produced a generalized disease that is almost always lethal. Myxomatosis was
deliberately introduced into Australia in 1950 and into Europe in 1952. It was
first spectacularly successful in controlling the rabbit pest, but biological adjust-
ments occurred in the virulence of the virus and the genetic resistances of the
rabbits. After 30 years of interaction, natural selection has resulted in a balance
at a fairly high level of viral virulence. (Fenner 1983)
The initial annual mortality rates were very high in Australia, over 95%, but these
dropped progressively over the next few years. There is a widespread perception
that the rabbits and the disease accommodated to each other and, therefore, that
myxomatosis provided only a temporary respite. This is not so. The rabbit density
at equilibrium with the disease is considerably lower than the mean density in the
absence of myxomatosis.
Parer et al. (1985) demonstrated the controlling effect of this virus. They used a
relatively benign strain of Myxomato immunize rabbit populations against the more
virulent field strains that swept through the study area in most years. Rabbit densi-
ties increased by a factor of 10 under this treatment. Even after the rabbits and the
virus had reached an accommodation with each other, the disease was apparently
holding mean density of rabbits to about 10% of the densities prevalent before intro-
duction of the Myxomavirus.
Most parasites and pathogens have little effect on their hosts. When a parasite jumps
from one host species to another, it is the “naivety” of the new host to the parasite
or pathogen which is responsible for the reaction of the new host individual or the
new host population to the parasite. In both meningeal worm in cervids, other than
white-tailed deer, and liver fluke infection in wombats it is the dramatic host
immunological response to the new parasite which is responsible for the debilita-
tion in the animals. Such a response has been dampened down over time as the
meningeal worm evolved in white-tailed deer and liver fluke evolved in sheep, and
so we do not see the same level of debilitation in the “normal” host species.
The key points from the epidemiology of parasites and pathogens are that the fate
of an infection is determined by only a few traits of the host and parasite, and there
is a critical density of the host that allows the infection to persist and spread. Efforts
to reduce the effects of parasites and pathogens can be at their most important in
the management of small populations of endangered species, be they in the wild or
in captivity. Diseases of harvested wildlife are more rarely controlled unless they
present a potential hazard to people. Few attempts to use parasites and pathogens to
control pest wildlife have been successful.
PARASITES AND PATHOGENS 195
11.13 Summary
