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The species jumping process may also operate the other way, with wildlife acting as
reservoirs of parasites and pathogens transmitted to domestic stock. The controver-
sies over brucellosis in bison, and its transmission to domestic stock both in the USA
and Canada, and the transfer of tuberculosis (Mycobacterium bovis) from European
badgers to cattle are obvious examples (Peterson et al. 1991; Clifton-Hadley et al.
2001). The appearance of SARS in humans in 2002 is thought to have arisen because
people in southern China keep civets (Viverra zibetha) in captivity and eat them.

We explore in Chapter 18 the general consequences of degraded habitats and frag-
mentation for conservation. One particular effect of habitat fragmentation is that it
increases exposure to parasites. In birds, and perhaps in other animal groups, Loye
and Carroll (1995) suggest three mechanisms:
1 Increased edge habitat due to fragmentation increases the contact rate between species
in adjacent habitats and exposes those in fragments to new vectors and new para-
sites to which they are more susceptible.
2 Loss of habitat could force birds to reuse old nests, exposing them to higher
numbers of fleas, ticks, or other nest-living parasites.
3 As a special case in birds, fragments expose birds not only to predators commut-
ing from the surrounding agriculture, but also to brood-parasite birds such as the
brown-headed cowbird (Molothrus ater) of North America.
Some of these mechanisms are illustrated by Loye and Carroll (1995) for the Puerto
Rican parrot (Amazona vittata). This species is restricted to a single fragment of
high-elevation forest. Habitat degradation, harvesting for the pet trade, and novel
parasites have been factors in its decline. In particular, fatal parasitism of nestlings
by muscid botflies became a problem after the pearly eyed thrasher (Margarops
fuscatus) invaded the forest fragment in about 1950. The thrasher nestlings are host
to abundant blood-feeding botfly maggots. The introduced native thrasher, therefore,
brought in its endemic parasite that then spread to a new but rare host, the parrot.

Parasites and pathogens can be a factor driving the decline of an endangered species
(see Section 17.2.8) and can become an issue in the recovery of endangered species.
Parasites and pathogens can hinder or thwart attempts to establish captive breeding
populations. Thorne and Williams (1988) review the well-known example of the first
attempts to establish a captive breeding colony of black-footed ferrets (Mustela
nigripes) in the USA. A previous attempt to establish a breeding colony in the early
1970s failed because canine distemper virus (CDV) killed the only two litters. The
source colony also disappeared. The extreme susceptibility of the black-footed
ferrets to CDV became apparent when four of six black-footed ferrets died after being
vaccinated for CDV in the 1970s. The vaccine had been previously shown to be safe
in domestic ferrets. In 1981 the species was rediscovered in Wyoming, and the colony’s
vulnerability to disease was quickly realized. Precautions were taken to minimize human
introductions of disease, especially CDV and influenza. The population declined from
an estimated peak population of 128 in 1984 to only 16 in 1985. The decline spurred
an attempt to start a captive breeding colony, but the first six ferrets captured rapidly
succumbed to canine distemper. Despite all precautions CDV infected the colony and
most of its members died from it. The few surviving eventually formed a breeding
population. Nonetheless, as Thorne and Williams (1988) note, “The captive breed-
ing program went from a carefully planned approach with ideally selected, unrelated

PARASITES AND PATHOGENS 193

11.11.2The
alteration of habitat


11.11.3Captive
breeding and
reintroductions

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