mycotoxins Flashcards
moldy feed
-mold in feed doesn’t aways mean myctoxins or no mold in feed there still could be
moldy feed is:
* Less palatable + lower nutritional value
* Production losses*
* Respiratory issues
* Mycotic abortion
* Aspergillus spp
aflatoxin where/what and target organ, species
Aspergillus flavus, penicillium spp (yellow appearance of corn)
- Substrates: peanuts, corn**, maize, cereals (wheat, barley)
- Target organ: liver
- Major human health problem – cause of liver cancer**
- Acute or chronic liver damage
species: all susceptible- poultry are the most susceptible (turkey X disease)
acute alflatoxicosis
- Acute liver failure: (1-2 days)
- Vague initial presentation: anorexia, lethargy, vomiting
- Jaundice
- Petechiation and ecchymoses
- Ascites
PM: liver enlarged, yellow
- Management: no antidote - symptomatic and supportive care (Silymarin, antioxidants, fluids, vitamin K, blood transfusion)
- Prognosis: guarded to poor
chronic alflatoxicosis
Herd level
Chronic hepatic insufficiency:
* Feed refusal, poor feed intake, decreased feed efficiency, diarrhea → weight loss
* Rough hair coat
* Impaired reproductive efficiency
* Photosensitization
* Impaired clotting → bruising, hematoma
-immunocompermized
-prognosis: poor
alfatoxin diagnosis, ddx
- Diagnosis: feed testing (LC/MS/MS) – send-out test
-tissues: liver, GI contents send out
acute liver failure ddx: blue green algea, chronic cu toxicosis
human health implications of alfatoxins
- IARC 1B – known human carcinogen: hepatocellular carcinoma
- Transfer of aflatoxins to edible animal tissues: milk, eggs
trichothecene mycotoxins targets
- Substrates: corn, cereals (wheat, barley, rye, oats) pink tinge
-T-2 toxin, HT-2 toxin, DON, DAS
Target organs: rapidly dividing cells (“radiomimetic” effect)
* GIT
* Hematopoietic system - lymphoid tissue/immune system, bone marrow
* Fetus
* Skin
t-2 toxin, Ht-2 toxin (trichothecene mycotoxins) species and clinical
- Most potent trichothecene mycotoxins
- Species sensitivity: poultry > monogastrics > ruminants
- Clinical features – chronic poisoning
- Feed refusal, decreased feed efficiency, impaired growth
- Poor reproductive performance
- Dermatitis
- Bloody diarrhea, vomiting
deoxynivalenol (DON) a trichothecene mycotoxin
- “Vomitoxin”
- Species sensitivity: pigs > other livestock
- Clinical features:
- Acute poisoning: vomiting, diarrhea, hypersalivation
- Chronic poisoning: feed refusal, decreased weight gain, decreased feed efficiency, altered immune function
trchothecenes toxins management and diagnosis
management:
* No specific antidote
* Remove contaminated feed
* Symptomatic and supportive care
Diagnosis: feed analysis (send-out) and compatible clinical signs
clin path: APLASTIC PANCYTOPENIA cats
ergot alkaloids tox and mechanism
- Substrate: cereal grains and grasses
- Seasonality: cool, wet spring
- Agonists and partial agonists of biogenic amine receptors: Norepinephrine, serotonin, dopamine
- Excessive stimulation of these receptors
- Alpha-1 adrenergic receptors: peripheral vasoconstriction***
- Anterior pituitary: decreased prolactin**
ergot alkaloids species differences
ergot alkaloids clinical features Gangrenous ergotism
-herd level problem
-develops over months/ several weeks
-decreased feed intake/ efficiency and feed refusals
* Shaggy hair coat
- Gangrenous ergotism**
- Hindlimb lameness
- Loss of ear tips, tail tips
- Loss of hooves
- Poultry: blackened combs and wattles, toes
- Weather: cold weather exacerbates vasoconstriction, livestock eat more during the winter
ergot alkaloids clinical features hyperthermic ergotism
- Can occur during mild weather
- Impaired thermoregulation due to peripheral vasoconstriction
- Decreased performance – not eating or drinking
- Shade-seeking, water-seeking
- Elevated core body temperatures
- Increased respiratory rate
ergot alkaloids clinical features Reproductive ergotism in horses
horses*
* Fescue toxicosis in USA – grazing endophyte infected tall fescue
* Poor mammary gland development
* Prolonged gestation with secondary dystocia
* Red bag
* Thickened placenta, retained placenta
* Decreased or absent milk production
* Poor doing foals (dysmaturity
ergot alkaloids clinical features Reproductive ergotism in pigs
- Poor mammary development
- Decreased litter size
- Decreased birth weights
- Agalactia → neonatal mortality
ergot alkaloid management
- No antidote → remove suspect feed**
- Gangrenous ergotism:
- Sloughing ears, tail tips: supportive care
- Sloughing hooves: euthanasia
- Reproductive ergotism:
- Place on high quality, EA negative feed
- Domperidone
- Hyperthermic ergotism:
- Cool down affect animals
- Provide lots of water
ergot alkaloid diagnosis
- Clinical signs of ergotism + presence of high concentration in feed
- Feed testing
-CFIA guideline
tremorgenic mycotoxins toxin and target
Compost poisoning, moldy fold poisoning
* Moldy dairy, nuts, bread
* Rotting organic material: garbage
- Penicillium spp.
- Toxins: roquefortine C + penitrem A
- Target organ: CNS species is dogs
- Toxicity: <0.5 mg/kg BW causes poisoning in dog
tremogenic mycotoxins clinical features
- Onset: within a few hours of ingestion
- Vomiting, diarrhea
- Tachypnea, tachycardia
- Tremors, ataxia, seizures**
- Hyperesthesia**
- Nystagmus
- Sublethal exposures: weeks to months of tremors**
tremogenic mycotoxins management
- No antidote
- Decontamination
- Limited window for induction of emesis
- Gastric lavage – can have a full stomach
- Symptomatic and supportive care
- Tremor management (methocarbamol, fluids
-IVLE
tremorgenic mycotoxins diagnosis
- History of ingestion or potential access to garbage/compost, acute neuroexcitation (tremors, hyperesthesia)
- Detection of penitrem A and/or roquefortine in tissues:
- Antemortem: stomach contents, vomitus, serum, urine
- Postmortem: liver, kidney, brain
