Chapter 12 Muscle Flashcards

1
Q

What is inflammatory myopathy in horses?

A

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.

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2
Q

What is infarctive purpura hemorrhagica (IPH)?

A

A severe form of vasculitis associated with purpura hemorrhagica that produces ischemia and complete infarction of portions of skeletal muscle and other organs.

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3
Q

What are common clinical signs of IPH?

A

Painful lameness, limb swelling, muscle stiffness, abdominal pain, petechiae, depression, well-demarcated limb edema, and focal firm swellings within muscles.

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4
Q

What are the typical hematologic and biochemical abnormalities in IPH?

A

Leukocytosis with neutrophilia and toxic changes, hyperglobulinemia, hypoalbuminemia, marked elevations in serum CK activity (>47,000 U/L), and elevated AST (>960 U/L).

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5
Q

What immunologic mechanisms are involved in IPH?

A

IgM- or IgA-streptococcal M protein immune complexes deposit along vessels, activating complement and causing leukocytoclastic vasculitis, vascular necrosis, occlusion, and infarction.

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6
Q

What is the treatment for IPH?

A

Aggressive antibiotic and corticosteroid treatment, including intravenous potassium penicillin, NSAIDs, and a tapering course of dexamethasone and prednisolone.

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7
Q

What is rhabdomyolysis associated with Streptococcus equi?

A

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.

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8
Q

What are the proposed immunologic mechanisms for S. equi rhabdomyolysis?

A

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.

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9
Q

What are the diagnostic findings in S. equi rhabdomyolysis?

A

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.

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10
Q

What is the treatment and prognosis for S. equi rhabdomyolysis?

A

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.

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11
Q

What is immune-mediated myositis (IMM) in Quarter Horse-related breeds?

A

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.

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12
Q

What are common clinical signs of IMM in Quarter Horse-related breeds?

A

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.

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13
Q

What immunologic mechanisms are proposed for IMM?

A

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.

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14
Q

What are the diagnostic findings for IMM?

A

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.

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15
Q

What is the treatment for IMM?

A

Anti-inflammatory doses of corticosteroids, with dexamethasone followed by prednisolone, and preventing exposure to respiratory infections and monitoring for early signs of atrophy.

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16
Q

What is systemic calcinosis?

A

A fatal syndrome of systemic dystrophic calcification associated with signs of malaise, mild fever, stiffness, muscle atrophy, hyperfibrinogenemia, hyperphosphatemia, and diverse organ failure.

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17
Q

What are common clinical signs of systemic calcinosis?

A

Mild fever, malaise, stiffness, loss of muscle mass, cough, tachypnea, mild ventral edema, progressive weakness, respiratory distress, laminitis, and gastrointestinal inflammation.

18
Q

What are the hematologic and biochemical abnormalities in systemic calcinosis?

A

Hyperfibrinogenemia, mild leukocytosis, elevated product of calcium multiplied by phosphorus (>65), and elevated serum CK activities.

19
Q

What immunologic mechanisms are associated with systemic calcinosis?

A

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

20
Q

What are the diagnostic findings for systemic calcinosis?

A

Muscle biopsies showing dystrophic calcification of muscle fibers, multinucleated giant cells, and calcification in various tissues including pulmonary, cardiac, renal, and vascular tissues.

21
Q

What is the prognosis for systemic calcinosis?

A

Poor, often resulting in euthanasia due to progressive weakness, inability to remain standing, respiratory distress, laminitis, or other underlying disease.

22
Q

What is uncharacterized immune-mediated and inflammatory myopathies?

A

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.

23
Q

What is sarcocystis myositis?

A

An inflammatory myositis associated with sarcocysts within skeletal muscle, leading to malaise, anorexia, weakness, muscle atrophy, and inflammatory reaction in muscle biopsies.

24
Q

What are the diagnostic findings for sarcocystis myositis?

A

Presence of sarcocysts in muscle biopsies, associated with lymphocytes and macrophages, and possibly eosinophils, serologic titers, and clinical signs.

25
Q

What is the treatment for sarcocystis myositis?

A

Antiprotozoal drugs such as pyremethamine/trimethoprim-sulfa or diclazuril.

26
Q

What are the signalment and clinical signs of IPH?

A

No known breed, gender, or age predilection. Primary presenting complaints include painful lameness, limb swelling, muscle stiffness, and sometimes abdominal pain.

27
Q

What are the diagnostic methods for IPH?

A

Hematologic and biochemical analysis, ELISA titers for S. equi serum M protein, peritoneal fluid analysis, ultrasonography of swollen muscles, and muscle biopsy.

28
Q

What are the immunologic mechanisms of S. equi rhabdomyolysis?

A

Streptococcal superantigens causing toxic shock-like reaction, or bacteremia with secondary multiplication of S. equi in skeletal muscle causing myodegeneration.

29
Q

What are the proposed mechanisms for IMM development?

A

Loss of self-tolerance to muscle cell antigens, cytokine-induced MHC class II expression on myoblasts, and altered autoantigen expression by target or antigen-presenting cells.

30
Q

What are the diagnostic criteria for IMM?

A

Muscle biopsies showing lymphocytic infiltrates, lymphocytic vasculitis, anguloid atrophy, fiber necrosis, multinucleated giant cells, and elevated serum CK and AST activities during the acute phase.

31
Q

What is the role of corticosteroids in IMM treatment?

A

Anti-inflammatory doses halt muscle atrophy, and recovery of muscle mass usually occurs over 2-3 months.

32
Q

What are the immunologic mechanisms in systemic calcinosis?

A

Cytokines such as TNF-alpha and IL-6 activate RANK-L, leading to bone resorption, hyperphosphatemia, and dystrophic calcification.

33
Q

What are the histopathologic findings in systemic calcinosis?

A

Dystrophic calcification of muscle fibers, multinucleated giant cells, and calcification in various tissues including pulmonary, cardiac, renal, and vascular tissues.

34
Q

What is the clinical presentation of uncharacterized immune-mediated and inflammatory myopathies?

A

Muscle atrophy, lymphocytic infiltrates in muscle biopsy specimens, and possible history of recent infection.

35
Q

What are the clinical signs of sarcocystis myositis?

A

Malaise, anorexia, weakness, asymmetric atrophy of some muscles, and symmetric atrophy of gluteal, epaxial, and quadriceps muscles.

36
Q

What are the hematologic findings in sarcocystis myositis?

A

Few abnormalities, with diagnosis based on muscle biopsies showing sarcocysts and associated inflammatory reaction.

37
Q

What is the importance of early recognition and treatment in IPH?

A

Early recognition and aggressive antibiotic and corticosteroid treatment are essential to fight the high fatality rate.

38
Q

What are the hematologic findings in S. equi rhabdomyolysis?

A

Mature neutrophilia, hyperfibrinogenemia, serum CK activity >100,000 U/L, low S. equi M protein titers unless recently vaccinated.

39
Q

What are the clinical features of systemic calcinosis?

A

Severe atrophy of epaxial muscles, hyperfibrinogenemia, hyperphosphatemia, and diverse organ failure.

40
Q

What are the immunologic mechanisms of IMM?

A

Altered autoantigen expression, cytokine-induced MHC class II expression on myoblasts, and loss of self-tolerance to muscle cell antigens.

41
Q

What are the diagnostic features of uncharacterized immune-mediated myopathies?

A

Lymphocytic infiltrates in muscle biopsy specimens, clinical presentation of muscle atrophy, and possible history of recent infection.