Muscle Lab. - any chronic disease (avian tuberculosis, aspergillosis, amyloidosis, neoplasia)

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Muscle Lab Case 1. The tale of three Black Ducks. 1. What is going on with bird A? This bird is in extremely poor body condition and is emaciated. There is marked pectoral muscle atrophy caused by malnutrition and the keel is easily palpable. 2. What diseases might you be suspicious about? - any chronic disease (avian tuberculosis, aspergillosis, amyloidosis, neoplasia) - lead poisoning - emaciation/starvation due to inability to access food (e.g. mandibular fracture, extreme weather, inexperience foraging) 3. Describe the lesions seen in bird B. Diffuse, multiple rod shaped white foci (<0.5 cm x 1cm) randomly disseminated throughout the pectoral muscle. 4. Explain the pathogenesis and identify the agent. The agent is Sarcocystis rylei which is a protozoal parasite that used waterfowl as an intermediate host. The definitive host is a carnivore who ingests the cysts in muscle, goes through sexual reproduction including the differentiation into gametes and fertilization within the intestines of the definitive host that then develops into a sporulated oocyst that is excreted in the feces of the carnivore. The oocysts are then ingested by the waterfowl in food or water that is contaminated with carnivore feces where the merozoites hatch from the oocyst and invade skeletal muscle to produce a sarcocyst. 5. Is this zoonotic? Nope, but not very appetizing. Other species of sarcocysts are found in the muscles of cattle, sheep and pigs and are often not visible grossly.

Case 2. X1654-10 (MF) Adult, male snow shoe hare found incidently in a coyote snare. There is an area of subcutaneous tissue and muscle (found over the left sacral and abdominal region) that contains a large mass that is firm, attached to the muscles and easily separated from the overlying skin. The surface was faintly granular and, on cut surface, the mass is composed of numerous cavities filled with 1-2 cm in diameter cysts that contain several small white nodules floating in clear fluid. The mass was firmly attached to the muscles, so that its removal resulted in the removal of the left abdominal wall. 2. What is the underlying agent? This is a coenurus (contains larval forms of the tapeworm), from Taenia serialis serialis 3. Explain the pathogenesis. This species of cestode uses rabbits and hares as the intermediate host and, usually, the red fox as the definitive host. In the fox, the adult parasite produces eggs that are shed through feces and contaminate vegetation that is then consumed by the hares or rabbits (intermediate hosts). In the hares, the parasites become encysted forming what is known as a coenurus (a larval cyst with multiple parasite heads or scolices), that lodges itself in the abdominal cavity, subcutis or muscle. It can remain there, in a viable state ready to infect a carnivore, for up to 2 years. When the hare is eaten by a predator, in this case most likely a red fox, the larvae are consumed as well and can mature into adults in the intestine of the fox. This starts the cycle again. 4. What did this mean for this animal? Although this appears to be a severe lesion, the animal was caught in a snare and did not die on its own, so the affect on the hare was likely minimal (although, maybe a little itchy). A carnivorous predator who then eats the hare and subsequently, the larval cestodes would develop an intestinal tapeworm (which is also probably not that big of a deal for them either). 5. Is it zoonotic? It is very unlikely for this parasite to cause disease in humans, particularly if the obvious cysts are discarded and the meat is cooked thoroughly. One thing worth noting is that dogs can become infected with the parasite if they consume hares that carry the larval forms, the coenurus. Other species of Taenia are zoonotic and are of concern in developing countries, but are more likely to be transmitted by fecal/oral transmission of eggs and not ingestion of cysticerci.

Case 3. B-19773-98 Black leg History: A male, 600lb (6 months old) calf, was found dead on pasture. He was acting dopey and weak last night. 3 other calves have dies on the same farm in the past week. 1. Describe the lesion and give a morphologic diagnosis. This animal was in good body condition. The muscles of the pectoral and pelvic girdles, thorax and diaphragm are dark red and fibers are separated by gas bubbles. Some areas of muscle are wet and exude red watery fluid on section, others are dry. The thoracic cavity contains red watery fluid and the costal and parietal pleura are covered by a layer of redstained, friable material up to 1cm thick. Morph: severe, acute hemorrhagic and emphysematous myositis 2. What is the underlying etiology. This is the classic lesion of black leg, caused by the bacterium (Clostridium chauvoei). 3. Explain the pathogenesis. Usually affecting the fasted growing animals, spores of C. Chauvei are ingested orally, pass into the blood stream from the intestinal mucosa and reach the skeletal muscles. They remain dormant in these areas until bruising or other trauma to the muscle result in anaerobic conditions that allow them to activate and produce toxins. The toxin damages endothelial cells which results in hemorrhage, edema and ischemic necrosis of regional myofibers as well as a generalized toxemia that results in death (usually within 24 hours). 4. How would you confirm your suspicion? Histopathology Fluorescent Antibody Test on fresh tissue Anaerobic culture (not always the best because of post mortem presence of Clostridia sp.) 5. What do you tell the farmer? This is usually a herd problem and usually due to improper or lack of vaccination in calves. Outbreaks are prevented by a 7-way or 8-way Clostridial vaccine and in an outbreak scenario all calves are usually vaccinated and treated with penicillin.

Case 4. B-29036-08 Poorly differentiated sarcoma History: Slaughterhouse cow Multifocal to coalescing firm, sometimes pedunculated white-yellow nodules of varying sizes cover and infiltrate the peritoneal surface of the body wall. 2. What are some differentials for this lesion? - neoplasia (lymphoma, sarcoma (fibrosarcoma, osteosarcoma, rhabdomyosarcoma), liposarcoma, neurofibroma) - granulomas (systemic fungal diseases such as histoplasmosis, blastomycosis, coccidiomycosis) - multiple abscesses (tuberculosis) 3. What are the tumors of skeletal muscle called? - rhabdomyomas (benign, usually found in the heart first) - rhadbomyosarcoma (malignant, most common in cow, sheep, dog and horse)

Case 5: History: Mixed breed, intact, 5 year old male dog with a history of neurologic signs. The right temporal muscle displays marked atrophy and is pale when compared to the left and the normal dog. 2. What are some differentials? - Neurogenic atrophy (peripheral neuropathy such as coon hound paralysis or tick borne disease) - Previous trauma to the head causing neurogenic atrophy - Disuse atrophy: couldn t move that side of the jaw for some reason - If it was bilateral: cachexia from chronic disease, Masticatory Muscle Myositis - If it was myolysis (degeneration or necrosis or swelling of the masticatory muscles consider autoimmune diseases such as canine polymyositis which causes degeneration and necrosis which would be diagnoses histologically) or dermatomyositis seen in Collies and Shelties usually causes myositis and pain in the masticatory muscles. 3. In a different dog that seems to have trouble eating, what disease would you think about? HINT: www.veterinaryradiology.net This animal has megaesophagus which is a condition involving dilation of the esophagus. The underlying disease can be Myastenia gravis which causes weakness and severe muscular fatigue because of dysfunction at the neuromuscular junction. There are two types (Hereditary- animals are born with a reduced number of acetylcholine (Ach) receptors and Acquired animals develop antibodies (IgG) against Ach receptors).

Case 6: White Muscle Disease History:A three week old, 112 lb, female calf in good body condition was sick last night and found dead this morning. She was breathing hard, had a fever and showed no improvement after treatment with antibiotics (Nuflor and Metacam). There are multifocal-coalescing irregular areas of palor located in skeletal muscles and throughout the ventricles of the heart which are more distinct on the left. 2. What are your morphologic diagnoses? Multifocal, necrotizing skeletal myopathy, marked-to severe, acute Multifocal myocardial necrosis, moderate to marked, acute 3. What is the underlying etiology and pathogenesis? This is an example of an underlying selenium deficiency causing a nutritional myopathy (white muscle disease). Selenium-containing enzymes (glutathione peroxidase and reductase) and Vitamin E are important free radical scavengers. In a situation of deficiency of these compounds, oxygen free radicals are free to cause damage and peroxidation of membranes which results in an influx of calcium into the sarcoplasm and mitochondria which the cells don t have enough energy to get out of the cell, causing the myofibers to degenerate. Type 1 fibers (more active) muscle is usually targeted because they produce more free radicals. 4. How would you confirm your suspicion? Test the liver for selenium level. Have an idea of areas of selenium-poor soils where animals should receive injections of vitamin E/Se at or shortly after birth. Do histology on affected or Type 1 muscles (diaphragm, intercostals). 5. What other species do we see similar lesions in? - pigs with Mulberry heart disease, can also see white muscle disease in sheep and less commonly in foals and goats - pigs with porcine stress syndrome would look similar (but usually affects Type II fibers) - horses that survive azoturia and have a polysaccharide storage disease (acute cases would be very dark and the animals might have myoglobinuria) - wildlife (especially ungulates) often associated with an exertional myopathy and tends to affect Type II fibers instead of Type I typical of WMD and tend to be more dark and hemorrhagic - birds can get exertional myopathy and also a compartment syndrome that causes deep pectoral myopathy resulting in a green colour to the surpacoracoid muscles due to ischemia and infarction.