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106 Cards in this Set
- Front
- Back
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What are some physical features of plants that defend them? Why do they have them?
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Thorns, spines, leaf hairs
Plant avoidance by herbivore |
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What are 2 chemical defense mechanisms of plants from herbivores?
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1) Reduces palatability
2) Adversely affects health of herbivore |
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What is an alkaloid?
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Typically an aromatic compound w/ nitrogen in the ring
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How many classes of alkaloids are there?
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10
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What are the 10 classes of alkaloids?
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1) Purine
2) Pyridine 3) Phenethylamines 4) Quinoline 5) Isoquinoline 6) Indole 7) Tropane 8) Terpenoid 9) Pyrrolidine 10) Vinca |
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What are two examples of an alkaloid that's a tropane?
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Atropine
Cocaine |
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What is an example of a compound that contains a quinoline alkaloid?
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Strychnine
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What are 2 examples of an alkaloid that's an isoquinoline?
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Morphine
Codeine |
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What are 2 examples of purine alkaloids?
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Xanthines
Caffeine |
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What are 2 examples of an alkaloid that a pyridine compound?
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Nicotine
Senecionine |
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What are 3 examples of indole alkaloids?
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1) Serotonin
2) Lolitrem B 3) Ergovaline |
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How are mycotoxins related to the 10 plagues of history?
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Postulated by scientists as the possible cause of plague #5 and plague #10
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What is St. Anthony's Fire?
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Earliest documented mycotoxicosis in humans in 10th century Europe
-Disease=ergotism, caused by Claviceps purpurea |
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The salem which trials could have been a case of ______.
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Ergotism
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What was the turkey "X" disease in England that represented modern mycotoxicology in the 1960s?
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An aflatoxin produced by Aspergillus flavus that was found in the feeds
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The Food and Agriculture Organization has estimated that 1/4 of the world's food crops are affected by___________.
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Mycotoxins
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What is the definition of mycotoxins?
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Toxic secondary metabolites produced by fungi (molds) that cause an undesirable effect (mycotoxicosis) when animals are exposed.
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What is the palatability, digestibility and energy content of moldy feeds?
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-Less palatable (reduce feed consumption)
-Reduced digestibility -Lower energy content |
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Mycotoxins cause what 6 abnormalities?
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1) Reduce nutrient utlization
2) Alter rumen fermentation 3) Suppressed immunity 4) Altered reproduction 5) Tissue irritation 6) Cellular death |
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Why do some mycotoxins produce symptoms that are different or more severe than expected?
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Mycotoxins can interact so the signs can be more severe than expected
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True or false. Drugs and antibiotics are effective in treating mycotoxicosis.
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False, drugs and antibiotics are consistently ineffective
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The signs of mycotoxins can all be associated to ________.
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Food or feedstuffs
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What is consistent about testing for mycotoxins?
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Testing of food / feedstuffs reveals fungal activity
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True or false. All mycotoxins are not transmissible to control subjects.
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True
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What are the 3 characteristics of the host that affect the degree of mycotoxin toxicity?
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Age, sex and nutritional status of the host
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What is the pattern related to mycotoxin outbreaks?
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Outbreak of symptoms is seasonal
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What kind of diagnostic testing is available for mycotoxins?
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Several commercial laboratories are available and provide screens for an array of mycotoxins
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What is the one downfall to mycotoxin screening?
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Cost of analyses has been a constraint but can be insignificant compared to the economic consequences of production & health losses related to mycotoxin contamination
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Why is prevention/ control of mycotoxin formation essential?
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There are few ways to completely overcome problems once mycotoxins are present
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What is the most important instigator of mold growth and mycotoxin formation in the field?
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Drought and insect damage
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What can you do to treat mycotoxicosis?
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-supportive treatment, reduction of stress and exposure to infectious diseases
-Mycotoxin binders |
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What is the theory behind mycotoxin binders?
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The binder decontaminates mycotoxins in the feed by binding them strongly enough to prevent toxic interactions
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What are 4 examples of mycotoxin binders (absorbent materials)?
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1) Activated carbon
2) Aluminosilicates -Clay, bentonite, etc 3) Complex indigestible carbohydrates e.g. cellulose 4) Synthetic polymers e.g. cholestryamine |
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True or false. Activated carbon is the only adsorbent product approved by the FDA for the prevention or treatment of mycotoxicoses.
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False, no adsorbent product is approved by the FDA
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What is the T-2 toxin?
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A Fusarium-produced type A mycotoxin
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What is the most toxic member of a large group of mycotoxins called trichothecenes?
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T-2 toxin
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What 7 types of feed is the T-2 toxin found in?
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1) Corn
2) Wheat 3) Barley 4) Oats 5) Rice 6) Rye 7) Sorghum |
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What conditions are conducive to T-2 toxin production?
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High humidity and moderate temperatures (6-24 C)
-Both in field & in storage |
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What is the mode of action of the T-2 toxin?
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Known to interfere w/ protein synthesis and suppress immunity
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What are the 2 clinical signs of T-2 toxin in swine?
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Oral lesions
Intestinal necrosis |
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What is the clinical sign of T-2 toxin in chickens?
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Oral lesions
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What happens to the T-2 toxin in ruminants? Does it cause clinical signs?
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Metabolized in rumen
-Associated w/ reduced feed consumption, loss in yield, gastroenteritis, intestinal hemorrhages & death |
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What is the toxic dose of T-2 toxin?
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No guidelines for T-2 toxin in feed, but avoiding levels above 100 ppb may be reasonable
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What is the treatment for T-2 toxin?
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-No antidote
-Supportive treatment, reduction of stress & exposure to infectious dz -Removal of ingested toxins by treatment w/ adsorbents such as superactivated charcoal |
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What is Deoxynivalenol?
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The proper name for type B trichothecene, often referred to as vomitoxin and produced by members of genus Fusarium
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What is deoxynivalenol most frequently found in? (4)
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1) Wheat
2) Barley 3) Rye 4) Oats -Occasionally in corn & potatoes |
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What conditions are conducive to deoxynivalenol production?
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Increases w/ cool, moist growing conditions & there is accumulation during improper storage
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What is the mode of action of deoxynivalenol?
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DON acts via the chemoreceptor zone of the medulla oblongata to affect brain neurochemistry (dopaminergic receptors)
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What are the 5 clinical signs of deoxynivalenol toxicity in swine?
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1) Feed refusals
2) Diarrhea 3) Emesis* 4) Reproductive failure 5) Death |
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What happens to cattle that ingest Deoxynivalenol
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*Detoxified in the rumen but has been associated w/ reduced feed intake and lower milk production
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What are the signs of deoxynivalenol toxicity in dogs & cats?
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Reduced feed intake at low levels and vomiting at higher levels
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What is the toxic dose of deoxynivalenol in dogs & cats?
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Clinical signs appear at 4 ppm
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What is the toxic dose of deoxynivalenol in beef cattle and sheep?
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Tolerated up to 21 ppm of dietary DON w/o obvious effects
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True or false. The FDA does not have restrictions for deoxynivalenol levels in feed.
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False, has advisory levels for vomitoxin in livestock feed
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What is the treatment for deoxynivalenol?
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-No antidote
-Supportive treatment, reduction of stress & exposure to infectious diseases -Removal of ingested toxins by treatment w/ adsorbents such as superactivated charcoal |
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What is Lolitrem B?
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Indole diterpene alkaloid produced by the endophytic fungus, Neotyphodium lolii
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What plant has lolitrem B? Where is it most concentrated?
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Concentrated in lower leaf sheaths of perennial ryegrass (Lolium perenne)
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How are Lolitrem B and peramine related?
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Peramine is a lot more toxic to insects than lolitrem B, if take away peramine then increase lolitrem B -changes the alkaloid back an forth to protect the plant
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What is the mode of action of Lolitrem B?
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Alters neurotransmitter GABA
-Alters Na+, K+ and Ca2+ channels |
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What can be seen on histopathology of brain samples from animals with Lolitrem B toxicity?
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Vacuolated Purkenje cells cerebellum
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What are the 4 clinical signs of Lolitrem B toxicity?
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1) Look nearly normal while lying down
2) Tremors; especially head & neck 3) Incoordination 4) Hypermetria |
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What is the toxic dose of lolitrem B in horses, cattle & sheep?
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Horses: not determined
Cattle: 1800-2000 Sheep: 1800-2000 |
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What is the final resting place for Lolitrem B in the body? Why does this matter?
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Adipose tissue
-Concerns have been raised about the public health safety of lolitrem B residues in beef fat |
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How do you diagnose Lolitrem B toxicity?
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-Exposure to perennial ryegrass (especially in fall pastures)
-Measurement of Lolitrem B in feed -No post mortem lesions |
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What are 6 differential diagnoses for lolitrem B?
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1) Aminoglycoside antibiotics
2) Ohio buckeye (Aesclus) 3) Dutchman's breeches (Dicentra) 4) Locoweed (astragalus) 5) Mercury 6) Metaldehyde |
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What is the treatment for Lolitrem B toxicity?
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Remove from contaminated feed, protect from accidental and sun damage
- supplement good quality feed |
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What is the prognosis of Lolitrem B toxicity?
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Good
-Deaths accidental, often drowning when drinking from pond or stream, or due to inability to forage for food and water, misadventure |
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How do you prevent Lolitrem B toxicity?
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Check quality of feed
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What are tremorgens?
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Tremorgenic mycotoxins are part of a structurally diverse group of fungal secondary metabolites called the indole-diterpenes
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What are the 4 tremorgens we are most concerned about?
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1) Paxilline
2) Lolitrems 3) Penitrems 4) Roquefortine |
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What is the disease caused by tremorgens that we care about most?
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Ryegrass staggers
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Where are tremorgens located?
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Tremorgenic intoxications occur worldwide
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What is the mode of action of Penitrem A?
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Blocks an inhibitor of large conductance of Ca2+- sensitive K+ channels, affecting vasodilation
-also neurotoxic |
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What is the mode of action of Roquefortine C?
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Potentially a neurotoxic compound that activates and inhibits detoxification enzymes P-glycoprotein and cytochrome p450-3A respectively
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What are the early (2-4 h post exposure) clinical signs of tremorgens in small animals?
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Hypersalivation, vomiting, panting, restlessness, and tremors around head & neck progressing to whole body tremors
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What are the clinical signs of tremorgens in small animals at high doses?
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Tremors are more severe with seizures, hyperthermia, tachycardia & death
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What are the 3 clinical signs of tremorgens in large animals?
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1) Early sign, fine muscle tremors around head & neck
2) When excited or exercised tremors are exaggerated 3) When forced to run, animals have exaggerated flexure of forelegs & incoordination |
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What is the pathophysiology of Penitrem A and roquefortines in small animals?
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Affect nervous system--> tremors, seizures & ataxia
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What are 8 DDX for tremorgens?
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1) Locoism (astragalus spp.)
2) Strychnine 3) Metaldehyde 4) Ethylene glycol 5) Cholinesterase inhibitors 6) Methylxanthines 7) Medications such as pseudoephedrine hydrochloride 8) Illicit drugs such as amphetamines |
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How do you diagnose tremorgens in small animals?
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CBC, serum chemistry profile and UA to rule out other causes of tremors
-Submit suspect food or stomach contents for LCMS analysis for tremorgenic mycotoxins |
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How do you diagnose tremorgens in large animals (Perennial ryegrass staggers)?
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Detection of Lolitrem B > 2000 ppb
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What are the 4 components of tremorgen treatment in small animals?
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1) Control severe tremors caused by tremorgenic mycotoxins, methocarbamol should be administered
2) Seizures- treat w/ diazepam followed by methocarbamol 3) Gastric lavage and activated charcoal administered to limit further absorption of toxins 4) Supportive therapy |
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What does treatment for tremorgens in large animals consist of?
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Replace contaminated forage and place animals in a quiet, secure environment until they recover
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What is the prognosis for tremorgen toxicity in small animals?
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Good w/ early treatment and recovery in 24-48 h
-Exposure fatal if lethal dose is consumed and decontamination delayed |
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What is the prognosis for tremorgen toxicity in large animals?
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Morbidity is high, but mortality is low
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How do you prevent tremorgen toxicity?
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-Restrict access to moldy food for dogs
-Removal of livestock from infected pastures |
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What is the mode of action of macadamia nut toxicity?
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Unknown
-Involves motor neurons, neuromuscular junctions, muscle fibers or neurotransmitters |
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How long does it take for the clinical signs of macadamia nuts to appear? How long does it take for the signs to resolve?
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Within 3-12 hours of ingesting nuts and tend to resolve over 24 hours
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What are the clinical signs of macadamia nut toxicity?
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Lethargy, vomiting, and hyperthermia w/ progression to ataxia or hind-limb paresis
-Also see tremors, abdominal pain, lameness, joint stiffness and pale mucous membranes |
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What is the toxic dose of macadamia nuts?
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1 g / lb of BW
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What is the general treatment for macadamia nut toxicity?
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Induce vomiting, gastric lavage, *activated charcoal especially if nuts were covered w/ chocolate
-w/ large amounts may do enema |
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What is the supportive treatment for macadamia nut toxicity?
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Severe cases-IV fluids
-Monitor and treat hyperthermia and protect animal from injury during ataxia/paresis |
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What is the prognosis of macadamia nut toxicity?
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Good
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At least nine ochratoxins have been identified, but which one is the most common and has the greatest toxicological significance?
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Ochratoxin A
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What produces ochratoxin A?
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Aspergillus sp. in warm climates
Penicillium sp. in cool climates |
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The highest levels of ochratoxin A is found in what?
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Cereal grains such as corn, barley, wheat and rye
-also found in coffee, dried fruit & red wine |
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What are the 5 modes of action of Ochratoxin A?
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1) Intefere w/ synthesis of tRNA, mRNA, and proteins
2) Inhibition of phenylalanine metabolizing enzymes 3) Binds strongly to proteins 4) Promotion of lipid peroxidation 5) Inhibition of mitochondrial ATP production |
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What are the clinical signs of acute ochratoxin A poisoning?
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Gastroenteritis, diarrhea, emesis, tenesmus, depression, anorexia, dehydration
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*Chronic exposure to ochratoxin A results in what?
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Slow onset with signs of *kidney disease
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What happens ochratoxin A in ruminants?
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OTA is rapidly metabolized in the rumen
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What happens to pre-ruminant calves that ingest ochratoxin A?
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Primarily a kidney toxin, but can also cause liver damage
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What long term damage can ochratoxin A cause other than kidney disease?
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Considered to be a carcinogen and causes kidney tumors
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True or false. There are no FDA restrictions on ochratoxin A levels.
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True, no FDA action, advisory or guidance levels has been established in US feed
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What is the EU Commission recommendations for Ochratoxin?
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Cereals and cereal products, 0.25 mg/kg
Complementary and complete feedingstuffs, 5.0 mg/kg |
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How do you diagnose Ochratoxin A toxicity?
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Lab tests reveal evidence of kindey involvement w/ elevated BUN and creatinine levels
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What are the gross lesions of ochratoxin A toxicity upon necropsy?
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Nephropathy w/ degeneration of proximal renal tubules
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