Lecture 18 Flashcards

(33 cards)

1
Q

What are the characteristics of vomitoxin aka the DON?

A

-found in corn, wheat, and barley
-fungus grows best in the field while the DON increases during storage
-ideal conditions for the DON are cool, wet falls with delayed harvest

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2
Q

What is the pathophysiology of the DON?

A

-induces emesis by direct stimulation of chemoreceptor trigger zone in medulla oblongata
-inhibits protein synthesis
-may lead to poor production and/or immunosuppression

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3
Q

What are the clinical signs of the DON?

A

-emesis
-diarrhea
-feed refusal
-decreased feed intake
-impaired nutrient absorption
-poor production

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4
Q

How does the DON affect different species?

A

-swine are more susceptible
-ruminants are more resistant; require higher conc.

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5
Q

What are the clin path abnormalities seen with the DON?

A

-low Na
-low K
-dehydration
-metabolic alkalosis

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6
Q

What is the diagnosis, treatment, and prevention for the DON?

A

*diagnosis:
-detection in feed

*treatment:
-remove the DON
-provide supportive care

*prevention:
-do not feed the DON
-binders to reduce absorption

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7
Q

What are the characteristics of zeralonone?

A

-produced by same fungus as the DON
-found in corn and other grains
-produced in cooler temperatures compared to the DON
-estrogenic compound

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8
Q

What are the signs of hyperestrogenism in swine caused by zeralonone?

A

-swollen vulva and mammary glands
-prolapsed rectum
-overdeveloped repro. tracts
-nymphomania
-pseudopregnancy
-early embryonic death/infertility in older sows; smaller litters
-estrogenization of males; reduced testicular weight, ridden by other males

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9
Q

Why is zeralenone toxicity worse in swine compared to other species?

A

-delayed detoxification
-enterohepatic recirculation

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10
Q

What are the signs of zeralenone toxicity in dairy heifers?

A

-anestrous/delayed estrus
-swollen vulva

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11
Q

What are the characteristics of ralgro?

A

-synthetic zeralenol growth implant for beef steers
-use improves rate of gain by an additional 40 lbs

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12
Q

What is the treatment and prevention for zeralenone?

A

-remove offending feed
-use binders to prevent absorption

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13
Q

What are the characteristics of fumonisins?

A

-grow on corn
-highest concentrations in screenings and broken kernels
-severely affect horses and pigs

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14
Q

What is the pathophysiology of fumonisins?

A

-inhibit sphingolipid synthesis in neuron, myocardial and hepatocyte cell membranes
-cause liquefactive necrosis of myelinated neurons (chronic)
-induce myocardial necrosis and resulting heart failure and pulmonary edema
-cause direct hepatoxicity (acute, high conc.)

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15
Q

What are the characteristics of equine leukoencephalomalacia?

A

-moldy corn disease
-due to fumonisins
-liquefactive necrosis of white matter of cerebrum in horses
-occurs at small concentrations over chronic exposures

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16
Q

What are the clinical signs of equine leukoencephalomalacia?

A

-altered mentation; depression to excitability
-head pressing
-ataxia
-blindness
-seizures
-death; always fatal/leads to euthanasia

17
Q

What are the characteristics of fumonisins in pigs?

A

-causes pulmonary edema and left-sided heart failure
-damage to left ventricle induces congestive pulmonary hypertension and edema
-clinical signs include sudden death, dyspnea, and cyanosis

18
Q

What are the characteristics of acute fumonisin exposure?

A

-can cause hepatoxicity in any species
-clinical signs include icterus, ill thrift, and poor production
-clin. path. shows elevated cholesterol, AST, bilirubin, SDH, and GGT

19
Q

What is the treatment for fumonisin toxicity?

A

there is no treatment

20
Q

What are the characteristics of ochratoxin?

A

-potent nephrotoxic mycotoxin
-found in cereal grains, dried fruit, coffee, and wine

21
Q

What is the pathophysiology of ochratoxin?

A

-damages proximal convoluted tubule cells
-lesions include hyaline casts, dilated tubules, and renal fibrosis
-ruminants break down ochratoxin and are less sensitive

22
Q

What are the clinical signs of ochratoxicity?

A

-uremia
-depression
-anorexia
-reduced production
-diarrhea
-dehydration
-anuria/oliguria
-acute renal failure

23
Q

What are the clin. path. findings in ochratoxicity?

A

-elevated BUN and creatinine
-excess protein in urine
-hyposthenuria
-casts in urine

24
Q

What is the treatment for ochratoxicity?

A

-no specific treatment
-remove offending feed
-fluids and electrolyte correction for supportive care

25
What are the grass species that can produce tremorgens?
-perennial ryegrass -dallisgrass -bahia grass -bermuda grass
26
Which grass is this?
perennial ryegrass
27
Which grass is this?
bermuda grass
28
Which grass is this?
dallisgrass
29
Which grass is this?
bahia grass
30
What is the pathophysiology of tremorgens/stagger toxins?
-stimulate GABA-receptors in CNS -impairs motor neuromuscular control -causes tremors and incoordination -ruminants are most commonly affected
31
What are the clinical signs of grass staggers?
-staggers/ataxia -muscle fasciculation -weakness -proprioceptive defecits -misadventures
32
What is the treatment for grass staggers?
-none necessary -remove cattle from offending pastures -signs resolve in 2 to 3 days
33
What is the prevention for grass staggers?
-clip seed heads -provide hay -limit grazing in suspected pastures