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→Diagnosis
==Diagnosis==
==Diagnosis==
Where animals present with clinical signs of bluetongue a presumptive diagnosis may be made, especially in regions where bluetongue is endemic. Post-mortem examination can be used to confirm the diagnosis. However, many cases of bluetongue are mild or subclinical and so laboratory confirmation of disease is required. Cattle in particular show few clinical signs.
===Clinical Signs===
===Clinical Signs===
The course of the disease in sheep can vary from peracute to chronic, with a mortality rate of 2-30%. Peracute cases die within 7-9 days of infection, mostly as a result of severe pulmonary edema leading to dyspnea, frothing from the nostrils, and death by asphyxiation. In chronic cases, sheep may die 3-5 wk after infection, mainly as a result of bacterial complications, especially pasteurellosis, and exhaustion. Mild cases usually recover rapidly and completely. The major production losses include deaths, unthriftiness during prolonged convalescence, wool breaks, and possibly reproductive loss. In sheep, bluetongue virus causes vascular endothelial damage, resulting in changes to capillary permeability and subsequent intravascular coagulation. This results in edema, congestion, hemorrhage, inflammation, and necrosis. The clinical signs in sheep are typical. After an incubation period of 4-6 days, a fever of 105-107.5°F (40.5-42°C) develops. The animals are listless and reluctant to move. Clinical signs in young lambs are more apparent, and the mortality rate is higher (up to 30%). About 2 days after onset of fever, additional clinical signs such as edema of lips, nose, face, submandibular area, eyelids, and sometimes ears; congestion of mouth, nose, nasal cavity, conjunctiva, and coronary bands; and lameness and depression may be seen. A serous nasal discharge is common, later becoming mucopurulent. The congestion of nose and nasal cavity produces a “sore muzzle” effect, the term used to describe the disease in sheep in the USA. Sheep eat less because of oral soreness and will hold food in their mouths to soften before chewing. They may champ to produce a frothy oral discharge at the corners of the lips. On close examination, small hemorrhages can be seen on the mucous membranes of the nose and mouth. Ulceration develops where the teeth come in contact with lips and tongue, especially in areas of most friction. Some affected sheep have severe swelling of the tongue, which may become cyanotic (‘blue tongue”) and even protrude from the mouth. Animals walk with difficulty as a result of inflammation of the hoof coronets. A purple-red color is easily seen as a band at the junction of the skin and the hoof. Later in the course of disease, lameness or torticollis is due to skeletal muscle damage. In most affected animals, abnormal wool growth resulting from dermatitis may be observed.
The course of the disease in sheep can vary from peracute to chronic, with a mortality rate of 2-30%. Peracute cases die within 7-9 days of infection, mostly as a result of severe pulmonary edema leading to dyspnea, frothing from the nostrils, and death by asphyxiation. In chronic cases, sheep may die 3-5 wk after infection, mainly as a result of bacterial complications, especially pasteurellosis, and exhaustion. Mild cases usually recover rapidly and completely. The major production losses include deaths, unthriftiness during prolonged convalescence, wool breaks, and possibly reproductive loss. In sheep, bluetongue virus causes vascular endothelial damage, resulting in changes to capillary permeability and subsequent intravascular coagulation. This results in edema, congestion, hemorrhage, inflammation, and necrosis. The clinical signs in sheep are typical. After an incubation period of 4-6 days, a fever of 105-107.5°F (40.5-42°C) develops. The animals are listless and reluctant to move. Clinical signs in young lambs are more apparent, and the mortality rate is higher (up to 30%). About 2 days after onset of fever, additional clinical signs such as edema of lips, nose, face, submandibular area, eyelids, and sometimes ears; congestion of mouth, nose, nasal cavity, conjunctiva, and coronary bands; and lameness and depression may be seen. A serous nasal discharge is common, later becoming mucopurulent. The congestion of nose and nasal cavity produces a “sore muzzle” effect, the term used to describe the disease in sheep in the USA. Sheep eat less because of oral soreness and will hold food in their mouths to soften before chewing. They may champ to produce a frothy oral discharge at the corners of the lips. On close examination, small hemorrhages can be seen on the mucous membranes of the nose and mouth. Ulceration develops where the teeth come in contact with lips and tongue, especially in areas of most friction. Some affected sheep have severe swelling of the tongue, which may become cyanotic (‘blue tongue”) and even protrude from the mouth. Animals walk with difficulty as a result of inflammation of the hoof coronets. A purple-red color is easily seen as a band at the junction of the skin and the hoof. Later in the course of disease, lameness or torticollis is due to skeletal muscle damage. In most affected animals, abnormal wool growth resulting from dermatitis may be observed.