Post by Deleted on Sept 17, 2012 22:37:24 GMT -5
Thousands of whitetail deer died across the country in 2011 as an epidemic spread across the land. But interestingly enough, many hunters were completely unaware that it was happening.
The outbreak was the work of two very similar diseases--epizootic hemorrhagic disease (EHD) and Blue Tongue--and even though more deer succumb to these diseases in a given year than any other ailment, they have traditionally taken a back seat to Chronic Wasting Disease, a less deadly but far more publicized deer disease.
EHD and blue tongue are caused by viruses, and the symptoms through which the diseases manifest themselves are not altogether unlike the Ebola virus in humans. In most cases, the infection stems from a gnat bite on the exposed portion of a whitetail's belly. The deer is exposed to the viral pathogens via the insect bite, and about two weeks later, the animal will experience a very high fever, followed by the death of tissues in the mouth, esophagus, stomach, intestines and other organs.
The infection amounts to a wholesale shutdown of almost every organ system in the whitetail's body. Blood vessels break and blood fills the intestines and body cavity, giving the disease the "hemorrhagic" portion of its name. In as little as 24 hours, the deer will die, usually at or near a water source.
The viruses responsible for EHD and Blue Tongue are closely related but share a number of important distinctions from each other. Both are common in hoofed animals, including wild and domesticated sheep. However, while farmers are able to immunize their herds of domesticated animals, it is virtually impossible to do the same for wild animals like whitetail deer, and even if we could immunize whitetails, we'd have to do so at least biannually, given the number of viral strains of EHD and Blue Tongue and their propensity to adapt and flair up.
Similar to the human flu, different strains of the diseases appear, spread and then disappear on a periodic basis. The disease spreads across the land in waves, invisible to the eye, but very obvious to the observant biologist.
For example, in 2011, I was fully aware that a particular strain of EHD--specifically EHD 6--was spreading across the southeast months before it manifested itself in the herd. The evidence came as desperate phone calls from landowners and managers in Alabama, then Mississippi and Louisiana. It hit eastern Texas in October, but then there was strange, new information. We heard about dead deer in southern Wisconsin, the Dakotas, Montana and even Kansas. My email file filled up with photos of dead deer, sent to me by folks wanting to know what was going on.
By the time the first frosts occurred, effectively removing the gnat vectors, a silent killer had left a trail of carnage across the land. Montana's Milk River Valley herd was hit especially hard, following a heavy winter die-off the previous year. Montana suspended or reduced tag sales.
The impact of hemorrhagic diseases, as with many diseases, is related to the density of animals in the population. Where would you expect the next epidemic of swine or bird flu--Hong Kong or Hutchinson, Kansas? The answer is obvious, Hong Kong. The reason, of course, is there are more people per square unit in Hong Kong than in the entire state of Kansas. The probability of one individual coming in contact with an infected individual is much higher.
So, why did the disease show up last year in Kansas? Good question! Have you noticed how the monster buck hotspots tend to move about the country? Have you thought about the reason?
Over the years, I have seen the title of "monster buck hotspot" move from state to state, occurring as herds began to grow in these areas. Once a herd saturates an area, however, there seems to be a decline in trophy buck abundance. For some time, Kansas has been the place to kill a big buck. I hunt there every year with my friend John Butler (Buck Forage Oats) and will continue to do so. Yet, Kansas' deer herd has been steadily increasing, mostly in response to changing land use and an aging human population.
Five years ago, I was warning about a potential loss of deer in Kansas from hemorrhagic disease. So, obviously one answer to reducing the impacts of these diseases is proper herd management. That means hunters need to harvest more does, an activity still not popular with hunters.
The drought of 2011 was "Biblical" in proportions throughout much of Texas and the Midwest. Drought leads to drying ponds and streams, leaving exposed mud or moist soil. Gnat larvae (maggots) thrive in such conditions, and are ready and waiting for a meal when deer come to water. In Montana, the problem was exacerbated by heavy spring rains, producing additional muddy areas during the summer.
So, what on earth can you do about that? Over the last three years, we have been conducting research on the effectiveness of supplemental water sources for deer. Using simple storage tanks and water troughs, we learned they would help spread deer out, pulling them away from the muddy flats adjacent to natural water. By spreading the deer out, we reduced the population density, thereby reducing the probability of an infected individual spreading the disease.
Supplemental feeding, where legal, can both help and hurt the spread of hemorrhagic disease. You never want more than a dozen animals using one feeder. This means you have to evenly distribute feeders over your land. Never put a feeder near water, as this is just asking for trouble.
I noted above effective immunization against viruses often requires a "booster" shot. Nature actually has a way of doing just that. Although there are different strains of the disease, some more virulent than others, if an individual comes down sick from one of the less damaging strains, that imparts some immunity against the more dangerous strains.
So, as a manager I like to see some hemorrhagic disease in my herd every year. As part of my record-keeping program, I examine every deer harvested from properties I manage to see if they have any of the tell-tale signs of having survived hemorrhagic disease.
The simplest way is to look at the tips of the hooves. Because the disease often erodes the lining of the rumen, digestive efficiency is affected; producing a period when the animal does not eat. If it survives and begins eating again, this causes a growth interruption in the hoof. A distinct line across the hoof is a clear indication the deer has survived the virus. Often the disease strikes just at the end of antler development. Loss of appetite and fever will stop antler growth and/or mineralization, producing sponge-like tips on the main beams and last antler points.
The percentage of animals with these indicators is a good indication of the resistance your deer herd has against hemorrhagic disease.
The bottom line is that deer will continue to contract diseases. In that regard, they're no different from humans or any other animals. The best approach is to manage our deer in balance with their habitat, paying careful attention to population density on our hunting lands.
BY DR. JAMES C. KROLL
The outbreak was the work of two very similar diseases--epizootic hemorrhagic disease (EHD) and Blue Tongue--and even though more deer succumb to these diseases in a given year than any other ailment, they have traditionally taken a back seat to Chronic Wasting Disease, a less deadly but far more publicized deer disease.
EHD and blue tongue are caused by viruses, and the symptoms through which the diseases manifest themselves are not altogether unlike the Ebola virus in humans. In most cases, the infection stems from a gnat bite on the exposed portion of a whitetail's belly. The deer is exposed to the viral pathogens via the insect bite, and about two weeks later, the animal will experience a very high fever, followed by the death of tissues in the mouth, esophagus, stomach, intestines and other organs.
The infection amounts to a wholesale shutdown of almost every organ system in the whitetail's body. Blood vessels break and blood fills the intestines and body cavity, giving the disease the "hemorrhagic" portion of its name. In as little as 24 hours, the deer will die, usually at or near a water source.
The viruses responsible for EHD and Blue Tongue are closely related but share a number of important distinctions from each other. Both are common in hoofed animals, including wild and domesticated sheep. However, while farmers are able to immunize their herds of domesticated animals, it is virtually impossible to do the same for wild animals like whitetail deer, and even if we could immunize whitetails, we'd have to do so at least biannually, given the number of viral strains of EHD and Blue Tongue and their propensity to adapt and flair up.
Similar to the human flu, different strains of the diseases appear, spread and then disappear on a periodic basis. The disease spreads across the land in waves, invisible to the eye, but very obvious to the observant biologist.
For example, in 2011, I was fully aware that a particular strain of EHD--specifically EHD 6--was spreading across the southeast months before it manifested itself in the herd. The evidence came as desperate phone calls from landowners and managers in Alabama, then Mississippi and Louisiana. It hit eastern Texas in October, but then there was strange, new information. We heard about dead deer in southern Wisconsin, the Dakotas, Montana and even Kansas. My email file filled up with photos of dead deer, sent to me by folks wanting to know what was going on.
By the time the first frosts occurred, effectively removing the gnat vectors, a silent killer had left a trail of carnage across the land. Montana's Milk River Valley herd was hit especially hard, following a heavy winter die-off the previous year. Montana suspended or reduced tag sales.
The impact of hemorrhagic diseases, as with many diseases, is related to the density of animals in the population. Where would you expect the next epidemic of swine or bird flu--Hong Kong or Hutchinson, Kansas? The answer is obvious, Hong Kong. The reason, of course, is there are more people per square unit in Hong Kong than in the entire state of Kansas. The probability of one individual coming in contact with an infected individual is much higher.
So, why did the disease show up last year in Kansas? Good question! Have you noticed how the monster buck hotspots tend to move about the country? Have you thought about the reason?
Over the years, I have seen the title of "monster buck hotspot" move from state to state, occurring as herds began to grow in these areas. Once a herd saturates an area, however, there seems to be a decline in trophy buck abundance. For some time, Kansas has been the place to kill a big buck. I hunt there every year with my friend John Butler (Buck Forage Oats) and will continue to do so. Yet, Kansas' deer herd has been steadily increasing, mostly in response to changing land use and an aging human population.
Five years ago, I was warning about a potential loss of deer in Kansas from hemorrhagic disease. So, obviously one answer to reducing the impacts of these diseases is proper herd management. That means hunters need to harvest more does, an activity still not popular with hunters.
The drought of 2011 was "Biblical" in proportions throughout much of Texas and the Midwest. Drought leads to drying ponds and streams, leaving exposed mud or moist soil. Gnat larvae (maggots) thrive in such conditions, and are ready and waiting for a meal when deer come to water. In Montana, the problem was exacerbated by heavy spring rains, producing additional muddy areas during the summer.
So, what on earth can you do about that? Over the last three years, we have been conducting research on the effectiveness of supplemental water sources for deer. Using simple storage tanks and water troughs, we learned they would help spread deer out, pulling them away from the muddy flats adjacent to natural water. By spreading the deer out, we reduced the population density, thereby reducing the probability of an infected individual spreading the disease.
Supplemental feeding, where legal, can both help and hurt the spread of hemorrhagic disease. You never want more than a dozen animals using one feeder. This means you have to evenly distribute feeders over your land. Never put a feeder near water, as this is just asking for trouble.
I noted above effective immunization against viruses often requires a "booster" shot. Nature actually has a way of doing just that. Although there are different strains of the disease, some more virulent than others, if an individual comes down sick from one of the less damaging strains, that imparts some immunity against the more dangerous strains.
So, as a manager I like to see some hemorrhagic disease in my herd every year. As part of my record-keeping program, I examine every deer harvested from properties I manage to see if they have any of the tell-tale signs of having survived hemorrhagic disease.
The simplest way is to look at the tips of the hooves. Because the disease often erodes the lining of the rumen, digestive efficiency is affected; producing a period when the animal does not eat. If it survives and begins eating again, this causes a growth interruption in the hoof. A distinct line across the hoof is a clear indication the deer has survived the virus. Often the disease strikes just at the end of antler development. Loss of appetite and fever will stop antler growth and/or mineralization, producing sponge-like tips on the main beams and last antler points.
The percentage of animals with these indicators is a good indication of the resistance your deer herd has against hemorrhagic disease.
The bottom line is that deer will continue to contract diseases. In that regard, they're no different from humans or any other animals. The best approach is to manage our deer in balance with their habitat, paying careful attention to population density on our hunting lands.
BY DR. JAMES C. KROLL
