I bet every deer hunter or reader does Outdoor news Heard of chronic wasting disease. The two obvious concerns about this always fatal deer and elk disease are:
1) Will this drastically reduce deer numbers? And 2) Can humans contract a similar disease from eating infected game?
Departments of Natural Resources have devoted many hours and dollars to managing CWD in deer populations, but last week’s viral media coverage of a scientific abstract has revisited troubling question No. 2.
A compact abstract by Jonathan Trout and colleagues from the University of Texas San Antonio Long School of Medicine was published in the journal Neurology on April 9, 2024, titled: “Two Hunters from the Same Lodge Affected by Sporadic CJD: Is Chronic Wasting Disease to blame?”
Stories about the study spread virally on news outlets like The Daily Mail, and a syndicated version of the Yahoo study appeared on social media across the country.
There was immediate skepticism in the scientific community over the rush to claim that zombie deer were infecting humans. National Deer Association replied last Thursday with the following headline: “NDA urges deer hunters to consider new CWD report with caution” and calls the online neurology report “sketchy.”
“Nothing in this new report changes current knowledge or guidelines regarding CWD in cervids. There is still strong evidence that CWD in deer and elk does not cause disease among hunters who eat infected animals. Because science is not 100% certain and prion diseases are still not fully understood, experts continue to recommend CWD testing of all deer harvested in known CWD areas and avoid consumption of CWD-infected game to minimize risk.”
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Additionally, deer biologist and wildlife science coordinator for the Arizona Game and Fish Department, Jim Heffelfinger, – she wrote in a post on Instagram last Thursday (his the handle is deer walnut): “This is not a study and it is not a scientific article. The whole thing is only 344 words long and is simply a mention of two hunters who died of Creutzfeldt-Jakob disease and both ate deer from the same deer population. There is no evidence of hunters contracting CWD.”
But to be clear, the work in question is an abstraction; it was never advertised as a peer-reviewed scientific work, the gold standard in science.
Therefore, the fault lies with the media, which takes the information presented in the abstract at face value and treats it as an crucial scientific publication. Is not. The summary should be treated as a suggestion only and not as something final.
A quick summary of CWD
CWD was first observed in the mid-1960s in Colorado in mule deer kept in captivity with sheep. The disease spread to at least 32 states and several Canadian provinces and prompted feeding bans.
It belongs to a family of neurodegenerative diseases called transmissible spongiform encephalopathies. TSEs include, but are not circumscribed to, mad cow disease (technically: bovine spongiform encephalopathy, BSE), scrapie, and variant Creutzfeldt-Jakob disease (in humans).
Essentially a naturally occurring protein, a prion changes in shape and becomes an infectious prion that accumulates upon contact between infectious and normal proteins, eventually clogging the central nervous system and causing death.
Sporadic CJD, or Creutzfeldt Jakob disease, is the human equivalent of CWD. Unlike vCJD (the v stands for “variant”), which appears to result from eating beef in mad cow disease, sporadic CJD is thought to originate in the body rather than being acquired from an external source (like infected beef).
Sporadic CJD is thought to occur naturally at an incidence of approximately 1 in a million people worldwide, with an average age of onset of 62 years. It is a fatal disease, just like CWD. But it could be triggered by eating a deer with CWD, at least in theory.
Neurology report
Trout and colleagues report that in 2022, a 72-year-old man who frequently consumed venison from a herd of CWD-affected deer developed symptoms consistent with sporadic CJD (rapid confusion and aggression on set) and rapidly deteriorated, dying within a few days. one month from the onset of symptoms.
An autopsy confirmed that he died of CJD. A friend of the deceased also died of CJD and was a recurrent consumer of deer from the same population. The study did not indicate where the deer eaten by hunters were caught. However, these observations motivated Trout and colleagues to pay attention to these cases given the potential implications.
The authors wrote: “Although causality remains unconfirmed, this group highlights the need for further research on the potential risks of consuming CWD-infected deer and its public health implications.” It is unclear whether two constitute a cluster.
This means that people who have not eaten game meat get CJD. We have a correlation which, as we always say, does not prove causation. A similar case occurred several years ago in Wisconsin, where three hunters were exposed to TSE and frequently consumed game, but transmission of the disease through contaminated game was ruled out.
Given the millions of deer eaten, many of them from CWD zones, and the few cases of CJD in game consumers, it is possible that these isolated cases are just correlations – that is, these people would unfortunately have died of CJD regardless of whether they had not eaten game.
I don’t want to say that time will tell, but given the potentially long incubation of TSEs (such as vCJD from beef) before disease occurs, this is a fair statement of what we know. It is also worth noting that we have only recently observed that the incidence of CWD-infected deer is very high and only in certain areas, so it is likely that exposure to infected deer is too recent to have led to many human TSE cases.
It is unlikely that deceased hunters ate deer that were clearly in the slow stages of near-death CWD when the clinical signs are obvious – stunning, emaciated condition, drooling, lack of fear, etc. It is more likely that If actually contracted sporadic CJD from a deer – massive if here – they became infected from deer that were infected with CWD, but the stage of infection was not advanced enough to show external symptoms of the disease.
There have been other studies on this topic. IN story for NDA last July, the group’s communications director, Lindsay Thomas, wrote about the data presented by Dr. Joe Abrams of the Centers for Disease Control in Atlanta. Speaking at the 4th International CWD Symposium held last summer in Denver, Abrams presented preliminary data from a survey of hunters in some of the oldest CWD hotspot areas among wild deer and/or elk in Colorado, Wyoming and Wisconsin.
The Colorado and Wyoming studies reviewed 30 years of data and examined records of more than 2 million hunters, including hundreds of thousands who hunted in CWD-endemic areas. It is likely that over the decades, many thousands of these hunters have consciously or unconsciously eaten game from CWD-infected animals that showed no outward signs of the disease.
The NDA has a long history on Abrams’ research, but the overall results did not show that hunters in these areas died at higher rates from prion diseases than in the general population.
Here, too, we should make clear that the NDA story represents a conference speech, not a peer-reviewed scientific article, which suggests caution in accepting its conclusions.
If we find more concentrated cases of sporadic CJD in zones where deer have CWD and have been eaten by people dying from CJD, it becomes likely that some external influence is at work – there may be something in the water or, more likely, in the water. deer. It’s worth staying vigilant.
Lindsay Thomas will join Outdoor News Editor-in-Chief Rob Drieslein for an interview on this topic on the Outdoor News Radio show and podcast.
