By Dr. James C. Kroll
It is curious to me how many people seem to think wildlife don't die from diseases! Yet, wild animals are no different from humans, and are beset with a host of pathogens and parasites. In the early days of my career, the only deer disease or parasite of concern was anthrax and screwworm. Anthrax was well-known to Texans, ravaging southwest Texas cattle, horse and sheep herds in areas where buffalo had over-wintered. In 1946 — the year I was born — the screwworm was named chief of insects affecting both man and animals. Building on the fact that this insect only mated once, government researchers sterilized male flies with radiation, and released them throughout infected areas. Elimination of the screwworm allowed deer populations to increase rapidly into the 1960s. Today, screwworm is a thing of the past and anthrax is limited to small areas in Texas and Mississippi.
I grew up during the longest drought of the 20th Century. Water was so scarce that we hauled water twice a day from the Brazos River to our cattle. But, the drought was not a Texas phenomenon — much of the U.S. suffered the same fate from 1952-1957. During this time — 1954 to be exact — a new deer disease was discovered, first in New Jersey and then in Michigan. Deer were found dead and dying around the few watering places available. The culprit turned out to be an Orbivirus carried by biting gnats (midges) plaguing deer watering in the evening. Initially identified as one of the known viruses, collectively called Epizootic Hemorrhagic Disease (EHD) — epizootic meaning “wide spread in a population,” and hemorrhagic identified as the breakdown of blood vessels and tissues. A deer dying from this disease is not a pleasant sight! Only anthrax kills more cruelly than EHD. There is an incredibly high fever, followed by mouth ulcers, death of internal organs and the rumen lining, and bleeding from body orifices. Deer die within a few hours of developing symptoms.
The virus strain — or serotype — causing the initial infection was given the designation EHDV-1. Later, two more strains were identified, EHDV-2 (Ibaraki, Alberta strain) and EHDV-6 (Australian, Indiana strain). All in all, there now are 6-7 strains of EHDV known in the U.S. EHDV-6 was isolated from dead deer in a 2006 outbreak in Indiana and Illinois.
Until 2007, biologists and managers considered it a southern disease, and professional biologists didn't even consider EHD as a problem in the north. In 2011, state biologists in Kansas and Wisconsin informed me their deer were free from EHD. Well, that didn't last long as it then showed up in a host of northern states. In 2012, I received a frantic call from a Wisconsin game official, asking my advice about how to inform the public in light of the chronic wasting disease (CWD) conversation in the area. The Southeastern Wildlife Disease Cooperative map below vividly shows that the disease is broadly distributed across the U.S. There have been two misconceptions among professional biologists: The first is that disease has a 5-7 year cyclic occurrence, beginning in the southeast and proceeding to the northwest into early fall. The second is that the net impact is not significant, killing no more than 25% of the population. Both are false! Ask hunters in Montana, Kansas, Missouri, Indiana, Illinois and Iowa!
The term EHD is not exactly accurate — it should be called Hemorrhagic Disease (HD), because a related virus also is involved: Bluetongue virus. BT was known of long before EHD. Its name is descriptive — one of the major symptoms is swelling of the tongue and a bluish appearance. Sheep have long been consider a carrier, which led to near extinction of local wild-sheep populations. Even identifying which virus a deer may have died from is quite difficult given the fact most deer have been dead for some time before discovery. Unfortunately, the range of BT (see map below) is just as extensive as EHD with 29 known strains — two of which (13 & 17) are most important to deer.
Deer populations in North America have declined by about 20 percent since 2000. Is it because of HD or CWD? Deer mortality factors are much more complex today. Deer have a host of mortality agents, including predators, disease, over-harvest, habitat degradation, etc. Yet, I do know that HD has a significant impact on deer herds. One noted biologist recently asserted that CWD was the real problem and not HD, because the former was unnatural and the latter natural. That is curious since EHDV-2 and EHDV-6 arrived here by way of Asia and Australia! CWD is not an exotic disease, and we have yet to document massive die-offs from CWD. To add to the problem, we have learned that EHDV-2 and EHDV-6 both have the ability to undergo reassortment, with new viruses "created” by borrowing chemical elements between strains. It once was true that local deer populations could build up short-term immunity after an outbreak, but today deer are faced with an ever-changing pathogens, thwarting development of immunity.
So, what can you do about any of this? There are no vaccines, and even if there were, how could we get them into the deer? Here at the Institute, we learned how to mitigate impacts by taking advantage of what we know about midges/biting gnats. They develop as maggots in mud or wet organic material. High fever is an early symptom, and deer go to water to reduce body temperature. Transmission occurs when gnats emerge from mud and bite a deer on the hairless part of their under bellies before then carrying the disease to another one. We have found, by implementing artificial water sources such as troughs, we spread deer out and eliminate mud from the equation! In 10 years, our deaths from HD at properties we manage have been significantly reduced. This is the only mitigation strategy we recommend. HD will always be with us, and like many animal diseases, the solution is management of mitigating factors.