Exam 2- Mycotoxin Flashcards
What are mycotoxins
Secondary metabolites of fungi
Economic cost of $0.5-5 Billion/year
What are influences on mycotoxin production
plant varieties, climate and weather, crop monoculture, seed coat damage, insect damage, storage quality, milling practices
How does fungi develop in grain bins?
Moisture migration and bin condensation
What is the common source for Aflatoxin?
Aspergillus flavus
source; high energy grains -> use energy from kernel
Corn peanuts, milo, cottonseed
Waht factors favor Aflatoxin
Temp 78-90
drought stress
insect damage
High humidity and moisture
Mechanism of Action associated with Aflatoxin
AFB1 metabolized by eposide. Epoxide binds to nucleic acids (DNA and RNA), Inhibition of protein synthesis, cell processes are disrupted, cell death -> necrosis
What are predisposing factors to Aflatoxin
low protein diet, low antioxidants, low vitamin A, low choline/methionine
clinical signs associated with Aflatoxin
Acute: anorexia, depression, emesis, bloody diarrhea, hemorrhage, icterus
chronic: decreased weight gain/production, immune suppression, Teratogenic, Carcinogenic, hepatic damage
Acute Lesions associated with Aflatoxin
Liver- tan to yellow, multi-organ hemorrhage
Microscopic: hepatocellular vacuolization, centrilobular congestion and necrosis, renal tubular necrosis
Chronic lesions associated with Aflatoxin
Nutmeg liver
hepatocellular vacuolization, hepatic fibrosis, bile duct proliferation
Human health concerns associated with Aflatoxin
Considered carcinogenic: FDA actino level is 0.5ppb
no treatment or antidote
Tricothecene Mycotoxins favored conditions
Cool temperatures or alternatign cool and warm temps
high moisture
Effects of Tricothecene
wide range of effects on the body- dependent on toxin
hematopoetic, dermal, lymphoid, GI
T2 toxin effect
Dermal and mucosal necrosis
Affects rapidly dividing cells
Causes immunosuppression: Lymphoid depletion, thymic involution, pancytopenia
Deoxynivalenol source, and conditions
corn
wet and cool conditions
What is Deoxynivalenol produces with
Zearalenone
Called a “vomitoxin”
Clinical effects in swine of Deoxynivalentol
Swine are the msot sensitive species -> younger pigs are more sensitive (feed averson, vomiting, feed refusal)
Neurochemical effect (increased serotonin): learning period of feed refusal
ruminants and horses are resistant!
How is the presence of Deoxynivalenol diagnosed?
History and presence of vomitoxin in feed
Source, conditions associated with Zearalenone
Corn is the main source
Optimal conditiosn: cool wet environments
Estrogenic conditions
** Zearalenone and vomitoxin are typically found together **
MOA of Zearalenone
binds to estradiol receptor -> promotes signs of estrogenism: decreased folicular maturation, inhibtion of ovulation
clinical effects of Zearalenone
Reproductive issues:
Females: hyperestrogenism, anestrus, embryonic losses, mammary gland development (NOT ABORTIVE!!!)
Males: decreased libido and semen quality
Fumosin species susceptible
Equine and swine are the most affected species
MOA of fumosin
inhibits sphingolipid synthesis
sphingolipids: components of cell membranes, and nervous tissues
clinical effects of Fumosin
Swine: Respiratory- dyspnea, cyanosis, weakness, acute death
Equine: neurologic - blind, ataxia, depressed
Lesion in swine associated with Fumosin
wet heavy edematous lungs
Pulmonary edema- expanded interlobular septa
Tan friable liver
Microscopic lesions: pulmoanry edema, centrilobular necrosis, portal fibrosis, fatty disposition
Lesions associated with Equine and fumosin
Gross lesions are necrosis of the white matter
Leukoencephalomalacia
Brown-yellow liver
Microscopic lesions include: neuronal vacuolization: expansion and edema
Clinical pathology associated
inidcators of hepatic insult
elevated liver values
