Breaking Down the Hemorrhagic Disease Outbreak

Published on: Jun. 17, 2013

The 2012 deer season might already be a distant memory; however, your next deer season may benefit from observations made during 2012–13. In 2012, more than 10,000 suspected hemorrhagic disease (HD) cases were reported, from all 114 counties, to Conservation Department sta ff, but the actual number of cases is unknown, and the severity will vary locally. To understand how and why this is the case, you must know a little more about the disease.

Understanding the Disease

Hemorrhagic diseases include both the bluetongue and epizootic hemorrhagic disease (EHD) viruses. Although the majority of confirmed-infected deer had the EHD virus, the bluetongue virus was also detected in Missouri. These viruses have indistinguishable symptoms, so we group them together for simplicity and refer to them as hemorrhagic diseases, or HD. Symptoms can appear similar to other diseases that affect deer, including chronic wasting disease (CWD). Therefore, it is important to notify the Conservation Department when sick or unexplained dead deer are found.

Hemorrhagic diseases are expressed in three different forms, with each causing a variety of symptoms. The three forms of HD are peracute, acute, and chronic (not related to chronic wasting disease) and dictate the length that a deer can survive. The peracute form progresses rapidly and causes death within a week after infection, which is the quickest of the HD forms. This form can cause swelling, or edema, when fluid accumulates in the head, tongue, neck, and lungs. Therefore, deer that die due to the peracute form often appeared healthy with very few clinical signs.

The acute form causes death within one to two weeks and symptoms include swelling and bleeding, or hemorrhages, throughout the body, including heart, rumen (portion of the stomach), and intestines. Sores, or ulcers, can also form on the deer’s tongue, dental pad (front portion of the roof of the mouth) and portions of the stomach. Both peracute and acute forms can cause deer to become lethargic, lose fear of humans, and develop a high fever. It is this fever that causes deer to seek relief in the form of water, but as the infection progresses they become disoriented and lose coordination, often dying in or in close proximity to these water sources. Research suggests that approximately 85 percent of the deer in Missouri that contract HD will have either the peracute or acute form.

Although the chronic form of HD is less common in Missouri, it can become more noticeable during widespread, intense outbreaks such as that seen in 2012. The chronic form is unique in that deer survive the HD virus, but the resulting tissue damage and secondary infections can lead to death. For example, if a deer survives the HD virus, but experienced rumen damage, then this can inhibit the proper digestion of food, causing the deer to eventually starve to death. However, HD is not always fatal, as some deer can survive HD and secondary infections, with the only remaining evidence being the occasional growth interruptions or sloughing of hooves. Does that survive the HD virus will pass maternal antibodies to their offspring the following year which adds a level of immunity to the population.

Life Cycle of HD

Hemorrhagic diseases are spread primarily by a biting midge in the genus Culicoides, which are commonly referred to as “no-see-ums” due to their small size (much smaller than mosqui-toes); however, there are likely other unknown vectors of transmission. Midges can transmit the HD virus to a deer (or the virus can be transmitted to a midge) when the female midge bites a deer for a blood meal, which is used to produce eggs. The eggs are laid in muddy areas and once they become larvae, they live within shallow water. As they mature they leave the water, develop wings, and complete the life cycle when they be-gin to breed. The life cycle of a midge is approximately 4–5 weeks, so as the summer progresses, the midge population can grow exponentially.

Theoretically, once a hard frost kills the adult midges, deer cannot become newly infected with HD because deer can only contract HD from the bite of a midge. However, warm spells after the first frosts can cause midge activity to continue, potentially allowing the virus to be spread to additional deer. Also, chronic forms of HD can cause mortality well into the winter. The Department of Conservation received reports of dead or sick deer that were typical of chronic HD into March of 2013. It is reassuring to know that the virus dies very quickly (less than 24 hours) once a deer dies, therefore, carcasses do not pose a threat for spreading HD. Additionally, the virus is only viable within a deer’s bloodstream for 50 days, with peak virus activity within a deer occurring between days four and 10, so an infected deer is unlikely to be a permanent reservoir for the disease in Missouri.

One question remains: How and where does the HD virus survive over winter? While there are several theories, none have been proven.

Implications for Humans and Other Wildlife

Hemorrhagic disease is not infectious to humans or non-ruminant animals like dogs and cats. Therefore, the virus itself poses no threat to humans. However, secondary infections in deer arising from the effects of the HD virus can pose human health risks if consumed or improperly handled. This provides further justification for normal precautionary measures to be taken when field dressing, butchering, and preparing venison to reduce any potential health risks. The Department of Conservation recommends not consuming venison from known diseased animals.

While infrequent, domestic ruminant species, like cattle and sheep, can become susceptible to specific HD viruses dependent on the animal species. For example, cattle can exhibit varying severity of symptoms from either EHD or blue-tongue, but it is infrequent. However, domestic sheep are generally unaffected by EHD, but bluetongue can have serious health implications.

Weather Intensified the Outbreak

The intensity of the 2012 HD outbreak in Missouri was a result of several weather conditions. While it is only a theory that warm winters allow the virus to be maintained from one year to the next, the 2011–12 winter was the third-warmest winter on record in Missouri. In March of 2012 the rainfall was slightly above average, causing the ponds and other water bodies to fill with water, which would provide ample breeding area for midges during the summer. Plus, March 2012 was the warmest on record at 14 degrees warmer than the long-term average! This warm weather continued, making the 2012 spring the warmest on record and likely causing midges to become active much earlier than normal.

Weather extremes continued into the summer with a combination of record heat and drought conditions, causing ponds and other water sources that filled up during early spring to dry up. The exposed mud flats created the ideal breeding areas for midges. The drought conditions also caused deer to visit these water sources more often because of lower water content in the plants they consumed and fewer free-standing water sources. Furthermore, nutrification of these sites because of livestock loafing in small ponds results in increased midge production. Additionally, both deer and midges are most active at dawn and dusk, further increasing the chance of contact.

But, it doesn’t stop there — warmer temperatures cause female midges to lay more eggs, thus producing more midges. For example, females produce about 22 eggs at 50 degrees, but when the temperatures increase to nearly 90 degrees, females produce 100 to 200-plus eggs! Additionally, the virus replicates quicker in warmer temperatures, increasing the chances of virus transfer when a midge takes a blood meal.

However, even with all that information we cannot reliably predict when and where an HD outbreak will occur because these conditions do not cause HD, but rather intensify an outbreak. Even if we could predict an outbreak, there are no proven actions that can protect a deer from contracting the virus.

Realistic Prevention?

While there is no way to completely protect deer from hemorrhagic diseases, there are a few management practices that could possibly reduce contact rates between midges and deer. These management practices are not absolute and effectiveness is dependent on the prevalence of HD in the area, size of your property, home range of deer in your area, and management on surrounding properties. However, after seeing the potential impact that hemorrhagic diseases can have on an area, these practices might be worth considering.

The most promising efforts for reducing potential contact between midges and deer are practices that reduce favorable conditions for midges around water and minimize unnecessary visits for deer to water sources. Efforts that promote vegetation surrounding water sources decrease the amount of mud flats that are exposed during droughts, thus reducing midge-breeding areas. Also, fencing o livestock from ponds is an ideal practice because livestock ponds are perfect breeding areas for midges. This is because livestock remove surrounding vegetation, thus exposing more mud, and excrete in the water and surrounding area, further increasing nutrient levels. While landowners have good intentions when placing feed or salt near water sources during the summer, this can cause deer to visit these water sources more often, increasing the probability of encountering midges. Most insects are unable to survive in water with high salt content; however, midges are the exception. Therefore, salt blocks near water can eliminate the majority of other insects, thus reducing competition for midges. The removal of salt and feed near water sources can reduce the risk of a deer encountering midges.

While preventative measures might have some a on the severity of the outbreak in a local area, post-outbreak management efforts, such as assessing local conditions and adjusting doe harvest as appropriate, is the most critical.

Population Effects

The way HD affects a population can vary greatly based on the size and make-up (i.e., sex ratio) of the population and severity of the outbreak, which is often not fully expressed in changing harvest until two to three years following an outbreak. Typically, the year following an HD outbreak hunters harvest the same number of deer as before the outbreak resulting in a greater proportion of deer being removed from the population because the pre-season population has already been reduced due to hemorrhagic mortality, thus leading to population declines. The declines will likely be intensified due to the record-low acorn crop, subsequently making deer more vulnerable to harvest in heavily forested areas. Alternately, in some areas where local harvest rates are typically low, the additional HD mortality will have little affect on long-term population size.

In next month’s Conservationist, we will discuss the potential population effects of the 2012 hemorrhagic disease outbreak, along with other factors that are influencing regional deer population trends.

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