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.Thedivided between two species of trematodes and ces- models used to describe parasitic helminthes addtodes, and often five species of nematodes.considerably more detail in that they consider, notAcanthocephalans are less ubiquitous, but at least whether a patch is occupied, but the numbers ofone species is associated with every other host pop- individuals of each species occupying each patch,ulation.This suggests that most free-living verte- these are usually described by a series of frequencybrates will be parasitized by at least one parasitic distributions.It is possible to compare the structureworm species during the course of their life, many of a range of different host pathogen models withwill harbour a community of parasitic organisms.those for metapopulation models.This suggests thatMore detail can be added to this picture by look- all these models describe a spectrum of complexitying at some data put together by Clive Kennedy, Al and detail that starts out with the basic models firstBush, and John Aho (Kennedy et al.1986b), who com- described by Levins and Culver (1971), and thenpared the species richness of helminth communities passing through different types of models forin fish, birds, and mammals.Their work suggests that host parasite systems (Dobson 2003).PARASI TI SM, BI ODI VERSI TY, AND CONSERVATI ON 137It is important to notice here that a large number similar effects may be occurring in temperateof  free-living organisms will have population forests (Packer and Clay 2000).structure and dynamics that correspond to one of The spatial dynamics of these systems can read-the frameworks previously described.For example ily be modelled in one dimension.First assume thatthe fish and invertebrates that occupy different the seeds produced from a tree decline exponen-parts of a coral can be considered as organisms that tially in abundance with increasing distance fromuse patches of coral as habitat.Like parasitic the tree.When these tree seeds germinate theirhelminths they may reduce the fitness of the coral, mortality is determined by whether they arebut their fitness will in turn also be dependent infected with a fungal pathogen.Their probabilityupon the dynamics of the coral and the ability of of acquiring the pathogen is a simple function oftheir offspring to locate a new patch of coral to col- the density of infected individuals in their immedi-onize.Many insects that feed on plants, or even car- ate vicinity.If we assume that we can divide therion, will also have a similar population dynamic area around the parent tree into an array ofstructure (Ives and May 1985; Anderson 1989).The  patches within which pathogen transmissionfactors that determine community composition and occurs, then we can describe the dynamics of therelative abundance in these communities will be fungal pathogen in each patch by the magnitude ofsimilar to those in the host pathogen models: the its basic reproductive number, R0.vital dynamics of the plant hosts, the statistical distri-Sbution of each insect species across the plant popu- R0.( )lation, and the birth, death, and dispersal rates ofthe different insect species.Here S is the density of seeds in a patch, is thetransmission rate of the pathogen, is the intrinsicrate of seedling mortality, and is the additional8.6.3 Fungal pathogens and forest diversitymortality due to infection with the fungalIf parasitism is so ubiquitous in the natural world, pathogen.Within any patch the proportion of seedsand parasites have the potential to regulate or alter that survive infection (SS) is approximately giventhe dynamics of their hosts, then this implies they by the following expressionmay play subtle and important roles in food webs(see also Chapter 4) and may even make significant SS e R0.contributions to indirect competitive interactionsbetween species (see Section 8.2 of this chapter).It is then relatively trivial to determine the pat-Work by Augspurger s on the role of fungal tern of recruitment of surviving seedlings at differ-pathogens in tropical forests illustrated that fungal ent distances from the parent.This mechanismpathogens have the potential to create spatially produces a classic  Janzen Connell recruitmentlocal patterns of frequency dependent recruitment curve.The high abundance of seedlings close to the(Augspurger 1983, 1984a).Janzen and Connell had tree produces high levels of disease that minimizeposited that a mechanism of this form might be their chances of recruiting.Seedlings are only ableimportant in mediating the coexistence of different to survive at distances where seed abundance hastree species in tropical forests (Janzen 1970; Connell fallen to sufficiently low levels that the pathogen1978).Augsburger s work showed that rates of dies out.Providing the fungal pathogen is specificseedling death were significantly higher in the to one host species then individuals of other speciesvicinity of the parent tree than they were at a dis- can recruit into these areas.It is important to noticetance removed from the tree (Augspurger 1984b).that we are again dealing with a threshold phe-The majority of the deaths occurred in shaded nomena, recruitment of seedlings can only occur atregions where  damping-off diseases caused by densities where the basic reproduction rate of thefungal pathogens were the main source of mortal- pathogen is less than unity.If seed productionity.Recent work on black cherry has illustrated that varies from year to year, then seedlings will tend to138 PARASI TI SM AND ECOSYSTEMrecruit closer to the parent tree in years of low seed rinderpest virus in East Africa (Sinclair 1979b;abundance, and further from the tree in years when Plowright 1982; Dobson 1995a,b).Rinderpest is aseed crop is high.Here, it is interesting to speculate morbillivirus that is closely related to canine dis-about how the recruitment patterns of tropical trees temper and human measles (Plowright 1968).Themight be affected by changes in the abundance of evolutionary split between the three pathogensspecies that feed on seeds [ Pobierz całość w formacie PDF ]