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-...

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.

Exotic diseases and parasites have caused extinctions on islands and continents, particularly when they spread through assemblages of immunologically naïve species. Hawaii has lost a substantial part of its endemic bird fauna since the introduction of avian malaria at the beginning of the 20th century. In contrast, the Galápagos archipelago still possesses its entire endemic avifauna. Several of these Galápagos bird populations are in decline, however, and wildlife managers seek guidance to counteract a potential man-made ecological disaster. We recommend that endemic birds be tested for susceptibility to disease outside the Galápagos so that protection efforts can be better designed to deal with actual threats. At present, the best and perhaps only management option is to protect the isolation of these island communities because treating or vaccinating wild bird populations against diseases is almost impossible. If the isolation of the Galápagos Islands is successful, we will preserve the complete avifauna of an archipelago for the first time in the history of human colonization in the Pacific eco-region

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.

The evolution of parasite resistance can be influenced by the abundance of parasites in the environment. However, it is yet unresolved whether vertebrates change their investment in immune function in response to variation in parasite abundance. Here, we compare parasite abundance in four populations of small ground finches (Geospiza fuliginosa) in the Galapagos archipelago. We predicted that populations exposed to high parasite loads should invest more in immune defence, or alternatively use a different immunological defence strategy. We found that parasite prevalence and/or infection intensity increased with island size. As predicted, birds on large islands had increased concentrations of natural antibodies and mounted a strong specific antibody response faster than birds on smaller islands. By contrast, the magnitude of cell–mediated immune responses decreased with increasing parasite pressure, i.e. on larger islands. The data support the hypothesis that investments into the immune defence are influenced by parasite–mediated selection. Our results are consistent with the hypothesis that different immunological defence strategies are optimal in parasite–rich and parasite–poor environments.