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Epizootic Hemorrhagic Disease (EHD) in White-Tailed Deer
Epizootic hemorrhagic disease (EHD) is an acute, infectious, often fatal viral disease of some wild ruminants. This malady, characterized by extensive hemorrhages, has been responsible for significant epizootics in deer in the northern United States and southern Canada. A similar hemorrhagic disease called bluetongue also occurs throughout the U.S. and Canada. The two diseases are antigenically different.
Since 1890, deer die-offs from diseases which might have been EHD have occurred in various parts of North America. These early die-offs were variously diagnosed as blackleg, blacktongue, bluetongue, mycotic stomatitis or hemorrhagic septicemia or they were undetermined. The causative agents were never confirmed. A review of the case histories, signs and lesions, seasonal occurrence, and lack of a bacterial agent suggests that they might have been EHD.
The first occurrence and subsequent identification of EHD occurred in 1955 when several hundred white-tailed deer (Odocoileus virginianus) succumbed in both New Jersey and in Michigan. It was considered a new disease of deer and the name 'epizootic hemorrhagic disease' was suggested to describe its main clinical and pathological features.
Since the initial 1955 outbreak, this malady has occurred primarily among white-tailed deer, although occasionally mule deer (O. hemionus) and pronghorn antelope (Antilocapra americana) have succumbed. EHD has been present in the United States for over 50 years now and large-scale regional deer population decreases have not been observed. Additional die-offs attributed to EHD occurred in Michigan in white-tailed deer in 1974, 2006, 2008, 2009, 2010, 2011, 2012, 2013, 2016, 2017, and 2018. The 1974 die-off occurred in several counties and resulted in approximately 100 deer dying. The 2006 die-off occurred in the southwestern portion of the state in Allegan County and involved 50-75 animals. In 2008, the die-off occurred in the southeastern portion of the state in Oakland and Macomb counties and involved 150-200 deer. In 2009, the die-off took place in the southwestern/southcentral portion of the state in Livingston County and involved 300-450 deer. In 2010, the die-off occurred in the southwestern portion of the state in Allegan, Berrien, Cass, Ottawa, St Joseph, and Van Buren Counties with an estimated mortality of 1,025 deer. In 2011, the die-off occurred in the southwestern portion of the state again in Cass and St. Joseph Counties with an estimated mortality of 300 deer. In 2012, the die-off occurred in 30 counties across the southern half of the Lower Peninsula with 14,898 deer reported dead. In 2013, the die-off occurred in the southwestern portion of the state in Allegan, Berrien, Ionia, Muskegon, Oceana, and Ottawa Counties with an estimated mortality of 140 deer. There were no confirmed cases of EHD in the state in 2014 or 2015. In 2016, a small number (8) of deer died in Berrien, Cass, and Van Buren Counties. In 2017, 265 deer died from EHD in 13 counties in the northern portion of the Lower Peninsula, and in 2018, a small number (4) of deer were diagnosed to have died from EHD in Calhoun and Kent Counties.
Transmission and Development
The mode of transmission of EHD in nature is via a Culicoides biting fly or midge. Culicoides variipennis is the most commonly incriminated vector in North America. A deer must be bitten by a midge carrying the virus to become infected. The disease is not transmitted directly from one deer to another but must go through the insect vector. A common observation in outbreaks involving large numbers of deer is that they are single epizootics which do not recur. Die-offs involving small numbers of deer occur almost annually, and the disease appears to be enzootic in these areas. All documented outbreaks of EHD have occurred during late summer and early fall (August-October) and have ceased within two weeks of the onset of frost, which kills the midge.
Experimentally, the disease can be transmitted to susceptible deer by the inoculation of virus-laden material from infected deer by subcutaneous, intramuscular, intravenous or oral routes.
Clinical signs of EHD and bluetongue are very similar.
White-tailed deer develop signs of illness about 7 days after exposure. A constant characteristic of the disease is its sudden onset. Deer initially lose their appetite and fear of humans, grow progressively weaker, often salivate excessively, develop a rapid pulse and respiration rate, and fever (affected animals frequent bodies of water to lie in to reduce their body temperature) and finally become unconscious. Hemorrhage and lack of oxygen in the blood results in a blue appearance of the oral mucosa, hence the name 'bluetongue'. Eight to 36 hours following the onset of observable signs, deer pass into a shock-like state, become prostrate and die.
The gross and histological lesions of EHD have been characterized by, as its name implies, extensive hemorrhage. Extensive hemorrhaging is the result of interference with the blood-clotting mechanism together with degeneration of blood vessel walls. Endothelial cells that line the blood vessels are damaged, resulting in blood leaking through the walls, resulting in hemorrhages. The hemorrhages range from pinpoint to massive in size and involve different tissues and organs in individual animals. No organs appear to be exempt from hemorrhage, with the most regularly involved being the heart, liver, spleen, kidney, lung, and intestinal tract. Generalized edema and increased pericardial fluid are consistently found in EHD. These changes also reflect the widespread interference with normal blood circulation.
The virus can be recovered from a variety of tissues of animals which have succumbed to EHD. These include blood, liver, spleen, kidney, lung, heart, and muscle.
A combination of case history, characteristic signs and lesions, and the isolation of the virus is necessary for a diagnosis of EHD. Useful aids in obtaining a diagnosis are the epizootic nature of the disease, its seasonal occurrence, its spectacular hemorrhagic lesions, and the extensive edema. Because of the similarity of its symptoms to other diseases, such as bluetongue and malignant catarrhal fever, the isolation and identification of the virus is essential.
Methods to be used for virus isolation are: (1) inoculation of cell cultures; (2) inoculation of susceptible sheep or deer combined with serologic monitoring; and (3) intravenous inoculation of embryonating chicken eggs.
Treatment and Control
There is no known effective treatment or control of EHD. Theoretically, an oral vaccine could be developed for administration through a supplementary winter-feeding program, but this is presently impossible, impractical and unwarranted.
Because of its very high mortality rate, EHD can have a significant effect upon the deer population in a given area, reducing numbers drastically. A common observation in outbreaks involving large numbers of deer is that they are single epizootics which do not recur. Die-offs involving small numbers of deer occur almost annually, and the disease appears to be enzootic in these areas.
Hemorrhagic disease can be transmitted to other wild ruminants. The EHD virus can infect domestic animals, most commonly hoof stock, but rarely causes disease.
The edibility of the venison is not impacted by the disease. There is no evidence that humans can contract the EHD virus either from the midge or from handling and eating venison. Pets and wildlife cannot be infected by either midges or from EHD infected deer carcasses.
For questions about wildlife diseases, please contact the Michigan DNR Wildlife Disease Laboratory.
First figure: Edema (yellowish fluid) underneath the skin. Second figure: Hemorrhages on the organs, diaphragm, and musculature.