This fact sheet was updated on March 21st, 2020.
This fact sheet was updated on March 21st, 2020.
Hemorrhagic Disease (HD) is caused by two closely related viruses; Epizootic Hemorrhagic Disease Virus (EHD) or Bluetongue Virus (BT). The disease features produced by both of these viruses are indistinguishable and therefore the term, hemorrhagic disease, is used when the specific virus is not known.
Outbreaks of disease similar to HD have been described since 1890, but the virus was not isolated until an outbreak in New Jersey white-tailed deer in 1955. The BT virus was isolated from white-tailed deer and bighorn sheep with HD in Texas in 1966. There is recent evidence that new variants of the EHD virus are now present in North America and that the virus, and possibly its vector, are expanding their ranges.
Hemorrhagic disease is the most common infectious diseases of white-tailed deer in the eastern United States and can cause a significant number of deaths during an outbreak. It is considered an emerging disease in other parts of North America.
Both wild and domestic ruminants can be infected by EHD and BT viruses but neither of these viruses is known to cause disease in humans. BT is generally more common in domestic species and EHD is more common in wild species.
White-tailed deer and mule deer are the primary wildlife species affected by EHD. It has caused severe mortality in at least one outbreak in bighorn sheep. Elk can become infected with this virus, but they do not seem to be as susceptible as white-tailed deer. Moose are not thought to be susceptible.
While BT is a well-known disease of sheep, cattle, goats, and can infect domestic dogs, it is also occasionally associated with the deaths of pronghorn antelope.
EHD and BT viruses are found worldwide in temperate and tropical climates, but they have only been reported in free-ranging wildlife in North America. In the United States, HD has been confirmed in most eastern and southeastern states as well as several states in the Midwest, the plains states, and northwest. There have also been sporadic cases reported in British Columbia, Alberta, and Saskatchewan in Canada.
The EHD and BT viruses are both transmitted by direct contact through biting flies or midges from the Culicoides group, or genus. Female midges take up the viruses by ingesting the blood of an infected animal and then transmit the virus when they feed on a naive susceptible animal. Midges preferentially breed in mud; therefore, outbreaks of hemorrhagic disease usually occur when deer congregate at water sources during the driest part of late summer and early fall when seasonal midge activity is at its peak and water levels are at or near their lowest points. Dead or dying deer near water in later summer or early fall are a common characteristic of an HD outbreak. Outbreaks end when the first hard frosts kill the midges.
Though these insects do not occur naturally in all parts of the United States, they are known for their ability to be transported to new areas on wind currents. Animals that live in areas where this primary vector is usually absent do not have any built-up immunity to the virus. As a result, when outbreaks of HD do occur, there are high mortality rates among white-tailed deer populations in these areas. In areas where the vector is found normally, immunity is more prevalent and mortality rates are lower.
Clinical signs of hemorrhagic disease can be highly variable and range from very rapid illness resulting in death within 36 hours, to a longer chronic course where animals remain ill for several weeks or months. Variation in clinical signs between individuals is not fully understood, but it appears that maternal antibodies, innate host resistance, the particular type of EHD and previous immunity are at play. White-tailed deer usually develop clinical signs about 5-10 days following infection with the EHD or BT virus, but some infected animals that have previously conferred immunity may remain asymptomatic.
EHD and BT viruses cause disease by damaging the lining of blood vessels, making them weak, leaky or destroying them. Clinical signs include swelling of the face or neck, loss of appetite, lethargy, weakness, lameness, respiratory distress, high fever, and excessive salivation. Infected animals may develop swollen, bluish tongues. Others will bleed from ulcers in the mouth and may also bleed from the nose. Frequently, deer will go into shock and die within 8 to 36 hours of the onset of clinical signs. Necropsy examination of animals that die of HD will often reveal extensive hemorrhage of the internal organs, including the heart, liver, kidneys, lungs, spleen, and intestines. Those that survive may exhibit hoof overgrowth and have indentations or cracks in the walls of their hooves (see photos).
Diagnosis is based on clinical signs and laboratory tests, particularly virus isolation from infected tissue. Blood, spleen, and lung are preferred samples for virus isolation.
There is currently no treatment for hemorrhagic disease in wildlife populations.
Hemorrhagic disease can cause high local mortality rates and is considered the most important viral disease of white-tailed deer in the United States. Both free-ranging and captive deer and elk are at risk of contracting HD and transporting infected animals to areas where HD is not yet present has spread the disease. The impact of this disease on local deer populations is not thought to be long lasting, but it is important to test suspect cases in order to identify outbreaks of HD. Insect control could theoretically decrease transmission of EHD and BT viruses in captive herds, but it has not proven to be feasible or effective in the past. An autogenous vaccine has been developed for use in captive white-tailed deer populations, but its efficacy is poor.