Infarctive Purpura Hemorrhagica:
Purpura hemorrhagica is an immune mediated vasculitis associated with sensitization and cross-reactivity to proteins in the
cell wall of Strep equi. It is type three hypersensitivity, and is characterized by leukocytoclastic vasculitis of the skin. Infarctive purpura hemorrhagica
is a severe form of purpura hemorrhagica that is characterized by severe leukocytoclastic vasculitis in numerous tissues (not
just skin) that progresses to infarction. Infarctive purpura hemorrhagic in horses has a high mortality. Infarctive purpura
hemorrhagica may be mediated by IgA, and is similar to Henoch-Schonlein purpura in humans. Henoch-Schonlein purpura is an
immune complex disease, and is most common in children.
Clinical signs and History:
History and clinical signs include some of the typical signs that occur with classic purpura in horses. Previous exposure
or infection with Strep equi is usually reported. Clinical signs consistent with purpura include edema (limbs or ventral abdomen)
and petechial or ecchymotic hemorrhages on mucous membranes. Clinical signs of infarctive purpura include severe lameness,
stiffness, and swelling of muscles. Colic can be an initial complaint. Once clinical signs develop, the clinical course is
rapid, and a high mortality rate is reported.
CBC- most horses have leukocytosis and mature neutrophila, with a high fibrinogen. Chemistry profile: high muscle enzymes
(CK ranges from 50,000 to > 200,000 U/L). Conformation of purpura can be further supported via a skin biopsy (for evidence
of leukocytoclastic vasculitis) and/or a serum titers of antibodies against M protein of Strep equi (ELISA SeM > 1:6,400).
Early recognition and treatment with antibiotics and corticosteroids (dexamethasone 0.1 mg/kg IV SID to BID) with weaning
doses over 1-2 weeks. Some clinicians will than switch to prednisolone for an additional 1-2 weeks. Antibiotic therapy should
be directed against Strep equi. Other recommended treatments would include intravenous fluids, NSAID, and gastroprotectants.
Immune Mediated Myositis- IgG Mediated
Signalment and History:
Predominately Quarter horses. Age includes two groups (less than 8 years and greater than 17 years. Exposure to horses with
infectious respiratory disease before clinical signs is common.
Clinical signs include rapid muscle atrophy (days to 1-2 weeks duration). The muscle atrophy can be symmetric to asymmetric
and most commonly involves the epaxial and gluteal muscles. Depression, stiffness and fever are reported in some horses.
CBC and serum chemistry is normal, other than the exception of slightly- to moderate increase in CK (mean 9,700 U/L, range
of 260-140,000 U/L) and AST (mean 2,880 U/L, range of 350-9,000 U/L). Histology of the affected muscles reveals a lymphocytic
inflammatory myopathy. Histology reveals macrophages and lymphocytes within myofibers as well as surrounding blood vessels,
atrophied fibers, and regenerative myofibers.
Horses respond favorably to corticosteroid therapy (dexamethasone or prednisolone). The duration of steroids usually ranges
between 4 to 8 weeks (with decreasing doses and alternate day therapy). Horses should be evaluated for ongoing or subclinical
respiratory infections (Strep equi or zooepidemicus). Antibiotic therapy should be considered in cases in which there is a
suspected nidus (abscess). Recurrence of muscle atrophy is reported, which may result in further treatment.