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1. Toxicology > Mycotoxins > Flashcards

Mycotoxins Flashcards

1
Q

Mycosis

A

Invasion in the organism by some part of the fungus

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2
Q

Mycotoxicosis

A

Mold growth is not directly involved in the host

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3
Q

Field Fungi

A

Fusarium, Pullaria, Alternaria
Grows under conditions prior to harvest
Die under usual storage conditions

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4
Q

Requirements for field fungi

A

Humidity over 80%
Moisture over 22%

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5
Q

Storage Fungi

A

Aspergillus, penicillin
Don’t invade intact grain prior to harvest
Humidity @ 70%, moisture 14-24%

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6
Q

Mycotoxins storage and transport

A

Dry samples: oven dry 176F-194F for 3 hrs
Reduce moisture to 12-23%
Long term: dry samples <12% and seal in moisture proof containers

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7
Q

Mycotoxin containers

A

Paper/ cloth bags
Avoid plastic bags

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8
Q

T/F: Mycotoxins have no specific treatment

A

TRUE

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9
Q

Mycotoxin prevention

A

Avoid contiaminated feed
Cleaning
Drying (13-25%)
Diluting with clean grain

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10
Q

Sources of alfatoxins

A

Aspergillus flavus, A. parasiticus
Corn, milo, cottonseed, peanuts

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11
Q

What enhances alfatoxin production

A

High humidity, grain moisture, drought stess
Fungal growth

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12
Q

Alfatoxin MOA

A

Inhibits and impairs protein synthesis
Interferes with transcription and fat metabolism

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13
Q

Hepatic Steatosis for alfatoxins

A

Due to lack of formation of lipid acceptor protein

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14
Q

What does hepatic steatosis lead to?

A

Decreased cellulose digestion
Reduced volatile fatty acid formation
Inhibition of proteolysis
Necrosis occurs

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15
Q

Alfatoxin B1

A

Most common and toxic
Forms covalent adducts with DNA,RNA and proteins

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16
Q

Alfatoxin M1

A

Carcinogenic potential
Milk, urine, tissues
Metabolite of B1

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17
Q

Alfatoxins species susceptibility

A

More severe in young
Poultry and monogastrics susceptible
Swine, dairy cattle, nutritionally deficient animals

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18
Q

Signs of alflatoxicosis (acute toxicosis)

A

Depression, anorexia, WL, malabsorption, bloody stools, ↓ milk production, subnormal temp.

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19
Q

Chronic alfatoxicosis in poultry

A

Pale bird syndrome, ↓ feed efficiency, stetarrhea, ↓ growth rate, ↑ capillary, bruising

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20
Q

Chronic alfatoxicosis in swine

A

Ascites, mild anemia, icterus, slow growth, anorexia, unthriftiness

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21
Q

Chronic alfatoxicosis in cattle

A

Reduced production and reduced rumen motility

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22
Q

Alfatoxicosis pathology

A

Liver is the major target organ
Degeneration and necrosis
Fatty change, bile duct proliferation

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23
Q

Testing and analysis of alfatoxins

A

Black light test
Thin layer chromatography
Gas-liquid chromo.
Mass Spectrometry

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24
Q

Alfatoxins black light test on corn

A

UV light gives a bright yellow fluorescence due to kojic acid marker
Fluorescence: broken or damaged grains

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25
Q

Alfatoxins tissue analysis

A

Milk and urine: M1 detectable 7-15d
Liver and kidney: excreted 72-96h and residue dissipates after 14d

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26
Q

Alfatoxin treatment

A

Hydrated sodium calcium alumino-silicate
Vit. E and Selenium

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27
Q

Alfatoxin prevention

A

Anhydrous ammonia (treat grain 10-14d)
Mold inhibitors

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28
Q

FDA guidelines for alfatoxins

A

Actionable level 0.5 ppb in milk (1%)

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29
Q

Zearalenone sources

A

Fusarium roseum and F. monilforme
Corn, wheat, barely, milo

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30
Q

Zearalenone fungal growth

A

Pink ear rot, scab

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31
Q

Zearalenone MOA

A

Alters DNA and RNA synthesis
Weak estrogenic effects
Inhibits FSH and ovarian maturation

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32
Q

Zearalenone susceptibility

A

Swine (prepubertal females/ gilts)

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33
Q

Zearalenone in swine

A

Hyperestrogenism
Swelling, edematous vulva, enlarged mammary gland, tenesmus, rectal/ vaginal prolapse

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34
Q

Zearalenone in mature cows

A

Nymphomania syndrome
Prevents follicular development
Pseudopregnancy/ anestrus syndrome

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35
Q

Lesions produced by Zearalenone

A

Edema or uterus, ovarian atrophy, follicular atresia, hypertrophy of uterus

36
Q

Zearalenone Treatment

A

AC, prostaglandin F2 alpha

37
Q

Slaframine

A

Indolizidine alkaloid in dried and sun-cured forages
R. leguminicola causng black path disease

38
Q

Slaframine MOA

A

Binding to AcH receptors
Parasympathomimetic properties
Mimics AcH

39
Q

Slaframine species susceptibility

A

All, but horses commonly affected
Cattle, sheep, goats susceptible

40
Q

Slaframine toxicosis signs

A

Rapid within 1-3hr
SLUD
Bloat, stiffness, cessation of milk production

41
Q

Ochratoxins and citrinin

A

From corn, barley, wheat, rye
Renal tubule: ↓ metabolite clearance and urine concentration ability

42
Q

What is the most common ochratoxin?

A

Ochratoxin A

43
Q

Ochratoxins and citrinin subacute/ chronic signs

A

PUPD, immunosepression, teratagenic, carcinogensis

44
Q

Ergotism

A

Invades the ovary of the grass flower during maturation and formation
Rye, barely, wheat, oats

45
Q

species most affected by erogotism

A

All, mostly cattle, sheep, swine and poultry

46
Q

Ergotism MOA

A

Ergot alkaloids mimic the action of dopamine in CNS
Targets uterus, small arteries (uterine contractions)

47
Q

Ergot toxicosis

A

Lameness
Swelling and tenderness of fetlock and pastern (loss of sensation)
Dry gangrene
Tip of tail/ ears necrotic and slough

48
Q

Treatment of Ergot toxicosis

A

Domperidone (horses)

49
Q

Fescue toxicosis

A

Ergot poisoning like
Ergot alkaloids (ergovaline) produced by endophyte fungus
Lolium arundinaceum/ Festuca arundinacea

50
Q

Syndromes produced by fescue toxicosis

A

Fescue lameness, summer fescue toxicosis, fat necrosis

51
Q

What causes Fescue foot/ lameness

A

Ergot alkaloids: ergovaline

52
Q

Fescue lameness/ fescue foot

A

Lameness (hindlimbs), necrosis
Swelling/ reddening
Knuckling, arching back, shifting wt
Happens in late fall/ winter

53
Q

Summer Slump cause

A

Endophyte fungus: Neotyphoidium coenophialum

54
Q

Summer Slump

A

Affects cattle&raquo_space; sheep and horses

55
Q

Signs of summer slump

A

Reductions: feed, milk production, weight
↓ immune response
Delayed shedding, bleaching
Reduced heat transfer

56
Q

Fescue toxicosis: Fat necrosis (lipomatosis)

A

Hard masses of necrotic fat in abdomen and pelvic areas in cattle over 2
Sites: omentum, mentary and peritoneal fat

57
Q

Fat necrosis toxic effects

A

Compression of abdomen, obstruct birth canal

58
Q

Diagnosis of fat necrosis

A

rectal palpation, ultrasound, biopsy, laparotomy

59
Q

Equine Fescue toxicosis

A

In mares
Stillborns, retained placenta, ↑ placental weight and thickness, ↓ prolactin and progesterone

60
Q

Equinr fescue toxicosis treatment

A

Domperidone (dopamine antagonist, normalize prolactin)

61
Q

Fescue toxicosis management

A

Endophyte free grass
Rotation (off fescue in hot summer)
Dilution: interseeding with red or white clover

62
Q

Tremorgenic grass staggers

A

Sheep and cattle
Infected ryegrass- endophyte A. lolii
Fine tremors, stiffness, ataxia, hypermetria, seizures

63
Q

Tremorgenic pentitrema A

A

Indole alkaloids
Walnuts, cream cheese, old moldy foods
Reduces GABA and glycine

64
Q

Tremorgenic pentitrema A signs

A

Tremors, stiffness, ataxia, seizures, opisthotonos

65
Q

Tremorgenic pentitrema A treatment

A

Anticonvulsants: pentobarbitol
Decontemination (emesis and lavage)

66
Q

Trichothecenes

A

Milo, wheat, corn, rye, barely, cereal crops
Occurs in late- harvested and over- wintered grain

67
Q

Trichothecenes MOA

A

Inhibits protein, DNA and RNA synthesis in cells
Cytotoxic to cells in vitro
Dermonecrotic effect

68
Q

What species is most sensitive to Trichothecenes?

69
Q

Trichothecenes clinical signs

A

Dermal and oral irritation + necrosis
Epithelial necrosis (mouth or beak)
Hemorrhage, anemia, hypoproteinemia

70
Q

Acute high levels of type A Trichothecenes

A

GIT ulceration, enteritis, ulceration of lymphoid follicle
Small and misshaped feathers

71
Q

Chronic exposure to type A Trichothecenes

A

Lymphoid depletion
Small and misshaped feathers

72
Q

Fumonisins (Moldy corn poisoning)

A

Caused Fusarium Verticilloides (F. moniliforme, F. proliferatum)
White and yellow corn
Potential carcinogen

73
Q

Fumonisin moldy corn poisoning susceptibility

A

Most domestic animals
Horses most sensitive
Also in swine

74
Q

Fumonisin moldy corn poisoning neurotoxicosis

A

Blindness, ataxia, circling, facial and pharyngeal paralysis, elevated liver enzymes, death

75
Q

Equine leukoencephalomalcia

A

From moldy corn poisoning and fatal
Softening and liquefaction of cerebral white matter, lesions, collapse of gray matter, hemorrhage

76
Q

Fumonisin moldy corn poisoning in swine

A

Acute progressive respiratory disorder
Acute pulmonary edema
Hepatic lesions
Focal pancreatic necrosis

77
Q

Fumonisin moldy corn poisoning diagnosis

A

Serum sphinganine: sphingosine ratio
↑ liver values (cholesterol, AST, ALT, BR)

78
Q

Phomopsins: Mycotoxic Lupinosis

A

Diaporthe toxia → lupine plants (moldy)
Sheep primarily and cattle
Summer and autumn

79
Q

Phomopsins MOA

A

Phomopsins A & B
Cytotix and antimitotic mycotoxins

80
Q

Toxic effects of Phomopsins

A

Hepatotoxicosis, abortions, jaundice, death, photosensitization, lacrimation, etc.

81
Q

Lupinosis fungus

A

Diaporthe toxia (Phomopsis leptostromiformis)
Causes Phomopsis stem-blight
Produces phomopsin mycotoxins

82
Q

Toxic lupine (bitter) plants- Lupine poisoning

A

Arthrogyposis and birth defects

83
Q

Pithomycotoxicosis: Facial Eczema

A

From Pithomyces chartarum
Sporidesmins mycotoxins
Causes toxic liver photodermatitis

84
Q

Pithomycotoxicosis: species

A

Cattle, sheep, goat, farmed deer

85
Q

Pithomycotoxicosis: MOA

A

Liver injury and blockage of bile ducts

1. Toxicology (14 decks)

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