Diseases / List of Miscellaneous / Metabolic / Multifactorial Diseases / Disease description:

Capture Myopathy (with special reference to Waterfowl and Cranes, and notes on Elephants)

INFORMATION AVAILABLE

GENERAL INFORMATION

CLINICAL CHARACTERISTICS & PATHOLOGY

INVESTIGATION & DIAGNOSIS

TREATMENT & CONTROL

SUSCEPTIBILITY & TRANSMISSION

ENVIRONMENT & GEOGRAPHY

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General and References

Disease Summary

GENERAL

Usually acute, signs vary from muscle stiffness to paralysis, sometimes with cardiac and/or respiratory signs, and death; may develop following capture or other physical stress.

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Alternative Names (Synonyms)

  • Exertional Myopathy
  • Stress Myopathy
  • Exertional Rhabdomyolysis
  • Overstraining Disease
  • Polymyopathy
  • White Muscle Disease
  • Transport Myopathy
  • Spastic Paresis
  • Muscle Necrosis
  • Leg Paralysis
  • Muscular Dystrophy
  • Degenerative Myopathy
  • Idiopathic Muscle Necrosis
  • White Muscle Stress Syndrome

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Disease Type

 Miscellaneous / Metabolic / Multifactorial

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Infectious/Non-Infectious Agent associated with the Disease

  • Physiological imbalances following excessive exertion, struggle and stress, frequently associated with capture, confinement and transport, particularly if a prolonged chase or struggling occurs. May occur associated with both physical capture and chemical immobilisation.
  • Intense muscular activity leads to anaerobic glycolysis, elevated lactic acid levels and metabolic acidosis. Also increased plasma potassium (hyperkalaemia) and catecholamine release, together resulting in reduced cardiac output, reduced tissue perfusion, severe muscle hypoxia and necrosis.
  • Selenium deficiency or vitamin E deficiency may predispose to the development of capture myopathy.
  • Has been seen in waterfowl struggling due to salt encrustation in hypersaline lakes. (B20.16.w13)

(B15, B20.16.w13, B35.9.w3, B36.51.w51, B39.w2)

  • In at least one crane following entrapment in mud. (P87.9.w3)

Infective "Taxa"

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Non-infective agents

Physical agents

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References

Disease Author

Debra Bourne MA VetMB PhD MRCVS (V.w5); Gracia Vila-Garcia DVM, MSc, MRCVS (V.w67)
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Major References / Reviews

Code and Title List

B20.16.w13, B36.51.w51, B39.w2
J1.23.w10, J1.23.w11

Waterfowl:
B15

J1.23.w2, J1.29.w9, J7.48.w1
P4.1992.w1
V.w6

Elephants:
B20
.16.w13, B35.9.w3, B214.3.7.w3

Cranes:
B12.56.w14, B115.8.w4, B703.10.w10
J1
.19.w11, J1.39.w6, J2.36.w3, J312.21.w2
P1.1981.w6, P1.1989.w2, P20.1998.w12, P87.7.w8, P87.9.w3, P87.9.w5

Other References

Code and Title List

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Clinical Characteristics and Pathology

Detailed Clinical and Pathological Characteristics

Variable from hyperacute to chronic; paresis, paralysis or sudden death, usually with pale lesions in skeletal and sometimes cardiac muscle.

Clinical Characteristics

IN MAMMALS/BIRDS IN GENERAL
  • Variable, depending on time course and severity. Elevated body temperature, increased heart rate and respiratory rate, depression, decreased responsiveness, ataxia and incoordination, weakness, muscle stiffness, tremors, torticollis, recumbency, shock and death may be noted. Four syndromes have been described:
  • Hyperacute: collapse and death within minutes of capture (cardiac fibrillation and circulatory collapse).
  • Acute: muscular stiffness, depression, increased heart rate, increased respiratory rate, death may occur in about 12 hours from pulmonary oedema.
  • Subacute: paresis or paralysis, may die from renal failure.
  • Chronic/ 'delayed peracute': sudden death, following a second stressful event several weeks after the original capture or stress.

(B15, B20.16.w13, B35.9.w3, B39.w2).

WATERFOWL
  • Stiffness, reluctance to fly, inability to fly, inability to walk and limb paralysis have been noted in waterfowl with capture myopathy. Depression was noted in some waterfowl, while others appeared bright and alert (J1.23.w2, J7.48.w1, B15, B35.9.w3, P4.1992.w1)
  • Clinical pathology: Raised creatine kinase (CK) and aspartate aminotransferase AST. Normal levels are CK less than 250 IU/litre, AST less than 20 IU/litre. May be dramatic increase, e.g. in affected Black-bellied whistling duck Dendrocygna autumnalis CK 23,680 IU/litre at 48 hours after capture, compared to 862 IU/litre in the clinically normal mate which had been captured simultaneously and 93-525 IU/L in four other ducks sampled (J1.23.w2, J1.29.w9, J7.48.w1).
CRANES
  • Variable clinical signs:
    • Peracute death (cardac failure);
    • Painful, stiff movements, swollen, hard muscles (warm to the touch);
    • Limb trauma due to struggling. (B12.56.w14)
    • After several days, weight loss and loss of fat stores. (B115.8.w4)

    (B12.56.w14, B115.8.w4, B703.10.w10)

  • Ataxia, paresis, paralysis. (J1.39.w6)
  • Inability to fly (unable to attain normal lift). (J1.39.w6)
  • Inability to rise from sternal recumbency or hock-sitting. (J1.39.w6)
  • Unusual posture (e.g. on back or side) and inability to recover from that posture. (J1.39.w6)
    • Clinical pathology:
      • Highly elevated creatinine kinase, lactic dehydrogenase and aspartate aminotransferase associated with muscle damage. (B12.56.w14, B115.8.w4, J1.39.w6)
      • Uric acid levels may be increased associated with renal failure due to increased lactic acid production, myoglobinuria and/or dehydration subsequent to reduced mobility. (B12.56.w14, B115.8.w4)
      • Elevated alanine aminotransferase. (B703.10.w10)

Cases:

  • In a wild greater sandhill crane Grus canadensis tabida (Grus canadensis - Sandhill crane) following capture by rocket netting and restraint for about one hour: (J1.19.w11)
    • Minimal movement in the four days after release (remained within 0.5 km); found dead on the fifth day. (J1.19.w11)
  • In four young adult Balearica regulorum - Grey crowned-crane after restraint (wrapped in burlap, with the legs flexed and tucked under the body for up to six hours) and anaesthesia for partial wing amputation, one bird was unable to stand when released back into its enclosure, and the others showed leg weakness and inability to stand after two to 10 days. The cranes sat and walked on their hocks. Initially they appeared generally bright, eating and drinking, but they gradually deteriorated and died at 15-16 days (three birds) while the fourth appeared to recover after six days, became ambulatory for three weeks, then became recumbent again and died. (P1.1981.w6)
    • Clinical pathology: greatly elevated creatine phosphokinase, lactate dehydrogenase and serum glutamic oxaloacetic transaminase. Elevated CPK was noted also in another individual restrained for about six hours which did not show clinical signs of capture myopathy. (P1.1981.w6)
  • A wild greater sandhill crane Grus canadensis tabida (Grus canadensis - Sandhill crane) was found unable to stand the day after capture using alpha-chloralose followed my manual restraint. (P20.1998.w12)
  • In a six-month-old Grus americana - Whooping crane, ataxia and inability to stand after restraint and handling; the crane remained alert but was found dead within 14 hours of handling. (J2.36.w3)
    • Clinical pathology: Initilly normal; not sampled again before death. (J2.36.w3)
  • In a five-month-old Grus americana - Whooping crane which had collided with an ultralight aircraft and become entangled in its rigging for two minutes before being freed, collapse into sternal recumbency after standing briefly, weakness and ataxia, initially able to stand but with progressive leg weakness and stiffness, developing to inability to stand, toe knuckling, and development of spastic leg movements by day 12; the crane was then euthanised. (J2.36.w3)
    • Clinical pathology: Initially (two hours post trauma) hyperkalaemia and raised pH; later (days four and nine) hypoproteinaemia, hyperkalaemia, elevated ALT, AST, CK and LDH. (J2.36.w3)
  • In a 16-month-old Grus americana - Whooping crane released the previous year, following capture and restraint in hot weather, initial slow, careful walking, collapse into sternal recumbency 30 minutes post release. Development of anorexia and dehydrated necessitated tube feeding. Inability to weight-bear on the legs progressed to tarsal rigidity and toe knuckling. Euthanased on day 12 following development of respiratory problems due to food regurgitation and aspiration. (J2.36.w3)
    • Clinical pathology: elevated ALT, AST, CK and LDH on day of capture and on days three and eight; hyperkalaemia and raised uric acid on days three and eight. (J2.36.w3)
  • Of 56 wild greater sandhill cranes (Grus canadensis - Sandhill crane) captured using alpha chloralose followed by manual restraint, two adults were alert but unable to stand the day after capture, and could stand only briefly when placed on their feet at 48 hours. A juvenile was hock-sitting and alert but unable to stand at 24 hours after capture. (J312.21.w2)
    • Creatine kinase (CK, aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) enzymes were all raised, with CK peaking in the juvenile at three days post capture while by day seven levels were half that at 24 hours post capture; levels in the adult female reached 353,520 U/L at three days and levels in the male appeared to show a similar trend (less samples taken). In the juvenile, AST and LDH varied, with a rise from day 1 to 2, a fall to day three then a further rise before falling (and another rise in AST at day seven). In the female, AST and ADH appeared to peak about day three. AST was still higher than reference at the time of release in all three cranes. (J312.21.w2)
ELEPHANTS
  • Inability to rise. (B214.3.7.w3)
  • Urine severely haemorrhagic. (B214.3.7.w3)
  • Death the following day. (B214.3.7.w3)

Clinical pathology:

  • Myoglobinuria detected. (B214.3.7.w3)

Incubation

Minutes or hours to days or weeks (B15, B20.16.w13, B35.9.w3, B39.w2).

Mortality / Morbidity

Sporadic incidence. High mortality if clinically apparent (B20.16.w13).

Pathology

IN MAMMALS/BIRDS IN GENERAL

Gross Pathology: lesions are typically bilateral but not symmetrical.

  • Acute: slight pallor of skeletal muscles, hepatic congestion, pulmonary congestion.
  • Subacute: pale, dry, friable muscles. Pale streaking in heart muscle (J1.23.w2, J7.48.w1).
  • Chronic: areas of fibrosis in skeletal and cardiac muscle.
  • Note: In at least some species, lesions of capture myopathy may not be evident at gross necropsy. (J1.23.w10)

Histopathology:

  • Acute: lysis and fragmentation skeletal muscle fibres, pulmonary congestion and oedema, centrilobular hepatic degeneration.
  • Subacute: swelling, hyalinization, lysis and disintegration of skeletal muscle fibres, mineralization of necrotic tissue, hyalinization and fibre fragmentation in cardiac muscle, may be necrotic foci in muscle.
  • Chronic: severe myofibril degeneration and necrosis; associated mineralization and interstitial hypercellularity – fibroplasia, macrophages, sometimes multinucleate giant cells. Dense fibrous connective tissue scarring.

(B15, B20.16.w13, B35.9.w3, B39.w2).

WATERFOWL Gross Pathology:
  • Skeletal muscle - Pale streaking to extensive pale, dry areas, particularly leg muscles and deep pectoral muscles.
  • Heart muscle - Pale streaks.

Histopathology:

  • Skeletal muscle - Severe degeneration of myofibres with hyalinization and fragmentation of fibres. Necrosis associated with mineralization and hypercellularity of interstitial areas.
  • Heart - Hyaline degeneration and necrosis of myocardial fibres.
  • N.B. lesions more apparent in individuals surviving longer.

(J1.23.w2, J7.48.w1, B15).

CRANES Gross pathology
  • Skeletal muscles and cardiac muscle: pale, streaked areas. (B115.8.w4)
  • Renal lesions (e.g. urate nephropathy). (B115.8.w4)
  • In a wild greater sandhill crane Grus canadensis tabida (Grus canadensis - Sandhill crane) following capture by rocket netting and restraint for about one hour: (J1.19.w11)
    • General: Severe weight loss (from 5.25 kg five days earlier down to 3.8 kg), complete absence of subcutaneous fat and marked pectoral muscle atrophy. (J1.19.w11)
    • Muscular: In the biceps femoris muscles, bilateral areas of pale streaking. (J1.19.w11)
    • Renal: Kidneys pale and mottled. (J1.19.w11)
    • Splenic: Spleen congested. (J1.19.w11)
  • In a three-year old, captive-reared Mississippi sandhill crane (Grus canadensis - Sandhill crane) found caught in a leg-hold trap two years after release. (P1.1989.w2)
    • Muscular: Pale streaked areas in the skeletal muscles. (P1.1989.w2)
  • In four young adult Balearica regulorum - Grey crowned-crane after restraint: (P1.1981.w6)
    • General: Fat depletion.
    • Muscular: Tibial, particularly the gastrocnemius muscles, were pale, with extensive yellow-white streaking.
    • Cardiac: In one bird, streaking of the ventricular myocardium.
    • Renal: In one bird, grossly visible urate deposition in the kidneys.
  • In a six-month-old Grus americana - Whooping crane,no significant gross lesions, but haemorrhages in one lobe of the thymus at the thoracic inlet. (J2.36.w3)
  • In a five-month-old Grus americana - Whooping crane: (J2.36.w3)
    • Muscular: Muscles of the legs, around the shoulder joints and elbows, and along the base of the neck, were diffusely pale or pale streaked, some with fine, white chalky streaks. (J2.36.w3)
      • Hip flexors and rotators, stifle flexors, and hock and digit flexors and extenders were most severely affected. (J2.36.w3)
  • In a 16-month-old Grus americana - Whooping crane: (J2.36.w3)
    • Muscular: Leg muscles (those moving the hip, stifle, hock and digit) diffusely pale or pale-streaked. Pectoral muscles (superficial and deep, near the shoulders) pale streaked. 
    • GIT: Proventriculus and ventriculus impacted with food and sawdust. 

Histopathology

  • Skeletal muscle and cardiac muscle: degeneration and necrosis with secondary inflammation. (B115.8.w4)
  • In a wild greater sandhill crane Grus canadensis tabida (Grus canadensis - Sandhill crane) following capture by rocket netting and restraint for about one hour: (J1.19.w11)
    • Muscular: Severe necrosis. Swollen myofibres; cytoplasm fragmented and in some fibres slightly mineralised. In a few fibres, proliferation of nuclei. Within a given primary bundle, all or only a single fibre were affected. (J1.19.w11)
    • Renal: Centrilobular congestion, moderately severe nephrosis; in some distal convoluted tubules and collecting ducts, aggregates of eosinophilic debris (urate spherules) and partialy mineralised debris. In the interstitium and tubules, mild granulocytic infiltrate. (J1.19.w11)
  • In a three-year old, captive-reared Mississippi sandhill crane (Grus canadensis - Sandhill crane) found caught in a leg-hold trap two years after release. (P1.1989.w2)
    • Muscular: Severe diffuse necrosis and degeneration of 90-100% of myofibres. (P1.1989.w2)
  • In four young adult Balearica regulorum - Grey crowned-crane after restraint: (P1.1981.w6)
    • Muscular: Extensive myodegeneration and necrosis: loss of striations, hyaline degeneration, granular degeneration, segmental swelling of myocytes, central vacuolatio, nuclear pyknosis, sarcoplasmal fragmentation, aggregation of sarcolemmel cells, interstitial fibrosis. Also in some areas interfascial haemorrhage and oedema.
    • Cardiac: In one bird, myodegeneration and necrosis as in the skeletal muscles.
  • In a six-month-old Grus americana - Whooping crane with peracute myopathy: (J2.36.w3) 
    • Muscular: In leg and pectoral muscles, individual myofibres, widely dispersed, were necrotic: lack of striations, swollen, with hyaline or flocculent degeneration. (J2.36.w3)
  • In a five-month-old Grus americana - Whooping crane: (J2.36.w3)
    • Muscular: In skeletal muscles, 70-90% of myofibres were necrotic or regenerative, with normal fibres or bundles interspersed. Most affected areas were highly cellular, with macrophages, myoblasts and narrow regenerative myofibres which contained rows of nuclei. A few necrotic, hyalinised or fibrotic fibres remained, most of which were mineralised. The regenerating areas were moderately disorganised with clustered nuclei in the centre of globoid regenerative fibres, indicating a non-ideal regenerative response. (J2.36.w3)
    • Cardiac: Left ventricular myocardial focus of fibroplasia and mineralisation. (J2.36.w3)
  • In a 16-month-old Grus americana - Whooping crane: (J2.36.w3)
    • Muscular: In skeletal muscles, up to 100% of myofibres were necrotic or regenerative. Some persistent necrotic fibres with diffuse mineralisation. Small foci of fibroplasia were found. (J2.36.w3)
    • Cardiac: Left ventricle, one small necrotic focus. (J2.36.w3)
    • Renal: Renal tubular epithelial cells contained golden cytoplasmic granules, suggesting occurrence of myoglobinuria. (J2.36.w3)
    • GIT: Oesophageal and proventricular muscle, mineralised foci and aggregations of multinucleated giant cells (either due to or the cause of the gastric impaction). (J2.36.w3)
    • Respiratory: Chronic laryngitis with bacterial and fungal infection (indicative of aspiration). (J2.36.w3)
ELEPHANTS --

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Human Health Considerations

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Susceptibility / Transmission

General information on Susceptibility / Transmission

  • A wide variety of bird species appear to be susceptible, as well as mammals. May also occur in amphibians and fish.
  • Nervous and/or wild individuals may be more susceptible than calm and/or tame individuals.
  • Individuals with marginal vitamin E/Selenium levels may be more susceptible.
  • Fear, stress, anxiety, overexertion, hyperthermia, metabolic acidosis and vitamin E/selenium deficiency all have been associated with development of capture myopathy.

(B20.16.w13, B35.9.w3, J1.23.w11, J2.36.w3)

Waterfowl:

  • Capture myopathy has been seen in waterfowl struggling due to salt encrustation in hypersaline lakes (B20.16.w13).

Cranes:

  • Cranes, as with other long-legged birds, may be relatively susceptible to capture myopathy. (P1.1989.w2, B12.56.w14)
  • Susceptibility may be increased in hot conditions. (J1.39.w6, J2.36.w3)
  • When seen in cranes during capture using Alphachloralose Sedation, it was noted that individuals more lightly sedated were more likely to develop capture myopathy. (P87.9.w5)

Elephants:

  • For Loxodonta africana - African Elephant being translocated within Africa, is has been noted that development of capture myopathy is more likely in individuals with metabolic acidosis due to recent dietary change (which occurs when there is a flush of vegetation after rains) or when elephants run excessively during the capture process. (B459.A.w3)

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Disease has been reported in either the wild or in captivity in:

[N.B. Miscellaneous / Traumatic Diseases tend to be under-reported and the majority are likely to affect all species, given exposure to the related disease agents/factors.]

GENERAL:

  • Capture myopathy has been reported in a wide variety of species of mammals and birds and particularly in deer (cervidae) and other ungulates. (B20.16.w13, J1.23.w11, P8.3.w3)

BIRDS

Waterfowl:

  • Snow goose Anser caerulescens and Ross’s goose Anser rossii, associated with rocket-net capture, holding for banding and being kept penned overnight. (B15).
  • Canada geese Branta canadensis trapped by salt encrustation on a hyper-saline lake (J1.23.w2).
  • Black-bellied whistling duck Dendrocygna autumnalis after 'strenuous' capture for transfer between collections (J7.48.w1).
  • 'Various waterfowl' struggling due to salt encrustation in hypersaline lakes (B20.16.w13).
  • Canada geese Branta canadensis following driving, trapping, handling and translocation (B35.9.w3).

Cranes:

  • Four young adult Balearica regulorum - Grey crowned-crane after restraint (wrapped in burlap, with the legs flexed and tucked under the body). (P1.1981.w6)
  • A wild greater sandhill crane Grus canadensis tabida (Grus canadensis - Sandhill crane) following capture by rocket netting and restraint for about one hour. (J1.19.w11, Th12)
  • Suspected in a wild young-of-the-year Grus americana - Whooping crane, with rapid breathing, appearing anxious, with its legs wrapped to its body, and suffering a "shock like death", following capture for banding in hot weather (about 30 C). (P1.1988.w1)
  • In Grus americana - Whooping cranes at Patuxent Wildlife Research Center, 1982-1995, capture myopathy was diagnosed as the cause of death in one chick and one adult (2/103 total fatalities). (P87.7.w8)
  • A wild greater sandhill crane Grus canadensis tabida (Grus canadensis - Sandhill crane) was found unable to stand the day after capture using alpha-chloralose followed my manual restraint. (P20.1998.w12)
  • A three-year old, captive-reared Mississippi sandhill crane (Grus canadensis - Sandhill crane) found caught in a leg-hold trap two years after release. Additionally, Aspergillosis was noted, which probably contributed to the crane's death. (P1.1989.w2)
  • In 3.7% of Grus canadensis - Sandhill crane captured by sedation with oral alpha-chloralose; this was seen in seven birds during 188 captures, with four of the affected birds successfully treated and re-released. (J1.39.w6, P87.9.w5)
  • Three Grus americana - Whooping cranes, following (respectively) routine handling, collision with and entanglement with a microlight, and capture and handling the year after release. (J2.36.w3)
  • In Grus canadensis - Sandhill cranes which became trapped in mud, one crane which was rescued died due to capture myopathy. (P87.9.w3)

MAMMALS:

Elephants:

Loxodonta africana - African Elephant:

  • Capture myopathy has been reported in Loxodonta africana - African Elephant. (B20.16.w13, B35.9.w3)
  • Capture myopathy occurred in a female elephant following a long rail journey: "the intense muscular activity involved in attempting to free itself led to this muscle degeneration in an animal unaccustomed to exercise." (B214.3.7.w3)

Further information on Host species has only been incorporated for species groups for which a full Wildpro "Health and Management" module has been completed (i.e. for which a comprehensive literature review has been undertaken). Host species with further information available are listed below:

Host Species List

BIRDS 

MAMMALS

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Disease has been specifically reported in Free-ranging populations of:

[N.B. Miscellaneous / Traumatic Diseases tend to be under-reported and the majority are likely to affect all species, given exposure to the related disease agents/factors.]

BIRDS:

  • Snow goose Anser caerulescens, Ross’s goose Anser rossii, associated with rocket-net capture, holding for banding and being kept penned overnight. (B15).
  • Canada geese Branta canadensis trapped in a hyper-saline lake (J1.23.w2).
  • 'Various waterfowl' struggling due to salt encrustation in hypersaline lakes (B20.16.w13).
  • In Grus canadensis - Sandhill crane which became trapped in mud, one crane which was rescued died due to capture myopathy. (P87.9.w3)

MAMMALS:

Elephants:

Loxodonta africana - African Elephant:

Further information on Host species has only been incorporated for species groups for which a full Wildpro "Health and Management" module has been completed (i.e. for which a comprehensive literature review has been undertaken). Host species with further information available are listed below:

Host Species List

WATERFOWL 

MAMMALS

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Environment/Geography

General Information on Environmental Factors/Events and Seasonality

  • Hot weather (high ambient temperature) is recognized as a predisposing factor (B20.16.w13).
  • Has been seen associated with salt encrustation, in which considerable masses of salt may be deposited on the feathers, severely weighing down the bird (J1.23.w2, B20.16.w13).
  • Sometimes may be associated with areas with low levels of selenium in plants (B20.16.w13).

In cranes:

  • Either hot or cold weather may increase risks when cranes are captured with alpha chloralose (Alphachloralose Sedation of Cranes), as this drug can alter thermoregulation. (J1.39.w6)
  • Cranes may be more susceptible to development of capture myopathy if only lightly sedated with alpha chloralose (due to ingestion of only a small about of treated bait); this may occur when food resources are highly available post harvest. (J1.39.w6)

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Regions / Countries where the Infectious Agent or Disease has been recorded

Potentially worldwide. Recorded in waterfowl in North America. Reported in various mammal and bird species in Africa, UK, North America, Australia. (B20.16.w13, B35.9.w3).

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Regions / Countries where the Infectious Agent or Disease has been recorded in Free-ranging populations

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General Investigation / Diagnosis

General Information on Investigation / Diagnosis

  • History (pursuit, capture or restraint with struggling, and/or chemical immobilisation).
  • Clinical signs, clinical pathology, particularly raised creatine kinase and aspartate aminotransferase.
  • Gross and histopathological lesions.

(B35.9.w3)

  • Capture myopathy should be suspected after restraint of long-legged birds with the legs folded for long periods. (P1.1981.w6)
  • Cranes: 
    • In the field, suspect a problem such as capture myopathy in recently caught and released birds if the crane shows "inability to attain normal lift when attempting to fly, inability to stand from a sternal or hock sitting position, and inability to recover from an awkward position (i.e., on back or side)." (J1.39.w6)
    • Diagnosis is based on combinations of clinical signs of ataxia, paresis or paralysis; significantly elevated blood creatine kinase (CK), aspartate amintransferase (AST) or lactate dehydrogenase (LDH), or pathological findings of extensive skeletal/cardiac muscle necrosis. (J1.39.w6)

Related Techniques

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Similar Diseases (Differential Diagnosis)

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Treatment and Control

Specific Medical Treatment

Sodium bicarbonate 4 meq/kg body weight (0.32gm/kg) in balanced electrolyte solution, by intravenous or intraperitoneal injection over 5-10 minutes. Glucocorticoids, selenium/Vitamin E and vitamin B complex may be useful adjuncts to this treatment. (B20.16.w13, B35.9.w3).

Related Techniques

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General Nursing and Surgical Techniques

General supportive care: fluids (enteral and/or parenteral), dextrose, corticosteroids, NSAIDs, vitamin E, selenium, antibiotics, sodium bicarbonate and muscle relaxants have all been given; also physical support (appropriate bedding, slings, supplemental heat, turning to prevent further muscle damage, physical therapy). (B20.16.w13, J1.23.w11, J2.36.w3)
  • Both supportive care and physical therapy appear to be important for recovery. (J312.21.w2)

Cranes:

  • Note: Treatment is often unrewarding; prevention is important. (B12.56.w14, J2.36.w3)
  • Supportive care: intravenous fluids, corticosteroids, antibiotics, vitamin E, selenium, nursing care including sling support if required, and physical therapy. (B12.56.w14, B115.8.w4)
    • If blood pH is below normal, give intravenous sodium bicarbonate (if acidosis is suspected but values are not available, give sodium bicarbonate at 4-6 mEq/kg bodyweight). (B12.56.w14, B115.8.w4)
    • Initial corticosteroids (dexamethasone 1-2 mg/kg every 12 hours subcutaneously or intramuscularly for 1-2 days). (B703.10.w10)
    • Vitamin E/selenium (0.06 mg/kg selenium IM, MU-SE, Schering, Union, New Jersey, USA). (B703.10.w10)
    • Initial intravenous fluids, followed by subcutaneous fluids (60-180 mL lactated Ringer's solution) every 12 hours until the crane is drinking. (B703.10.w10)
    • Nutritional support with an easily-digested supplement e.g. Emeraid Nutri-support (B703.10.w10) or Ensure (Ross Products Division, Abbott Laboratories, Columbus, Ohio, USA) (J312.21.w2) by gavage using a red rubber feeding tube, until the crane is self-feeding. (B703.10.w10, J312.21.w2)
  • Supportive care, including supplemental heat, nutritional support, physical support (bedding, slings), frequent turning to prevent further muscle damage, physical therapy including range-of-motion exercises and assisted walking. (J2.36.w3)
    • In three greater sandhill cranes, successful treatment included physical therapy every 1-2 hours for chicks, every 8-12 hours for adults. (J2.36.w3)
  • In three wild greater sandhill cranes (Grus canadensis - Sandhill crane): (J312.21.w2)
    • For the first two days dexamethasone 1-2 mg/kg subcutaneously every 12 hours, with selenium/vitamin E 0.06 mg/kg intramuscularly on day one, repeated day seven in the juvenile and adult females. (J312.21.w2)
    • Fluids: Lactated Ringer's solution was given subcutaneously, 60-180 mL every 12 hours for the first 2 - 5 days. (J312.21.w2)
    • Nutritional support: Gavage feeding was carried out using 30-120 mL Ensure (Ross Products Division, Abbott Laboratories, Columbus, Ohio, USA) via a red rubber feeding tube, and 10-12 live minnows were force-fed to each crane daily. (J312.21.w2)
      • The male was self-feeding on minnows from a small pool by day six, after which assisted feeding stopped. (J312.21.w2)
      • Note: nutritional support was essential; despite this support, the male (the first to be treated) lost 1.25 kg; the female lost 0.5 kg and the juvenile 0.35 kg. (J312.21.w2)
    • Physical therapy:  (J312.21.w2)
      • For the juvenile, initially, days 1-3, placed on its feet every time it was found in sternal recumbency. On day 4, the crane appeared weaker and unable to stand for more than a few minutes, drooping its wings and appearing to have problems balancing. thereafter every 1-2 hours during the day its legs were moved manually, assisted walking was carried out, and it was placed in a hock-sitting position. By day nine it was able to stand and balance for 1-2 hours at a time; on day 11 it stood for 12 hours and on day 12 it rose to its feet independently, but when taken to its place of origin (female parent foraging nearby), fell and was unable to rise. It was returned to rehabilitation with further gavage feeding, and released successfully on day 15, close to where its female parent and other cranes were foraging, and was observed foraging with and flying with the flock for the next two days, but was not seen thereafter. (J312.21.w2)
      • For the adults, assisted walking 2-3 times daily, using a towel to support the body, and passive movement of the legs. Leg strength increased in the male of days 7-11; he was able to stand and walk by day 12, and was released on day 17, by which time he was pacing and wing-flapping. In the female, leg strength increased over days 5-7, she was able to stand and walk on day eight and was released on day 10, by which time she was pacing and wing-flapping. Both adults were seen with their mates within two weeks of release and survived and reared chicks in following years. (J312.21.w2)
  • Note: Continued deterioration indicates a poor prognosis; euthanasia may be required if there is no obvious improvement after about 12 days. (J2.36.w3)

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Preventative Measures

Vaccination

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Prophylactic Treatment

  • Use shade and/or water to cool individuals becoming hyperthermic during handling (B20.16.w13).
  • Ensure diets contain adequate levels of Vitamin E /Selenium (V.w6)

Cranes

  • Note: holding wild cranes overnight in a quiet pen in which they can be watched without disturbing them may be advantageous following capture and restraint, to detect effects of myopathy that might not be visible immediately, thereby reducing the risk of affected cranes being released prematurely and dying following release. (J312.21.w2)

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Environmental and Population Control Measures

General Environment Changes, Cleaning and Disinfection

  • Organise capture to minimise chase-time, struggling, time with human contact, amount of struggling and heat stress. Blindfolds may be useful.
  • Avoid arranging captures in hot weather.
  • Use adequate anaesthesia rather than physically restraining a struggling, partially-sedated animal.
  • Ensure appropriate crate sizes (including adequate room for the animal to stand) and transport conditions.
  • If vitamin E or selenium status is considered low or borderline, supplement before immobilisation or transport.

(B20.16.w13, B35.9.w3, J1.23.w11)

In cranes:

  • Take particular care when trapping, handling, chemically immobilising or transporting cranes. (B12.56.w14, B115.8.w4)
  • Minimise handling. (B115.8.w4)
  • Avoid restraint of cranes and other long-legged birds with the legs folded for long periods. (P1.1981.w6)
  • Avoid excessive chasing, particularly in hot weather. (P1.1988.w1, J2.36.w3)
  • Conduct procedures in cool conditions if possible. (J2.36.w3)
  • Ensure correct handling and restraint, with proper leg positioning. (B115.8.w4, J2.36.w3)
  • Ensure correct transportation. (B115.8.w4)
  • Provide adequate dietary vitamin E and selenium. (B115.8.w4)
  • Minimise stressors, including using hoods. (J2.36.w3)
  • Avoid development of hyperthermia if possible, and treat this promptly if it occurs. (J2.36.w3)
  • If anaesthetising, ensure an adequate plane of anaesthesia. (J2.36.w3)
  • Ensure transport arrangements are appropriate. (J2.36.w3)
  • Avoid catching wild cranes using alpha chloralose (Alphachloralose Sedation of Cranes) in hot weather or cold weather. (J1.39.w6)
  • When catching cranes using alpha chloralose, take measures to achieve heavier sedation (light sedation may increase the risk of development of capture myopathy: (J1.39.w6)
    • avoid capture at times of the year when behavioural factors may make cranes more likely to ingest less of the drug; (J1.39.w6)
    • ensure the social group to be caught is consistently on the bait and remaining comfortably at the bait site for an hour before adding the drug to the bait. (J1.39.w6)

In elephants:

  • Avoid excessive chasing during capture. (B459.A.w3)
  • Avoid capturing individuals with metabolic acidosis due to recent dietary change (which occurs when there is a flush of vegetation after rains). (B459.A.w3)

Population Control Measures

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Isolation, Quarantine and Screening

  • Wild cranes should be monitored in the days after capture and release, so that development of problems such as capture myopathy can be detected and possibly treated. (J1.39.w6)
    • Note: holding wild cranes overnight in a quiet pen in which they can be watched without disturbing them may be advantageous following capture and restraint, to detect effects of myopathy that might not be visible immediately, thereby reducing the risk of affected cranes being released prematurely and dying following release. (J312.21.w2)
  • Avoid using alpha chloralose (Alphachloralose Sedation of Cranes) to re-capture cranes which have previously developed capture myopathy following capture, in case these individuals are intrinsically more susceptible to the development of this problem. (J1.39.w6)

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