28 – Mycotoxins Flashcards
(37 cards)
1
Q
What are mycotoxins?
A
- Toxins of fungal/mold origin
- Global problem for animals and humans
- Produced in field and/or during storage
- Animals exposed through ingestion
- Rage of disease
o PRODUCTION LOSSESS - Removal of contaminated feed is KEY
- Often no specific treatment or antidote
2
Q
What are some important things to know with mycotoxins?
A
- *presence of mold does NOT mean there are mycotoxins
- *lack of visible mold DOES NOT mean mycotoxins are not present
- Many are not destroyed by processing
3
Q
Moldy feed
A
- Different problem
o Less palatable and lower nutritional value (PRODUCTION LOSSES) - Respiratory issues
- Mycotic abortion (Aspergillus spp.)
- Mold spore counts
o >1M cfu/g=feed with caution
o >5M cfu/g=do NOT feed
4
Q
Aflatoxin
A
- Aspergillus flavous, etc.
- Yellow appearance of mold
- Conditions for growth: high T, drought stress, damage due to insects
- Substrates: CORN, maize, cereals
- More in US “corn belt”
5
Q
Aflatoxin: target organ
A
- LIVER
- Major health problem: cause of liver cancer
- Acute or chronic liver damage
6
Q
Aflatoxin: toxicity and mechanism
A
- All species susceptible (POULTRY most susceptible)
- Bioactivation in liver
o Impaired protein and nucleic acid synthesis, oxidative damage=acute liver failure
o Carcinogenic, immunosuppressive
o Potential effects on kidney, reproductive system and other tissues
7
Q
Acute aflatoxicosis
A
- ACUTE LIVER FAILURE
o Anorexia, lethargy, vomiting
o Jaundice
o Hematemesis, melena
o Petechiation, ecchymoses
o Ascites
o Increased liver enzymes and indicators of failure - PM: enlarged, pale yellow, friable
- Histo: hepatic lipidosis, bile stasis, biliary hyperplasia, necrosis and steatosis
8
Q
Acute aflatoxicosis: management and prognosis
A
- No antidote
- Symptomatic and supportive are
o Hepatoprotectants, fluids, vit K, blood transfusion - Prognosis: graded to poor
9
Q
Chronic aflatoxicosis
A
- Herd level
- Chronic hepatic insufficiency
o Feed refusal, poor feed intake
o Rough hair coat
o Impaired reproductive efficiency
o Photosensitization
o Impaired clotting
o Poor immunocompetence - Prognosis: poor in advanced stages of diseases
10
Q
Aflatoxin: diagnosis
A
- Feed testing: send out test
- Detection in tissues: liver, GI contents (send-out test)
11
Q
**What are the human health implications with aflatoxin?
A
- IARC 1b: known human carcinogenic: hepatocellular carcinoma
- Transfer of aflatoxins to edible animal tissues (milk, eggs)
12
Q
Trichothecene mycotoxins
A
- Mostly produced by Fusarium spp.
o Fusarium head blight (‘pink tinge’) - Substrates: corn, cereals
- Ideal conditions for growth
o High humidity (>70%)
o Wet grain in storage
o Cool to moderately warm climates
o Production in field and during storage
13
Q
Trichothecene mycotoxins: mechanism
A
- Inhibition of macromolecule synthesis (DNA, RNA, protein), oxidative damage, induction of apoptosis
- Direct cytotoxicity
14
Q
Trichothecene mycotoxins: target organs
A
- *RAPIDLY DIVING CELLS
o GIT
o Hematopoietic system: lymphoid tissue/immune system, bone marrow
o Fetus
o Skin
15
Q
Trichothecene mycotoxins: T-2 toxin, HT-2 toxin
A
- Most potent ones
- POULTRY>monogastrics>ruminants
- Clinical features: chronic
o Feed refusal, impaired growth
o Poor reproductive performance
o Dermatitis
o Bloody diarrhea, vomiting
o Mucosal lesions: oral, esophageal, GIT
o Abortion
o Increased susceptibility to secondary infections, vaccination failure
16
Q
Trichothecene mycotoxins: deoxynivalenol (DON)
A
- “vomitoxin”
- PIGS>other livestock
- Clinical features
o Acute: vomiting, diarrhea, hypersalivation
o Chronic: feed refusal, decreased weight gain, decreased feed efficiency, altered immune function
17
Q
*Trichothecene mycotoxins: clinical pathology
A
- *APLASTIC PANCYTOPENIA
18
Q
Trichothecene mycotoxins: management
A
- No specific antidote
- Remove contaminated feed
- Symptomatic and supportive care
o Transfusion may be required
o Gastroprotectants
o Fluids
o Erythropoietin
19
Q
Trichothecene mycotoxins: diagnosis
A
- Feed analysis and compatible clinical signs
- NO tissue test available
20
Q
Ergot alkaloids
A
- Claviceps purpurea: common in western Canada
- Fescue toxicosis: USA
- Substrate: cereal grains and grasses (rye, barley, wheat)
- Seasonality: cool, wet spring
- Flowering period of growing cycle
o Honeydew: sclerotia (aka ergot bodies)
21
Q
Ergot alkaloids: mechanism
A
- Ergopeptine alkaloids=seem to be the most common
- Agonists and partial agonists of biogenic AMINE RECEPTORS
- EXCESSIVE stimulation of the receptors
o Alpha 1 adrenergic: PERIPHERAL VASOCONSTRICTION
o Anterior pituitary: DECREASED PROLACTIN
22
Q
Ergot alkaloid: species differences
A
- Cattle: gangrenous, hyperthermic
- Small ruminants and poultry: gangrenous
- Horses and pigs: reproductive
- Companion animals: not reported
23
Q
Ergot alkaloids: clinical features
A
- Herd-level problem
- Develops over several weeks to months
- Decreased feed intake, feed refusal, decreased feed efficiency
- Shaggy hair goat
- GANGRENOUS ERGOTISM
- HYPERTHERMIC ERGOTISM
- REPRODUCTIVE ERGOTISM: horses and pigs
24
Q
*Gangrenous ergotism
A
- Hindlimb lameness
- Loss of ear tips, tail tips
- Loss of hooves
- Poultry: blackened coms and wattles, toes
- **Weather: cold weather exacerbates vasoconstriction and livestock each more during the winter
- *humane euthanasia
25
*Hyperthermic ergotism
- Can occur during mild weather
- Impaired thermoregulation due to peripheral vasoconstriction
- Decreased performance
- Shade-seeking, water-seeking
- Elevated core body temperatures
- Increased RR
26
*Reproductive ergotism: horses
- Fescue toxicosis in USA
- Poor mammary gland development
- Prolonged gestation with secondary dystocia
- Red bag
- Thickened placenta, retained placenta
- Decreased or absent milk production
- Poor doing foals
27
*Reproductive ergotism: pigs
- Poor mammary development
- Decreased litter size
- Decreased birth weights
- Agalactia: neonatal mortality
28
Ergot alkaloids: management
- NO antidote
- **REMOVE SUSPECT FEED
29
Gangrenous ergotism: management
- Supportive care: ears, tails
- Sloughing hooves=euthanasia
30
Reproductive ergotism: management
- Place on high quality, ergot alkaloid negative feed
- Domperidone (will help to increase prolactin)
31
Hyperthermic ergotism: management
- Cool down affected animals
- Provide lots of water
- May take several days to weeks to recover
32
Ergot alkaloids: diagnosis
- Clinical signs of ergotism and presence of high concentration in feed
- FEED TESTING
33
Tremorgenic mycotoxins
- Compost poisoning, moldy food poisoning
o Moldy dairy, nuts bread
o Rotting material: garbage, compost
- Penicillium spp
- *TARGET ORGAN: CNS
- Mechanism: interference with inhibitory neurotransmission (GABA, glycine, glutamine)
- DOGS
34
Tremorgenic mycotoxins: clinical features
- Vomiting, diarrhea
- Tachypnea, tachycardia
- TREMORS, ataxia, seizures
- HYPERESTHESIA
- Nystagmus, hyperthermia
- Clin path: lactic acidosis (high AG metabolic acidosis)
- Sublethal exposures: WEEKS TO MONTHS OF TREMORS
35
Tremorgenic mycotoxins: management
- No antidote
- Decontamination
o Limited window
o Gastric lavage
- Symptomatic and supportive care
o Tremor management
o Lipophilic: can consider ILE
o Enterohepatic circulation prolong treatment might be required
36
Tremorgenic mycotoxins: diagnosis and prognosis
- History of ingestion or access to compost/garbage
- Acute neuroexcitation
- Detection of penitrem A and/or roquefortine in tissues
- Prognosis: good with aggressive symptomatic and supportive care
37
What is the target organ of Ochratoxin?
- KIDNEYS
