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Y4 - Large animals > Farm animal Toxicology > Flashcards

Farm animal Toxicology Flashcards

1
Q

What samples can be taken to check for toxicology?

A
  • Urine
  • Liver
  • Kidney
  • Blood
  • Stomach contents
  • Feed
  • Bone / hair
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2
Q

How would you treat a toxic case?

A
  • Remove source
  • Limit absorption / hasten elimination
  • Symptomatic + supportive Tx
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3
Q

What are common mineral poisonings?

A
  • Lead
  • Copper
  • Selenium
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4
Q

What are clinical signs of lead poisoning?

A
  • Acute poisoning = young calves - neuro signs, muscle tremors + twitching, hyperthermia, salivation, rolling eyes, bellowing, blindness, stiff gait, convulsions w opisthotonos + pupillary dilation
  • Sub-acute = adult cattle + sheep - neuro signs = dullness, anorexia, salivation, blindness, incoordination, staggering, circling, muscle tremors, colic, ruminal atony, recumbency
  • Chronic = lambs w access to soils in high lead = nephrosis, ill-thrift + gait abnormalities, osteoporosis, abortion + infertility
  • Subclinical = chronic exposure at low levels = no clinical signs
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5
Q

How is lead poisoning diagnosed?

A
  • CS
  • Heparin - >0.48umol/litre
  • Kidneys lead levels = gold standard
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6
Q

What is Tx of lead poisoning?

A
  • Chelation therapy
  • Thiamine hydrochloride
  • Supportive therapy
  • Rumenotomy
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7
Q

How is lead poisoning prevented / controlled?

A
  • Remove animals from source
  • Good waste management on farm
  • Check old buildings for paint, flashing etc
  • More difficult if soil contamination
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8
Q

When do cows tend to get copper poisoning?

A
  • If access to pig feed or grazer pasture fertilised with pig manure
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9
Q

What are clinical signs of copper poisoning in cattle/sheep?

A
  • Sudden onset
  • Depressed
  • Anaemia
  • Jaundice + haemoglobinuria
  • Ataxia
  • Recumbency + death
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10
Q

What’s seen on PME of copper poisoning?

A
  • Pale / jaundice carcase
  • Dehydrated
  • Liver = pale tan
  • Kidneys = dark red / gun metal grey
  • Urine dark red / black, secondary lung consolidation
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11
Q

How is copper poisoning diagnosed?

A
  • Hx, CS + PME
  • Kidney copper conc used to confirm Dx
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12
Q

What is Tx of copper poisoning?

A
  • Supportive tx
  • Copper antagonists = molybdenum / sulphur
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13
Q

What are clinical signs of selenium poisoning?

A
  • Toxic damage to CV, Resp + urinary systems + Damage secondary lymphoid tissue
  • None specific = staggering gait, dyspnoea, tympany, colic, diarrhoea, recumbency, cyanosis, death
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14
Q

What is seen on PME of selenium poisoning?

A
  • Sub-cut haemorrhages
  • Straw coloured fluid in pericardium
  • Severe pulmonary oedema
  • Abomastitis
  • Intestinal + hepatic congestion
  • Brainstem haemorrhages
  • Destruction of renal cortices
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15
Q

How is selenium poisoning Dx?

A
  • Elevated selenium in liver, heart + kidneys
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16
Q
  • What is Tx + Px of selenium poisoning?
A
  • Tx = NO TREATMENT
  • Px = ensure correct doses when giving supplements + proper mixing
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17
Q

What are clinical signs of anticoagulant rodenticide poisoning?

A
  • Anaemic
  • non-pyrexic
  • weak
  • haemorrhages
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18
Q

What is aetiology of nitrate / nitrite poisoning?

A
  • Excessive intake of nitrate
  • Rumen bugs = nitrate => nitrite => Ammonia => Bacterial protein
  • If lots of nitrate consumed = accumulation of nitrite which is absorbed into bloodstream + converts haemoglobin into methemoglobin which cannot transport oxygen
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19
Q

What are CS of nitrate + nitrite poisoning?

A
  • Due to lack of oxygen
  • Anoxia, cyanotic mucosae tachypnoea, weak + rapid pulse
  • Sub acute + chronic forms more vague in signs
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20
Q

How is nitrate / nitrite poisoning diagnosed?

A
  • CS / Hx
  • Blood - plasma protein bound nitrite
  • Chocolate-brown discoloration of blood
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21
Q

What is Tx of nitrate/nitrite poisoning?

A
  • Methylene Blue IV
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22
Q

What is aetiology of botulism?

A
  • Often associated with the use of broiler litter as fertiliser (ingestion of pre formed toxin - rotten carcass’s types C and D, rotten plant material type B)
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23
Q

What are clinical signs of botulism?

A
  • Often found dead, or if alive often found recumbent with
    flaccid paralysis or ataxic
24
Q

Dx of botulism?

A
  • CS / Hx
  • PME = botulism toxin test
25
Q

Tx of botulism?

A

NONE

26
Q

How is botulism prevented / controlled?

A
  • Take care with broiler litter - animal by-product order
  • Clinically affected animals should NOT go into food chain
27
Q

What is mycotoxins? CS?

A
  • Produced by fungi
  • May be involved in non-specific disease syndromes
28
Q

What is the financial impact of mycotoxins of farm?

A
  1. Reduced crop yields
  2. Product rejection
  3. Reduced animal performance
  4. Increased Health Issues
29
Q

How is mycotoxins diagnosed?

A
  • Difficult - due to lack of tests
30
Q

How can mycotoxin risk be prevented / controlled?

A
  • Reduce exposure to mycotoxin
  • Prevent production of mycotoxins - influenced by temp, CO2 + water levels
  • Ensure grain is dried to correct moisture content
  • Prevent exposure of silage to oxygen by ensuring adequately compacted and covered
  • With big bale silage handle with care to avoid damaging the wrap
  • Keep straw dry
  • Avoid feed, forage or bedding with visual mould or spoilage!
  • Clean crop storage areas between batches
  • Consider adding a mycotoxin binder to ration – monitor impact on stock
31
Q

What is the aetiology of aflatoxins?

A
  • Aspergillus fungi
  • occur in field prior to harvest / postharvest if drying delayed, insect / rodent infestation
32
Q

What are CS of aflatoxins? Tx?

A
  • Primarily hepatic disease
  • Decreased feed intake
  • Decreased milk yields
  • Recurrent infection - immune suppression
  • Tx = NONE - remove source
33
Q

What is aetiology of deoxynivalenol?

A
  • Fusarium fungi
  • High prevalence in UK cereals - corn, wheat, barley, oats
34
Q

What are Clincal signs of deoxynivalenol? Tx?

A
  • Lower feed intake
  • Lower milk production
  • Diarrhoea
  • Immune alterations
  • Tx = NONE - remove source
35
Q

What is aetiology of Zearalenone poisoning?

A
  • Fusarium fungi
  • Production enhanced by high temp
  • Pigs more susceptible
36
Q

What are clinical signs of zearalenone? Dx? Tx?

A
  • CS = hyperoestrogenism, hyperemia, swelling of vulva, mammary glands, nymphomania, rectal + vaginal prolapses, poor libido in boars
  • Dx = CS + Hx
  • Tx = NONE - remove source
37
Q

What is aetiology of facial eczema?

A
  • Ingestion of sporidesmin, produced by the fungus Pithomyces chartarum found in the mat of leaf litter in shaded pasture
  • Occurs in humid, warm weather
  • Toxin concentrates in the liver causing epithelial necrosis of the bile ducts
38
Q

CS of facial eczema?

A
  • Ill thrift, reduced fertility
  • Severely affected animals develop photosensitisation. Signs include: photophobia, swelling of the face and ears
39
Q

Dx, Tx + Px of facial eczema?

A

Diagnosis
* History
* Serum gamma glutamyltransferase (GGT) concentration can be used to diagnose subclinical disease
* Can measure pasture spore counts
Treatment
* No specific treatment available
Prevention / Control Measures
* Oral administration of zinc salts prior to exposure
* Feed hay, or brassica crops during high risk periods and
avoid close grazing.
* Remove stock from high risk areas
* Breed for resistance

40
Q

Aetiology of ryegrss staggers?

A
  • Ingestion of mycotoxin lolittrem produced by acremonium loliae found on periennial ryegrass
41
Q

CS of ryegrass staggers?

A
  • Neurological signs 1-2 weeks after the introduction to toxic pasture and include:
  • Fine tremors of the head and neck at rest, head nodding,
    jerky movements of the neck and limbs, alteration in stance. Severely affected animals can collapse head first before rolling into lateral recumbency, with their necks arched back and limbs extended. Tetanic spasma can persist for several minutes before apparent recovery
42
Q

Px of ryegrass staggers?

A
  • Remove from affected pasture
  • Avoid close grazing, consider feeding supplementary hay / reseeding
43
Q

What is aetiology of ergotism?

A
  • Ingestion of ergot alkaloids produced by Claviceps purpurea a parasitic fungus of rye and other small grain crops.
  • Ergots are the resting stage of the fungus and can be seen as dark horn like structures which replace grass seeds
44
Q

CS of ergotism?

A
  • Capillary damage with extremities of affected animals appearing painful, inflamed then cold with numbness and the development of dry gangrenous lesion’s in the lower legs, ears and tail. Affected animals may loose weight, have reduced milk yields and painful udders. Irritation of the digestive tract can also occur with abdominal pain and vomiting
45
Q

What are common plant poisoning associated with?

A
  • Poor pasture viability
  • Overgrazing
  • Incorporation into conserved forages
  • Use of herbicides
  • Increased accessability - dumping of hedge cutting and garden waste, clearing ditches + leaving plants wilt
  • Transportation
46
Q

How is plant poisoning diagnosed?

A
  • Consider exposure, time frame, risk factors (overgrazing), clinical signs
47
Q

What is ragwort?

A
  • Aetiology = pyrrolizidine alkaloids - hepatotoxic
  • CS = weight loss, oedema, straining diarrhoea, Photosensitisation, Pigs quite resistant to ragwort toxicity
  • Dx = Liver Biopsy = fibrosis, vein occlusion, bile duct proliferation
48
Q

What are bluebells?

A
  • Aetiology = scillaren glycoside alkaloids
  • CS = abdominal pain, vomiting diarrhoea
  • Hard dry faeces and bloat in cattle
  • Weak pulse, milk drop
  • Dx = Evidence - CS
49
Q

What are classed as brassicas?

A
  • Broccoli
  • Cauliflower
  • Beet
  • Kale
  • Cabbage
  • Rape
  • Turnips
50
Q

What are Ra[e + Kale? Aetiology? CS?

A
  • Aetiology = Ingestion of a variety of substances found in common feed associated plants (fodder beets, kale, rape, turnips) including S-methylcysteine sulfoxide (SMCO), nitrate / nitrites, goitrogens, oxalates, Some evidence for inherited predisposition e.g. Zwarbles to oxalate deposition
  • CS = SMCO – causes haemolysis, anaemia, haemoglobinuria, pallor, jaundice, tachycardia
  • Nitrates (as before)
  • Hypothyroidism, goitre and hypocalcaemia
51
Q

What plants cause photosensitisation? Tx?

A
  • St John’s Wort
  • Ragwort, Bog asphodel
  • Tx = Move affected animals into shade anti-inflammatories + antibiotics - Supportive therapy for liver
52
Q

Rhododendron = Aetiology? CS? Dx?

A
  • Aetiology = Grayanotoxins bind sodium channels in excitable cells, thereby exerting their main effect on cardiac and skeletal musculature and the nervous system.
  • Access to woodland or ornamental shrubs
  • CS = Abdominal pain, vomiting (pathognomonic), tremors, staggering, recumbency, paddling, death
  • Diagnosis = Clinical signs and presence of plant in rumen
53
Q

Acorns + Oak, aetiology? CS?

A
  • Aetiology = Ingestion of phenols and tannins following windy conditions in the autumn
  • CS = Alimentary signs: colic, anorexia, weight loss, ascites, oedema, constipation replaced by black tarry faeces. Haematuria
  • On PME – gastrointestinal ulceration and haemorrhage, nephritis, liver degeneration
  • Bloods – raised urea and creatinine, raised liver enzymes
    *Pigs are more resistant, can be used to clear acorns
54
Q

Bracken aetiology? CS? Dx?

A
  • Aetiology = Cyanogenic glycoside, thiaminases
  • CS = Vary! Different toxins affect species differently
  • Enzootic haematuria in cattle
  • Depression, weakness, anorexia, haemorrhagic syndrome (blood in faeces, urine and haemorrhages on mousuc membranes). Pancytopenia with agranulocytosis leucopenia and thrombopenia
  • Tumours of the bladder wall
  • Thiamine deficiency in pigs – heart enlargement
  • Bright blindness in sheep (retinal degeneration)
  • Diagnosis = History, clinical signs, blood results
55
Q

Yew aetiology? CS? Dx?

A
  • Aetiology = Yew contains the alkaloid and the heterocide taxicatoside, toxicity is considered maximal in winter.
  • The lethal oral dose of fresh plant material per
  • kg of bodyweight is reported to be 1 to 10 grams.
  • Very acute! Ingestion of yew
  • CS = Sudden death, Cardiac depression, dyspnoea, abdominal pain, muscle tremor, weakness
  • Diagnosis = Presence of plant in rumen or mouth
56
Q

Hemlock water dropwort aetiology? CS? Dx?

A
  • Aetiology = Oenanthotoxin
  • CS = Sudden death, Nervous signs: salivation, dilated pupils, convulsions, Diarrhoea occurs with sublethal exposures
  • Dx = Grows in ditches – history of access to exposed tubers, which often occur after ditching or following flooding
  • Presence of plant in rumen
57
Q
A

Y4 - Large animals (78 decks)

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