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

Exam 2- Feed, ionophores, etc. Flashcards

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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
Gossypol intoxication source
cotton seeds
26
Gossypol mechanism of action
speculated: Inhibition of protein synthesis Disrupts ETC -> tissue degeneration & necrosis Decreased reproduction through inhibition of spermatogenesis chelates iron- binds to iron in egg yolk
27
Gossypol species susceptibility
Monogastrics and pre-ruminants are more susceptible than adults calves- heart failure Ruminants & horses- generally resistant
28
Clinical signs associated with Gossypol intoxication
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
29
Sample collection associated with Gossypol intoxication
Heart, liver, lungs
30
What gross lesions are there asssociated with Gossypol intoxication
Widespread congestion & edema (ascites, hydrothorax) Heart- enlarged, pale, streaking Liver- pale, friable, and swollen Skeletal muscles may be pale
31
Microscopic lesions associated with Gossypol intoxication
heart- myocardial degeneration and necrosis Lungs- interlobular edema Liver- centrilobular hepatic necrosis
32
Diagnosis of Gossypol intoxication
Presence of gossypol in feed- test for the free form | History of exposure
33
Treatment for Gossypol intoxication
Remove source form diet (reproductive effects reversed) Decrease stressors Supplementation: Iron, protein, Vitamin A, Lysine
34
Urea/Non-Protein Nitrogen sources
Feed, fertilizers
35
Urea metabolism and positive effects Normal
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
urea MOA In an intoxication situation
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
what are the conditions of optimal activity for Urease Potential methods for intervention
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
Casues of Urea/Non-Protein Nitrogen intoxication
Feed associated- misformulations/excess, Direct feeding of protein pellets etc. Urea based fertilizers Water- fertilizer tanks used for water
39
Predisposing factors to Urea/Non-Protein Nitrogen intoxication
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
Clinical signs associated with Urea/Non-Protein Nitrogen
``` 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
Urea/Non-Protein Nitrogen Sample Collection and testing
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
Treatment for Urea/Non-Protein Nitrogen intoxication
Stop further ammonia production Decrease urease activity (decrease temp and acidify rumen contents) Triage (urinarination = still converting ammonia to urea = improve prognosis)
43
consumption of Raw soybeans is associated with:
``` ammonia toxicosis Lactic acidosis (acute carbohydrate fermentation ```
44
Clinical signs associated with Consumption of Raw soybeans
Lethargy, depression, salivation, polyuria, increased RR, death
45
Diagnosis of overconsumption of Raw soybeans
history of exposure | Elevated rumen or ocular ammonia
46
Treatment for overconsumption of Raw soybeans
Treat the ammonia toxicosis | >8hrs post ingestion- treat carbohydrate overload and rumen acidosis
47
Ammonated forages common term
Bonkers syndrome
48
Mechanism of action for Ammonated forages
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
Clinical signs associated with Ammonated forages
``` trembling Stampeding I"nterupted periods of calm Dilated pupils Rapid respiration urination, salivation, defecation Bellowing and seizures Star gazing ```
50
Diagnosis for Ammonated forages
Remove feed- rapid recovery | Assay for imidazoles in forage, milk, or serum- not routinely offered. Gross lesions consistent with traum
51
Treatment for Ammonated forages
Sedatives, thiamine
52
Nitural toxicants in Feed
Nitrate and cyanide
53
Nitrate sources
Plants- forage material- nitrate accumulators Stunted planted growth causes accumulation over time Stressors- drought/dry weather, increased manure etc.
54
where on the corn stalk do you find the highest concentrations of Nitrate
The lower on the stalk, the higher the Nitrate
55
Nitrite sources
Fertilizer, pickling and curing brines, gunpowder, explosives
56
Nitrate MOA
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
What animals are most susceptible to Nitrate toxicity
Ruminants are most susceptible- rumen microflora rapidly converts nitrate to nitrite. horses pigs dogs and humans are RESISTANT to nitrate
58
What animals are most susceptible to nitrite toxicity
All sepecies are susceptible to ingetion of nitrite because nitrite enters the blood stream.
59
Predisposing factors to nitrite intoxication
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
Clinical Signs associated with nitrate intoxication
Rapid onset- within minutes to several hours | Cyantoic, weakness & ataxia, collapse, respiratory distress, aboritons , death
61
Sample Collection & testing for Nitrate
Ocular fluid... aqueous OR vitreous >20ppm indicates poisoning feed and forage- Nitrate/Nitrate on a dry matter masis Water- fertilizer tanks, wells, ponds
62
Lesions associated with nitrate
Tissues may appear congested and muddy
63
Diagnosis of Nitrate intoxication
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
Traetment of Nitrate intoxication
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
Prevention of nitrate intoxication
provide readily utilized energy source Introduce ruminants to high risk forages slowly ID and understand the major sources and circumstances for nitrate risk
66
what human health concerns are there with nitrate toxication?
Blue Baby syndrome: methemaglobinuria
67
Cyanide sources
fumigants, pesticides, cyanide salts, fires, plants
68
Cyanogenic Plants
Bamboo, Elderberry, Apricots, Cherries, Clovers
69
When is the greatest cyanide potential in forages
During the early growth phases, and then declines
70
Cyanide in forages
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
Cyanide in Plants
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
MOA of cyanide
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
What species are at risk for cyanide toxicity
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
Clinical signs associated with Cyanide
Rapid onset: minutes to <1 hr Anoxia, dyspnea, excitement & muscle tremors, collapse, seizures -> death, Bright cherry red mucous membranes
75
Sample collection and testing for Cyanide
Whole blood- bright red venous blood, rumen stomach contents (almost odor) Brain, liver, forage/plant material
76
Treatment for Cyanide
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
what human health concerns does Cyanide have?
Gasseous form is used as a terrorist/warfare agent

Toxicology (7 decks)

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