Nutrition and GI: Toxicology Flashcards

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1
Q

What is the name for a disease state that results from exposure to a poison?

A

Toxicosis

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2
Q

What samples can be used for clinical pathology of toxins?

A
  • Urine
  • Liver
  • Kidney
  • Blood
  • Stomach contents
  • Feed
  • Bone/hair
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3
Q

What is the general treatment for toxicosis?

A
  • Remove source
  • Limit absorption/hasten elimination
  • Symptomatic and supportive
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4
Q

What are common mineral poisoinings?

A
  • Lead
  • Copper
  • Selenium
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5
Q

What is the role of the APHA in toxicoloty?

A
  • Screening programmes
  • Wildlife incident investigation scheme
  • Emergency response- fire/flooding
  • Animal disease outbreaks
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6
Q

What are the acute and subacute clinical signs of lead poisoning?

A

Acute
* young calves- typically
* found dead within 24hr
* Neurological signs- tremors, twitching, hyperthermia, salivation, rolling etes, blindness

Subacute
* Adults cattle and sheep
* Live for several days
* Neurological- dullness, anorexia, blindness, incoordination
* Staggerining, circling, muscle tremors

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7
Q
  1. When does chronic lead poisoning occur?
  2. How is lead poisoning diagnosed?
A
  1. Typical in lambs with high lead in soil- nephrosis is common, ill thrift, gait abnormalities, lameness
  2. Dx
    * Clinical signs
    * Heparin levels in blood
    * Kidney lead levels gold standard, liver can also be used
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8
Q

How is lead poisoning treated and prevented?

A

Treatment
* Chelation therapy
* Thiamine hydrochloride
* Supportive therapy
* Rumenotomy

Prevention/Control Measures
* Remove animals from source
* Good waste managment on farm
* Check old buildings for paint, flashings etc

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9
Q

Following lead poisoning case what must farmers do?

A
  • Farmers are obliged to take measures to avoid contamination of the food chain- 16 weeks
  • If emergency slaughter in 16 weeks FCI saying offal discarded
  • If animals close to finishing- blood lead analysis < 0.15 ok
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10
Q
  1. When does copper poisoning in cattle occur?
  2. What are the clinical signs?
A
  1. Access to pig feed or pasture grazed with pig manure
  2. Sudden onset, depressed, anaemia, jaundice and haemoglobinuria, ataxia, recumbency
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11
Q

What does PM or copper poisoning show?
How is it diagnosed?

A

PM
* Carcase- pale or jaundiced
* dehydrated
* liver pale tan or bronze
* Kidneys dark red or gun metal grey
* Urine dark red/black
* Secondary lung consolidation

Diagnosis
* History, clinical signs and PM
* Kidney copper concentrations to confirm

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12
Q

How is copper poisoning treated?
How is it prevented?

A

Tx
* Supportive therapy
* Copper antagonism

Prevention/Control
* Remember poisoning id due to efficiency or absorption and dietary availability
* Care with copper foot baths

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13
Q
  1. When does selenium posisoning occur?
  2. What are the clinical signs?
A
  1. Acute toxicosis occurs due to excessive supplementation
  2. Toxic CV, resp and urinary damage- staggering, dyspnoea, colic, diarrhoea, cyanosis, death
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14
Q
  1. What does PM show for selenium poisoning?
  2. How is it diagnosed?
A
  1. Sub cut haemorrhage, straw coloured fluid in pericardium, pulmonary oedema, abomastitis, intestinal and hepatic congestion, brain stem haemorrhage
  2. Elevated selenium in the liver, heart and kidneys
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15
Q

What are the clinical signs of anticoagulant rodenticides?

What is the implication for humans?

A

Anaemic, non-pyrexic, haemorrhages

Residues can remain in tissues for a long time, affected livestock may never enter food chain

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16
Q

Fertiliser

What is the aetiology of nitrate and nitrite poisoning?

Therefore what are the clinical signs?

A
  • Excess intake
  • Rumen bacteria convert to bacterial protein
  • But if large quantities nitrate to nitrite which is absorbed into blood
  • Converts haemoglobin to methemoglobin

Lack of O2
* Anoxia
* Cyanotic mucosae
* Tachypnoea
* Weak/rapid pulse

17
Q

How is nitrate/nitrite poisoning diagnosed, treated and prevented?

A

Diagnosis
* Clincial signs/ history
* Blood- plasma bound nitrite
* Chocolcate brown blood

Tx
* Methylene blue IV

Prevention/Control
* Accidentally
* Can also be in docks and fat hen plants

18
Q
  1. What can cause botulism?
  2. What are the clinical signs?
  3. How is it diagnosed?
A
  1. Use of broiler litter as fertiliser
  2. Often dead, if alive, recumbent with flaccid paralysis
  3. Clinical signs/history, PME- botulusm toxin test

No treatment

19
Q

What is the aetiology of mycotoxins?

What are the financial impacts to the farm?

A

Aetiology
* produced by fungi
* Occur in feed routinely but usually at concentrations that do not impact health and performance

Financial impact
* Reduce crop yields
* Product rejection
* Reduced animal performance
* Increased health issues

20
Q

How is mycotoxicosis controlled?

A
  • Reduce exposure to mycotoxin
  • Prevent production of mycotoxins- temp, CO2, water
  • Ensure grain dried to correct moisture content
  • Prevent exposure of silage to O2
  • Big bale- avoid damage
  • Keep straw dry
  • Avoid feed, forage or bedding with visual mould
  • Clen crop storage between batches
  • Consider mycotoxin binder
21
Q
  1. What causes aflatoxins?
  2. What are the clinical signs
  3. How is it treated?
A
  1. Aspergillus fungi, occur in field prior to harvest or post harvest if drying delayed/insect
  2. Primarily hepatic disease, decreased feed intake, decreased milk yields, recurrent infection
  3. None- remove source
22
Q
  1. What causes zearalenone
  2. What are the clinical signs?
A
  1. Fusarium fungi- high temps, pigs more affected
  2. Signs of hyperoestrogenism, hyperaemia and swelling of the vulva, mammary glands, nymphomania
23
Q

What mycotoxin causes facial eczema?

A
  • Ingestion og sporidesmin, produced by the fungus
  • Occurs in humid, warm wather
  • Toxin concentrated in the liver causing epithelial necrosis of the bile ducts
  • Ill thrify, reduced fertility
  • Severly affected animals develop photosensitisation

Prevention/Control
* Oral administration of zinc salts
* Feed hay or brassica crops
* Remove stock from high risk areas
* Breed for resistance

24
Q
  1. What causes ryegrass staggers?
  2. What are the clinical signs?
A
  1. Ingestion of the mycotoxin lolittrem produced by acremonium loliae found on perennial ryegrass
  2. Neurological signs 1-2 weeks after- fine tremors head and neck, head nodding, alteration in stance, severely affected animals
25
Q

What does ingestion of ergoy alkaloids produced by claviceps purpurea

A

Ergotism

26
Q

What are the clinical signs of ergotism?

A
  • Capillary damage with extremities of animal appearing painful
  • Inflamed then cold
  • Dry gangrenous lesions
27
Q

What are common plant poisonings associated with?

A
  • Poor pasture availability
  • Overgrazing
  • Incorporation into conserved forages
  • Use of herbicides
  • Increased accessibility
  • Transportation- hungry on arrival
28
Q
  1. What plant is this?
  2. What does it cause?
  3. What are the clinical signs?
  4. How is it diagnosed?
A
  1. Ragwort
  2. Hepatotocixity- pyrrolizidine alkaloids
  3. Weight loss, oedema, straining diarrhoea, photosensitisation
  4. Liver biopsy- fibrosis, vein occlusion, bile duct proliferation
29
Q

What do brassica crops (rape and kale) cause?
What are the clinical signs?

A
  • Contin S-methly cysteine sulfoxide (SMCO)
  • Nitrites
  • Goitrogens
  • Oxalates

SCMO- haemolysis, anaemia, pallor, jaundice
Hypothyroidism, goitre, hypocalcaemia

30
Q

What can the following feed associated plants cause?
1. Clover
2. Linseed
3. Potatoes

A
  1. Oestrogens, cyanogenic, glycosides- frothy bloat
  2. Cyanogenic glycosides- death, salivation, sleepiness, staggering, convulsions
  3. Glycoalkaloids, phenolic compounds
31
Q
  1. What is this plant?
  2. What does it cause?
A
  1. St Johns wort
  2. Photosensitisation
32
Q
  1. What is this?
  2. What does it cause?
  3. What are the clinical signs?
A
  1. Rhododendron
  2. Grayanotoxinc bind Na channels- nervous, CV, muscles
  3. Abdominal pain, vomiting, tremors, staggering, recumbency, padding
33
Q

What do acors/oak cause?

A
  • Alimentary signs- colic, anorexia, weight loss, ascites, oedema
  • PME- GI ulceration, haemorrhage, nephritis, liver degeneration
34
Q
  1. What does braken ingestion lead to?
  2. What are the clinical signs?
A
  1. Cyanogenic glycoside, thiaminases
  2. Vary- Different toxins affect species differently, enzootic haematuria in cattle, depression, weakness, anorexia, tumours of bladder wall
35
Q

What does yew ingestion cause?

A

Contains taxicatoside
Sudden death
Cardiac depression, dyspnoea, abdominal pain, muscle tremour

36
Q
  1. What is this?
  2. What does it cause?
A

Hemlock water dropwort- oenathotoxin

Sudden death
Nervous signs
Diarrhoea with sublethal exposures