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Toxicology > Ionophore toxicosis > Flashcards

Ionophore toxicosis Flashcards

1
Q

5 uses of ionophores?

A
  • Anticoccidial in poultry, cattle, and goats
  • Growth promoter feed additive in cattle
  • Monensin is approved to improve efficiency of milk production in dairy cattle in the US
  • Reduction of bloat and rumen acidosis in ruminants
  • Prevention of tryptophan-induced atypical bovine pulmonary emphysema
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2
Q

Examples of ionophores?

A
  • Monensin
  • Lasalocid
  • Salinomycin
  • Narasin
  • Semduramicin sodium
  • Laidlomycin propionate potassium
  • Carboxylic acid derivatives antibiotics
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3
Q

Solubility?

A

Slightly soluble in water, soluble in organic solvents and oils

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4
Q

Form lipid-soluble complexes with what?

A

With polar cations (Na, Ca, K Mg) that are transported across cellular membranes

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5
Q

What is the most common source of ionophore toxicosis?

A

Monensin

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6
Q

What are 3 other sources of ionophore toxicosis?

A
  • Eating feeds that contain more than the recommended levels in chickens, cattle and swine
  • Eating feeds with added ionophores, accidentally or intentionally, in horses, sheep and dogs
  • Malicious poisoning in horses
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7
Q

Which animals are susceptible to ionophore toxicosis? Which species are the least, intermediate, and most sensitive?

A
  • All animals susceptible
  • Equine are the most sensitive, cattle are intermediate, and poultry are the least sensitive
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8
Q

T/F: Horses that ingest recommended ionophore levels for cattle are poisoned

A

FALSE–they are not poisoned

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9
Q

Concurrent administration of which drugs increases toxicosis?

A
  • Tiamulin
  • Chloramphenicol
  • Erythromycin
  • Sulfonamides
  • Cardiac glycosides
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10
Q

Toxicokinetics of monensin

Absorbence: ruminants vs. monogastrics?

A
  • Ruminants absorb about 50%
  • Monogastric animals absorb most of it
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11
Q

Toxicokinetics of monensin

Where is it distributed?

A

Throughout the body

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12
Q

Toxicokinetics of monensin

T/F: Blood and tissue levels are relatively small, but monensin accumulates in tissues of animals when given in high doses

A

FALSE–monensin does not accumulate in tissues when given in high doses (the rest is true)

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13
Q

Toxicokinetics of monensin

Metabolization and excretion?

A

Rapidly metabolized by P-450 oxidative demethylation enzymes in the liver (slow metabolism in equines because they have the lowest oxidative demethylases) and excreted mainly in bile

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14
Q

Mechanism of action

What does ionophore toxicosis disrupt?

A

Disrupts transmembrane electrochemical gradients

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15
Q

Mechanism of action

What are the main targets?

A

The mitochondria of highly energetic tissues (myocardium, skeletal muscles, and the kidney)

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16
Q

Mechanism of action

Ionophore toxicosis causes an influx of what?

A

Influx of the sodium-ionophore complex increasing intracellular Na accompanied by increasing intracellular Ca

17
Q

Mechanism of action

Ionophore toxicosis causes sequestering of, inhibition of, and decreased what? What does this lead to?

A

Sequestering of Ca by mitochondria and inhibition of mitochondria and decreased ATP and energy–> increased cytoplasmic Ca

18
Q

Mechanism of action

What is the cell death due to?

A

Disrupting homeostatic mechanisms

19
Q

Mechanism of action

Ionophore toxicosis also causes catecholamine release, which results in what?

A

Oxidation products and free radicals causing sarcolemmal membrane damage

Disruption of ion concentrations in excitable cells (neurons, myocardium, skeletal muscles, smooth muscles) alters their functions

20
Q

Pretty chart explaining mechanism of action

(actually it’s pretty ugly/boring)

A
21
Q

Clinical signs in horses?

A
  • Rapid onset
  • Anorexia, profuse sweating, colic, depression, incoordination, hyperventilation, tachycardia, tachyarrhythmias, prostration, and death
22
Q

Clinical signs in cattle?

A

Anorexia, diarrhea, depression, labored breathing, ataxia, prostration, and death

23
Q

Clinical signs in poultry?

A

Anorexia, diarrhea, ataxia, resting on the knees with wings and legs directed outward, decreased egg production

24
Q

Clinical signs in dogs?

A

Ataxia, muscle weakness of hind limbs, respiratory paralysis, dysuria, constipation, and depression

25
Q

Lesions?

A
  • Mainly cardiac muscle lesions in horses (pale cardiac muscles, white streaks of necrosis in the myocardium), and also skeletal muscle lesions
  • Mainly skeletal muscle lesions in sheep, swine, and dogs (pale skeletal muscles)
  • Both skeletal and cardiac muscle lesions in cattle and poultry
26
Q

Chemical analysis for ionophores (detection, best samples, other samples)?

A
  • Methods detect ppb levels
  • Best sample is feed
  • Other samples are GI contents, liver, and feces
27
Q

Which enzymes are elevated following ionophore toxicosis?

A
  • Creatinine phosphokinase (CPK)
  • Aspartate transaminase (AST)
  • Lactic dehydrogenase (LDH)
  • Alkaline phosphatase (ALP)
28
Q

What is decreased on the clinical pathology? What remains unchanged? What is increased (besides enzymes)?

A
  • Decreased serum Ca and K (during first 12hrs)
  • No change in Na
  • Increased PCV
29
Q

Diagnosis?

A
  • History of feed-related problem
  • Clinical signs
  • Lesions
  • Lab diagnosis
30
Q

DDx

General (all species)?

A

Include other myopathy and neuropathy conditions

31
Q

DDx

Horses

A
  • Colic
  • Blister beetle ingestion (cantharidin toxicosis)
  • Azoturia
32
Q

DDx

Cattle?

A

Vitamin E/selenium deficiency

33
Q

DDx: poisonous plants

Plants affecting skeletal muscle?

A
  • Coffee senna (Senna occidentalis)
  • Coyotillo (Karwinskia humboldtiana)
  • White snakeroot (Eupatorium rugosum)
34
Q

DDx: poisonous plants

Plants that are cardiotoxic?

A
  • Oleander
  • Taxus spp.
  • Milkweed
  • Vetch
35
Q

DDx

Poultry

A
  • Nutritional myopathy
  • Coffee senna toxicosis
  • Botulism
  • Na-water deprivation toxicosis
  • Mycotoxicosis (moniliformin cyclopiazonic acid)
  • Round-heart disease
  • Downer syndrome (viral arthritis)
36
Q

Is there a specific antidote for ionophore toxicosis?

A

Nope, that’d be too easy

37
Q

Treatment

A
  • Remove medicated feed
  • Decreasing absorption
    • Activated charcoal
    • Mineral oil
    • Saline cathartics
38
Q

Symptomatic treatment

A
  • IV fluids and electrolyte therapy (to correct hypovolemia and support cardiovascular and renal functions)
  • Potassium to correct hypokalemia (<2 mEq/L)
  • Monitor cardiac function for several months
  • Horses should not be ridden or stressed for several months
  • Vitamin E and selenium may decrease muscle damage especially in cattle and swine
39
Q

Prognosis?

A
  • Horses that survive may suffer myocardial scarring and necrosis
  • Horses may not reach previous performance

Toxicology (22 decks)

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