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behaviors. Other general responses are unusual levels of activity, disorientation, and
altered responses to stimuli.
Three lines of evidence support the hypothesis that modified behavior of hosts is
a strategy adapted to increase transmission (Lafferty and Morris 1996). First, hosts
infected by transmissible stages of parasites often behave differently. Second, experi-
mentally infected prey are more readily eaten by predators in laboratory experiments;
and third, infected prey are eaten by predators more frequently than expected in field
studies. We mentioned above that parasitized snowshoe hares in spring were more
likely to be eaten by predators (Murray et al. 1997). Conspicuous behaviors exhib-
ited by killifish (Fundulus parvipinnis) were linked to parasitism by larval trematodes.
Field experiments showed that parasitized fish were heavily depredated by birds, the
final hosts (Fig. 11.3).

Unlike enzootic diseases, epizootic ones have intermittent effects on host populations.
There are outbreak phases with rapid spread and high mortality followed by periods
of quiescence when they lie dormant in host species. The great majority of the pathogens
causing epizootics are microparasites such as viruses and bacteria. Some case stud-
ies illustrate their behavior.

Rinderpest is a virus from the Morbillivirus group (genus Morbillivirus, family Para-
myxoviridae) that produces measles in humans and canine distemper in dogs, cats,
and hyenas. It is probably the oldest member of the group, from which others evolved.
Predators can develop cross-immunity to distemper by feeding on herbivores infected
with rinderpest (Rossiter 2001). Its natural host is cattle and it is endemic to Asia.
It is highly contagious through droplet infection via licking and sneezing. It causes
high fever, and inflammation and lesions of the alimentary and respiratory passages.
Rinderpest, as far as evidence goes, was absent from Africa until it was introduced
during the 1880s from Egypt to southern Sudan and Ethiopia. By 1889 it was caus-
ing epidemics in eastern Africa where it killed 95% of the cattle and similar propor-
tions of closely related wildlife, especially African buffalo but also wildebeest, and
less closely related giraffe, warthog , greater and lesser kudu, and other antelope species
(Rossiter 2001). By 1896 the epidemic had reached the tip of South Africa and the
West African coast causing similar mortality. Thereafter rinderpest reappeared at roughly
20-year intervals producing slightly less virulent epizootics. Mortality of susceptible
animals was at least 50%.

186 Chapter 11


100

80

60

40

20

0
Uninfected Low infection High infection

% depredated

Fig. 11.3Parasitized
killifish are more
heavily depredated by
birds than are
unparasitized fish
(adapted from Lafferty
and Morris 1996.


11.7 Epizootic diseases


11.7.1Rinderpest

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