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Toxicology > Exam 2- Feed, ionophores, etc. > Flashcards

Exam 2- Feed, ionophores, etc. Flashcards

1
Q

Sodium ion toxicosis- water deprivation causes

A

Extensive periods without water followed by unrestricted access. Swine are the most commonly affected species.
Cattle: restricted water
Dogs: cured meats, homemade playdough, sea water

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2
Q

Sodium ion toxicosis- mechanism of action

A

Na+ moves into neurons with dehydration -> increased brain Na+: decreased glycolysis -> decreased energy in neuron -> ATPase pump impaired -> Na+ unable to escape -> unrestricted water acess -> H20 moves into neurons -> edema and brain swelling

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3
Q

Sodium ion toxicosis clinical signs

A

Swine: rapid onset, thirst, constipation/dry feces, recumbent and paddling, blindness, head pressing, jaw chomping

Cattle: tremors, ataxia, recumbent and paddling, circling

Dogs: GI upset, vomiting, diarrhea, PU/PD Tremors

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4
Q

Sodium ion toxicosis sample collection and testing

A

Brain: Fresh brain Na+ Swine- Eosinophilic perivascular cuffing
Cattle- edema and neuronal degredation (polio)
Dogs: eosinophils and necrosis not present

Occular fluid
CSF and serum

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5
Q

sodium ion toxicosis treatment

A

shut off water
Rehydrate slowly- alternate water flow off/on
Use of hypertonic solution preferred to prevent further edema
Mannitol (25%) for edema
Furosemide- 2.2 to 4.4mg/kg PO, IV, or IM BID

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6
Q

Definition of an Ionophore

A

A substance that can transport ions across a lipid membrane within a cell
Feed efficiency and improved growth
Coccidiostat

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7
Q

Positive effects of ionophores

A

Improve feed efficiency- reduce gram + & favor Gram - bacteria
change in gram-/gram+ ratio (increasing proprionic acid- morei efficient energy)
Protein metabolism and energy is positively influenced

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8
Q

Ionophores and Mechanism of Action

A

Overdose -> hemostatic mechanisms fail resulting in an increase of Ca and Na influx.
Increased Ca influx -> Free radical formation -> oxidative damage to tissues
tiamulin potentiation: Directly inhibits CP450 enxzymes. Inhibition of the enzymes causing ionophore accumulation, and additional oxidative damage to tissues - eventual muscle necrosis

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9
Q

Monensin Toxicity

A

horses are the most susceptible species.

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10
Q

what are Causes of intoxication associated with Ionophores?

A

Mixing errors, delivery errors, history of eating cattle feed (dogs)
Barn break ins

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11
Q

Why are ionophore intoxications often mis-diagnosed in large animals

A

Delayed onset of clinical signs

Subtle/non-specific signs

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12
Q

Clinical signs of Ionophore toxicosis in horses

A

Anorexia, sweating, colic, progressive ataxia, posterior paresis, laterally recumbent, tachycardia, hypotensive
Death (within 24 hours)- can be delayed

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13
Q

Clinical signs of ionophore intoxication in cattle

A

Anorexia, diarrhea, weakness/ataxia, recumbent, dyspneic, death (2-5 days)

clinical signs are several days after exposure

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14
Q

Clinical signs of ionophore intoxication in Swine

A

Dog sitting, unable to rise/move, increased vocalization, centrally aware, anorexia, tremors

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15
Q

clinical Signs of ionophore intoxication in Dogs

A

Flaccid ascending paralysis
High dose results in respiratory paralysis
Alert
Appears like botulism

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16
Q

Clinical Signs of ionophore intoxication in Poultry

A

Anorexia & diarrhea, weak & ataxic, Drooped head & wings, Sternal recumbency, paralysis

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17
Q

ionophore sample collection and testing

A

Cattle and horses:
cardiac and skeletal muscle (left papillary muscle)
Swine, sheep, dogs: Skeletal muscle (diaphragm is a good muscle)
Collect muultiple sections!!! Cut into muscle-> never know what you wind

Feed- test for ionophores

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18
Q

Clincal pathology in ionophore intoxication cases

A

leukocytosis
Increased cardiac troponins, Increased AST, CPK, Protein
Decreased K, NA, Ca
urine: increased Glucose, protein, myoglobin, hemoglobin
Decreased USG

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19
Q

Lesions associated with Ionophore intoxication

A

Myocardial necrosis
Skeletal muscle necrosis

ascited, hydrothorax, pulmonary edema, hepatic congestion

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20
Q

Lesions associated with ionophore intoxication and Poultry

A 
Cardiac and skeletal muscle necrosis
Pulmonary and hepatic edema
Gastroenteritis
Ascites and hydro pericardium
Gross lesions are not commonly observed
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21
Q

tiamulin and ionophores

A

Tiamulin is a common antibiotic utilized in swine to treat respiratory disease
Inhibits metabolism of ionophore: accumulation results in toxicosis

situations:
tiamulin in water + ionophore in feed
tiamulin + ionophore in feed
Tiamulin + other ionophore

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22
Q

Diagnosis of ionophores

A

History of exposure
Corresponding clinical signs and lesions
Presence of ionophore in feed

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23
Q

Treatment of ionophore intoxication

A 
Remove source
No antidote
Reduced stress (decrease cardiac load)
Vitamin E/Selenium(limits oxidative damage, doesn't reverse damage) (Vitamin E would be the safer option, because Selenium has a narrow margin of safety)
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24
Q

Prevention of ionophore intoxication

A

Good milling practices
Correct storage of materials
communication- make sure the correct feed is going to the right place

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25
Q

Gossypol intoxication source

A

cotton seeds

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26
Q

Gossypol mechanism of action

A

speculated:
Inhibition of protein synthesis
Disrupts ETC -> tissue degeneration & necrosis
Decreased reproduction through inhibition of spermatogenesis
chelates iron- binds to iron in egg yolk

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27
Q

Gossypol species susceptibility

A

Monogastrics and pre-ruminants are more susceptible than adults

calves- heart failure

Ruminants & horses- generally resistant

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28
Q

Clinical signs associated with Gossypol intoxication

A

Affects are cumulative
swine- slow growth, weakness, dyspnea, generalized edema, death
Pre-ruminants- sudden deaths
Dogs and bulls- decreased fertility
Dairy cattle- ill thrift, decreased heat tolerance, decreased fertility

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29
Q

Sample collection associated with Gossypol intoxication

A

Heart, liver, lungs

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30
Q

What gross lesions are there asssociated with Gossypol intoxication

A

Widespread congestion & edema (ascites, hydrothorax)
Heart- enlarged, pale, streaking
Liver- pale, friable, and swollen
Skeletal muscles may be pale

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31
Q

Microscopic lesions associated with Gossypol intoxication

A

heart- myocardial degeneration and necrosis
Lungs- interlobular edema
Liver- centrilobular hepatic necrosis

32
Q

Diagnosis of Gossypol intoxication

A

Presence of gossypol in feed- test for the free form

History of exposure

33
Q

Treatment for Gossypol intoxication

A

Remove source form diet (reproductive effects reversed)
Decrease stressors
Supplementation: Iron, protein, Vitamin A, Lysine

34
Q

Urea/Non-Protein Nitrogen sources

A

Feed, fertilizers

35
Q

Urea metabolism and positive effects

Normal

A

urease rapidly converts urea to ammonia
Ammonia synthesized to microbial protein by the rumen microbes.

in an alkaline environment, Ammonia is absorbed into the blood stream. -> Liver -> Urea -> Urine

In acidic environment, ammonia is converted to ammonium - not absorbed into the blood stream

36
Q

urea MOA

In an intoxication situation

A

Urease hydrolyzes urea ato ammonia in the rumen. H+ protonates ammonia to ammonium and the pH begins to increase (alkaline pH results in ammonia being favored)

Ammonia is absorbed into the blood
Excessive ammonia overwhelms the liver, and can’t convert to urea
Elevated blood ammonia crosses the BBB

37
Q

what are the conditions of optimal activity for Urease

Potential methods for intervention

A

Temperature 120 degrees F
pH 7.7-8.0
Peak NH3 .5-2hrs

Treatment: cool the rumen down, and make the diet more acidic

38
Q

Casues of Urea/Non-Protein Nitrogen intoxication

A

Feed associated- misformulations/excess, Direct feeding of protein pellets etc.
Urea based fertilizers
Water- fertilizer tanks used for water

39
Q

Predisposing factors to Urea/Non-Protein Nitrogen intoxication

A

poor carbohydrate diet: Decreased energy for rumen bacteria resulting in a decreased conversion of ammonia to protein

Inadequate adaptation- rumen microbes not accustomed to high amounts

high rumen pH and temp- optimal conditions for urease -> increased conversion to ammonia

Heaptic insufficiency- capability to eliminate ammonia from blood

Unrestricted access to supplements

40
Q

Clinical signs associated with Urea/Non-Protein Nitrogen

A 
Rapid onset: 10 min- hours post consumption
Salivation & bruxism (grinding)
Muscle tremors and incoordination
Polyuria
Weakness
Tachypnea
Violent spasms/seizures
Acute death - often found this way
41
Q

Urea/Non-Protein Nitrogen Sample Collection and testing

A

Ocular fluid (post mortem sampling)
rumen content
Serum

water
Feed or forage- urea concentration

time is of the essence- collect, seal, and freeze samples ASAP following death

42
Q

Treatment for Urea/Non-Protein Nitrogen intoxication

A

Stop further ammonia production
Decrease urease activity (decrease temp and acidify rumen contents)
Triage (urinarination = still converting ammonia to urea = improve prognosis)

43
Q

consumption of Raw soybeans is associated with:

A 
ammonia toxicosis 
Lactic acidosis (acute carbohydrate fermentation
44
Q

Clinical signs associated with Consumption of Raw soybeans

A

Lethargy, depression, salivation, polyuria, increased RR, death

45
Q

Diagnosis of overconsumption of Raw soybeans

A

history of exposure

Elevated rumen or ocular ammonia

46
Q

Treatment for overconsumption of Raw soybeans

A

Treat the ammonia toxicosis

>8hrs post ingestion- treat carbohydrate overload and rumen acidosis

47
Q

Ammonated forages common term

A

Bonkers syndrome

48
Q

Mechanism of action for Ammonated forages

A

Imidazoles form from browning reaction with amino groups and a reducing compound (sugar)
Reaction is more rapid at higher temps and pH

Multiple imidazoles form

49
Q

Clinical signs associated with Ammonated forages

A 
trembling
Stampeding
I"nterupted periods of calm
Dilated pupils
Rapid respiration
urination, salivation, defecation
Bellowing and seizures
Star gazing
50
Q

Diagnosis for Ammonated forages

A

Remove feed- rapid recovery

Assay for imidazoles in forage, milk, or serum- not routinely offered. Gross lesions consistent with traum

51
Q

Treatment for Ammonated forages

A

Sedatives, thiamine

52
Q

Nitural toxicants in Feed

A

Nitrate and cyanide

53
Q

Nitrate sources

A

Plants- forage material- nitrate accumulators
Stunted planted growth causes accumulation over time
Stressors- drought/dry weather, increased manure etc.

54
Q

where on the corn stalk do you find the highest concentrations of Nitrate

A

The lower on the stalk, the higher the Nitrate

55
Q

Nitrite sources

A

Fertilizer, pickling and curing brines, gunpowder, explosives

56
Q

Nitrate MOA

A

Nitrate becomes nitrite - some is converted to ammonia and is used for microbial growth
Excessive nitrate - increases nitrite -> Excessive nitrite overwhelms bacteria.
nitrite in the blood causes an accumulation of methemaglobin

Death by anoxia- blood appears chocolate brown

57
Q

What animals are most susceptible to Nitrate toxicity

A

Ruminants are most susceptible- rumen microflora rapidly converts nitrate to nitrite.
horses pigs dogs and humans are RESISTANT to nitrate

58
Q

What animals are most susceptible to nitrite toxicity

A

All sepecies are susceptible to ingetion of nitrite because nitrite enters the blood stream.

59
Q

Predisposing factors to nitrite intoxication

A

Rate of consumption- small amounts ingested over time does not necessarily result in intoxication
Low energy diets (decreased energy for rumen bacteria results in a decreased conversion of nitrite to ammonia)
Lack of adaptation- rumen microbes not accustomed to high amounts = overwhelmed

60
Q

Clinical Signs associated with nitrate intoxication

A

Rapid onset- within minutes to several hours

Cyantoic, weakness & ataxia, collapse, respiratory distress, aboritons , death

61
Q

Sample Collection & testing for Nitrate

A

Ocular fluid… aqueous OR vitreous
>20ppm indicates poisoning

feed and forage- Nitrate/Nitrate on a dry matter masis
Water- fertilizer tanks, wells, ponds

62
Q

Lesions associated with nitrate

A

Tissues may appear congested and muddy

63
Q

Diagnosis of Nitrate intoxication

A

Chocolate brown blood, history of exposure, high ocular fluid or serum nitrate/nitrite concentrations, Detection fo high nitrate/nitrite levels in suspected materials

Bovine abortions: Fetal ocular fluid nitrate >20ppm

64
Q

Traetment of Nitrate intoxication

A

Prevent further exposure
Methylene blue 1% (repeat as needed every 6-8 hours0
Cold water and oral penicillin: Decreased rumen microbe activity-> Decreased nitrate reduction to nitrite

65
Q

Prevention of nitrate intoxication

A

provide readily utilized energy source
Introduce ruminants to high risk forages slowly
ID and understand the major sources and circumstances for nitrate risk

66
Q

what human health concerns are there with nitrate toxication?

A

Blue Baby syndrome: methemaglobinuria

67
Q

Cyanide sources

A

fumigants, pesticides, cyanide salts, fires, plants

68
Q

Cyanogenic Plants

A

Bamboo, Elderberry, Apricots, Cherries, Clovers

69
Q

When is the greatest cyanide potential in forages

A

During the early growth phases, and then declines

70
Q

Cyanide in forages

A

physical damage to the plant, causes the release of intrinsic enzymes -> Hydrolyze CG -> HCN. Toxic levels of HCN may remain in large hay bales where forage is immediately baled

Properly ensiled silage loses cyanide potential

71
Q

Cyanide in Plants

A

Thiosulfate combines with HCN -> thiocyanate -> urinary excretion. Animals can safely consume small amounts of these plants

ruminants constantly exposed: Effects are NOT cumulative -> tolerance does not develop
need a severe overload

72
Q

MOA of cyanide

A

Occurs within the mitochondira
cyanide ion combines with Fe in cytochrome oxidase system-> inhibits reducetion of O2 within ETC -> inhibited transfer of O2 to tissues. -> Inhibited cellular respiration -> anoxia

73
Q

What species are at risk for cyanide toxicity

A

Ruminants- higher risk: rumen microbes - rapid hydrolysis of CGs to HCN
Monogastrics - lower risk: lower gastric pH -> decreased hydrolysis of CGs. Must consume raw plant material

All species are susceptible to cyanide gas

74
Q

Clinical signs associated with Cyanide

A

Rapid onset: minutes to <1 hr

Anoxia, dyspnea, excitement & muscle tremors, collapse, seizures -> death,

Bright cherry red mucous membranes

75
Q

Sample collection and testing for Cyanide

A

Whole blood- bright red venous blood, rumen stomach contents (almost odor)
Brain, liver, forage/plant material

76
Q

Treatment for Cyanide

A

Must have rapid intervention
Sodium nitrite combination with sodium thiosulfate
mehtylene blue can be utilized as well- use when you suspect either cyanide or nitrate intoxication

Mechanism: Na Nitrite -> methemablobin -> CHMetHb -> Cn binds to thiosulfate -> excreted as thiosulfate

77
Q

what human health concerns does Cyanide have?

A

Gasseous form is used as a terrorist/warfare agent

Toxicology (7 decks)

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