Johannes Foufopoulos

Anthropogenic land use changes drive a range of infectious disease outbreaks and emergence events and modify the transmission of endemic infections. These drivers include agricultural encroachment, deforestation, road construction, dam building, irrigation, wetland modification, mining, the concentration or expansion of urban environments, coastal zone degradation, and other activities. These changes in turn cause a cascade of factors that exacerbate infectious disease emergence, such as forest fragmentation, disease introduction, pollution, poverty, and human migration. The Working Group on Land Use Change and Disease Emergence grew out of a special colloquium that convened international experts in infectious diseases, ecology, and environmental health to assess the current state of knowledge and to develop recommendations for addressing these environmental health challenges. The group established a systems model approach and priority lists of infectious diseases affected by ecologic degradation. Policy-relevant levels of the model include specific health risk factors, landscape or habitat change, and institutional (economic and behavioral) levels. The group recommended creating Centers of Excellence in Ecology and Health Research and Training, based at regional universities and/or research institutes with close links to the surrounding communities. The centers' objectives would be 3-fold: a) to provide information to local communities about the links between environmental change and public health; b) to facilitate fully interdisciplinary research from a variety of natural, social, and health sciences and train professionals who can conduct interdisciplinary research; and c) to engage in science-based communication and assessment for policy making toward sustainable health and ecosystems.

The first part of this paper surveys emerging pathogens of wildlife recorded on the ProMED Web site for a 2-year period between 1998 and 2000. The majority of pathogens recorded as causing disease outbreaks in wildlife were viral in origin. Anthropogenic activities caused the outbreaks in a significant majority of cases. The second part of the paper develops some matrix models for quantifying the basic reproductive number, R(0), for a variety of potential types of emergent pathogen that cause outbreaks in wildlife. These analyses emphasize the sensitivity of R(0) to heterogeneities created by either the spatial structure of the host population, or the ability of the pathogens to utilize multiple host species. At each stage we illustrate how the approach provides insight into the initial dynamics of emergent pathogens such as canine parvovirus, Lyme disease, and West Nile virus in the United States.

One of the central questions of conservation biology is what life‐history traits render a species prone to extinction. We addressed this problem by calculating extinction rates for 35 species of turtles and squamates (lizards and snakes) occurring on 87 land‐bridge islands in the Mediterranean Sea. We calculated extinction rates in two ways: first, by incorporating the known sequence of historical island separations and second by ignoring history and assuming that the islands became isolated simultaneously. The second procedure is simpler and more frequently used in the literature and produces estimates of extinction rates that are similar to the first, more complex procedure. We then determined the relationship between extinction rates (calculated using both methods) and body mass, longevity, habitat specialization, and population abundance using two methods: first, by accounting for the phylogenetic relationships among species and, second, by ignoring them. Only population abundance and habitat specialization explained a significant amount of the observed variation in species extinction rates. Body mass itself did not explain variation in extinction rates, although it was strongly correlated with abundance. These conclusions were obtained using both procedures for calculating extinction rates and both procedures for correlating extinction rates with life‐history traits.

Wikelski, M., Foufopoulos, J., Vargas, H., Snell, H. 2004. Galápagos Birds and Diseases: Invasive Pathogens as Threats for Island Species. Ecology and Society 9(1): 5. https://doi.org/10.5751/ES-00605-090105

1 Phenotypic plasticity may allow an organism to respond to temporally variable opportunities for growth and risks of mortality. However, life-history theory assumes that there are often trade-offs between the benefits afforded by plasticity in one trait and the consequences of that plasticity on other traits that affect fitness. In organisms with a complex life cycle, trade-offs may occur between larval and post-metamorphic traits. 2 Many amphibians metamorphose in temporary ponds, and may accelerate larval development to avoid mortality when a pond desiccates. A younger age at metamorphosis often results in reduced body size, but may also facilitate a trade-off with physiological traits that are linked to fitness in the adult stage. 3 We investigated a potential trade-off between desiccation-driven acceleration of development rate and immune system responsiveness in a species that breeds exclusively in temporary ponds. We exposed Rana sylvatica (wood frog) tadpoles to four possible desiccation regimes and then assayed the cell-mediated immune response to a standardized foreign antigen, phytohaemagglutinin (PHA), injected 3 weeks after metamorphosis. We also quantified total leucocyte numbers from haematological smears to obtain a secondary measure of individual immunological condition. 4 Animals exposed to desiccation had shorter development times, weaker cellular immune system responses to PHA and lower total leucocyte numbers than animals from control groups. Both measures of immune response showed a decrease with increasing severity of the desiccation treatment. 5 It is currently unclear whether the observed depression in immune response is transient or permanent. However, even temporary periods of immune system suppression shortly after metamorphosis may lead to greater susceptibility to opportunistic pathogens or parasites.