4.3 Feed and Water Toxicants Flashcards
what are ionophores used for? what are common examples?
Used as coccidiostats and growth promotants
Examples include:
Monensin, Lasolacid, Salinomycin
comparative toxicity of ionophores to different species?
Most toxic: Horses
Mid: Cattle, Sheep, Dogs
Least: Chicken, Turkeys
Monensin: Mechanism of Toxicity
Mechanisms are not fully explained
Likely sustained Na+-induced Ca++ effect in myocytes Muscle contraction > necrosis
How do we diagnose Monensin toxicity?
Serum biomarkers
increased AST, CK, AP
Cardiac troponin ❤
Reduced Ca++ and K+
Chemical Analysis
Ionophore screen in feed/tissue
Cattle > 33 ppm, Poultry >110 ppm
Rapidly metabolized in tissue residues
Differentials for Monensin toxicity?
White muscle disease (selenium deficiency)
Cardiotoxins (yew, oleander)
treatment for Monensin toxicity
Feed change, supportive care, detoxification, decontamination
Avoid cardiorespiratory exertion (putting cattle in a chute)
Target organs of Monensin toxocity in various species
=>muscle necrosis
Cardiac muscle
Horses Donkeys Cattle
Skeletal muscle
Sheep Pigs Dogs
clinical signs of Monensin toxicity in cattle
- Anorexia, decreased milk production
- Mild diarrhea and depression
- Dyspnea, ataxia, death from cardiac failure
what factors contribute to acute nitrate/nitrite toxicity in ruminants?
High nitrate intake
Plants (>1%) and/or water (>1000ppm)
Season and climate
Some plants have high nitrate content
More likely in spring (use of nitrate fertilizer), or after frost damage or drought
Roots take up more nitrate as soil warms
Reduced photosynthesis slows nitrate utilization
Mismanagement
Hungry animals eat more
Reduce proportion of high nitrate components in mix
what is the mechanism of nitrate/nitrite toxicity in ruminants? what is the result?
Nitrates (water contamination, young green feed, etc)
>Convert to nitrite (rumen flora)
>Nitrite binds to Fe3+ in heme Oxidation to methemoglobin
>Hypoxia and vasodilation (nitric oxide/NO)
=>Methemoglobinemia
clinical and necropsy signs of acute nitrate/nitrite toxicity in ruminants
Weakness and collapse, ataxia, death
Acute death, cyanosis, dark brownish blood (variable)
Nitrate (>20 ppm) in ocular fluids (rapidly degraded)
Abortions 3-7 days after fetal hypoxia
treatment for acute nitrate/nitrite toxicity in ruminants
IV methylene blue (1 or 2%: 1-10 mg/kg IV)
> Reverses methemoglobinemia
prevention of acute nitrate/nitrite toxicity in ruminants
Monitor feed nitrates, pasture levels, and intake in critical periods
Safe levels < 0.5%
how does salt poisoning occur?
High sodium intake during water deprivation
Precipitated by renewed access to water
***what is the mechanism of salt toxicity? what are the dehydration and rehydration phases?
Dehydration phase [water deprivation]
1. Dehydration increases Na+ in plasma - 135 increase to 160+ mEq/L
2. High Na+ by equilibration in astrocytes and CSF
“salty brains”
Rehydration phase
Water moves into the salty brain!
1. Rapid rehydration reduces Na+ concentration in plasma
2. Water influx into astrocytes and CSF [brain edema] because excretion of Na+ is slower
3. Intracranial pressure increases
4. Perfusion decreases - ischemia and necrosis
5. Polioencephalomalacia (grey matter necrosis), especially in pigs
clinical diagnostic signs of salt toxocity? lab signs? necropsy signs?
Clinical Signs:
* Circumstantial: recent water restriction and increased salt intake
* Typical CNS signs: dog sitting, wandering, bump into objects, circling,
seizures, opisthotonus, paddling in a coma
* Death within several to 48 hrs
Laboratory signs:
* High Na+ in serum and CSF
* Na+ analysis of feed (or water)
Necropsy signs:
* Polioencephalomalacia
* Eosinophilic meningoencephalitis transiently in pigs
how can we manage and prevent salt toxicity?
Treatment
-No effective treatment
Prevention
-Reduce salt intake
-Gradually resupply water
Differentials for salt toxicity?
Differentials: insecticide poisoning, pseudorabies, arsenic, Se intoxication, anything causing CNS signs
Non-protein nitrogen (NPN) toxicosis mechanism and clinical signs?
Urea, ammonium acetate, ammoniated feeds, etc
NPN > converted to ammonia > amino acids in rumen
Overload causes hyperammonemia Rapid onset salivation, ataxia, muscle spasms, convulsions, death within
hours of access to new feed mix.
how can we diagnose non-protein nitrogen toxicosis?
-High rumen pH (8-10) (but samples are unstable)
-Feed analysis
how can we treat non-protein nitrogen toxicosis?
-Cold water (slows rumen metabolism)
-5% acetic acid orally before recumbency
>2-6 L for cattle, 0.5-1 L for sheep and goats
what are cyanobacteria? when do we encounter them?
- Primitive photosynthetic bacteria
- Blooms under conditions favoring competition with plant algae
- Warm sunny weather (summer and fall)
- Eutrophication (animal wastes, phosphates)
- Water - pH 6 to 9
Are generally hepatotoxic and/or neurotoxic
what are some toxic forms of blue-green algae? what tissue do they affect?
-Microcystis (M. aeruginosa) and Nodularia (N. spumigen) effect liver
-anatoxin produced by anabaena is neurotoxic
what is the mechanism of microcystis and nodularia toxicity?
Inhibit protein phosphatases
-Disrupts cytoskeleton leading to endothelial separation in hepatic sinusoids and zonal hemorrhage/necrosis
clinical signs of Microcystis (M. aeruginosa) and Nodularia (N. spumigen) toxicity?
-Vomiting in some species, colic, diarrhea (often bloody)
-Sudden death from hepatic encephalopathy
Microcystin Hepatotoxicity mechanism?
-Inhibits protein phosphatase 2A
-Cellular hyperphosphorylation
-Cellular injury and necrosis
-Loss of structural associations
Anatoxin Neurotoxicity effects?
Anatoxin-a produced by Anabaena (cyanobacteria)
Acute anterior paralysis and sudden death
what are mycotoxins? what do they do?
Toxic secondary metabolites produced by fungi
* ~7 groups are important in animal toxicoses (over 400 exist)
* Ranking depends on agricultural practice and climate
* Residues with human risk important to feed producers
=>toxin production depends on various conditions
under what conditions do fungi flourish? which are likely to be found in fields vs storage?
Fungi flourish in high moisture conditions
Field contamination by plant pathogens e.g. Fusarium
Storage contamination by saprophytes e.g. Aspergillus
Grains (especially corn), nuts or vegetation (pasture, hay)
25% of world’s crop harvests are contaminated with fungi
Levels usually below those responsible for overt toxicity
Factors affecting mycotoxin production
Plant substrate
Plants favor selected pathogens and saprophytes
Composition (e.g. starch)
Damage (stress, insects, other fungi, etc)
Growth conditions
Humidity
Temperature
pH
Oxygen
Geographic locations
Type of mycotoxins consumed
Exposure
Animal susceptibility
Feeding systems
zearalenone - where is it found? what is it? what animals does it affect? what are the sings/symptoms?
-found in northern corn areas, including Ontario
-estrogenic mycotoxin
-affects pigs > cattle > > poultry
-vulvar hypertrophy in gilts, infertility, rectal prolapse, mammary hypertrophy
trichothecenes - where is it found? what is it and what types are there?
found in continental climates with cold winters
-Over 170 structurally related compounds
-Few of these are important as animal toxins, but few are very potent
-Produced by fungi that grow in cool, damp conditions
-Fusarium spp
Type A: T-2 toxin, diacetoxyscirpenol (DAS), etc
Type B: Deoxynivalenol (vomitoxin), etc
Also have type C and D
Fungi proliferate on plants in the field Further fungal growth in feed storage
-Toxins produced under cool moist conditions
Over wintered grain and forage
Moisture >15%
T-2 toxin + vomitoxin @ 6-12°C
(whereas is Zearalenone 19-20°C)
zearalenone diagnosis
Estrogenic lesions or infertility
Pink Fusarium mould contamination of grain, corn Conditions for production (cool, high moisture) Zearalenone analysis
Pigs >1 ppm (gilts) > 3 ppm (sows) > 9 ppm (boars)
Cattle > 12 ppm (heifers)
Poultry (very resistant)
zearalenone treatment/prevention?
Withdraw or dilute feed
Divert feed to cattle (not dairy) or poultry
Prevent moisture and fungal contamination
trichothecenes clinical signs
**1. Poor growth/production
**2. Feed refusal (or vomition)
- Irritation of skin and mucosal membranes
- Cytotoxic to replicating cells @ higher doses
* Immunosuppression
* Impaired hematopoiesis
what animals are particularly susceptible to fumonisins?
Fumonisins - pigs and horses are particularly susceptible
=>Horses fed mouldy corn
what type of toxic effects and clinical effects do fumonisins have?
Hepatotoxic, vasotoxic, and neurotoxic
**Acute porcine pulmonary edema (PPE)
**Cardiotoxic in pigs
-Hepatotoxicity in various species
-Hepatocarcinogenic in rats
-Nephropathy in rats, rabbits, and lambs
-Linked to esophageal cancer in humans
what animal is resistant to fumonisins?
poultry
what conditions favor fumonisin growth?
Fusarium verticillioides (syn. F. moniliforme)
Toxic mold in warm conditions
what is the mechanism of fumosisin toxicity?
fumonisins inhibit ceramide lipid synthesis
=>cause buildup of sphingosine, which causes:
-CNS vasogenic edema
-inhibits Ca++ channels > cardiac failure
what are alfatoxins produced by? how can we see them? where? what species do they affect and how?
Produced by Aspergillus flavus and A. parasiticus
Blue (AFB) or green (AFG) fluorescence UV
Mainly on corn, sorghum, peanuts, small grains
Grow in storage (or in field) in humid, warm conditions
Highly potent human toxins
Hepatotoxic, immunosuppressive, and hepatocarcinogenic
Wide variation in susceptibility among species
Dogs: chronic hepatopathy (eventual cirrhosis)
effects of aflatoxin on the liver?
Acute: hepatic necrosis
Chronic: cirrhosis and cancer
what are ochratoxins? how are they produced and what do they do? what species are susceptible or resistant?
Produced by Aspergillus ochraceus and Penicillium viridicatum
Nephrotoxic, hepatotoxic, carcinogenic
Pigs and dogs most susceptible > chickens
> Porcine nephropathy in Denmark
> Consider meat residues (clear in a few weeks)
Cattle are resistant (toxin degraded in rumen)
what are tremorgens? what do they do and what species are susceptible? what are a few examples?
Neuro-excitatory toxins
-Tremors and convulsions if severe
-Sheep, cattle, dogs most susceptible
Penitrem A - Penicillium spp - Tremors in dogs
Roquefortine - P. roqueforti - (walnuts, garbage)
Paspalitrem - Claviceps paspali - Paspalum staggers
what is ergot and where is it found? what does it produce? what effects does it have?
-Ergots are sclerotia (dark resting body, mass of hyphal threads) of Claviceps spp
-Grows in various grains Produce toxic ergot alkaloids
Indole alkaloids, lysergic acid, and ergotamine
-Constrict arterial smooth muscle
-Ischemia of extremities
-Exacerbated by cold
