of the prehistoric and historic Indians and caught the eye (and trigger finger) of the
early European explorers. California condors ranged from the Columbia River south
into New Mexico in the 1800s but by 1940 their range had contracted to a small
area north of Los Angeles. Koford’s (1953) estimate, based on sightings, of only 60
individuals surviving by the early 1950s was probably low. Annual surveys by simul-
taneous observations of known concentrations were begun in 1965 but abandoned
in 1981 because they were judged to be subject to unacceptable error. Photographic
identifications were then used to generate a total count of 19–21 birds in 1983 (Snyder
and Johnson 1985). The decline continued until, in 1985, the last eight wild indi-
viduals were caught and added to the captive flock.
The causes of the initial decline were probably shooting and loss of habitat, but
the supporting evidence is anecdotal. Low productivity caused by an insufficiency of
food was suggested as a cause of the decline during the 1960s. Road-killed deer were
cached at feeding stations in 1971–73 to alleviate the perceived shortage of food (Wilbur
et al. 1974). That program was run for an insufficient time to determine whether
supplementary feeding was associated with increased productivity.
The connection between toxic organochlorines and eggshell thinning in birds was
established in the late 1960s, but the resulting flurry of studies focused on bird-
eating and fish-eating birds because avian scavengers were assumed to be less at risk.
The possibility of a causal association between environmental toxins and the later
decline of the condor was recognized in the mid-1970s, but determination of the specific
role of organochlorines in that decline was delayed (Kiff 1989). Eggshell samples from
California condors had been collected in the late 1960s but for various reasons, includ-
ing mishaps to the samples, analyses were delayed until the mid-1970s. The negative
correlation between eggshell thickness and DDE (dichlorodiphenyldichloroethane)
levels was significant: the shells were thinner and their structure different from shells
collected before 1944.
It was known that condor eggs often broke but the cause was open to debate. Even
the monitoring activities themselves were suspected as being the cause. The evidence
for organochlorines was circumstantial but it led Kiff (1989) to conclude that “DDE
contamination probably had a very serious impact on the breeding success of the
remnant population in the 1960s, leading to a subsequent decline in the number of
individuals added to the pool of breeding adults in the 1970s.” In 1972 DDT was
banned in the USA. The few eggs measured after 1975 had thicker eggshells and this
led to guarded optimism. In March 1986, however, an egg laid by the last female to
attempt breeding in the wild was found broken. Its thin shell was suspiciously rem-
iniscent of the “DDE thin-eggshell syndrome.” In the meantime, analysis of tissue
from wild condors found dead in the early 1980s revealed that three of the five had
died from lead poisoning, probably from ingesting bullet fragments in carrion. Other
condors had elevated lead levels in their blood (Wiemeyer et al. 1988). Recognition
of the deleterious effects of yet another toxin in the condor’s food supply led to pro-
vision of “clean” carcasses just before the last condors were taken into captivity.Extinctions caused by disease are particularly difficult to identify in retrospect.
Moreover, on theoretical grounds disease is unlikely to be a common agent of extinc-
tion. In their review of pathogens and parasites as invaders, Dobson and May
(1986b) noted the improbability of a parasite or pathogen driving its host to extinc-
tion unless it had access to alternative hosts.320 Chapter 18
18.2.9The effect of
introduced diseases