Detecting and assessing outbreaks

[Extract] An infectious disease outbreak is defined as a situation whereby the rate at which new hosts become infected increases. In other words, it is an unexpected increase in disease or mortality where it does not normally occur, or is at a frequency greater than previously observed. In Figure 5.1, we provide an example of outbreak dynamics for human diseases. As demonstrated in this graph, once the infected host population reaches a critical size, the number of new cases increases exponentially. As more individuals within a population are exposed to the disease, the number of new cases eventually declines, either through host recovery and immunity or death. The disease then becomes a long-term aspect of the population dynamics, becoming endemic and either reaching equilibrium with few occasional cases, or undergoing periodic outbreaks

Costs, benefits and inducible defences: a case study with Daphnia pulex

Phenotypic plasticity is one major source of variation in natural populations. Inducible defences, which can be considered threshold traits, are a form of plasticity that generates ecological and evolutionary consequences. A simple cost–benefit model underpins the maintenance and evolution of these threshold, inducible traits. In this model, a rank-order switch in expected fitness, defined by costs and benefits of induction between defended and undefended morphs, predicts the risk level at which individuals should induce defences. Here, taking predator-induced morphological defences in Daphnia pulex as a threshold trait, we provide the first comprehensive investigation into the costs and benefits of a threshold trait, and how they combine to reflect fitness and predict the switchpoint at which induction should occur. We develop reaction norms that show genetic variation in switchpoints. Further experiments show that induction can confer a survival benefit and a cost in terms of lifetime reproductive success. Together, these two traits combine to estimate expected fitness and can predict the switchpoint between an undefended and a defended strategy. The predictions match the reaction norm data for clones that experience these costs and benefits, and correspond well to independent field data on induction. However, predictions do not, and cannot, match for clones that do not gain a benefit from induction. This study confirms that a simple theory, based on life history costs and benefits, is a sufficient framework for understanding the ecology and evolution of inducible, threshold traits

Review: Marine Ecology - Emerging Marine Diseases - Climate Links and Anthropogenic Factors

Mass mortalities due to disease outbreaks have recently affected major taxa in the oceans. For closely monitored groups like corals and marine mammals, reports of the frequency of epidemics and the number of new diseases have increased recently. A dramatic global increase in the severity of coral bleaching in 1997-98 is coincident with high El Nino temperatures. Such climate-mediated, physiological stresses may compromise host resistance and increase frequency of opportunistic diseases. Where documented, new diseases typically have emerged through host or range shifts of known pathogens. Both climate and human activities may have also accelerated global transport of species, bringing together pathogens and previously unexposed host populations

Substantial changes in the genetic basis of tadpole morphology of Rana lessonae in the presence of predators

Predator-induced morphological plasticity is a model system for investigating phenotypic plasticity in an ecological context. We investigated the genetic basis of the predator-induced plasticity in Rana lessonae by determining the pattern of genetic covariation of three morphological traits that were found to be induced in a predatory environment. Body size decreased and tail dimensions increased when reared in the presence of preying dragonfly larvae. Genetic variance in body size increased by almost an order of magnitude in the predator environment, and the first genetic principal component was found to be highly significantly different between the two environments. The across environment genetic correlation for body size was significantly below 1 indicating that different genes contributed to this trait in the two environments. Body size may therefore be able to respond to selection independently in the two environments to some extent