim at understanding more about the mechanisms connecting these phenotypic traits. HighlightsCo‐variation between behavioral and immune traits has been found in many studies.Causal linkages between behavior and immunity remain unresolved.Influence of genes, prenatal, early/adult environment, and microbiota are reviewed.

LPS and neuroinflammation: a matter of timing

Lipopolysaccharide (LPS) administration has been repeatedly shown to elicit central inflammation, regardless of the route of administration. In a recent study, Tiwari et al. (Inflammopharmacology 10.1007/s10787-016-0274-3, 2016) dispute the potential of peripheral administration of LPS to induce neuroinflammation. Here, I summarise literature indicating that the neuroinflammatory effects of LPS are time dependent, and suggest that their findings can be explained by the time at which they chose to measure neuroinflammation.

A novel symbiotic relationship between sociable weaver birds (Philetairus socius) and a new cheliferid pseudoscorpion (Pseudoscorpiones : Cheliferidae) in southern Africa

Abstract. Birds harbour a wide array of other taxa in their nests or in their plumage, which either have an ectoparasitic or commensal relationship with the host. We report on the discovery of a cheliferid pseudoscorpion found in the plumage and nests of the sociable weaver bird (Philetairus socius) in southern Africa. The nests of these communal birds are the largest of any bird, and may contain up to 500 individuals. The pseudoscorpion is likely to have a mutualistic relationship with the birds, most likely preying on other small invertebrates in the nests. Molecular data derived from two populations of the pseudoscorpion found divergence levels of 1.1% in cytochrome oxidase 1 (CO1), and an analysis of CO1 and two rRNA genes (18S and 28S) found a close relationship with Chelifer and Parachelifer in the tribe Cheliferini, which is supported by the morphology of the male genitalia. The molecular analysis also suggests that Beierius may not belong to the Cheliferini. The pseudoscorpion found in association with the sociable weaver represents a new genus and species, Sociochelifer metoecus Harvey, sp. nov.