and coughing. In some cases, lesions form in the skin as well as the mucous membranes. This form is commonly called . As the disease progresses the infection concentrates in the tissue of the lymph nodes, lungs, liver and spleen. This causes the formation and discharge of yellow-gold, mucopurulent discharge from the nasal and lacrimal ducts as well as pyogranulomatous abscesses in lymph vessels and nodes that may rupture externally and exude discharge. Systemic signs include fever, anorexia, lethargy, weight loss, septicemia / bacteremia, convulsions, coma and death within days to months. There is no treatment of glanders. Symptomatic care would include antibiotics, wound drainage & dressings and pain management. Euthanasia of positive cases is required. Prognosis is grave. It is considered a fatal disease. Those who survive the acute stage of disease are considered chronic carriers and may be responsible for the transmission of disease. Prevention includes early diagnosis and proper quarantine practices. Unfortunately, there is no vaccine available. Glanders commonly affects horses and other equine species, but may infect cows, donkeys, mules, dogs, cats, goats and humans. Glanders is considered an disease as it has been eradicated from North America and Western Europe. In North America Glanders is a reportable disease as it causes a high mortality rate in humans and livestock alike.
Hendravirus
Equine hendra virus, is an infrequent & sporadic disease only seen in
, since
the mid-1990s.
It is now believed to be caused by an RNA virus similar to the Nipah virus of the paramyxoviridae family. (The old theory linked it to a morbillivirus). are the reservoir and that their urine or reproductive fluids are involved in transmission to horses. Direct contact is required for zoonosis via infected body secretions, fluids or tissues. It is suspected that It is believed that the pathogenesis for Hendra virus is dependent on route of transmission. It was regarded as an acute respiratory disease but that is proving less and less true. When respiratory infection is present, the virus attacks the alveolar walls. It has been shown that the virus has an affinity for tissue resulting in lesions, edema & hemorrhage. Lesion have been noted in vasculature of the cerebrum, kidney, stomach, spleen & heart. The virus can also be neurotropic resulting in neuronal necrosis. Affected horses developed systemic signs with the time from onset of signs to death, being only 1–3 days. Pyrexia, anorexia, and depression are the initial signs after an incubation period of 8– 11 days. Signs of respiratory disease such as nasal discharge, increased respiratory rate, dyspnea and edema & congestion of lungs. Neurological signs include ataxia, blindness, head tilt, circling,
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