Mycotoxins Flashcards
Mycotoxins
Toxins of fungal/mold origin = secondary metabolites
Results in production losses
What factors affect mycotoxins?
Many not destroyed by processing
-multiple mycotoxins present
-production of mycotoxins affected by substrate, temperature, oxygen, humidity
Does the presence of mold mean mycotoxins?
No and lack of mold does not mean mycotoxins are not present
Moldy feed
- Less palatable and lower nutritional value= production losses
- resp issues
- Mycotic abortion = Aspergillus spp
Aflatoxin
Yellow appearance of mold
-grow with high temperature, drought stress, damage due to insects
What feed carries aflatoxin?
-peanuts
-corn
-maize
-cereals (wheat, barley)
Target organ of aflatoxin
Liver
-causes liver cancer or acute/chronic liver damage
Where is aflatoxin found?
Not routinely found in Canada, found in USW corn belt
Aflatoxin mechansim
aflatoxin B1, B2, G1, G2
-toxins undergo bioactivation in liver= oxidative damage= acute liver failure
*carcinogenic
Species susceptible to aflatoxins
All species susceptible (*especially poultry! Turkey X disease!)
Acute aflatoxicosis
Acute liver failure
-anorexia, lethargy, vomiting
-jaundice
-hematemesis, hematochezia, melena
-petechiation and ecchymoses
-ascited
Clinical pathology of aflatoxins
Increased liver enzymes, indicators of liver failure
Post mortem of acute aflatoxicosis
enlarged, pale yellow, friable liver, generalized icterus
Histo acute aflatoxicosis
-hepatic lipidosis
-bile stasis
-biliary hyperplasia
-hepatocellular necrosis and steatosis
Management of acute aflatoxicosis
-No antidote
-symptomatic and supportive care
Prognosis of aflatoxicosis
Guarded to poor
Chronic aflatoxicosis
**At herd level
-chronic hepatic insufficiency = feed refusal, poor feed intake, decreased feed efficiency, diarrhea= weight loss
-rough hair coat
-impaired reproduction efficiency
-photosensitization
-impaired clotting= bruising, hematomas
-poor immunocompetence= increased susceptibility to infection
Chronic aflatoxicosis prognosis
Poor in advanced stages of disease
Aflatoxin diagnosis
-Feed testing = send out test
-detection in liver, GI contents
DDx in aflatoxins
-acetaminophen
-blue green algae
-Amanita mushrooms
-chronic copper toxicosis
-iron
xylitol in dogs
-alsike clover in horses
Trichothecene mycotoxins
-Fusarium spp often found in corn, cereals (wheat, barley, rye, oat)
Ideal conditions for trichothecene mycotoxin growth
-high humidity
-wet grain in storage
-cool to moderately warm climates
-production in field and during storage
Mechanism of trichothecene mycotoxins
Inhibits macromolecule synthesis = direct cytotoxicity
Target: fast dividing cells = GIT, hematopoietic system (lymphoid tissue/immune system, bone marrow), fetus, skin
T-2 toxin, HT-2 toxin
Most potent trichothecene mycotoxins
-Most sensitive are poultry> monogastrics > ruminants
Clinical signs of T-2 and HT-2 toxins
Chronic poisoning
-feed refusal
-decreased feed efficiency
-impaired growth
-poor reporductive performance
-dermatitis
-bloody diarrhea, vomiting
-mucosal lesions (oral, esophageal, GIT)
-abortion
-increased susceptibility to secondary infections, vaccine failure
Deoxynivalenol (DON)
Vomitoxin
*most sensitive in pigs> other livestock
Clinical signs of DON
Acute poisoning: vomit, diarrhea, hypersalivation
Chronic: feed refusal, decreased weight gain, decreased feed efficiency, altered immune function
Clinical pathology signs of trichothecene mycotoxins
Aplastic pancytopenia
Management of trichothecenes
-no antidote
-remove contaminated feed
-symptomatic and supportive care (transfusions, gastroprotectants, fluids, erythropoietin)
Diagnosis of trichothecenes
Feed analysis (Send out) and clinical signs
*no tissue test available
Ergot alkaloids
Claviceps purpurea - common in western canada
Where is ergot common?
cereal grains and grasses (rye, triticale, barley, wheat)
Ergot seasonality
Cool wet spring
-flowering period of growing cycle = honeydew (sclerotia or ergot bodies)
Ergot alkaloids mechanism
Excessive stimulation of:
-alpha 1 adrenergic receptors= peripheral vasoconstriction
-anterior pituitary= decreased prolactin
Species differences with ergot alkaloids
Clinical signs of ergot alkaloids
Herd level problem
-develops over several weeks to mths of consuming contaminated feed
-low feed intake
-shaggy hair coat
-gangrenous ergotism = hindlimb weakness, loss of ear tips, tail, loss of hooves
-Poultry= black combs and wattles, toes
*cold weather makes it worse= animals eat more in winter and vasoconstriction worse
Hyperthermic ergotism
Can occur in mild weather
-impaired thermoregulation due to peripheral vasoconstriction
-decreased performance (not eating or drinking)
-shade seeking, water seeking
-high core body temp
-increased resp rate
Reproductive ergotism in horses
-fescue toxicosis= grazing endophyte infected tail fescue
-poor mammary gland development
-long gestation with secondary dystocia
-red bag
-thick placenta, retained placenta
-decreased or absent milk production
-poor doing foals (dysmaturity)
Reproductive ergotism in pigs
-poor mammary development
-decreased litter size
-decreased birth weights
-agalactia= neonatal mortality
Ergot management
-no antidote= remove suspect feed
-gangrenous ergotism= sloughing ears, tail than supportive care, but sloughing hooves= euthanasia
-reproductive ergotism= place on high quality feed, and give domperidone
-hyperthermic ergotism= cool down affected animals, provide water; several weeks to recover
Diagnosis of ergot alkaloids
-clinical signs and high concentration in feeds
-feed testing= not counting or weighing ergot sclerotia in feed
Tremorgenic mycotoxins
From Penicillium spp
Compost poisoning and moldy food poisoning = dairy, nuts, bread, garbage, compost
Mechanism of tremorgenic mycotoxins
Interference with inhibitory neurotransmission (CNS)
-GABA, glycine, glutamate
Onset of tremorgenic mycotoxins
Within few hours of ingestion
Clinical signs of tremorgenic mycotoxins
-vomit, diarrhea
-tachypnea, tachycardia
-tremors, ataxia, seizures
-hyperesthesia
-nystagmus
-hyperthermia
**at sublethal doses, weeks to months of tremors may occur
Clinical pathology of tremorgenic mycotoxins
-lactic acidosis (high anion gap metabolic acidosis)
Management of tremorgenic mycotoxins
-no antidote
-decontamination= limited window for emesis, gastric lavage
-symptomatic and supportive care = tremors methocarbamol, fluids, antiemetics. ILE
*enterohepatic circulation= prolonged treatment may be needed
Diagnosis of tremorgenic mycotoxins
-history of ingestion of garbage/composition
-detection of toxins in tissues
DDX of tremorgenic mycotoxins
-strychnine
-OP/carbamates
-bromethalin
-metaldehyde
-lead
-stimulants
-pyrethroids
Prognosis of tremorgenic mycotoxins
Good with aggressive symptomatic and supportive care
