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Path 2 - Muscles - Myositis, Neoplasia, NMJ, Tendon

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sihirlifil's version from 2017-04-29 15:02

Myositis

Question Answer
What is notable about bacterial myositis?Muscle is poor medium for most bacterial infections (even w/ overwhelming septicemia, repeated)
**Which bacteria grows well in muscle?Clostridium (anaerobic conditions
How common is viral infection? Which viruses?COMMON!
Porcine encephalomyelitis (corona), hog cholera
Canine distemper
Feline panleukopenia
FMD, bluetongue
Newcastle
Hemorrhagic myositis: Blackleg Caused by? What happens?Clostridium chauvoei
Ingestion of spores, dormant in muscles via bloodstream --> Activation of spores w/ muscle injury --> proliferation of bacilli --> toxin production --> vascular damage, edema, hemorrhage, necrosis, myositis, emphysema (crepitant muscles)
Hemorrhagic myositis: Lesions of blacklegLarge muscles of pectoral & pelvic girdle +/- heart, tongue, diaphragm, masticatory are crepitant with sweetish/rancid odor
Wet: dark, red, wet
Dry: black, spongy
Often endocarditis, fibrinohemorrhagic pleuritis
Hemorrhagic myositis: Malignant edema caused by? happens in who? What happens?Clostridium septicum, perfringens in horses, ruminants, swine
Spores in soil --> wound contamination of devitalized tissue --> activation of spores, bacilli proliferate --> toxin production -->vascular damage, hemorrhage, edema, necrosis, *GAS GANGRENE*
Deep wounds more suitable (less oxygen)
Effects of exotoxins in both blackleg and malignant edema?Toxic injury to capillary endothelium = altered permeabiliy = edema, hemorrhage
Lysis of myocytes = necrosis
Gas bubbles produced during bacterial replication
**Suppurative myositis caused by? Results in?Pyogenic bacteria (Trueperella pyogenes, Corynebacterium pseudotuberculosis) via direct penetration, hematogenous (embolic foci!), spread from adjacent tissue
Localized or diffuse suppuration, myofiber necrosis, resolution, abcessation
Eosinophilic myositis: caused by?Sarcocystis
Immunologic injury (autoimmune against type IIc of masticatory muscles)
Idiopathic
Eosinophilic myositis in ruminants: cause? looks like?Idiopathic (+/- hypersensitivity to sarcocystis?)
Focal necrosis, eosinophilic infiltration, well-demarcated green foci that fades to off-white when exposed to air (chronic --> eosinophilic granuloma)
**Eosinophilic myositis: Masticatory muscle myositis (MMM) happens in? what is happening?Dogs (GSD)
Autoimmunity against Type IIc muscle fibers (masseter, temporalis)
Antibodies to myosin isoform; Acute = eosinophilic myositis, chronic = atrophic myositis
**Eosinophilic myositis: Masticatory muscle myositis (MMM) clinically looks like?Recurrent, painful, mandibular immobility, muscle swelling (temporal, masseter, zygomatic), mouth held partially open, painful eating
Attack lasts 1- 3 weeks; muscles become progressively more atrophied
**Eosinophilic myositis: Masticatory muscle myositis (MMM) acute vs. chronicAcute: swollen, dark red, doughy, hard w/ yellow/pale streaks/foci
Chronic: Atrophy, fibrosis, numerous plasma cells
Immune-mediated myositis: Polymyositis of dogs- what's going on?T-cell mediated
Acute/chronic progressive; lymphoplasmacytic inflammation against myofibers = necrosis
Immune-mediated myositis: Polymyositis of dogs- lesions?Megaesophagus, atrophy, degeneration, necrosis
Infiltration of lymphocytes, plasma cells, occasional eosinophilia
**Immune-mediated myositis: Purpura hemorrhagica- happens in? when?Horses
Post-streptococcal infection (Strep equi)
**Immune-mediated myositis: Purpura hemorrhagica- what does it look like?Edema of head and limbs, leukocytoclastic vasculitis, petechiae (mucosa, musculature, viscera), +/- glomerulonephritis
**Immune-mediated myositis: Purpura hemorrhagica- what's going on?Immune complexes in serum containing IgA & S. equi-specific antigens
Immune-mediated myositis: Dermatomyositis in dogs- who specifically? what happens?Collies, shelties
Dermatitis, myositis (atrophy of masticatory muscles) --> spontaneous recovery
Granulomatous myositis: looks like?Focal or multiple granulomas:
White firm masses, caseous to necrotic centers, "sulfur granules"
Granulomatous myositis: caused by?Tuberculosis
Higher bacteria
Systemic mycoses
Metazoan parasites (trichinosis, cysticercosis)
(Roeckl's granuloma in cattle)
Granulomatous myositis: infective agents (specifically)Tuberculosis: Mycobacterium bovis
Wooden tongue: **Actinobacillus lignieresii
Lumpy jaw: **Actinomyces bovis
Botryomycosis: Staphylococcus aureus
Fungal: Blastomyces dermatitidis
Viral myositis: caused by? lesions?RNA viruses
Small foci, streaks; infarcts from vasculitis (e.g. bluetongue); multifocal necrosis from direct effect on myofibers (enteroviruses, FMD)
**Most important parasitic myopathy? Others?Trichinella spiralis
Ancyclostoma caninum larva migrans
Toxocara canis (focal granulomas)
Dirofilaria immitis (thromboembolism)
What is special about Trichinella?ONLY nematode to ENTER CELLS as part of life cycle!!
How does Trichinella get into muscles?Adult stage in intestines of carnivores, females deposit larvae into lymphatics --> bloodstream --> myocytes
How does immunity affect Trichinella?Aquired during enteric stage; may REDUCE number of larvae reaching muscle but DOESN'T affect migration, encystment, larval development
Lesions of trichinosis?Disoriented myofibrils
Myofilaments detached, frayed at Z line
Most organelles degenerate, disappear (especially mitochondria, lysosomes)
Cytoplasm filled with SER
Larvae free in cytoplasm with hyaline cyst wall
**Which cestodes cause myopathy?Taenia solium = Cysticercus cellulosae (pigs)
Taenia saginata = Cysticercus bovis (cattle)
Which protozoa cause myopathy?Toxoplasma gondii in cats
Neosporum caninum in dogs
Sarcocystis in sheep, cattle, pigs, ducks
(Segmental necrosis, necrotizing myositis)
How does **Sarcocystosis appear?Parasites form elongated spindle-shaped structures
Groups of organisms surrounded by thick cyst wall of both parasite & host origin (white dots, streaks)
Which muscles are affected by Sarcocystis? What is the disease like?Skeletal, tongue, heart, esophagus, diaphragm
Disease is apparently harmless with no clinical signs and no inflammatory reaction around encysted parasites
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Neoplasia

Question Answer
Primary neoplasms: how common?EXTREMELY RARE
**Rhabdomyoma: who gets it? how does it behave? Looks like?Congenital in cow, sheep, pig
Benign; origin = heart 66%
Large pedunculated mass in the heart, cross-striation
**Rhabdomyosarcoma: who gets it? how does it behave? looks like?Cow, sheep, dog, horse; NOT reported in PIG (they like to get the benign one)
Malignant,
distant metastasis to lung, spleen, lymph nodes, kidneys
Poorly encapsulated~ spherical pink/gray nodules
How do you diagnose primary neoplasms?Demonstration of myofibrils or cross-striations in neoplastic cells (Ddx: regenerative muscle fibers)
Where does a botryoid rhabdomyosarcoma come from? Who gets it?Sites with no striated muscle (kidney, urinary bladder trigone, urethra) from rests of embryonic myoblasts
Young large breed (especially St Bernard) (unlike TCC, which is old)
INFILTRATIVE, metastasis
(Botryoid = shaped like bunch of grapes)
Secondary neoplasms: (6)Lymphoma (bovine)
Marek's disease (avian)
Hemangiosarcoma (dog)
Malignant melanoma
SCC (dogs vulva & pelvis, cattle extraocular & orbicularis oculi muscle)
Canine mammary adenocarcinoma & MCT (cutaneous muscle)
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NMJ & Tendon

Question Answer
Myasthenia gravis: in who? what happens?Dogs and cats
Muscle weakness & fatigue from deficiency of acetylcholine receptors (congenital or required)
**What's going on in acquired myasthenia gravis?Post-synaptic membrane is distorted, lower concentration of ACh receptors on muscle end-plate; antibodies are attached to the membrane
*ACh is released normally*
What's going on in congenital myasthenia gravis?Deficiency of ACh receptors (no evidence of auto-immune disease)
Lesions of myasthenia gravisMegaesophagus
Dysphagia
Secondary aspiration pneumonia
Thymoma
**Botulism: caused by?Toxins produced by Clostridium botulinum, ingested from feed or produced in gut
Botulism: who is affected?Horses and ruminants
**Botulism: what's going on?Toxins bind irreversibly to the presynaptic nerve terminals, preventing release of acetylcholine
Botulism: what does it look like?General flaccid paralysis
Dysphagia, tongue weakness, aspiration pneumonia
Recumbency --> ischemia, focal necrosis
How do tendons heal?Slow, by scar formation (relatively avascular)
What does tendon disease look like clinically?Lameness, abnormal posture, joint collapse
Tendons: congenital anomalies = Congenital flexure of pasterns (contracted tendons) - lambs, foals
Tendons: rupture, laceration, strain occurs how?Overstretching by exertion, deep laceration (wire cuts, mowing machines)
Sever
Sequelae = collapse of joint, slow healing (after sx)
Tendons: how do birds get perosis? What does it look like?Dietary deficiency of Mn or choline
Lateral displacement of gastrocnemius tendon, collapse of hock
Tendonitis: caused by?Strain, physical injury, viral (reovirus in chickens)
Tenosynovitis: caused by?Trauma, penetrating wound (serous, fibrinous, pirulent)
Which parasite can affect the tendon?Onchocerca spp
Brisket, abdominal wall, ligamentum nuchae; fibrous nodules
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