If it does turn out to be an auto-immune problem (eosinophilic myositis also known as Masticatory myositis), do tell the breeder - it can be (tho' not always - and it's very hard to pin down) related to specific lines of dogs in a number of breeds and it's important that the breeder knows that it's happened.
It's always hard to say exactly the cause, but if it happens a lot, they can begin to narrow down the genetic lines that predispose to it.
and - well done to your vet for recognising it.
here's an extract from a paper which tells more about it:
IMMUNE MEDIATED MUSCLE DISEASES
Canine polymyositis is usually seen in large breed dogs (incidence in females is greater than males). It is an acute disease causing progressive weakness of the head, trunk, and limbs. The clinical signs include pain, undulating fever, dysphagia, and megaesophagus. Diagnosis is by eosinophilia on the CBC, leukocytosis, increases in ALT, LDH, and CPK. Fifty percent of cases will have immunofluorescence for ANA or antisarcolemmal antibodies.(15) Biopsies demonstrate Type I and II fibres with multifocal necrosis with vacuolization and hyalinization. Treatment is with corticosteroid at 0.5 mg–1 mg/kg q12h. If a response is noted after one week, the prognosis is good.(15)
Masticatory myositis involves antibodies directed at the type 2M fibres unique to the muscles of mastication: the temporalis, masseter and pterygoid. Embryologically these muscles are derived from mesoderm.(16) By two weeks postpartum, these muscles have developed the unique 2M fibres.
There are two distinct disorders in masticatory myositis: 1) acute eosinophilic myositis; and 2) chronic atrophic myositis.
Eosinophilic myositis is prevalent in German Shepherds and Dobermans of a young age (less than four years). The acute phase lasts two to three weeks followed by remission and recurrent attacks. Peripheral eosinophilia is noted. Histology reveals large numbers of eosinophils, plasma cells infiltrating the muscles, hemorrhage, and necrosis. Chronic lesions demonstrate scar tissue. Treatment involves use of corticosteroids at 0.5–1 mg/kg.(17)
Atrophic myositis has no breed, sex, or age predilection. There is usually a single less dramatic attack followed by progressive atrophy and fibrosis. Peripheral eosinophilia is not a feature. Eosinophils are less predominant in histology. Treatment is less effective and the prognosis is guarded.(17)
Masticatory myositis has been described as a result of infection with the protozoa Leishmania infantum.(18) Leishmania is transmitted by the sandfly and is zoonotic. The disease is endemic in the Mediterranean and Portugal with sporadic reports in Europe and the United Kingdom. Muscle fibre necrosis, atrophy, mononuclear infiltrates, vasculitis, and amastigotes within macrophages are histological features. IgG immune complexes have been detected.(18)
good luck
ms
It's always hard to say exactly the cause, but if it happens a lot, they can begin to narrow down the genetic lines that predispose to it.
and - well done to your vet for recognising it.
here's an extract from a paper which tells more about it:
IMMUNE MEDIATED MUSCLE DISEASES
Canine polymyositis is usually seen in large breed dogs (incidence in females is greater than males). It is an acute disease causing progressive weakness of the head, trunk, and limbs. The clinical signs include pain, undulating fever, dysphagia, and megaesophagus. Diagnosis is by eosinophilia on the CBC, leukocytosis, increases in ALT, LDH, and CPK. Fifty percent of cases will have immunofluorescence for ANA or antisarcolemmal antibodies.(15) Biopsies demonstrate Type I and II fibres with multifocal necrosis with vacuolization and hyalinization. Treatment is with corticosteroid at 0.5 mg–1 mg/kg q12h. If a response is noted after one week, the prognosis is good.(15)
Masticatory myositis involves antibodies directed at the type 2M fibres unique to the muscles of mastication: the temporalis, masseter and pterygoid. Embryologically these muscles are derived from mesoderm.(16) By two weeks postpartum, these muscles have developed the unique 2M fibres.
There are two distinct disorders in masticatory myositis: 1) acute eosinophilic myositis; and 2) chronic atrophic myositis.
Eosinophilic myositis is prevalent in German Shepherds and Dobermans of a young age (less than four years). The acute phase lasts two to three weeks followed by remission and recurrent attacks. Peripheral eosinophilia is noted. Histology reveals large numbers of eosinophils, plasma cells infiltrating the muscles, hemorrhage, and necrosis. Chronic lesions demonstrate scar tissue. Treatment involves use of corticosteroids at 0.5–1 mg/kg.(17)
Atrophic myositis has no breed, sex, or age predilection. There is usually a single less dramatic attack followed by progressive atrophy and fibrosis. Peripheral eosinophilia is not a feature. Eosinophils are less predominant in histology. Treatment is less effective and the prognosis is guarded.(17)
Masticatory myositis has been described as a result of infection with the protozoa Leishmania infantum.(18) Leishmania is transmitted by the sandfly and is zoonotic. The disease is endemic in the Mediterranean and Portugal with sporadic reports in Europe and the United Kingdom. Muscle fibre necrosis, atrophy, mononuclear infiltrates, vasculitis, and amastigotes within macrophages are histological features. IgG immune complexes have been detected.(18)
good luck
ms
