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Toxicology > 4.3 Feed and Water Toxicants > Flashcards

4.3 Feed and Water Toxicants Flashcards

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1
Q

what are ionophores used for? what are common examples?

A

Used as coccidiostats and growth promotants
Examples include:
Monensin, Lasolacid, Salinomycin

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2
Q

comparative toxicity of ionophores to different species?

A

Most toxic: Horses
Mid: Cattle, Sheep, Dogs
Least: Chicken, Turkeys

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3
Q

Monensin: Mechanism of Toxicity

A

Mechanisms are not fully explained
Likely sustained Na+-induced Ca++ effect in myocytes Muscle contraction > necrosis

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4
Q

How do we diagnose Monensin toxicity?

A

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

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5
Q

Differentials for Monensin toxicity?

A

 White muscle disease (selenium deficiency)
 Cardiotoxins (yew, oleander)

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6
Q

treatment for Monensin toxicity

A

 Feed change, supportive care, detoxification, decontamination
 Avoid cardiorespiratory exertion (putting cattle in a chute)

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7
Q

Target organs of Monensin toxocity in various species

A

=>muscle necrosis

Cardiac muscle
Horses Donkeys Cattle

Skeletal muscle
Sheep Pigs Dogs

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8
Q

clinical signs of Monensin toxicity in cattle

A
  • Anorexia, decreased milk production
  • Mild diarrhea and depression
  • Dyspnea, ataxia, death from cardiac failure
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9
Q

what factors contribute to acute nitrate/nitrite toxicity in ruminants?

A

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

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10
Q

what is the mechanism of nitrate/nitrite toxicity in ruminants? what is the result?

A

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

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11
Q

clinical and necropsy signs of acute nitrate/nitrite toxicity in ruminants

A

 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

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12
Q

treatment for acute nitrate/nitrite toxicity in ruminants

A

 IV methylene blue (1 or 2%: 1-10 mg/kg IV)
> Reverses methemoglobinemia

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13
Q

prevention of acute nitrate/nitrite toxicity in ruminants

A

 Monitor feed nitrates, pasture levels, and intake in critical periods
 Safe levels < 0.5%

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14
Q

how does salt poisoning occur?

A

High sodium intake during water deprivation
Precipitated by renewed access to water

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15
Q

***what is the mechanism of salt toxicity? what are the dehydration and rehydration phases?

A

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

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16
Q

clinical diagnostic signs of salt toxocity? lab signs? necropsy signs?

A

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

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17
Q

how can we manage and prevent salt toxicity?

A

Treatment
-No effective treatment

Prevention
-Reduce salt intake
-Gradually resupply water

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18
Q

Differentials for salt toxicity?

A

Differentials: insecticide poisoning, pseudorabies, arsenic, Se intoxication, anything causing CNS signs

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19
Q

Non-protein nitrogen (NPN) toxicosis mechanism and clinical signs?

Study These Flashcards
A

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.

20
Q

how can we diagnose non-protein nitrogen toxicosis?

Study These Flashcards
A

-High rumen pH (8-10) (but samples are unstable)
-Feed analysis

21
Q

how can we treat non-protein nitrogen toxicosis?

Study These Flashcards
A

-Cold water (slows rumen metabolism)
-5% acetic acid orally before recumbency
>2-6 L for cattle, 0.5-1 L for sheep and goats

22
Q

what are cyanobacteria? when do we encounter them?

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A
  • 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
23
Q

what are some toxic forms of blue-green algae? what tissue do they affect?

Study These Flashcards
A

-Microcystis (M. aeruginosa) and Nodularia (N. spumigen) effect liver
-anatoxin produced by anabaena is neurotoxic

24
Q

what is the mechanism of microcystis and nodularia toxicity?

Study These Flashcards
A

Inhibit protein phosphatases
-Disrupts cytoskeleton leading to endothelial separation in hepatic sinusoids and zonal hemorrhage/necrosis

25
clinical signs of Microcystis (M. aeruginosa) and Nodularia (N. spumigen) toxicity?
-Vomiting in some species, colic, diarrhea (often bloody) -Sudden death from hepatic encephalopathy
26
Microcystin Hepatotoxicity mechanism?
-Inhibits protein phosphatase 2A -Cellular hyperphosphorylation -Cellular injury and necrosis -Loss of structural associations
27
Anatoxin Neurotoxicity effects?
Anatoxin-a produced by Anabaena (cyanobacteria) Acute anterior paralysis and sudden death
28
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
29
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
30
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
31
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
32
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)
33
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)
34
zearalenone treatment/prevention?
Withdraw or dilute feed Divert feed to cattle (not dairy) or poultry Prevent moisture and fungal contamination
35
trichothecenes clinical signs
**1. Poor growth/production **2. Feed refusal (or vomition) 3. Irritation of skin and mucosal membranes 4. Cytotoxic to replicating cells @ higher doses * Immunosuppression * Impaired hematopoiesis
36
what animals are particularly susceptible to fumonisins?
Fumonisins - pigs and horses are particularly susceptible =>Horses fed mouldy corn
37
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
38
what animal is resistant to fumonisins?
poultry
39
what conditions favor fumonisin growth?
Fusarium verticillioides (syn. F. moniliforme) Toxic mold in warm conditions
40
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
41
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)
42
effects of aflatoxin on the liver?
Acute: hepatic necrosis Chronic: cirrhosis and cancer
43
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)
44
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
45
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

Toxicology (11 decks)

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