Epizootic hemorrhagic disease

The distribution of EHD depends greatly on the distribution and abundance of the biting midge (Culicoides variipennis), the level of existing immunity in deer, and the genetic variations in susceptibility.[5] EHD is found in North America, Australia, Asia, and Africa. Seropositive animals have also been found in South America. It occurs most often in the southern United States, although its distribution is not uniform.[6] In the south, the disease is characterized as frequent and mild, whereas in the north, the disease is characterized as infrequent, severe, and capable of high mortality.[5] EHD can occur throughout Indiana. Outbreaks in Indiana of the disease can be characterized by both significant outbreaks that occur on a 5-10 year cycle that affect the entire state and smaller outbreaks that may only involve a few counties.

Transmission of EHD occurs by a host being bitten by a virus-carrying fly or midge. There are many different species of culicoides that can carry this virus, however, the most common carrier is thought to be Culicoides variipennis. Epizootic hemorrhagic disease can only be transmitted by a vector, meaning that EHD cannot be transmitted from animal to animal but only through the initial bite by a vector. Ordinarily, EHD outbreaks will reoccur within an area primarily during seasonal dry spells. Outbreaks will typically result in large die-offs, smaller and more isolated outbreaks can be common.[7]

The midge larvae hatches and lives near the water's edge in the bank. They will grow and typically remain in the submerged mud in water that is less than 2 inches deep. They will continue to live in eutrophic areas as these areas provide the highest likelihood of survival for the larvae as well as the midge as it matures. The midges do not survive long after the first seasonal frost.[8]

Deer may become infected with peracute, acute, or chronic EHD infections. Deer can develop clinical signs in as little as 7 days after exposure and this is most constantly characterized by sudden onset of the 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 include 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.[2] The head and neck of infected deer may swell. 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 chronic EHD often become lame due to these hoof problems.[4] Although they are ill for several weeks, they can eventually recover. 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.[2] Death is also common in deer with acute EHD, which is generally comparable to peracute EHD and is characterized by excessive salivation, nasal discharge, and hemorrhaging of the skin.[9] Cattle that develop EHD typically have subclinical signs. These infections are less severe than the infections in deer, but they may still exhibit fever, oral ulcers, excessive salivation, lameness, and coronitis (inflammation of the coronary band in hoofed animal). Sheep rarely develop clinical signs, and experimentally infected goats have never been shown to exhibit any signs of EHD.[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.

Epizootic hemorrhagic disease (EHD) has been around for many years. It is believed that EHD can be 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 analysis the true causative agent was never confirmed. After further review of the case history and other telltale signs and lesions, seasonal occurrence, and lack of a bacterial agent suggests that they might have been EHD.[14]

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