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→Clinical Signs
===Clinical Signs===
===Clinical Signs===
BT is primarily a disease of sheep but when these animals have positive BTV
serology, care must be taken to avoid confusing clinical BT and diseases with similar
clinical signs.
6.2 The clinical signs in sheep can be very variable, ranging from acute to subclinical.
The acute signs begin with fever, which may last about a week. The
incubation period, generally 4–8 days, is possibly influenced by the dose of virus
received. Within 24–36 hours of the onset of fever the lining of the mouth and nose
becomes hyperaemic. Excess salivation and a clear nasal discharge accompany this.
Over the next few days the discharge becomes thick with mucus and pus and may be
blood stained. It eventually dries to form a crust around the nostrils.
In acute cases, the lips and tongue become very swollen and oedema may extend over
the face to include the ears and intermandibular space. The hyperaemia becomes more
intense and tiny, flat, red or purple (petechial) haemorrhages appear on the mouth,
nose and conjunctival linings. The clinical feature that gives the disease its name, a
deeply cyanotic (blue) tongue, occurs in only a small percentage of cases.
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).
Breathing becomes difficult. Profuse bloody diarrhoea occurs in some cases. Vomiting
may also occur and lead to inhalation pneumonia.
Foot lesions, on one to four feet, may appear towards the end of the fever period.
There is acute reddening and petechial haemorrhages on the coronary band at the top
of the hoof. Affected sheep stand with arched backs and are reluctant to move.
There is rapid weight loss and weakness due to loss of appetite and specific muscular
necrosis. Spasmodic twisting of the head and neck to one side (torticollis) is
sometimes a late sign.
6.3 The mortality rate is variable: in highly susceptible sheep it can be up to 70%.
Deaths may occur at any stage up to a month or more after the onset of signs.
Convalescence in surviving sheep is prolonged. Breaks occur in wool, which add to
the production losses.
6.4 Infection of pregnant ewes may lead to abortions, mummified foetuses, or the
birth of stillborn or weak lambs, which may have congenital defects.
6.5 Goats are less commonly, and less severely, affected than sheep. The
pathogenesis is similar and the clinical signs are milder.
6.6 Infection in cattle, although of great epidemiological significance, is generally
sub-clinical. A report from the United States suggested only 0.01% of cattle infected
with BTV show clinical signs. These include inflammation and mucosal erosions in
the mouth and nose, mild laminitis and a stiff gait. Infection of early pregnant animals
may lead to embryonic death and resorption.
Technical Review - Bluetongue: The Virus, Hosts and Vectors
___________________________________________________________________________
15.
Version 1.5; 21 November 2002
6.7 Severe disease and mortalities occur in white-tailed deer in the United States
where the pathogenesis and clinical signs are indistinguishable from the closely related
EHD virus.
6.8 Other species of farmed or wild feral deer may have BTV antibodies, but
usually no disease is observed.
In the face of bluetongue virus infection, sheep display characteristic clinical signs<sup>14</sup>. After a 4-6 day incubation period animals develop a pyrexia of 40.5-42°C and become depressed. 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.
In the face of bluetongue virus infection, sheep display characteristic clinical signs<sup>14</sup>. After a 4-6 day incubation period animals develop a pyrexia of 40.5-42°C and become depressed. 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.