Farm animal toxicology Flashcards
1
Q
What are some key questions to know if toxicology is relevant in your case?
A
2
Q
What are soem contributing factors to toxicities in prod animals?
A
-> Management factors
- PAsture management
- Weed control
- Hedging and drainage
- Housing - garden waste
-> Nutrition
- Feed shortage
- Conserved forages
- Inapprorpiate feeding
-> Human error / negligence
- Garden refuse disposal
- Fly tipping
- Ration formulation errors
-> Animals factors
- Age
- Boredom
- Unfamiliar surroundings
3
Q
What are out general principles of tx?
A
-> Reduce toxin absorption
- > Speed toxin elimination
- >Symptomatic tx
- >antagonists
4
Q
Detail reducing toxin absorption?
A
- Absorbants (e.g. activated charcoal)
- Purgatives
- Oral fluid therapy
- Rumenotomy and rumen lavage
5
Q
Detail Speed of toxin elimination
A
- Forced diuresis : IVFT, diuretics
6
Q
Antagonists?
A
- Rarely available
- e.G. Ca disodium EDTA for lead poisoning
7
Q
Make a big map of what signs are caused by what plants?
A
8
Q
Describe occurence of sudden death from yew tox?
A
- sPoradic
- Hx of access to tree or clippings
9
Q
CLS of YEw tox? (Although not usually alive)
A
- Dyspnoea
- Muscle tremors
- Collapse
- Bradycardia
- Rapid, sudden death
10
Q
Which plant poisonings have an IMMEDIATE onset?
A
- Yew
- Laurel
- Potato
- Hemlock
- Water dropwort
- Lush pasture
- (fog fever, frothy bloat)
11
Q
Which plant poisonings have a delayed onset?
A
- Bracken
- Sheep – Bright blindness
- Cattle – Carcinoma
- Ragwort
- Photosensitising species
- Oestrogenic species
- Brassica species
12
Q
Aetiology of Ragwort tox (Neuro)?
A
- Pyrrolizidine alkaloids
- Dose dependant severity
- Hepatotoxicity leading to liver failure
- Clinical signs of hepatic encephalopathy
13
Q
Occurrence of Ragwort tox?
A
- Relatively common
- At grazing or when fed conserved forage
14
Q
CLS of Acute Ragwort tox?
A
=> Neurological signs due to hepatic
encephalopathy
* Blindness
* Excitability
* Ataxia
=> Gastrointestinal signs
* Diarrhoea
* Faecal tenesmus
* Rectal prolapse
* Colic
15
Q
What subacute clinical signs of ragwort?
A
- Photosensitisation
- Dullness
-Weight loss - Icterus
16
Q
Diagnosis of Ragwort?
A
- History of grazing pasture with ragwort
- Clinical signs
- Raised liver enzymes (AST, GGT and GLDH)
- PME (Icterus, Ascites and Cirrhosis)
17
Q
Control of ragwort?
A
- Improved pastures by hand pulling of ragwort
- Selective weed killers in spring
18
Q
What is the aetiology for Fog fever?
A
L-Tryptothan toxicity
19
Q
Pathogenesis of Fog Fever?
A
- Converted to Tri-methyl indole in the rumen
- Cytotoxic to lung tissue
- Atypical interstitial pneumonia with pulmonary oedema
20
Q
Clinical signs of Fog Fever?
A
- Mixed inspiratory / expiratory dyspnoea
- Mouth breathing, no coughing
- Generalised fluid crackles on auscultation
- No pyrexia
21
Q
Tx for Fog fever?
A
REMOVE CATTLE FROM PASTURE
- Diuretic: furosemide
- NSAID: meloxicam
22
Q
Aetiology of Oak tox?
A
Acorn poisoning
Oak leaf poisoning
23
Q
Pathogeneiss of Oak tox?
A
- Tannic acid in acorns
- GI ulceration
- Nephrotoxicity
24
Q
Occurence of oak tox?
A
- Sporadic
- Some cattle develop a craving
25
CLincial signs of oak tox?
* Gradual onset
* Anorexia and dullness
* Gastrointestinal
- Rumen atony
- Constipation
- Dark, hard faeces followed by black, tarry faeces
* Renal
- Haematuria
- Renal failure and polyuria
26
Clinical signs of rhododedrendon tox?
-> Gastrointestinal
* Salivation
* Retching
* Projectile vomiting
* Colic
-> Neurological
* Staggering
-> Sudden death
27
Tx for rhodedendron tox?
- OVFT
- Diuretics
- Rumenotomy and rumen lavage
28
Aetiology to bracken tox?
* Several toxic factors
* Bone marrow suppression
- Ingestion of large quantities over a short time frame
- Acute haemorrhagic disease
* Carcinogenic
- Chronic exposure to low levels
- Neoplasia of the upper alimentary tract or urinary bladder (Enzootic haematuria)
29
Occurrence of bracken tox?
marginal grazing
30
Main thing seen with braken tox?
red urine/ anaemia
31
What clinical signs for Acute harmorrhagic syndrome?
=> Enteric form
* Anaemia, leucopaenia and
thrombocytopaenia.
* Mucosa petechiation and epistaxis
* Pyrexia, anorexia, depression and
dysentery
* Death 1-5 days.
=> Laryngeal oedema
* Usually seen in calves
* Depression
* Roaring respiration and dyspnoea
32
What clinical signs for neoplastic form. ofbracken tox?
=> Urinary bladder (Enzootic haematuria)
* Haematuria
* Anaemia
* Weakness
=>Upper alimentary squamous cell
carcinoma
* Pharangeal neoplasia – ptyalism, halitosis,
coughing, nasal discharge
* Oesophageal neoplasia – ptyalism,
halitosis, chronic rumenal tympany,
diarrhoea
33
Photosensitisation can be ....
- Primary (type I)
- Secondary (Type III)
- Congenital porphyria (Type II)
34
Describe type I photosensitisation
■ Plants contain photoactive pigments
■ St Johns wort (common plant in hedgerows and rough grazing)
■ Bog asphodel
■ Hypericum species
35
Describe type II photoS?
■ Following liver dysfunction
■ Ragwort
36
What are some differentials for photoS?
-> Trauma -> physical or chemical
-> Ectoparasites -> psoroptic mange
-> Photosensitsation
37
TX for photosensitisation?
HOUSE AFFECTED CATTLE OUT OF SUNLIGHT!!
Tx:
- clean and debride raw areas
- Protect against fly strike
- NSAIDs
38
What risk factors to chemical poisoning?
* Innate curiosity
* Considerable appetite
* Non-selective licking and grazing habits
* Feeding mouldy grain
* Feeding grain treated with insecticides, fungicides or herbicides
* The accidental overdosing with trace elements or medicines
39
What is required for confirmation of a diagnosis of a specific poison?
chemical assay => samples (50g) of the suspect material, collected and frozen at -20°C pending analysis
- abomasal contents
- liver
- kidney
- urine
40
if there is any possibility of litigation arising ....?
duplicate sample should be taken and sealed in the presence fo a witness
41
Sources of LEad poisoning ?
- Lead, paint, pipes, car batteries
- Coil in certain areas
42
What do clinical signs of lead tox depend on?
- Rate of exposure
- Magnitude of exposure
- Body mass of animal
43
What signs of Lead tox?
NEUROLOGICAL -> acute high exposure and small body mass
GIT -> chronic low exposure and large body mass
44
Describe neurological signs with lead tox?
* Bilateral central blindness
* Muscle fasciculations
* Bruxism, jaw champing and bellowing
* Head pressing
* Hyperaesthesia and excitability
* Seizures
45
Describe GI signs ?
* Anorexia
* Colic
* Rumenal stasis and mild tympany
* Constipation followed by diarrhoea
* Weight loss and poor growth
46
What should you do if you are suspicious of LEAd tox?
INFORM APHA
47
Diagnosis of Lead?
- cLs
- Blood lead levels
- Kidney lead levels. onPME
48
TX for LEad tox?
- Supportive and symptomatic (xylazine and fluids)
- Oral salts to precipitate soluble lead (MgSO4)
- Lead chelating agents (IV Ca disodium EDTA)
49
Describe metabolism. andabsorption fo copper?
* Very high liver capacity for copper storage in cattle
* Influenced by the presence of antagonists
* (e.g. Molybdenum and sulphate)
50
Sources of copper tox?
* Supplemented in feed or through boluses
* Pig feed and manure
* Fungicides and molluscicides
* Wood preservatives
51
What causes acute presentations of xopper tox?
* Short term exposure to high levels (sheep > cattle)
* Chronic exposure exceeds liver storage
(cattle)
52
What clinical signs to copper tox ACUTE?
* Haemolytic crisis
* Abdominal pain and diarrhoea (blue-green
tinged)
* Sudden death
53
Chronic copper tox?
-> Herd
* Reduced milk yield
* Poor growth rates
* Increased mortality
-> Individual
* Anorexia
* Depression
* Jaundice
* Anaemia
* Haemoglobinuria
* Death
54
Pathology of Copper tox?
* Increased liver copper
* Reduced haemoglobin
* Reduced PCV
* Black enlarged kidneys
* Yellow carcase
55
Tx for copper tox?
supportibe; poor pg
56
Aetiology of Molybdenum tox?
* Copper antagonist, leading to copper deficiency
* Exacerbated by the presence of iron and sulphur
57
Occurence of molybdenum tox?
'teart pastures'
58
CLS of Molybdenum ?
* Diarrhoea often green or black with offensive odour
* Depigmentation
* Poor condition
* Stiff gait in young
* Poor milk yield
* Poor pregnancy rate
59
Diagnosis of Molybdenum tox?
* Challenging: cannot be excluded by a single measure
* Clinical signs
* Biochemistry: Copper and caeruloplasmin to copper ratios
* Liver copper levels
* Forage analyses: Copper and its antagonists
60
Tx & prevention?
Tx-> oral copper boluses
Prevention -> copper boluses & in-feed supplementation
