Our Stolen Futurea book by Theo Colborn, Dianne Dumanoski, and John Peterson Myers
 
 

 

  Johnson, PTJ, KB Lunde, EG Ritchie, AE Launer. 1999. The Effect of Trematode Infection on Amphibian Limb Development and Survivorship. Science 284: 802.

This 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.

  Johnson 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
 

 

Johnson 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.

One of the most compelling pieces of evidence for a parastic basis of deformities in the area they worked is summarized:

  Between 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).  

This is important for two reasons.

First, 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.

Second, 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.

Clearly, something different is going on where most of the deformities are occurring.

The other question Johnson et al. raise, without a great deal of comment, is whether variation in trematode number is a result of agrochemical contamination:

  "Accelerated 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."  

The 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.

One 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 parasite.

 

 

 

 
     

 

 

 

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