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Y4 FA - GIT and nutrition > Toxicology > Flashcards

Toxicology Flashcards

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1
Q

Define toxicosis

A

A disease state that results from exposure to a poison

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2
Q

Describe the generalised treatment needed for toxicology cases

A
  • Remove source
  • Limit absorption / hasten elimination
  • Symptomatic & supportive
  • A few specific antidotes available* check they can be used in food producing animals
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3
Q

Describe the APHAs role in toxicology

A
  • Screening programmes
  • The Wildlife Incident Investigation Scheme (WIIS), detects incidents that might be associated with the misuse or abuse of agrochemicals in relation to wildlife
  • Emergency response: Following an incident such as a fire or severe flooding
  • Animal disease outbreak: This forms part of their scanning surveillance.
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4
Q

How is food safety linked to toxicology in animals?

A
  • With any poisoning incident which involves food producing animals, it is essential that an assessment of safety in carried out.
  • Under the Food Safety Act 1990 and related legislation, farmers, as primary food producers, and their advisors are required to show due diligence to protect the food chain.
  • The key activity is making sure that incidents are detected.
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5
Q

Describe the clinical signs of acute lead poisoning

A

Typical in young calves
- Found dead or death occurring within 24 hours of sudden onset toxicity with neurological signs
- Muscle tremors and twitching (head and neck), hyperthermia, salivation, rolling eyes, bellowing, blindness, stiff gait, convulsions with opisthotonos and pupillary dilation.

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6
Q

Describe the clinical signs of subacute lead poisoning

A

Adult cattle and sheep most commonly affected
- Animals live for several days.
- Neurological signs include, dullness, anorexia, salivation, blindness, incoordination, staggering, circling, muscle tremors, colic, ruminal atony, recumbency

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7
Q

Describe the clinical signs of chronic lead poisoning

A

Most commonly seen in lambs with access to soils high in lead
- Nephrosis
- Ill thrift with gait abnormalities or lameness and paralysis due to fractures (osteoporosis).
- In pregnant animals: abortion and poor fertility

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8
Q

How can lead poisoning be diagnosed?

A
  • Clinical signs
  • Heparin levels in blood
  • Kidney lead levels provide diagnostic gold standard but liver can also be used (biopsy)
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9
Q

Why are further tests often required in lead poisoning cases?

A

To clarify food safety issues – lead can be detected in blood, faces, urine and milk, hair and wool can be used for subclinical and chronic lead poisoning cases

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10
Q

How is lead poisoning treated?

A

Chelation therapy
Thiamine hydrochloride
Supportive therapy
Rumenotomy

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11
Q

How can lead poisoning be controlled/prevented?

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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12
Q

What is the obligation of farmers in regards to lead poisoning?

A

Obliged to take measures avoid contamination of the food chain – 16 week voluntary withdrawal

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13
Q

Should emergency slaughter of any of the clinically unaffected cattle in the exposed group be required during the 16 weeks of voluntary withdrawal, what should happen to the carcass?

A

The animal should be accompanied by FCI stating that offal should be discarded

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14
Q

If blood lead analysis is
1. < 0.15 µmol/l
2. 0.15 µmol/l to 0.48 µmol/l
3. > 0.48 µmol/l
4. >1.21µmol/l
What further action is required?

A
  1. No further action required
  2. Provide food chain information (FCI) to the abattoir and ensure offal is discarded
  3. Provide FCI to the abattoir, ensure offal is discarded and make an additional risk assessment as to whether carcase meat requires testing prior to carcase release into the food chain
  4. Clinical toxicity is likely. Ideally a further withdrawal period should be observed. If slaughter is essential then provide FCI to the abattoir ensuring offal is discarded and that carcase meat is tested for lead residues prior to carcase release into the food chain.
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15
Q

Describe the aetiology of copper poisoning

A
  • More common in sheep
  • Chronic copper poisoning more common
  • Variation in breed susceptibility
  • Cattle tends to occur if have access to pig feed or graze pastures fertilised with pig manure
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16
Q

List the clinical signs of copper poisoning

A

Sudden onset
Depressed
Anaemia
Jaundice and haemoglobinuria
Ataxia, recumbency
Eventually death

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17
Q

How will an animal with copper poisoning present at post mortem?

A

Carcass - pale or jaundiced, dehydrated
Liver pale tan or bronze coloured
Kidneys dark red or gun metal grey
Urine dark red / black
Secondary lung consolidation

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18
Q

How is copper poisoning diagnosed?

A
  • History, clinical signs and post mortem findings
  • Kidney copper concs used to confirm diagnosis
  • If other animals in the group can check subclinical liver damage using AST
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19
Q

How is copper poisoning treated?

A

Supportive therapy
Copper antagonists – molybdenum or sulphur * care need to monitor to avoid deficiency!

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20
Q

How is copper poisoning prevented/controlled

A

Remember poisoning is due to a combination of efficiency of absorption and dietary availability
Care copper foot baths

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21
Q

What is the cause of selenium poisoning?

A

Acute toxicosis occurs due to excessive supplementation

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22
Q

What are the clinical signs of selenium poisoning?

A

None specific – staggering gait, dyspnoea, tympany, colic, diarrhoea, recumbency, cyanosis and death

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23
Q

Which organs/tissues are damaged in selenium poisoning?

A

Causes toxic damage to the cardiovascular, respiratory and urinary systems and damage to the secondary lymphoid tissue

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24
Q

How is selenium poisoning diagnosed?

A

Elevated selenium in the liver, heart and kidneys

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25
Q

How is selenium poisoning treated?

A

None

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26
Q

How is selenium poisoning prevented/controlled?

A

Ensure correct doses when giving selenium supplements
Ensure proper mixing of drenches or wormers containing selenium

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27
Q

What are the clinical signs of anticoagulant rodenticide poisoning?

A

Anaemic, non-pyrexic, weak, haemorrhages
Mainly seen in pigs

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28
Q

What are the implications of anticoagulant rodenticide poisoning?

A

Affected livestock may never be able to enter the food chain

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29
Q

Describe the aetiology of nitrate and nitrite poisoning

A
  • Excessive intake of nitrate
  • Rumen bugs convert: nitrate -> Nitrite -> Ammonia -> Bacterial Protein
  • BUT if ruminants consume lots of nitrate get accumulation of nitrite which is then absorbed into the bloodstream converts haemoglobin to methemoglobin which cannot transport oxygen
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30
Q

Clinical signs of nitrate/nitrite poisoning are due to?

A

Lsck of oxygen

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31
Q

What are the clinical signs of nitrate/nitrite poisoning?

A

Anoxia, cyanotic mucosae, tachypnoea, weak and rapid pulse – could be mistaken for neurological signs
Can get subacute or chronic forms – signs more vague

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32
Q

How is nitrate/nitrite poisoning diagnosed?

A

Clinical signs / history
Blood – plasma protein bound nitrite
Chocolate-brown discoloration of blood

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33
Q

How is nitrate/nitrite poisoning treated?

A

IV methylene blue

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34
Q

How is nitrate/nitrite poisoning prevented/controlled?

A

Usually occurs accidentally e.g. spilt fertiliser

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35
Q

Describe the 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)

36
Q

What are the clinical signs of botulism toxicity

A

Often found dead, or if alive often found recumbent with flaccid paralysis or ataxic

37
Q

How is botulism diagnosed?

A

Clinical signs / history
PME – botulism toxin test

38
Q

How is botulism treated?

A

None

39
Q

How is botulism prevented/controlled?

A

Take care with broiler litter (Animal By-Products Order)

40
Q

Why must botulism be controlled from a human health perspective? How is this managed?

A

Type B food safety concern.
Clinically affected animals should not be presented for slaughter into the food chain and shouldn’t use produce from affected animals.
Recovered cases should not be presented into the food chain for 18 days

41
Q

Mycotoxins are produced by?

A

Fungi

42
Q

What is the financial impact of mycotoxins on a farm?

A

Reduced crop yields
Product rejection
Reduced animal performance
Increased Health Issues

43
Q

Why is diagnosis of mycotoxins difficult?

A

Due to lack of tests to determine the presence of mycotoxins in feed or in the animal

44
Q

How are mycotoxins prevented/controlled?

A
  • Prevent production of mycotoxins: influenced by temperature, carbon dioxide and water levels – most likely to be an issue in warm, wet conditions
  • 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
45
Q

Describe the aetiology of aflatoxins

A

Aspergillus fungi
- Occur in field prior to harvest or postharvest if drying delayed, insect or rodent infestation
- Highest risk of contamination: corn (peanuts, cottonseed)

46
Q

What are the clinical signs of aflatoxins?

A

Primarily a hepatic disease
Decreased feed intake
Decreased milk yields
Recurrent infection – immune suppression

47
Q

How can aflatoxin toxicity be treated?

A

None
Need to remove the source

48
Q

Deoxynivalenol is also known as?

A

Vomitoxin

49
Q

Describe the aetiology of Deoxynivalenol (vomitoxin)

A

Recent study showed high prevalence in UK cereals (corn, wheat, barley, oats)
Caused by Fusarium fungi

50
Q

What are the clinical signs of Deoxynivalenol (vomitoxin) toxicity

A

Lower feed intake
Lower milk production
Diarrhoea
Immune alterations

51
Q

The production of Zearalenone toxins is enhanced by?

A

High temperatures

52
Q

What are the clinical signs of Zearalenone toxicity?

A
  • Signs of hyperestrogenism
  • Hyperemia and swelling of the vulva, mammary glands
  • Nymphomania
  • Other signs: rectal and vaginal prolapses, poor libido in boars
53
Q

Describe the 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
54
Q

What are the clinical signs of facial eczema caused by sporidesmin?

A

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

55
Q

How is facial eczema caused by sporidesmin diagnosed?

A
  • History
  • Serum gamma glutamyltransferase (GGT) concentration can be used to diagnose subclinical disease
  • Can measure pasture spore counts
56
Q

How is facial eczema caused by sporidesmin prevented/controlled?

A
  • 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
57
Q

What are the clinical signs 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

58
Q

Describe the 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

59
Q

Describe the clinical signs 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.

60
Q

How are the different mycotoxin toxicities treated?

A

All do not have specific treatments
Need to remove the source to prevent infection

61
Q

Plant poisonings are often associated with what factors?

A
  • Poor pasture availability i.e., heavy snow
  • Overgrazing
  • Incorporation into conserved forages
  • Use of herbicides
  • Increased accessibility i.e., dumping of hedge cuttings and garden waste, clearing ditches and leaving plants to wilt
  • Transportation – hungry on arrival!
62
Q

What needs to be considered when diagnosing plant poisonings

A

Commonly relies on plant identification, but plant alone not diagnostic!
Need to consider:
- Evidence of potential exposure
- Believable time frame
- Risk factors that may have contributed i.e. overgrazing
- Clinical signs

63
Q

Describe the general advice given in plant poisoning situations

A
  • Remove stock from suspected source
  • Give access to good quality forage – may dilute
  • Eliminate poison: rumenotomy or adsorption with activated charcoal
  • Treat symptomatically
64
Q

Describe the aetiology of ragwort poisoning

A

Ingestion over a prolonged period of time of Pyrrolizidine alkaloids: hepatotoxic
Rarely acute poisoning
Pigs quite resistant to ragwort toxicity

65
Q

What are the clinical signs of ragwort poisoning?

A

Weight loss, oedema, straining diarrhoea
Photosensitisation

66
Q

How is ragwort poisoning diagnosed?

A

Liver Biopsy: fibrosis, vein occlusion, bile duct proliferation

67
Q

Name two brassica crops

A

Rape
Kale

68
Q

Describe the clinical signs of rape/kale toxicity

A

Haemolysis, anaemia, haemoglobinuria, pallor, jaundice, tachycardia
Hypothyroidism, goitre and hypocalcaemia

69
Q

How is rape/kale toxicity diagnosed?

A

Clinical signs and history
Bloods – depends!
Can measure nitrate levels
Haematology – red blood cell inclusions on smears

70
Q

Other feed associated plants that can cause poisoning include…?

A

Clovers
Linseed
Potatoes

71
Q

What are the signs seen with clover toxicity?

A

Frothy bloat, laminitis, photosensitisation, infertility, goitre, abortions

72
Q

What are the signs seen with Linseed toxicity?

A

Sudden death
Salivation
Sleepiness
Staggering
Convulsions

73
Q

What are the signs seen with Potato toxicity?

A

GI signs
Nervous signs
Death

74
Q

Name some plant spp that cause photosensitisation

A
  • St Johns wort
  • Ragwort
75
Q

Describe the clinical signs seen with St Johns wort toxicity

A

Photosensitisation - erythema, swelling, skin necrosis in white areas (sunburn on hairless and un-pigmented skin, especially on the dorsal aspect.

76
Q

How is photosensitisation treated?

A

Move affected animals into shade, anti-inflammatories and antibiotics if required. Supportive therapy for liver

77
Q

Describe the clinical signs of Rhododendron toxicity

A

Abdominal pain, projectile vomiting (pathognomonic), tremors, staggering, recumbency, paddling, death

78
Q

Describe the clinical signs of acorn/oak toxicity

A

Alimentary signs: colic, anorexia, weight loss, ascites, oedema, constipation replaced by black tarry faeces. Haematuria

79
Q

How does an animal with acorn/oak toxicity present on PME?

A

Gastrointestinal ulceration and haemorrhage, nephritis, liver degeneration

80
Q

Describe the blood test results for an animal with acorn/oak toxicity

A

Raised urea and creatinine, raised liver enzymes

81
Q

Which spp is resistant and can be used to clear acorns?

A

Pigs

82
Q

Describe the clinical signs of Bracken toxicity

A

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)

83
Q

Describe the clinical signs of yew toxicity

A

Very acute
Sudden death
Cardiac depression, dyspnoea, abdominal pain, muscle tremor, weakness

84
Q

How is yew toxicity uniquely diagnosed?

A

Presence of plant in rumen or mouth!

85
Q

Describe the clinical signs of Hemlock water dropwort toxicity

A

Sudden death
Nervous signs: salivation, dilated pupils, convulsions
Diarrhoea occurs with sublethal exposures

Y4 FA - GIT and nutrition (11 decks)

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