Lecture 17 Flashcards

(34 cards)

1
Q

What are the general characteristics of mycotoxins?

A

-produced by fungi which contaminate feedstuff
-often found in cereal grains or forage
-number of potential toxins is unknown
-presence of fungus does not always mean mycotoxins are present

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2
Q

What are the ideal conditions for mycotoxin production?

A

-warm temperatures
-high moisture
-plant stressed and/or damaged

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3
Q

What are the two conditions in which mycotoxins tend to be produced?

A

-plants in the field that undergo stress
-feed stored inappropriately

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4
Q

Which factors can contribute to plant stress?

A

-drought
-flood
-extreme temps
-insects
-herbicide damage

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5
Q

What are the characteristics of grain screenings and fines?

A

-chaff and broken/damaged bits left over after cleaning
-contain the highest amounts of mycotoxin contamination

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6
Q

What are the characteristics of mycotoxin detection?

A

-lab sensitivity is so good that some mycotoxin levels are typically found regardless of if they are causative
-action level is the conc. at which mycotoxins are considered unsafe
-acceptable level is detectable concentrations below action levels for a specific product
-grains for human consumption have lower tolerance than those for animals

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7
Q

How does mycotoxicosis differ from mycosis?

A

mycosis: disease caused by fungal infection
mycotoxicosis: disease caused by mycotoxin exposure

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8
Q

Which animals are more and less susceptible to mycotoxicosis?

A

-ruminants are less sensitive
-monogastrics are more sensitive

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9
Q

What are the three factors contributing to mycotoxicosis severity?

A

-concentration
-duration of exposure
-species

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10
Q

What are the general characteristics of aflatoxins?

A

-found primarily in corn; also peanuts, cottonseed, and cereal grains
-fungal invasion of seeds/kernels and growth and toxin production
-occurs when plants are damaged and then exposed to warm, humid conditions or drought

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11
Q

What is the pathophysiology of aflatoxins?

A

-aflatoxin B1 (AB1) is present in highest concentration
-preformed aflatoxin is ingested
-aflatoxin goes to liver and caused direct damage to proteins, enzymes, and DNA
-result is cellular necrosis, immune suppression, mutagenesis, and neoplasm
-AM1 is excreted in milk and infiltrates muscle tissue

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12
Q

What are the clinical signs of acute aflatoxicosis?

A

-sudden death
-prolonged prothrombin time
-hemorrhage
-petechiation
-bloody diarrhea
-anorexia
-rumen atony
-ataxia
-tremors
-abortion
-liver failure

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13
Q

What are the clinical signs of chronic aflatoxicosis, which is more common?

A

-poor growth
-poor milk production
-poor feed conversion
-rough coats
-ill thrift
-immunosuppression
-hepatic fibrosis
-infertility
-carcinogenesis

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14
Q

Which species is affected at the lowest concentrations of aflatoxins?

A

poultry

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15
Q

What are the minimum database tests for aflatoxicosis?

A

*CBC:
-low RBC count
-low hemoglobin
-thrombocytopenia

*chem (liver failure):
-hypoalbuminemia
-high ammonia
-high bile acids
-high bilirubin

*chem (direct liver damage):
-high AST, ALT, SDH, GGT

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16
Q

Which conditions make an animal more susceptible to aflatoxins?

A

-growing animals
-high production animals
-poultry
-young piglets
-diets lacking protein, selenium, and/or vitamin E

17
Q

How does the exposure level of aflatoxin affect the presentation?

A

*low conc:
-hepatic insult and suboptimal growth in piglets
-decreased performance, depression, ataxia, and resp. infections in calves

*moderate conc:
-affects mature horses, cattle, and swine
-causes hepatic damage

*high conc:
-affects animals regardless of species or age
-causes coma, lateral recumbency, hepatic failure, and death

18
Q

What is the diagnosis of aflatoxins based on?

A

-clinical signs
-lesions
-toxic concentrations in the ration

19
Q

Which samples are taken for aflatoxin testing?

A

-5 kg (10 lb) of feed that is randomly selected and represents as much of the storage conditions as possible (perimeter and center, moving flow ideal)
-liver and kidney tissue samples

20
Q

What are the steps to treating aflatoxicosis?

A

-remove potentially contaminated feeds and replace with healthy feed
-supplement with trace minerals and free radical scavengers

21
Q

What are the prevention steps for aflatoxicosis?

A

-store grains at less than 12% moisture
-clean grains/screen before storing
-use water tight grain bins
-ammoniation of feed to reduce fungal colonization
-adding binders

22
Q

What are the two types of ergot alkaloids toxicities?

A

*fescue toxicosis:
-infected fescue that produces ergovaline

*ergotism:
-infected small grains that produce ergovaline

23
Q

What are the three pathologies of ergovaline?

A

-vasoconstriction
-hypoprolactemia
-fat necrosis

24
Q

How does ergovaline cause vasoconstriction?

A

-activates alpha1-adrenergic and serotonin receptors
-inhibits D1-dopamine receptors
-results in vasoconstriction of small vessels and poor peripheral blood flow
-effect is exacerbated by cold weather; leads to ischemia and necrosis
-in hot weather, animals cannot dissipate heat correctly

25
How does ergovaline cause hypoprolactemia?
-induces overstimulation of D2-dopamenergic neurons in hypothalamus -excess dopamine inhibits production and release of prolactin -decreased prolactin induces agalactia, prolonged gestation, and altered placental physiology
26
What is the suspected mechanism behind ergovaline causing fat necrosis?
vasoconstrictive necrosis
27
What are the "summer slump" signs of ergot alkaloid toxicity?
-hyperthermia due to hot weather -open-mouthed breathing -lethargy -unwillingness to graze -poor milk production -poor growth rates -infertility
28
What are the "fescue foot" signs of ergot alkaloid toxicity?
-exacerbated vasoconstriction due to cold weather -sloughing of feet, ear tips, tails, teats -swelling and erythema of affected tissues -lameness -mastitis -hippo cows/frostbite on ear tips
29
What are the main signs of fescue toxicity seen in mares?
-prolonged gestation -dystocia -agalactia
30
How is ergotism diagnosed?
testing suspect forage and feed
31
What is the treatment for ergot alkaloid toxicity?
-remove suspected feed -provide adequate shelter, shade, and water -antibiotics for secondary infections of ischemic tissue
32
What are the characteristics of domperidone?
-can mitigate hypoprolactinemia -D2-antagonist that blocks the excess dopamine effect -give to pregnant mares with known exposure in last 30 to 60 days of gestation
33
What are the prevention steps for ergot alkaloids?
*pastures: -clip seed heads -avoid excess fertilization -intermix with legumes -use endophyte free or novel endophyte fescue varieties *hay: -ammoniation to reduce ergovaline concentrations *mares: -eliminate fescue from diet for most or all of gestation *ergotism: -avoid or remove offending feed -only feed cleaned/screened grains
34
How have cattle adapted to the ergot alkaloids?
cattle raised in fescue environments can be adapted to the effects -no genomic selection markers to determine this