infection: (i) EIDs associated with a jump from domestic to wildlife populations
living nearby; (ii) those connected with direct human intervention through
translocation of host or parasite; and (iii) those with no human or domestic animal
associations.
1 The rinderpest is a clear case of the transfer of a virus from cattle to susceptible
wildlife hosts that had not met the disease before. Similarly, canine distemper has
spread into wild dog (Lycaon pictus) populations of Serengeti causing the local
extinction of that species (Ginsberg et al. 1995), into lions causing a 40% mortality,
and also into hyenas (Roelke-Parker et al. 1996). Most likely the rapidly expanding
human population surrounding the Serengeti ecosystem, with its associated domestic
dogs that carry the disease, are the source of these new outbreaks. Another example
is brucellosis (Meagher and Meyer 1994). This was introduced to North America with
the import of cattle, and the disease then jumped to elk and bison in Yellowstone
National Park, USA and Wood Buffalo National Park in Canada.
2 The translocation of wildlife for agriculture, hunting, and conservation has
increased exposure of wildlife to novel diseases. Translocation of fish and amphi-
bians may have caused the ranavirus epizootics now threatening many amphibian
populations (Daszak et al. 2000). Rabies epizootics in the eastern USA developed from
translocations of infected raccoons (Procyon lotor) from the southern USA where the
disease was enzootic (Rupprecht et al. 1995).
Zoos and captive feeding programs may inadvertently expose animals to novel
diseases due to the close proximity of neighboring hosts. Asian elephants (Elephas
maximus) in zoos have contracted a lethal herpes virus from neighboring African
elephants (Loxodonta africana) (Richman et al. 1999). There is considerable concern
that the agent for bovine spongiform encephalopathy (BSE) could be transferred to
zoo-held wildlife through contaminated food, and thereby to free-living wildlife (Daszak
et al. 2000).
3 Climate change may be having an effect on the emergence, frequency, and inten-
sity of epizootics. For example, African horse sickness in South Africa (Bayliss et al.
1999) and various aquatic diseases (Marcogliese 2001) have been affected by climatic
events. The fungal disease cutaneous chytridiomycosis is the cause of amphibian
mortality in Central American and Australian rainforests (Berger et al. 1998; Morell
1999). The synchronous emergence of this novel disease in widely spaced sites affect-
ing a wide range of species is thought to be the result of global climate change (Pounds
et al. 1999).
In general, the causes of EIDs are largely ecological. These are (i) movement and
migration of hosts and pathogens to new environments; (ii) the change of environ-
ment in situthrough global climate change; and (iii) a change in agricultural and
forestry practices that brings species into contact. Changes in genetic characteristics
of the pathogens play little if any part in EIDs except perhaps in their ability to jump
to new hosts (Krause 1992; Schrag and Wiener 1995).As we have seen, most endemic parasites interact with other factors such as food and
predators to reduce host population numbers. There are few examples where para-
sites, on their own, regulate the host population, that is act in a density-dependent
way. One clear example comes not from an endemic parasite, but from an emerging
epizootic disease. The poultry pathogen Mycoplasma gallisepticumhas entered a pre-
viously unknown host, the house finch (Carpodacus mexicanus) in North America.188 Chapter 11