12. Other feed and water contaminants

• Contaminants in animal feeds and livestock water include fungus, mycotoxins, environmental contaminants, and bacterial contaminants.

Mycotoxins

• Mycotoxins are metabolites produced by fungi, not essential for their growth, but produced under stress.
• They are low molecular weight, non-antigenic substances.
• They are produced on various substrates, including animal feeds at certain temperatures and moisture levels.
• There are over 300 identified mycotoxins from approximately 350 fungal species.
• In the field, mycotoxins are associated with conditions like facial eczema in New Zealand.
• Aflatoxin, Zearalenone (ZEN), and Deoxynivalenol (DON) are the three most reported mycotoxins in livestock production.
• Mycotoxicosis can be suspected if outbreaks show characteristics like a cause that is not readily identifiable, non-transmissibility and association with certain batches of feed.
• Outbreaks of mycotoxicosis can be seasonal, affected by weather conditions that promote mold growth.
• Biological action of a toxin in a host is often delayed.
• Diagnosis of mycotoxicosis depends on recognizing specific clinical signs, which may or may not be present.
• Toxins are not uniformly distributed, making them difficult to detect; detection methods are not always available.
• Toxins may have a short period of existence in the animal, further complicating diagnosis.
• Preventing and controlling mycotoxins requires good agricultural, manufacturing, and hygienic practices.
• Plant disease management, appropriate storage conditions, and chemical and physical decontamination are crucial control measures.

Aflatoxins

• Aflatoxins are produced by Aspergillus fungi.
• Aflatoxins are acutely toxic, hepatotoxic, immunosuppressive, mutagenic, teratogenic, and carcinogenic.
• AFB₁ produced by A. flavus is the most dangerous aflatoxin.
• AFB₁ is metabolized to AFM₁ in the mammalian liver.
• 2-6% of AFB₁ ingested by lactating animals is transmitted into milk as AFM1.
• Dairy animals can secrete carcinogenic metabolites (aflatoxin M series) in their milk after ingesting aflatoxin-contaminated feed.
• In Australia, rain-fed peanuts grown in the Burnett region of Southeast Queensland can have problems with aflatoxin.
• Cases of aflatoxicosis have been reported in poultry, sheep, pigs, cattle, and dogs in Australia.
• Aflatoxicosis is linked to peanut meals and by-products, moldy bread and bakery waste, and grain sorghum and maize stored with high moisture contents.
• Animal susceptibility decreases in the following order: ducks > turkeys > chicken > fish > pigs > cattle > sheep.
• Fetuses are very susceptible even to low toxin concentrations.
• Young and fast-growing animals and males are generally more susceptible.
• No animal species is resistant to acute toxic effects.
• Aflatoxins are passively absorbed from the gastrointestinal tract and absorbed from the intestinal tract into the hepatic portal system.
• Aflatoxin B1 can bind reversibly to albumin, with unbound aflatoxin B1 passing from circulation into tissues.
• Aflatoxins do not readily accumulate in tissues, although repeated exposures can generate toxic effects.
• Aflatoxins may cross the placenta and damage fetal tissue; they are eliminated through bile, feces, urine, milk, and eggs.
• Most species eliminate the toxin within 24 hours after exposure.
• GI dysfunction, reduced productivity (milk, eggs, weight gains), reduced feed utilization efficiency, anemia, and jaundice are general clinical signs of Aflatoxins.
• Aflatoxins are heat-stable molecules and cannot be eliminated through heat treatments, making prevention essential.
• Adsorbents like clinoptilolite, montmorillonite, bentonite, and aluminosilicate can be added to feed to bind aflatoxins thus decontaminating the feed.
• Microbial detoxification can decontaminate feed, especially in chickens.
• Butylated hydroxytoluene, Urtica diocia seed extract, grape seed proanthocyanidin extract, and poultry litter biochar are other additives that can counteract AFB1 in chickens.

Ochratoxins

• Ochratoxins are secondary metabolites produced by several species of Penicillium and Aspergillus.
• Ochratoxins block protein synthesis.
• Ochratoxin A is the most toxic, producing neurotoxic, nephrotoxic, teratogenic, hepatotoxic, and immunotoxic effects.
• Mild liver damage, enteritis, and immunosuppression can result from Ochratoxin.
• Poultry and pigs are acutely sensitive to Ochratoxin.
• Ochratoxins are generally not a significant risk to livestock in Australia.
• Ochratoxins enter the circulatory system through gastrointestinal adsorption.
• Ochratoxin A competes with phenylalanine-tRNA ligase, inhibiting protein synthesis.
• The mode of action includes DNA adduct formation, apoptosis, interference with the cytoskeleton, lipid peroxidation, and inhibited mitochondrial respiration.
• Absorption rate varies between species.
• Efficient degradation in the rumen results in low concentrations in cow milk.
• Non-toxic bacteria, yeasts, and fungi from soil, fruits, and vegetables can control ochratoxin-producing fungi.

Fusarium Toxins

• Capable of inducing both acute and chronic effects.
• Dose levels and duration of exposure determines the severity of Fusarium toxins.
• Types of Fusarium toxins: Trichothecenes, Zearalenone, and Fumonisin B1.

Trichothecenes

• Poisoning from type A is not diagnosed in Australia.
• Type B is DON.
• Inhibits protein synthesis.
• Results in the disruption of DNA & RNA synthesis.
• Affects actively dividing cells, also those lining the gastrointestinal tract, skin, and lymphoid and erythroid cells.
• Results in decreased immunoglobulins and cytokines.
• Intoxication results in irritation, hemorrhage, & necrosis in the gastrointestinal tract; and decreased regenerative processes in bone marrow & spleen.
• Impairs the immune system function.
• May cause reproductive changes.
• T2-toxin clinical signs are: weight loss, poor feed utilization, inappetence, vomiting, bloody diarrhea, abortion, and death in acute cases
• Guidelines dictate that pigs are more sensitive than chickens.
• Cattle & sheep are considered fairly tolerant.
• Guidelines for Australia: pig diets should contain 0.5 mg/kg DM, broiler, layer & duck diets: 2 mg/kg DM and sheep & cattle diets: 2 mg/kg DM.
• Inhibits reproductive performance & immune function.
• Pigs that have consumed contaminated feed (1mg/kg DM) typically vomit & persistently refuse feed.

Zearalenone

• A non-steroidal estrogenic mycotoxin implicated with infertility in pigs, cattle & sheep
• Low exposure causes an increased size of mammary glands & reproductive organs
• Higher doses or longer exposure interfere with conception, ovulation, implantation, fetal development & survival
• Young female pigs are very susceptible, because estrogenic effects can be produced at 0.2 mg/kg in diet
• Once young pigs consume sufficient to induce pseudo-estrogenism, lower concentration of Zearalenone can maintain the condition
• Guidance levels in Australia are 0.05 mg/kg DM for young pigs & breeding sows
• In ewes, it decreases ovulation rate, increases duration of estrus, and increases uterine weight
• Poultry is quite resistant, in which 10-800 mg/kg is required to produce significant effects

Fumonisin

• Present in maize in all Australian growing regions
• It is not regulated in Australia
• Risks for livestock appear low, given maize is rarely the main grain component of mixed diets
• FB₁ most common & toxic
• The major mode of action is interference with sphingolipid metabolism
• Fumonisins cause a wide range of illnesses such as Leucoencephalomalacia in horses and Pulmonary edema in pigs

Ergot Alkaloids

• Compounds produced by certain fungi
• Claviceps purpurea is predominantly found on rye, wheat & barley
• Epichloë species (formerly Neotyphodium species) - can infect perennial ryes grass & tall fescue
• Ergot alkaloids have different biological activities
• Ergots are only produced pre-harvest
• Biological activity is related to the similarity of the ergoline ring structure to serotonin, dopamine, noradrenaline, & adrenaline
• Ergot binds biogenic amine receptors and elicits effects such as decreased serum prolactin and vasoconstriction
• Vasoconstriction is associated with D₁-dopaminergic receptor inhibition, partial agonism of α₁-adrenergic & serotonin receptors
• Hypoprolactinaemia results from stimulation of lactotrophic D₂-dopamine receptors in anterior pituitary, and inhibition of prolactin secretion
• Ruminants are generally less affected as others that are non-ruminants
• Effects vary with species, breed, age, gender, *& physiologic state.
• In ruminants, vasoconstrictive effects are predominate and lead to both gangrenous and hyperthermic forms of ergot intoxication.
• Rectal temperatures of affected cattle are ~ 41-42°C, with an increase in respiration rate.
• Ergotism in feedlot cattle manifests as loss of ear tips, loss of tail & hyperexcitability, loss of tail & recumbency and episcleral congestion
• Severe meningeal congestion also caused in cattle due to hyperexcitability.
• Clinical signs of fat necrosis include cattle, goats, deer, pigs, and horses, and hard masses of necrotic fat in the mesentery of intestinal tract
• It can interfere with normal passage of digesta, reproductive capacities & parturition
• Effects in Mare: decreased conception or increased early embryonic mortality, abortions, prolonged gestation, decreased relaxin, dystocia, thickened, edema, retained placental membranes, Agalactia, and increased rates of newborn mortality
• Recovery unlikely in animals with clinical peripheral gangrene