JPC SYSTEMIC PATHOLOGY

MUSCULOSKELETAL SYSTEM

April 2025

M-M11

 

Signalment (JPC #2082440): An adult male great blue heron (Ardea geriduas).

 

HISTORY: This heron was unable to stand or fly.

 

HISTOPATHOLOGIC DESCRIPTION: Skeletal muscle: Diffusely distributed throughout the section, 50% of myocytes are either swollen with vacuolated sarcoplasm (degeneration) or hypereosinophilic with loss of cross striations (hyalinization), pyknotic nuclei, fragmentation of myofibrils, and occasional contraction bands (necrosis). Degenerate and necrotic myocyte sarcoplasm frequently contains densely basophilic granular material (mineral). Necrotic myocytes are often surrounded and occasionally infiltrated by macrophages, heterophils, and hypertrophic and hyperplastic satellite cells. Occasionally, satellite cells are clumped together, and myocytes have internalized, linearly arranged ("rowing") nuclei with increased sarcoplasmic basophilia (regeneration).

 

Feathered skin: Diffusely the subcutaneous adipose tissue is characterized by loss of differential staining with retention of architecture (coagulative necrosis), often admixed with acicular cholesterol clefts. Multifocally, numerous macrophages and heterophils infiltrate necrotic fatty lobules. Abundant eosinophilic necrotic cellular debris multifocally surrounds necrotic adipocytes. There are occasional 3-10 µm thick bands and globules of pale yellow to tan homogenous material (ceroid). Similar material is often within the cytoplasm of foamy macrophages. Few small arteries within the adipose tissue contain fibrin thrombi.

 

Heart: The epicardium is expanded 3-5 times normal with edema, fibrin, and low numbers of macrophages, lymphocytes, and plasma cells.

 

MORPHOLOGIC DIAGNOSES: 1. Skeletal muscle, myocytes: Degeneration and necrosis, polyphasic, diffuse, moderate, with mineralization and rare regeneration, great blue heron (Ardea geriduas), avian.

2. Feathered skin, panniculus adiposus: Steatitis, necrotizing and histiocytic, diffuse, with extracellular and intrahistiocytic ceroid.

3. Heart, epicardium: Epicarditis, lymphohistiocytic, diffuse, subacute, minimal.

 

ETIOLOGIC DIAGNOSIS: Nutritional myodegeneration and steatitis

 

ETIOLOGY: Vitamin E/selenium deficiency

 

SYNONYMS: Nutritional myopathy, white muscle disease, stiff lamb disease, rigid lamb disease, nutritional panniculitis, yellow fat disease

 

GENERAL DISCUSSION:

• Any animal is susceptible but the syndrome is most frequently seen in cattle, sheep, pigs, and horses; most often young animals, especially if there is rapid post-natal growth, but all ages are susceptible; seen in mature horses with equine masticatory myopathy; infrequent in carnivores
• Disease seen in late winter or early spring is most parts of the world for most livestock; sheep disease presentation is typically in the fall
• Vitamin E/selenium deficiency results in a broad spectrum of diseases in a variety of animal species, including myopathy, steatitis, hepatic necrosis (D-M10), and/or encephalomalacia (N-M28) because of increased oxidative stress on cells 
• The most common nutritional deficiency leading to nutritional myopathy in most species is a deficiency in selenium; vitamin E deficiency without a deficiency in selenium is uncommon in mammals, but may be more common in reptiles and birds
• Striated muscle changes in some species are referred to as nutritional “muscular dystrophy”, which is an inappropriate term according to some references 
• Nutritional deficiency of vitamin E and/or selenium may result from:
• Poor climate conditions/housing
• Prolonged winter feeding 
• Poor quality hay, grain, rancid food source (fish, cod liver oil)
• Increased oxidative stress (e.g. iron injections in neonatal pigs) à increased consumption/depletion of antioxidants 
• Malabsorption of fat (e.g. cholestasis, cystic fibrosis, and small intestinal disease)
• Competition from other elements (sulfur, zinc, silver, cadmium, tellurium, copper)

 

PATHOGENESIS:

• Vitamin E is an important antioxidant; it sequesters free radicals before they can initiate peroxidation of the polyunsaturated fatty acids of cell membranes or cause damage to cell protein molecules
• Diets that contain a large amount of polyunsaturated fats (e.g. fish oil) require greater amounts of dietary vitamin E
• May be low in compounded rations due to storage and/or formulation (using vitamin poor feedstuff)
• Selenium is an essential constituent of the intracellular antioxidant enzyme glutathione peroxidase, which prevents peroxides from causing cell membrane damage through reduction into hydroxy acids
• Selenium is more soluble in alkaline and well-aerated soils and has more bioavailability as selenates in growing plants; selenium content is diluted in lush forage; geographic regions of US have low selenium contents in soil 
• Organic selenium has greater protection that inorganic selenium; most dietary selenium supplements are inorganic
• It is considered that it is the primary cause of myofiber degeneration as skeletal and cardiac muscle high demand for oxygen makes it most prone to the oxidative injury and highly depended on the glutathione peroxidase system.
• Decreased selenium increased physiological demand for Vitamin E. 
• Free radical generation with deficiency of free-radical scavengers such as vitamin E and selenium (protective through its role in glutathione peroxidase and other selenoproteins) à oxidative damage, loss of cell membrane integrity and stability, loss of ability to maintain ion gradients
• Calcium ions enter the damaged cell from the extracellular compartment à increased demand for energy to move calcium from cytosol into mitochondria away from calcium-sensitive myofilaments à mitochondria become overloaded with calcium à energy depletion à excess calcium the cytosol à myofibril hypercontraction and degeneration
• Steatitis (yellow‑fat disease) may result from a combination of membrane damage and production and deposition of ceroid
• Ceroid: Similar to lipofuscin but is associated with a pathologic (oxidative) process often associated with vitamin E deficiency;  
• Muscle fiber necrosis occurs due to the damage to sarcolemma leading to calcium ions influx and hypercontraction of myofibrils and necrosis of myofibers

 

CLINICAL FINDINGS:

• Nutritional myopathy:
  • Bright, alert, but with muscle stiffness, weakness or irregular gait
  • +/- lethargy
  • +/- intercostal muscle involvement à dyspnea
  • +/- myoglobinuria à coffee-colored urine
  • +/- lingual, pharynx, and masticatory muscles à dysphagia
• Possible acute death with no previous clinical signs
• Steatitis:
• Pyrexia, malaise; pain or hyperesthesia on palpation
• Clinical pathology:
• Elevated CK, LDH, AST, ALT (large animals)
• Plasma alpha-tocopherol levels < 3.5 umol/L
• Myoglobinuria is usually absent in young animals (less skeletal muscle)
• Serum glutathione peroxidase is a good indicator of selenium levels

 

GROSS FINDINGS:

• Nutritional myopathy:
  • Bilaterally symmetrical lesions
  • Multifocal pale streaks parallel to fiber direction
  • Marked mineralization of skeletal/cardiac muscle
  • Heart lesion is seen frequently on the sub- epicardial and endocardial surface
• Steatitis:
  • Yellow to yellow-brown subcutaneous and cavitary fat
  • Firm, lumpy, gritty fat 
  • Subcutaneous edema
  • Fishy odor

 

LIGHT MICROSCOPIC FINDINGS:

• Nutritional myopathy:
  • Selective, random, segmental and polyphasic necrosis of myofibers +/- mineralization; myocyte degeneration (hyaline degeneration, loss of cross striations, segmental fiber fragmentation); basement membrane and satellite cells remain intact allowing for rapid myocyte regeneration
  • Unlike skeletal muscle, necrotic cardiomyocytes do not regenerate and are replaced by fibrous stroma 
  • Preferentially, but not exclusively, involves type I muscle fibers 
  • EM: Earliest detectable change it the degeneration of mitochondria
  • Nutritional steatitis:
• Edematous fat with areas of coagulative necrosis and infiltration by neutrophils, lymphocytes, macrophages, and multinucleate giant cells
• Ceroid deposition between adipocytes; found within macrophages of the liver, spleen, and lymph nodes; ceroid appears as yellow pigment and is positive for Sudan black, PAS, and acid-fast; immunohistochemistry may differentiate ceroid from lipofuscin but is a very laborious research tool and generally not used 

 

DIFFERENTIAL DIAGNOSES:

• Myodegeneration:
• Toxic myopathies (monensin [M-T01], Cassia [M-T02], Xanthium)
• Inherited muscular dystrophy (M-M06)
• Sarcocystosis (M-P04)
• Exertional rhabdomyolysis (M-M14; typically monophasic pattern)
• Steatitis: 
• Fat necrosis: Trauma, pancreatic enzymatic necrosis
• Cats: Sterile nodular panniculitis, lupus panniculitis

 

COMPARATIVE PATHOLOGY:

Vitamin E/selenium deficiency in other species:

• In order of susceptibility to vitamin E/selenium imbalance: cattle, sheep, pig > horse, goat > cat, dog
• Large domestic animals (cattle, pigs, sheep are most commonly affected by nutritional myopathy, also horses and goats): often it is actually selenium deficiency that is the cause of myofiber degeneration; most common in neonatal animals; affects striated muscle (both cardiac and skeletal)
  • Calves: 4-6 weeks of age, up to 6 months, then sporadically; precipitating event is unaccustomed physical activity that coverts subclinical to clinical disease; lesions found in left ventricle > right; large weight bearing muscles of the thighs and shoulders as well as tongue and neck of suckling calve; alopecia in calves seen with feeding of Vitamin E deficient milk substitute
  • Sheep: “White muscle disease”, “rigid lamb disease”, and “stiff lamb disease” terms used for spring lambs 2-4 weeks of age turned out onto first green pasture; similar muscles affected as in calves with the addition of respiratory muscles (diaphragm and intercostal); mineralization common
  • Horses: Foals up to 2 weeks of age; adults often present with trismus and inability to apprehend food due to temporal and masseter muscles that are swollen and stiff leading to impaired mastication, inappropriately termed “maxillary/masseter myositis”; presence of myocardial necrosis separates this syndrome from exertional, metabolic, and ischemic myopathy; diets low in Vitamin E can also cause equine degenerative myeloencephalopathy (N-M07), equine motor neuron disease (N-M24), and lipofuscin accumulation in the retinal pigmented epithelium with retinal degeneration
  • Foals may get nutritional panniculitis secondary to Vitamin E deficiency
  • Goats: Few reports; reared under less intensive agricultural practices; similar findings as in sheep;selenium deficiency can lead to periorbital alopecia and generalized seborrhea, this condition is described as Vitamin E responsive dermatosis
  • Pigs: 
  • Nutritional myopathy: Mostly in weaned pigs 6-20 weeks of age; skeletal muscle lesions microscopic; liver and heart lesions more prominent grossly; microscopically distinct central degeneration pattern within muscle fascicles
  • Hepatosis dietetica (see D-M10): Acute centrilobular to massive hepatic necrosis due to Vitamin E and Selenium imbalance with concurrent deficiencies of sulfur-containing amino acids; often in association with a combination of one or more of: nutritional panniculitis (yellow fat disease), nutritional myopathy, serous effusions (“exudative diathesis”), ulceration of the squamous mucosa of the stomach (pars esophagea), and mulberry heart disease
  • Mulberry heart disease: (see C-M06) (dietary angiopathy: Myocardial degeneration seen with Vitamin E and Selenium deficiency; important diagnostic feature is the fibrinoid necrosis of the arterioles seen in many organs
  • Nutritional panniculitis may occur secondary to Vitamin E deficiency
• Carnivores, primates, camelids: Nutritional myopathy is unusual, although: 
  • Cats and mink fed vitamin E-deficient diets develop steatitis (yellow fat disease); associated with feeding of fishmeal which have high concentration on unsaturated fatty acids
  • Dogs: Intestinal lipofuscinosis (AKA leiomyometaplasia, brown dog gut) can be induced by vitamin E deficiency in association with excess dietary lipids; grossly tan to dark brown intestinal serosal surfaces; histologically, accumulations of brown, granular, acid-fast, gray to brown granules (leiomyometaplasts) in the cytoplasm of smooth muscle cells in the tunica muscularis; lipofuscin accumulation in the retinal pigmented epithelium and retinal degeneration
  • Cocker Spaniels dogs have inherited storage disease generalized ceroid-lipofuscinosis which has both intestinal lipofuscinosis and hindlimb paresis and incoordination
  • Wasting marmoset syndrome: Has been associated with low Vitamin E; presents with profound weight loss, muscle atrophy (type II fiber), “cage paralysis”, chronic diarrhea, hair loss, colitis, panniculitis, steatitis, hemolytic anemia; Vit. E administration prevents this condition
• Avian: 
  • Gizzard myopathy, bursal atrophy and lymphoid depletion seen with Vitamin E deficiency
  • Captive fish-eating birds most susceptible 
  • Mineralization is a key differentiator between nutritional myopathy and toxicosis
  • Fowl: Vitamin E deficiency (+/- interaction with synthetic antioxidants, selenium, and sulfur-containing amino acids) causes 3 distinct syndromes:
    • Avian encephalomalacia (crazy chick disease, see N-M28): Often gallinaceous birds; swollen cerebellum with soft, dark, and/or hemorrhagic areas (cherry red cerebellum); malacia most severe on the folial tips; cerebellar surface hemorrhage is striking in turkey poults; fibrin thrombi in blood capillaries are an important diagnostic feature; bilateral symmetric necrosis of the spinal cord gray matter  
    • Exudative diathesis: Severe blood-stained edema of ventrum due to increased capillary permeability; pericardial effusion may cause sudden death; fluid may be green, brown, or red
  • “Muscular dystrophy”: Yellow-white skeletal muscle streaking of the breast, legs, +/- gizzard
  • Captive great-billed parrots have high incidence of vitamin E deficiency-associated muscle degeneration, encephalomalacia, gliosis, and neuronal necrosis primarily of the cerebellum
  • Ocular diseases, hyperkeratosis, and testicular and epididymal atrophy has been associated with Vitamin E deficiency
• Hamsters: Spontaneous hemorrhagic necrosis (SHN) of the CNS of fetal hamsters with necrohemorrhagic lesions most prominent in the prosencephalon, has been reproduced by feeding dams diets deficient in vitamin E
• Guinea pig: Nutritional myopathy is common and in some cases there is a clear relationship to selenium/vitamin E deficient diets; fetuses born to vitamin E-deficient sows may develop encephalomalacia
• Rabbits: Nutritional “muscular dystrophy”, neonatal mortality, infertility
• Wildlife, zoo animals: Multiple zoo animal species are susceptible to nutritional myopathy, but evidence is circumstantial; the Rottnest quokka (a small nocturnal wallaby), the nyala, Bazilian tapir are highly susceptible
  • Osteopathy with concurrent selenium deficiency reported in Patagonian huemul
  • Selenium deficiency which imparts bone growth though to be causative in periodontitis in ruminants
  • Vitamin E responsive hemolytic anemia and necrotizing myopathy seen in owl monkeys, marmosets, and gelada baboons
  • Hemolytic anemia and encephalomalacia reported in black rhinos
  • Pansteatitis seen in kiwis and red tailed hawks
• Rat and Mice: Cardiomyopathy seen due to vitamin E deficiency.

 

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