Changes

===Clinical Signs===

===Clinical Signs===

Bluetongue is primarily a disease of sheep, and in the face of infection these animals can display clinical signs ranging from acute to subclinical^{1, 14}. Acute disease follows an incubation period of about one week, which may depend on the infectious dose of virus received.  Signs begin with pyrexia of around 40.5-42°C, and hyperaemia of the oral and nasal mucosa is seen 24-36 hours later accompanied by hypersalivation and a serous nasal discharge. The nasal discharge quickly becomes mucopurulent and potentially blood-tinged, and dries to froms a crust around the nostrils. Facial oedema affects the nose, lips, tongue and submandibular areas. Severe swelling of the tongue results in protrusion and cyanosis, lending the disease its name. The oral mucosa becomes congested, petechiated and ulcerated which leads to inappetance, dysphagia and frothing at the mouth. A serous nasal discharge is later seen to become mucopurulent, and the conjuntiva are often injected. Inflammation of the coronet causes lameness, and the junction of the skin and hoof is purple-red in colour. Skeletal muscle damage in advanced disease may also contribute to lameness. The course of ovine bluetongue can vary from peracute to chronic, and mortality is between 2% and 30%. In peracute cases, severe pulmonary oedema leads to death by asphyxiation around one week after infection. Acute, mild cases normally have a rapid and complete recovery. In chronic cases, death occurs 3-5 weeks after infection due to exhaustion and bacterial complications such as pasteurellosis.

Bluetongue is primarily a disease of sheep, and in the face of infection these animals can display clinical signs ranging from acute to subclinical^{1, 14}. Acute disease follows an incubation period of about one week, which may depend on the infectious dose of virus received.  Signs begin with pyrexia of around 40.5-42°C, and hyperaemia of the oral and nasal mucosa is seen 24-36 hours later accompanied by hypersalivation and a serous nasal discharge. The nasal discharge quickly becomes mucopurulent and potentially blood-tinged, and dries to froms a crust around the nostrils. Oedema of the head occurs, which particularly affects the lips and tongue but may also spread to include the ears and submandibular areas. In a few cases the tongue becomes severely swollen and cyanotic, lending the disease its name. Petechial haemorrhages appear on the still-hyperaemic mucosaeThe oral mucosa becomes congested, petechiated and ulcerated which leads to inappetance, dysphagia and frothing at the mouth. A serous nasal discharge is later seen to become mucopurulent, and the conjuntiva are often injected. Inflammation of the coronet causes lameness, and the junction of the skin and hoof is purple-red in colour. Skeletal muscle damage in advanced disease may also contribute to lameness. The course of ovine bluetongue can vary from peracute to chronic, and mortality is between 2% and 30%. In peracute cases, severe pulmonary oedema leads to death by asphyxiation around one week after infection. Acute, mild cases normally have a rapid and complete recovery. In chronic cases, death occurs 3-5 weeks after infection due to exhaustion and bacterial complications such as pasteurellosis.

Necrotic lesions develop on the gums, cheeks and tongue 5–8 days after the onset of

Necrotic lesions develop on the gums, cheeks and tongue 5–8 days after the onset of

fever. These heal slowly under a membrane of pus and serum (diphtheritic membrane).

fever. These heal slowly under a membrane of pus and serum (diphtheritic membrane).