EHD vs. CWD: Which Deer Disease is Actually Deadlier?

When Chronic Wasting Disease (CWD) showed up in southern Wisconsin in 2002, it may have been the first time the average American hunter realized that deer have diseases! Yet, all animals and humans have a host of diseases, some of which can be restricted just to a single species or group (Endemic) or spread across several species, even to humans (Zoonotic).

The appearance of CWD sparked a general panic among the public, and the blame rests squarely on the outdoor media. For starters, it was falsely reported three men had died from eating CWD tainted venison. Later, anti-hunting groups applied the term “Zombie Deer Disease” to CWD, again reporting falsely that humans can contract the disease.

Recently, another group of diseases known as Epizootic Hemorrhagic Disease (EHD), or Blue Tongue (BT), again were dubbed “Zombie Deer Disease or Virus.” This left the average hunter totally worried and confused! Weekly, I receive emails and messages asking me if venison is safe to eat. Hence, the purpose of this article is to provide you with the documented scientific facts about both diseases; hopefully, putting your concerns to rest.

For over a million years, white-tailed and mule deer have dealt with a host of diseases and parasites, including a pretty long list! The most common ones are: pneumonia (viral and bacterial), respiratory virus (RSV, BRSV), hemorrhagic disease, Lyme disease, brain abscess, deer warts, leptospirosis, nematode worms, mange, fly bots and CWD. Of these, the number one killer of whitetails today, bar none, is Hemorrhagic Disease; and CWD is one of the rarest mortality agents to date. Let’s learn more!

Hemorrhagic Diseases

Hemorrhagic diseases are blood borne diseases that, as their name implies, cause wide scale hemorrhaging in the organs; followed by massive organ failure and blood loss. There are two closely related types of hemorrhagic disease, Epizootic Hemorrhagic Disease (EHD) and Blue Tongue (BT). They are double-stranded RNA viruses in the family Reoviridae, genus Orbivirus. They are classified in “serotypes,” with a total of 7 EHD serotypes and 27-29 BT serotypes.

They are found throughout the world, affecting livestock and other wildlife species; but there are only three serotypes of EHD and six BT serotypes (one exotic) active in the U.S. According to most scientists, technically viruses are not alive. They do not reproduce and need a host cell they “fool” into reproducing them! The most dangerous thing about RNA viruses, in my opinion, is they do not mutate, rather they can change through a process called “reassortment.” This is a process of genetic recombination caused when two or more serotypes infect the same cell, then shuffle gene segments to produce “novel” viruses. I know this is some pretty technical scientific talk, but it is important to what I am about to tell you!

As best we can tell, EHD was first reported among sick deer in New Jersey in 1955; and BT subsequently in the same area in 1960. There are anecdotal reports of deer dying as far back as the 1800s, but there is no evidence it was HD. Since then, the disease has been found in at least 40 states in the Continental U.S. The current range is from New York and Ontario, westward through the Midwest to Montana, into southern Canada, and the Pacific Northwest (California, Oregon and Washington). Changing climate seems to be allowing the HD to spread north into new areas with devastating effects.

Although the first reports of HD involved the EHDV-1 serotype, the most commonly reported infections today come from EHDV-2 (1999) and EHDV-6 (2006). The latter serotype is also called the “Indiana strain,” now considered an exotic serotype originating in Australia. EHDV-6 was first reported in cattle in Illinois, and probably came to the U.S. from the Caribbean and South America. It is called the Indiana Strain, because this novel reassortant strain of EHDV-6 first occurred in Indiana, originating from segments of EHDV-6 and EHDV-2 combined.

The result was a more virulent serotype of EHDV-6, dubbed “Indiana,” now killing large numbers of deer in the Midwest. EHDV-1 and 6 are endemic throughout the U.S. in both wild and domesticated ruminants, while EHDV-2 is primarily endemic in the Southeast; it is also the most commonly detected EHDV serotype in the U.S. It is interesting to note, some biologists have referred to EHD as a “natural” disease, when the deadliest is an exotic form. There also are five BT serotypes affecting whitetails — BTV-2, 10, 11, 13 and 17.

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How does EHD affect deer? Depending on the serotype and exposure history of each deer, the outcome of infection can be rapid death (peracute), slow morbidity (acute) or recovery with permanent organ damage (chronic). Deer generally cannot get EHD from contact with other deer; rather, it must be transmitted by biting flies (midges) of the genus Culicoides, known as “no-see-ums,” or gnats.

These insects live adjacent to small pools of standing water, stream banks and areas with high organic matter content such as feeding stations. Most infections occur during warmer parts of the year, and often are related to drought conditions. Once a significant frost occurs, most gnat activity disappears; however, the disease can still remain for some time.

The life cycle of the biting midges requires a female to secure a blood meal from a deer. She then lays her eggs in moist soil or mud with high organic matter, where the hatching larvae feed on a continuous supply of moist organic matter. After 6-12 months, the larvae pupate and emerge as new female midges in the late afternoon and night for a feeding flight of up to 1.25 miles. She prefers to feed on the soft underbelly of the deer, where the hair is not thick. Her mouth parts consist of a fleshy sheath inside of which are four, tiny cutting blades that lacerate the skin to make it bleed. She then laps up the flowing blood, where viruses are picked up by these mouth parts and spread to the next deer she feeds on.

Incubation period lasts from three to five days, with 5-24 days to detectable viremia. But sometimes viremia may not appear for 50-60 days; meaning even after a significant frost and cessation of midge flights, pathology can appear. The infectious conditions are: peracute, acute and chronic. The first sign of the disease is high fever, significantly exceeding the normal body temperature of 101.4° F (105° F considered hyperthermic).

That is why a characteristic indicator of EHD infection is an unusual number of dead deer in or near water; where they come to cool off. This also plays into the life cycle of the midge!

Peracute cases usually result in rapid death by 36 hours, often with few clinical signs of the disease. Acute cases have considerably more symptoms of disease, including significant hemorrhaging from orifices and internally bleeding around the heart, lungs and gastrointestinal tract (especially the rumen).

Ulcerated sores develop in the palate, dental pad and on the tongue, producing excessive salivation and nasal discharge. The tongue often swells and becomes bluish (hence the name for BT), hanging out of the mouth and preventing eating. Death usually occurs in five to 10 days. Chronic cases usually result in prolonged illness, which results in deer being off feed for a time, which produces the tell-tale growth interruption rings on their hooves. They may also slough off, crippling the deer.

The finger-like papillae in the lining of the rumen also are damaged, and the deer is never as thrifty as prior to infection. This affects completion of pregnancy, lactation and antler growth.

The ultimate impact of an infection will depend on several factors, including the serotype of the virus involved and the length of time since the last infection. In our research, we concluded we need some amount of infection every year (hopefully from a less virulent serotype), in order to develop herd immunity. Monitored blood titer studies suggested some genetic resistance is attainable in a localized herd. Studies also suggested the further north you go in the whitetail’s range, the greater the interval between viral challenges, and the greater the impact when a new outbreak occurs. Cyclicity ranges from five to 10 years in these regions.

Mortality rates are difficult to obtain from state agencies, but there are reports of mortality rates ranging from 25-90 percent. Some states are beginning to adjust bag limits based on observed EHD morbidity and mortality. Some southern populations seldom have significant losses, especially Texas. This may be due to continuous maintenance of herd immunity.

Variability may be caused by factors such as abundance and distribution of the insect vectors, EHD/BT serotype, existing herd immunity, and genetic variations in the susceptibility of deer. Surviving deer develop long-lived neutralizing antibodies. Nearly 100 percent of the deer population can be seropositive in some regions.

Here is what you wanted to hear! There has never been a case of deer EHD in a human, and there is no evidence this will ever happen. As with most viruses, once an animal is dead, they die themselves; so there is almost zero chance you will ever be exposed to them.

Chronic Wasting Disease

Chronic Wasting Disease (CWD) belongs to a group of diseases known as Transmissible Spongiform Encephalopathies (TSEs). Translation: they are infectious diseases that turn the animal’s brain to a sponge! Just as Hemorrhagic Disease is not caused by a living organism, CWD is caused by a misshapen protein called a prion.

A “normal prion” (PrPc) is a protein composed of long chains of amino acids linked together. They reside in nerve cells, but we are not sure what function they serve. Current thought is that normal prions play a role in intracellular signaling and cell adhesion. Yet, we do know what misshaped prions (PrPsc) can do, and it’s a great deal of damage to the brain.

The misfolded prion is not recognized by the body as a foreigner. Consequently, the body fails to mount an immune response. Also, the misshaped prions have the ability to create more “bad” prions; and, over time, their numbers increase and tend to be concentrated in the brain, where they do their damage.

The prions clump together to form amyloid plaques, leading to erosive brain damage. The erosion causes holes to form, especially in the brain stem, hence the name “spongiform.” The brain stem connects the brain to the spinal cord, and is responsible for maintaining balance and posture, regulating blood pressure, breathing, hearing and heart rhythms; all essential for life.

Deer are just one of a number of species, including human, that have TSE diseases! The best-known ones are Creutzfeldt-Jakob Disease (CJD) in man, Bovine Spongiform Encephalopathy (“mad cow disease” or BSE) in cows, Scrapie in sheep, Transmissible Mink Encephalopathy, Feline Spongiform Encephalopathy, Ungulate Spongiform Encephalopathy and Chronic Wasting Disease.

These are just the ones we know about at this time; and there are probably many more. They all have one thing in common: they are all rare in occurrence and mortality! For example, Creutzfeldt-Jakob disease in humans has a worldwide age adjusted death rate of one per 1.25 million per year!

I noted earlier EHD was first detected in New Jersey in 1955. As best we can tell, the first notice of CWD was at a state research facility at Ft. Collins, Colorado, around 1965. The map shown below indicates the first known distribution by 2007. Although we may never know how CWD appeared in that facility, we do know that in addition to deer and elk, there were sheep from a Scrapie research program in residence.

The deer were captured from the Rocky Mountains to the west and brought to the facility for nutrition research; then, some were released back into the wild. The next case location was the Sybille Research Center near Wheatland, Wyoming. There is evidence deer were moved from the Colorado facility to Sybille prior to discovery.

The website, deerfriendly.com, noted that, “At the minimum, Fort Collins acted as a super spreader...” of the disease.  Subsequently, it also can be traced from the Ft. Collins facility to Canada, and then to Wisconsin, where scientists were conducting CWD research in the late 1990s. Infected brain material was sent to the facility from Ft. Collins.

There is only anecdotal evidence this was the source of the Wisconsin outbreak. Whatever the final story on its origin, CWD since has spread to as many as 32 states and four Canadian provinces.

Until CWD appeared in Wisconsin in 2002, hunters and the public had paid little attention to the disease! When it was diagnosed in three white-tailed deer from the Mt. Horeb area of Iowa and Dane counties on Feb. 28, 2002, all heck broke loose! The WDNR immediately put together a “control program” — which resulted ultimately in the killing of as many as 172,000 deer in the southern farmland of Wisconsin.

In 2007, the Wisconsin legislature evaluated the program and declared it “unsuccessful.” Since then, the disease has remained mostly within the four initial CWD Zone counties (Dane, Iowa, Richland and Sauk), but has spread to more of Wisconsin’s 72 counties. As of 2022, 71.4 percent of cases still come from these four counties. After 20 years, there has been no scientific evidence CWD has significantly affected reproduction or survival of Wisconsin whitetail herds.

There are many reasons why the Wisconsin approach did not work. Capital among them were: CWD is not a density-dependent disease, and incubation time after infection often exceeds generation time for whitetails. As a respected colleague once pointed out, “…by the time a whitetail can become clinical, in most cases it is already dead from something else!”

CWD actually is more of a frequency-dependent disease. In a density-dependent disease, probability of infection is related to the density of individuals, while a frequency-dependent disease is affected by the frequency of contact between individuals. The innate social structure of whitetails defeats the density-dependent argument.

Therefore, killing thousands of deer will do nothing to eradicate CWD! Now, CWD certainly should never be taken lightly. I am not saying that; however, in 2002, I stuck my neck out and made a calculated statement that, unless you can answer “yes” to the following questions, CWD will remain off or low on the list of top whitetail mortality agents: 1. Will it devastate deer herds? 2. Can humans catch the disease?

After the 20-plus years since I made that statement, there has been no credible scientific evidence that the answer to either question is yes. Yet, is it “possible” someday a human may contract the disease? Sure, anything is possible, but Scrapie has been known to infect sheep for at least 250 years, with about 30 percent susceptible to Scrapie. Yet not a single human has ever contracted either Scrapie or a derivative of it by contact or eating sheep. Furthermore, published science supports a human barrier to CWD prion transmission.

Regarding negative effects of CWD on deer herds, there has not been a single peer-reviewed study to date reporting CWD had a negative effect on fecundity (fertility) or recruitment of whitetails. In fact, the Wisconsin DNR’s own data clearly show that, within the CWD Zone, fawn crops range 80-100 percent.

Now, let’s examine the information we have concerning infection and mortality rates in other states. Based on published data, CWD remains a rare disease in the majority of states. In the last 11 years, Texas has tested 110,256 free-range deer for CWD with 91 positives, a 0.08 percent apparent infection rate. Even when we include data from the three states with the highest infection rates (Colorado, Wyoming and Wisconsin), the average apparent infection rate for all states with CWD is around 2 percent.

And it’s important to note “apparent infection rate” does not convert to mortality rate, since it is one thing to test positive for CWD prions and another to have the disease.

Once infected, it may take 16-plus months for a deer to become clinical for CWD. The “chronic” nature of CWD does raise questions as to whether or not, with enough time, could we eventually see an impact, at least on mortality? Quantifying mortality in wild animals is quite difficult! Also, some scientists point out that a deer found dead from, say a predator, may have been rendered more susceptible to predation because of CWD; or a road killed deer may also have died for the same reason.

There is not a single state that can provide specific mortality data from CWD. Yet, I keep returning to the one question that raises the most doubts: Where are all the dead deer?

In the case of EHD, there certainly is no doubt when an epidemic occurs, since there have been properties where you literally can smell the death from far away. But landowners have yet to report significant numbers of dead deer in areas where CWD has been documented for years. It is curious to me there are only a handful of photographs of dead deer attributable to CWD, so few we keep seeing the same ones over and over.

Saul Has Slain His Thousands!

There is no doubt, in some years, EHD does indeed kill perhaps thousands of deer (whitetail and mule deer) over the range of the species. Landowners indeed know when die-offs occur, since they can see and smell the dead animals. In these areas it may take years for the herd to recover. Yet, we still have whitetails in these areas, and most herds eventually recover, a testament to the resilience of the whitetail.

Recently, biologists have reported higher mortality rates from EHD, which may present a problem when you factor in new mortality agents such as apex predators.

CWD has been known almost as long as EHD, but science has yet to answer the basic question: How much mortality can you attribute to CWD? Meanwhile, the majority of research funding and focus continues to reside with CWD.

Hence this section’s name! In the Bible (1 Samuel 18:7), it says: “As the troops were returning home after David had killed the Philistine, the women came out of all the cities of Israel to meet King Saul with singing and dancing, with joyful songs, and with tambourines and other instruments . . . And as the women danced, they sang out: ‘Saul has slain his thousands, and David his tens of thousands.’ And Saul was furious and resented this song. ‘They have ascribed tens of thousands to David,’ he said, ‘but only thousands to me. What more can he have but the kingdom?”’

Saul is CWD and David is EHD! The most important things I hope you have learned from this article are: EHD and CWD cannot infect humans; there is no way to control or eradicate either disease, and the white-tailed deer seems to be perfectly capable of adapting to both diseases. Rest easy, and eat plenty of heart-healthy venison, friends!

Epizootic Hemorrhagic Disease (EHD) Facts:

• The disease is caused by Obiviruses, of which there are different serotypes.
• These viruses have been around for millennia in some form but remain ever-changing to enhance virulence.
• The viruses also can be exotic in origin.
• EHD is spread by biting gnats.
• The impact of the disease on individual deer depends on the serotype and disease history of each deer.
• Mortality rates can be as high as 90 percent, yet to date, deer populations seem to recover.
• Deer populations can be sampled for blood titers to monitor the disease.
• There are no known treatments or immunizations for these diseases.

Chronic Wasting Disease (CWD) Facts:

• The disease is caused by misshaped proteins in the nervous system called prions.
• It first appeared in research facilities in Colorado, and since has spread throughout the U.S.
• As with all TSE diseases, it is a rare disease. CWD is chronic by nature and takes 16-plus months to become clinical.
• There is no empirical evidence that CWD affects reproduction in deer.
• It is not a density-dependent disease and cannot be reduced or controlled by reducing populations.
• There appears to be a barrier to the disease in humans.

About the Author

Dr. Kroll is founder and director of the Institute for White-tailed Deer Management & Research in Nacogdoches, Texas.