Hemorrhagic Disease: How to Combat the Deadliest Deer Disorder

In an earlier edition of North American Whitetail (Spring 2024), I compared and contrasted the two most important diseases in white-tailed deer, Chronic Wasting Disease (CWD) and Hemorrhagic Disease (HD). The column created quite a stir among hunters, landowners and the general public, since the majority of these folks were either uninformed or ill-informed about these diseases. Now, I’d like to go a step further in discussing HD, its history and efforts to combat this devastating disease.

HEMORRHAGIC DISEASE HISTORY

In 1955, several white-tailed deer were found dead adjacent to water in New Jersey; and at about the same time, also in Michigan and South Dakota. This was not the first time dead deer were found in that region, since there were reports dating back to the 1800s! Later, scientists identified the culprit as a strain (serotype) of viruses known as Epizootic Hemorrhagic Disease (EHD), dubbing it EHDV-1. In a few short years, the virus appeared in North Dakota, Alberta, Nebraska, Missouri, British Columbia, Iowa and Wyoming.

In 1966, another type of Hemorrhagic disease virus, “Bluetongue” (BTV), was isolated from white-tailed deer and bighorn sheep in Texas. Both EHD and BT had been known for years among livestock throughout the world. At present, there are a total of eight serotypes of EHD and 27 of BT that I am aware of. Of these, three EHD serotypes (EHDV 1, 2 and 6) have been reported in white-tailed deer. There also are five BTV serotypes reported to infect whitetails — BTV-2, 10, 11, 13 and 17.

When I began my wildlife career in 1972, I had not even heard of EHD or BT! By 1980, I was quite aware of the diseases, but most biologists believed it was primarily a southern disease, since that is where testing and reporting was strongest. In the late 1980s, North American Whitetail magazine’s managing publisher, Steve Vaughn, approached our Institute with the idea of establishing a research area at Ft. Perry, Georgia. The purpose would be to develop and test various habitat and population management strategies, the results of which would be shared with our readers.

The study area encompassed 2,000 acres. Things were going well until 1987, when HD hit our deer herd; we lost half of the herd that year. It was devastating to say the least. I was now fully aware of EHD and BT, and I have monitored the progression of the disease across North America ever since. It turned out that Georgia was the "epicenter" of the disease at that time.

The 1970s and 80s were a time of rapid deer population growth in the U.S., with the effects of large-scale stocking programs kicking in. By 2000, the U.S. was “fully stocked” with whitetails, and the common dogma then was that HD was a southern disease, and there was no need to worry about it.

In 2012, reports of deer dying in Iowa got a lot of folks’ attention. Since then, the disease has caused significant deer mortality in the state, particularly during drought conditions when deer congregate around limited water sources. Iowa experienced severe outbreaks in 2012, 2013, 2019, and 2023. Illinois was affected earlier in the late 1970s, but the big toll coincided with the 2012 outbreak in Iowa, with an estimated 2,043 cases reported in 76 counties. Then there was Montana!

The first documented large-scale outbreak of HD west of the continental divide occurred in the Missoula Valley in 2013. Dead deer were being reported commonly in the Missoula Valley, totaling 400 or more in a single month. The area continued to see repeated episodes, with mortality rates higher than ever seen before. In 2015, the Milk River deer herd had an estimated mortality rate of 90 percent. Professional biologists continued to maintain that HD, over the long haul, did not have a significant impact on deer population dynamics. Yet, hunters were reporting that it was difficult to find a mature buck Montana’s endemic area.

IS HD MANAGEABLE?

In my studies and teaching about wildlife diseases, I point out that the steps for dealing with a wildlife disease include identifying:

• The pathogen
• The host(s)
• Distribution of infected individuals, demographic relationships
• Mode of transmission
• Morbidity and mortality
• Control measures
• Prevention measures

In the case of CWD, there are still many knowledge gaps that have not been filled. In the case of HD, we have a much better understanding of the disease process.

The Pathogen: Hemorrhagic disease is caused by one of two types of viruses, Epizootic Hemorrhagic Virus and Bluetongue Virus. We know that these viruses can change by a process called Reassortment. This is where the virus uses segments of other strains to produce a new strain. Although the first reports of HD involved the EHDV-1 serotype, the most reported infections today are from EHDV-2 (1999) and EHDV-6 (2006). This hybrid serotype is also called the “Indiana strain,” now considered an exotic serotype originating from Australia.

EHDV-6 was first reported in cattle in Illinois, and it likely came to the U.S. from the Caribbean and South America (the infected Caribbean cattle would’ve originally been infected by the Australian cattle). It is called the Indiana strain because this novel reassortant strain of EHDV-6 first occurred in whitetails in Indiana. The Indiana strain now kills 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 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 BTV serotypes affecting whitetails—BTV-2, 10, 11, 13 and 17.

The Host: White-tailed deer, mule deer, antelope, elk and bighorn sheep are all known to contract one or more strains of HD.

The Distribution: Hemorrhagic disease is widely spread across the U.S. and Canada, but there are areas, such as Texas, where it occurs less. The range appears to be spreading.

Mode of Transmission: HD viruses are spread by biting midges or gnats that thrive in organic-rich, moist soils, especially those adjacent to water sources. The primary species of midge is Culicoides variipennis; however, other species can carry it.

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 six to 12 months, the larvae pupate and emerge as new, female midges in the late afternoon and night for a feeding flight of up to a half mile. 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 the mouth and spread to the next deer she feeds on.

Morbidity & Mortality: The three infectious conditions of HD are peracute, acute and chronic. The first sign of the disease is high fever, significantly exceeding the normal body temperature of 101.4 degress F (105 F considered hyperthermic). That is why a characteristic indicator of HD infection is an unusual number of dead deer in or near water, where they come to cool off.

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 from the mouth and preventing eating. Death usually occurs between five and 10 days.

Chronic cases usually result in prolonged illness, which results in deer being off feed for a time, producing the tell-tale growth interruption rings on their hooves. They may also slough off, crippling the deer. Mortality rates are difficult to obtain from state agencies, but there are reports of mortality rates ranging from 25 to 90 percent.

CONTROL & MANAGEMENT

If we accept what often is written in public education documents and social media about HD, there is nothing that can be done to control or manage these diseases. For example, here is what the Southeastern Cooperative Wildlife Disease Study brochure offers: “At present, there are no wildlife management tools or strategies available to prevent or control hemorrhagic disease. Although die-offs of whitetails due to hemorrhagic disease often cause alarm, past experiences have shown that mortality will not decimate local deer populations and that the outbreak will be curtailed by the onset of cold weather.” However, managing wildlife disease over the broad landscape and on smaller private lands can be quite different.

In managing a disease, we look for the greatest limiting factor among the above topics. We have learned that HD viruses have the ability to change and become more virulent; the Indiana strain is a prime example. Viruses are notorious for changing over time, increasing or decreasing host morbidity and mortality rates. In regard to the host (deer in this case), it seldom is practical to immunize free-ranging individuals. Recent studies have shown through monitored blood titer studies some genetic resistance is attainable in a localized herd. This is most likely in warmer climates where outbreaks are more frequent. 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. There also appears to be some innate genetic resistance in some populations, specifically through the Toll-Like Receptor 3 (TLR3) gene. However, long-term research and development will be needed for this, and I do not see agencies acquiring funds for such research.

So, that brings us to only two solutions that are feasible on private lands. We need to re-visit the two types of diseases: density-dependent and frequency-dependent. HD is a density-dependent disease; that means, if we maintain our deer herds at or below carrying capacity, we can reduce the probability of exposure to the virus. Where would you expect to hear about the next outbreak of Covid, New York City or some small, rural community? So, proper herd management is our first defense.

Next, let’s look at the primary mode of transmission — midges! Their life cycle includes moist, organically rich sites, usually around ponds or streams. What if we develop a management strategy that discourages deer from drinking at these water sources? Sound impossible? Over the last three decades, we have studied the use of “artificial” water sources, such as troughs. I have been writing about their use for over 25 years, and at first received a lot of criticism early on about my recommendation. In more recent times, more landowners and managers have adopted this practice.

Our research showed that deer prefer to drink in a secluded area, away from the social pressures created when large numbers of deer drink at one place. The right placement will also spread your deer out. We place troughs at a density of one per 40 to 80 acres, evenly spaced around the property. Further, a water trough will not produce the wet muddy soils we see around ponds as they dry up or draw down in late summer. We do not inset our troughs in the ground. Here at the Institute, we have a water trough about 100 yards away from a 3.5-acre impoundment; yet, our deer prefer to water at the trough. Other strategies involve constructing ponds without shallow water edges.

Recently, managers have begun to attack the midges themselves! There now are water and soil treatment chemicals that kill or impede larval development of midges. Utilizing beneficial bacteria and enzymes can break down organic matter and create unfavorable conditions for midge reproduction. Encouraging natural predators like insect-eating fish, dragonflies and birds can also help control midge populations.

We have deployed and evaluated these recommendations at the Institute for White-tailed Deer Management & Research, and we have not had a single case of EHD or BT in our deer herds for two decades! I hope this article gave you some hope in combating the most significant deer disease, Hemorrhagic Disease. In these times of panic over Chronic Wasting Disease, I wanted to give you encouragement that you can manage for less disease in the deer living on your property. While reviewing recent literature on EHD, I was pleased to see that even some die-hard deer conservation organizations now are giving advice on reducing the impact of HD.

EDITOR'S NOTE

Hemorrhagic disease is a serious threat to whitetail populations, and hunters should do everything in their power to fight it. Although we haven’t had the opportunity to test it for ourselves yet, we’re extremely excited to see the innovation from our friends at RakkFuel in developing a new product, EHD-fense. Designed to combat the midges themselves, EHD-fense accomplishes this through an all-natural three-step system (Catapult, LiveWater and D-Muck).

Part one, dubbed Catapult, is a liquid biocatalyst that helps decompose the organic muck that midges breed in. Then comes LiveWater, which consists of beneficial bacteria to produce an environment best for insects that prey on midges. Finally, to help prevent muck from encouraging new midge populations, D-Muck pellets release non-toxic microbiota to speed up the digestion of organic material.

---