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Large Animal Medicine > Muscle Diseases of Ruminants > Flashcards

Muscle Diseases of Ruminants Flashcards

1
Q

How does clostridial myositis present?

A

BLACK LEG = subcutaneous emphysema

MALIGNANT EDEMA = leg is cold to the touch, swollen, and edematous

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2
Q

What are the 4 causative agents of clostridial myositis?

A
  1. Clostridium chauvoei = black leg
  2. C. septicum = malignant edema
  3. C. novyi = black disease
  4. C. sordellii = sord
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3
Q

How do cattle become infected with clostridium?

A

exist as spores worldwide in the soil and manure and can be ingested via grazing or infect wounds

  • macrophages engulf spores and bring them to tissues, where they will release toxins when an anaerobic environment develops
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4
Q

What causes clostridial myositis signs following infection?

A

ANAEROBIC ENVIRONMENTS - bruising from fighting

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5
Q

What ages of cattle are most commonly affected by clostridial myositis?

A

YOUNG and WELL-MUSCLED —> < 2 y/o, especially black leg (emphysema)

  • suspected due to larger muscle mass
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6
Q

Is it likely for this cattle to be affected by clostridial myositis?

A

no

  • not a good doer
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7
Q

What is indicative of classing black leg in cattle?

A

SQ emphysema - C. chauvoei

+/- sudden onset of death

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8
Q

What are the chances these calves died of black leg?

A

unlikely - laying together near a tree, outbreaks uncommon —> lightning?

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9
Q

How are cattle diagnosed with clostridial myositis antemortem and postmortem?

A

based on clinical signs

  • impression smears with large G+ rods
  • areas of black muscle necrosis that smell of rancid butter
  • culture and sensitivity of aspirates of affected tissue
  • PCR
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10
Q

What is the drug of choice for treating black leg? What 3 additional treatments are considered?

A

high dose of procaine penicillin G —> systemic + local

  1. NSAIDs for pain and inflammation
  2. skin incisions to oxygenate the area
  3. humane euthanasia - slaughter not an option, need to prevent further cases rather than save one
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11
Q

What 2 populations should be vaccinated for black leg? What population is this not necessary in?

A
  1. pregnant cows 1-2 months from calving
  2. calves less than 2 years (can have maternal Abs up to 6 months)

older cattle > 2 y/o —> immunity due to exposure

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12
Q

How long does it take for the black leg vaccine to provide protection? What else can be done to protect young stock while waiting for vaccine protection?

A

2 weeks

prophylactic antibiotic treatments (PPG)

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13
Q

Is routine vaccination of herds for black leg economical? Is one sufficient?

A

YES —> only need to vaccinate susceptible populations

unlikely, recommended vaccinate 2 times a year

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14
Q

What time of year is associated with higher chances of clostridial myositis development?

A

late summer to early winter

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15
Q

How should bodies be properly handled following death from clostridial myositis?

A

burned or buried deep and covered with lime

  • filled with clostridium spores that can contaminate the pasture
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16
Q

What is clostridial myositis prognosis like?

A

guarded to grave —> even if animal survives, it can be permanently disabled

17
Q

What is a common development in downer cows? How does this develop?

A

crush syndrome

increased intramuscular pressure and muscle swelling blocks drainage of venous blood from muscles, leading to ischemic necrosis (hopeless prognosis at this point)

18
Q

How is crush syndrome relieved? What can be seen on necropsy?

A

get downer off of the muscles —> float tank, hip lift, sling, rolling (can be used to diagnose any neurologic disease)

blackened necrotic muscle

19
Q

What is the most common cause of nutritional myodegeneration in cattle? What 2 syndromes develop?

A

white muscle disease = dietary deficiency of selenium and/or vitamin E

  1. cardiac - sudden onset, death
  2. skeletal
20
Q

How does the skeletal form of white muscle disease compare to the cardiac form? How do these animals present?

A

slower onset of muscle weakness, stiffness, and trembling in limbs

  • swollen, hard, painful muscles of front and hindlimbs
  • recumbency, unable to stand
  • respiratory distress with increased abdominal effort due to DIAPHRAGM and INTERCOSTAL muscle involvement
21
Q

What are 3 signs of white muscle disease on clinical pathology? What is highly suggestive?

A
  1. elevated SCPK (CK) to the 1000s
  2. low whole blood selenium levels
  3. low glutathione peroxidase

history of typical clinical signs and lack of supplementation

22
Q

Where in the US is white muscle disease most common?

A

COASTAL STATES and river bottom pastures —> selenium is leeched into the water from the soil

  • most common in calves 2-4 months of age (young and rapidly growing!) during the spring and summer months
23
Q

What form of white muscle disease is amendable to treatment? What treatment is recommended?

A

skeletal

selenium products —> BO-SE (1 mg/kg in calves), MU-SE (5 mg/mL in adults)

24
Q

What is able to block selenium uptake?

A

sulfur blocks its uptake into the forage on pasture cows would be getting it from

25
Q

How is white muscle disease prevented, especially in selenium-deficient areas?

A

availability of selenium mineral content to herd all year round

  • intraluminal bolus
  • long-term selenium injections are labor-intensive
26
Q

How do cattle present with bilateral ruptures gastrocnemius?

A

plantigrade (dropped) hock with no weight bearing —> when hock is pulled on exam, stifle will not move

  • hopeless prognosis
27
Q

What is indicative of peroneus tertius rupture in cattle? What is the most common cause of this?

A
  • skidding/dragging of hindleg causes irregular wearing on the claws on the top
  • no resistance to pulling on legs

roping injury - yanking on leg

28
Q

What causes gossypol toxicosis? In what large animals is this most common?

A

infection of cottonseed feed (common protein)

swine (can affect cows!)

29
Q

What are the 2 major signs of gossypol toxicosis? What can be protective?

A
  1. cardiotoxic - diffusely pale, flaccid, dilated chambers
  2. multifocal myocardial and skeletal muscle necrosis

iron

30
Q

What are the major differentials for gossypol toxicosis?

A
  • monensin
  • selenium/vitamin E deficiency
31
Q

In what animals is doubling muscle (muscular hypertrophy) common? What does it commonly lead to?

A
  • Belgian Blue cattle
  • Piedmontese cattle
  • pigs
    myostatin gene mutation

Large Animal Medicine (34 decks)

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