Disease and the abundance and distribution of bird populations: a summary

Over the past few years, I have written several reviews about the effects of infectious diseases upon the distribution and abundance of their host populations. One general review and synthesis is in the fmd chapter of a book whose earlier chapters focus mainly on human diseases (Anderson & May 1991). A bird-specific discussion, with particular reference to conservation issues, is given by Dobson and May (1991). Broadly related questions about the invasion, persistence and spread of infectious diseases within animal communities are explored by Anderson and May (1986) and with emphasis on bird populations by Dobson and May (1986). Also relevant are a set of papers from the Society for Conservation Biology's first-ever symposium on Conservation and Disease (for an overview, see May 1988, Scott 1988).
Rather than burdening the literature with a recapitulation of these existing reviews, this paper gives a sign-posted guide for those who are not familiar with this particular literature. I first sketch reasons for believing that infectious diseases play an important part in the life history of birds. Next I point towards an analytic framework for understanding the dynamics of host-pathogen associations. Finally I list some of the implications for the conservation biology of bird populations.     

Stomatal Response to Humidity and Lanthanum

Lanthanum fed to the base of excised leaves of Sesamum indicum L. and Helianthus annuus L. was used as a tracer to investigate by electron microscopy the path of water in the apoplast of leaves. The generally random distribution of lanthanum in cell walls provided no support for the hypothesis that cuticular transpiration may be greater for guard cells than for adjacent epidermal cells. Occasionally, accumulations of lanthanum were observed in anticlinal walls of epidermal cells and at the outer surface of the plasma membrane but lanthanum was not observed in the symplast. The influx of ⁸⁶Rb to excised roots of sesame and sunflower was inhibited during incubation with 0.5 mM lanthanum or calcium for 15 or for 180 min. Stomata of sunflower partially closed when 2.5 mM lanthanum was supplied to the base of excised shoots in a potometer, whereas this treatment had little effect on stomatal conductance of sesame shoots maintained in a constant environment. Supplying 2.5 mM lanthanum to the base of sesame shoots strongly inhibited stomatal opening response to increase in ambient humidity but had little effect on stomatal opening response to light. It was concluded that stomatal opening response to increased humidity may be dependent upon some process, such as ion influx, that is inhibited by lanthanum, and that opening response to humidity may differ in mechanism from stomatal opening response to increased irradiance.