[7] Researchers also found that maternal antibodies against EHDV could be detected in Georgia deer up to 18 weeks, and seropositive fawns showed minimal clinical evidence of disease while seronegative fawns exhibited mild to moderate clinical signs of disease.
In general, deer infected with EHD lose their appetite, lose their fear of people, grow weak, show excessive salivation, develop a rapid pulse, have a rapid respiration rate, show signs of a fever, which includes lying in bodies of water to reduce their body temperature, become unconscious, and have a blue tongue from the lack of oxygen in the blood.
One of the most common characteristics of deer with the chronic form of EHD is the sloughing or breaking of the hooves caused by growth interruptions.
Deer with the peracute form of the disease may go into shock 8–36 hours after the onset of symptoms, and are found lying dead.
[4] Typically, EHD does not kill livestock, but it may affect the production industry negatively because of effects from the disease such as cattle weight loss and lameness.
EHD has been shown to not affect humans, and no evidence has been found that the epizootic hemorrhagic disease can be contracted through midge bites or by consuming venison that has been infected with the virus.
Animals that are sick may show obvious signs of extreme fatigue and illness, such as rapid weight loss or lesions or abscesses across the body.
Other signs include foaming or frothing of the nose and mouth (similar to rabies), as well as the decay of walls of their hooves.
However, preventive actions include stopping troughs from overflowing, making sure pipes are not leaking, and removing any standing pools of water.
EHD is thought to have been first found and tracked back to around 1890, and has been responsible for die-offs of many different species across North America.
Diseases such as blackleg, blacktongue, bluetongue, mycotic stomatitis, or hemorrhagic septicemia were thought to have been the cause of many of these die-offs.
After further review of the case history and other telltale signs and lesions, seasonal occurrence, and lack of a bacterial agent suggest that they might have been EHD.
[14] Current research is focused on the elucidation of mechanisms governing differences in response to EHDV among populations of white-tailed deer.
[8][7] Researchers in 2023 found that two single nucleotide polymorphisms had significant differences in frequency between EHD-positive and EHD-negative deer, suggesting a genetic component in susceptibility to EHDV.