08: Congenital Defects

Spastic paresis

Spastic contraction of gastrocnemius and superficial digital extensor

Demographic for spastic paresis

6 weeks - 1 year old

Cause of spastic paresis

Thought to be loss of normal inhibition of gamma motor neurons

CS of spastic paresis

Hyperextension of hock and stifle when bearing weight, but will let you flex the hind limb when they are laid down

Treatment for spastic paresis

Salvage or partial tibial nerve neurectomy

T/F: it is ok to breed your cow that had spastic paresis

NO, it is a recessive genetic disease

Spastic syndrome

Similar to spastic paresis

Demographic for spastic syndrome

3-7 year old cattle

CS of spastic syndrome

Hyperextension of hind limbs that progresses

Treatment for spastic syndrome

Salvage

Why might you have a hard time getting a cow with spastic syndrome through the commercial inspection process

It looks like neuro disease

Common congenital musculoskeletal disease in cattle

Arthrogryposis

If you have a calf with arthrogryposis, what else should you look for

Additional congenital defects: cleft palate, scoliosis, hydranencephaly

Causes of arthrogryposis

• Viral: BVD, Bluetongue, etc.

• Genetic

• Toxins: lupine, Sudan grass, senecio, locoweed

CS of arthrogryposis

Flexural, articular, and rotational deformities that are rigid and cannot be moved

Treatment for arthrogryposis

None, avoid similar breeding

Tibial hemimelia

Bilateral lack of development of the tibia

CS of tibial hemimelia

Short limb with no firm attachment to the upper limb

Other defects commonly seen with tibial hemimelia

Abdominal hernia and incomplete closure of the CNS

Muscular hyperplasia AKA double muscling

Increased number of normal sized muscle fibers

Cattle breeds that may carry genes for muscualr hyperplasia

• Piedmontese

• Belgian white & blue

• Charolais (largely bred out)

• Angus (largely bred out)

Primary disadvantages associated with muscular hyperplasia

• Dystocia → C-section basically required

• Underdeveloped repro system and delayed puberty

• Not super hardy

Nutritional myodegeneration AKA white muscle disease

Degradation and oxidative damage of muscle fibers

Cause of white muscle disease

Low selenium and vit E

Dietary predisposing factors for white muscle disease

• Acidic or volcanic soil

• High sulfur → inhibits Se uptake by plants

• Prolonged grain storage → decreases vit E

• Milk replacer with high PUFAs → increased vit E requirement

Areas in the United States with low soil selenium concentration

East and west coasts

Form of white muscle disease that will cause sudden death

Cardiac form

Form of white muscle disease that has a slower onset

Skeletal form

CS of skeletal form of white muscle disease

• Weak muscles, tremors

• Stiffness

• Swollen, firm, and painful muscles

• ± Might only be able to stand for short periods

• Resp distress if diaphragm and intercostal muscles are affected

Diagnosis for white muscle disease

• Increased muscle enzymes

• ± Myoglobinuria

• Low serum Se and vit E

Necropsy findings associated with white muscle disease

Pale, dry, white streaks in skeletal or cardiac muscles

Treatment for white muscle disease

Supplement Se and vit E

Effective ways to supplement Se and vit E

• Ration/mineral mix

• Intra-ruminal Se bolus

• Se injections

Primary cause of blackleg

Clostridium chauveoi

Blackleg pathogenesis

C. chauveoi spores ingested → migrates to lay dormant in muscles → trauma or ischemic environment → sporulation → production of necrotizing and hemolyzing toxins → more ischemia → viscous cycle

Likelihood of seeing a blackleg case alive

Not common, usually acute death

If you get a live blackleg case, what CS might you see

• Lame

• Febrile

• Systemically ill

• Swollen muscles

• Recumbent

Necropsy findings associated with blackleg

• SQ/muscular emphysema (abnormal in a fresh carcass)

• Black, dry muscle tissue

• Unique odor

• Large G+ rods on smear

Treatment for blackleg

Not recommended, but can try high doses of penicillin and muscle incisions to aerate tissues

Prognosis for blackleg

No bueno

T/F: we can readily prevent blackleg

Sure can: vaccines and good handling

Injury associated with large animals that are down for a while

Ischemic muscle and nerve injury

How soon can a large animal get crush syndrome from laying on a hard surface

6 hours

Diagnosis for crush syndrome

• Firm, swollen muscles

• Loss of function

• Increased CK and AST

Of the muscle enzymes, which one increases and decreases faster

CK

Treatment for crush syndrome

• Treat underlying cause for prolonged recumbency

• Soft bedding

• Frequent recumbency changes

• Slings, hip lifts, float tank

Secondary issue to avoid with crush syndrome

Get the CK down to avoid kidney injury

Non-equine demographic for exertional rhabdomyolysis

Camelids and small ruminants

Predisposing factor for exertional rhabdomyolysis

Inconsistent exercise

CS of exertional rhabdomyolysis

• Stiffness

• Sore, swollen, painful muscles

• Increased CK and AST

Treatment for exertional rhabdomyolysis

Rest, IVF, NSAIDs, and time

Cause of porcine stress syndrome

Recessive inherited myopathy

Inciting events for porcine stress syndrome

Stress or halothane anesthesia

CS of porcine stress syndrome

• Muscle rigidity

• Malignant hyperthermia (>107F)

• Sudden death

How does porcine stress syndrome result in economic loss

Can result in pale, soft, exudative pork

Treatment for porcine stress syndrome

• Stop anesthesia

• Decrease body temperature

• Supportive care

Specie most likely to have ionophore toxicosis

HORSES

CS of ionophore toxicity

• Death

• Anorexia and pica

• Diarrhea

• Ataxia

• Dyspnea

Necropsy lesions associated with ionophore toxicity

• Fluid everywhere: hydrothorax, ascites, pulmonary edema

• Muscular necrosis