Chapter 12 Muscle Flashcards
(41 cards)
What is inflammatory myopathy in horses?
A suspicion of inflammatory myopathy arises from clinical history, physical exam findings, hematologic findings, serum biochemistry profile, and bacterial cultures/PCR or serum titers. Muscle biopsies showing lymphocytes and macrophages within myofibers indicate inflammatory myopathy.
What is infarctive purpura hemorrhagica (IPH)?
A severe form of vasculitis associated with purpura hemorrhagica that produces ischemia and complete infarction of portions of skeletal muscle and other organs.
What are common clinical signs of IPH?
Painful lameness, limb swelling, muscle stiffness, abdominal pain, petechiae, depression, well-demarcated limb edema, and focal firm swellings within muscles.
What are the typical hematologic and biochemical abnormalities in IPH?
Leukocytosis with neutrophilia and toxic changes, hyperglobulinemia, hypoalbuminemia, marked elevations in serum CK activity (>47,000 U/L), and elevated AST (>960 U/L).
What immunologic mechanisms are involved in IPH?
IgM- or IgA-streptococcal M protein immune complexes deposit along vessels, activating complement and causing leukocytoclastic vasculitis, vascular necrosis, occlusion, and infarction.
What is the treatment for IPH?
Aggressive antibiotic and corticosteroid treatment, including intravenous potassium penicillin, NSAIDs, and a tapering course of dexamethasone and prednisolone.
What is rhabdomyolysis associated with Streptococcus equi?
A severe acute generalized rhabdomyolysis occurring in young Quarter Horses during a concurrent S. equi infection, leading to marked elevations in serum CK and AST activities and high mortality.
What are the proposed immunologic mechanisms for S. equi rhabdomyolysis?
Toxic shock-like reaction due to streptococcal superantigens causing massive inflammatory cytokine release, or bacteremia with secondary multiplication of S. equi in skeletal muscle causing myodegeneration.
What are the diagnostic findings in S. equi rhabdomyolysis?
Mature neutrophilia, hyperfibrinogenemia, serum CK activity >100,000 U/L, low S. equi M protein titers unless recently vaccinated, and muscle biopsies showing acute extensive myodegeneration.
What is the treatment and prognosis for S. equi rhabdomyolysis?
Flushing infected guttural pouches, draining abscessed lymph nodes, antimicrobial treatment, NSAIDs, and possibly high doses of short-acting corticosteroids. The mortality rate is very high.
What is immune-mediated myositis (IMM) in Quarter Horse-related breeds?
A condition causing malaise, rapid, pronounced atrophy of epaxial and gluteal muscles, and high serum CK and AST activities, typically responding to anti-inflammatory doses of corticosteroids.
What are common clinical signs of IMM in Quarter Horse-related breeds?
Dramatic muscle atrophy of epaxial and gluteal muscles, stiffness, general malaise, rapid progression of atrophy involving up to 40% of muscle mass within a week, and frequent periods of recumbency.
What immunologic mechanisms are proposed for IMM?
Loss of self-tolerance to antigens expressed by muscle cells, potentially due to cytokine-induced expression of MHC class II molecules on myoblasts and myotubes, leading to presentation of autoantigens to CD4+ cells.
What are the diagnostic findings for IMM?
Elevated serum CK and AST activities during the acute phase, muscle biopsies showing lymphocytic infiltrates, lymphocytic vasculitis, anguloid atrophy, fiber necrosis, and multinucleated giant cells.
What is the treatment for IMM?
Anti-inflammatory doses of corticosteroids, with dexamethasone followed by prednisolone, and preventing exposure to respiratory infections and monitoring for early signs of atrophy.
What is systemic calcinosis?
A fatal syndrome of systemic dystrophic calcification associated with signs of malaise, mild fever, stiffness, muscle atrophy, hyperfibrinogenemia, hyperphosphatemia, and diverse organ failure.
What are common clinical signs of systemic calcinosis?
Mild fever, malaise, stiffness, loss of muscle mass, cough, tachypnea, mild ventral edema, progressive weakness, respiratory distress, laminitis, and gastrointestinal inflammation.
What are the hematologic and biochemical abnormalities in systemic calcinosis?
Hyperfibrinogenemia, mild leukocytosis, elevated product of calcium multiplied by phosphorus (>65), and elevated serum CK activities.
What immunologic mechanisms are associated with systemic calcinosis?
Recognition of self or endogenous antigens. Synergistic effects of cytokines such as TNF-alpha and IL-6 on activation of RANK-L, leading to enhanced bone resorption and hyperphosphatemia, promoting dystrophic calcification.
Hyperphosohataemia causes passive calcification, increase pth secretion, causes smooth muscle to switch to osteogenic cells and interferes with renal vit d3 production
What are the diagnostic findings for systemic calcinosis?
Muscle biopsies showing dystrophic calcification of muscle fibers, multinucleated giant cells, and calcification in various tissues including pulmonary, cardiac, renal, and vascular tissues.
What is the prognosis for systemic calcinosis?
Poor, often resulting in euthanasia due to progressive weakness, inability to remain standing, respiratory distress, laminitis, or other underlying disease.
What is uncharacterized immune-mediated and inflammatory myopathies?
Individual cases of myositis in horses with suspected inflammatory or immune-mediated basis, often involving lymphocytic infiltrates in muscle biopsies and presenting with muscle atrophy.
What is sarcocystis myositis?
An inflammatory myositis associated with sarcocysts within skeletal muscle, leading to malaise, anorexia, weakness, muscle atrophy, and inflammatory reaction in muscle biopsies.
What are the diagnostic findings for sarcocystis myositis?
Presence of sarcocysts in muscle biopsies, associated with lymphocytes and macrophages, and possibly eosinophils, serologic titers, and clinical signs.
