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==Pathogenesis==
 
==Pathogenesis==
The condition is thought to occur due to both immediate (Type 1) and delayed (Type 4) hypersensitivity reactions to Culicoides salivary proteins. These proteins are injected during feeding and susceptible animals respond to them by producing IgE antibodies.
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The condition is thought to occur due to both immediate (Type 1) and delayed (Type 4) hypersensitivity reactions to Culicoides salivary proteins. The proteins are injected during feeding and IgE antibodies are produced in repsonse by susceptible animals.
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==Clinical signs==
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The cardinal sign of Sweet itch is extreme, intense pruritus with characteristic distribution patterns. Commonly affected areas include the head, mane, tail, withers and ventral abdomen. Primary lesions are papules but self-excoration may lead to the characteristic lesions of sweet itch including alopecia, broken hairs, erosions, ulcers. In the chronic stages, lichenification is  a common feature. 
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==Diagnosis==
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Diagnosis is often based on the animal's history, seasonal clinical signs and the site and nature of the lesions. Other important differential diagnoses that should be ruled out include psoroptic and sarcoptic mange, other insect-related  and dermatophilosis
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==Treatment==
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