Johnson, PTJ, KB Lunde, EG Ritchie, AE Launer. 1999. The Effect
of Trematode Infection on Amphibian Limb Development and Survivorship.
Science 284: 802.
paper establishes experimentally and through field observation that
in certain regions within the western US, a trematode parasite is
responsible for many of the frog deformities observed in nature.
Mechanisms of the trematode action are undetermined, but may involve
either chemical or mechanical disruption of development caused by
presence of the parasite.
et al. exposed tadpole Pacific tree frog (Hyla regilla)
to the cercaria of a trematode parasite, Ribeiroia. They
found that as the number of parasites per tadpoles rises, the
percentage of abnormalities increases while survival decreases.
adapted from Johnson et al. 1999
et al. show experimentally that the rate of deformity and
mortality is related to parasite density. They also show that the
density of parasites employed in laboratory experiments is comparable
to that measured in the field. And they demonstrate that the pattern
and type of deformities measured in the field is within the range
of deformities caused in the laboratory by the trematode parasite.
of the most compelling pieces of evidence for a parastic basis of
deformities in the area they worked is summarized:
1996 and 1998, we surveyed 35 ponds in Santa Clara County, California,
to determine the prevalence of abnormal amphibians. At 4 of
the 13 ponds supporting Pacific treefrogs, severely abnormal
frogs were observed. Intensive monitoring programs established
at two of these ponds consistently recorded high frequencies
(15 to 45%) of metamorphic frogs with polymely (extra limbs)
and other hindlimb deformitie... Water tests failed to detect
any pesticides, polychlorinated biphenyls (PCBs), or heavy metals,
and 200 H. regilla eggs collected from the ponds hatched and
developed normally in the laboratory (emphasis added).
is important for two reasons.
it indicates that contamination from obvious sources most likely
was not a problem. One constraint on the certainty of their conclusion
is that it can be very difficult to measure biologically available
contamination on the basis of water samples, because many contaminants
accumulate disproportionately in sediment and biological tissue.
Biologically relevant contamination can be present within sediment
and the trophic system without being detectable in the water column.
But the causative agent clearly was not transmitted from female
to offspring, not was it in the water column. Transmission from
sediment to egg masses would seem unlikely, unless the transmission
was via direct contact. Given the results with parasites, this would
seem to be a stretch.
it is important because it contrasts significantly with the details
of observations from Minnesota, the epicenter of frog deformities.
There, not only are a diversity of pesticides present, but in many
cases parasites are not. Moreover, the same experiment they conducted
with 200 H. regilla eggs, performed on Minnesota frogs, showed deformites,
even after the water was filtered to remove potential parasites.
something different is going on where most of the deformities are
other question Johnson et al. raise, without a great deal
of comment, is whether variation in trematode number is a result
of agrochemical contamination:
eutrophication due to organic pollution and the removal of molluscivorous
predators have both been shown to increase snail abundance and
the incidence of parasite infection."
implication here is that even if the causation of deformities in
the area where they worked is a natural parasite, the incidence
of the natural parasite and thus the frequency of deformity may
be due to human activity.
additional factor they do not address, but related to the last point,
is whether variation in immune
system function may relate to variation in resistance to the