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4th year > General Farm animals > Flashcards

General Farm animals Flashcards

1
Q

What is important to ensure with euthanasia to avoid pain and distress?

A

Immediate loss of consciousness

Followed by cardiac and respiratory arrest

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2
Q

What is taken into account when deciding if euthanasia is the right thing?

A

What is best for animal
Wellbeing of client
Financial constraints
Own conscience

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3
Q

Methods of euthanasia of farm animals?

A

Pentobarbitone
Shoot
-stunning (captive bolt) followed by pithing
-free bullet gun

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4
Q

Where to aim captive bolt to stun cattle?

A

Place muzzle 2cm lateral of the crossing point of two ‘lines drawn’ between lateral cants of eye and opposite horn base

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5
Q

Where to aim captive bolt to stun hornless and horned sheep/goats?

A

Hornless sheep - place muzzle in centre of top of head

Horned sheep/goats - behind ridge between horns, aim towards base of tongue

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6
Q

Where to aim captive bolt to stun pigs?

A

2cm above eyes, halfway across forehead, aiming up slightly

May be better to use shot gun - same as above or from behind ear aiming towards opposite eye

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7
Q

When can a farm animal have certified emergency slaughter to be transported to a slaughterhouse after? Rules?

A

Accidents/fresh lesions if can’t travel
Vet must carry out ante-mortem inspection and certify animal fit for human consumption
Must then be slaughtered within 2 hours
Only for acute problems - not when solar ulcer or joint infection
Animal must be clean
Vet must be present at the slaughter
Farmer to sort slaughtermen coming out
TSE tests to be carried out, blood to be collected
Large parts of carcass condemned
Rarely profitable
Anything else - euthanasia followed by disposal of carcass (fallen stock)

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8
Q

What is toxicosis?

A

A disease state that results from exposure to a poison

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9
Q

General methods of treatment for toxins?

A

Remove source
Limit absorption/hasten elimination
Symptomatic and supportive
Specific antidote

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10
Q

What are the main common mineral poisonings in farm animals?

A

Lead
Copper
Selenium

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11
Q

Clinical signs of lead poisoning?

A

Acute - typical in young calves, found dead or death within 24h of sudden onset of neurological signs:
- muscle tremor and twitching (head and neck)
- hyperthermia
- salivation
- rolling eyes
- bellowing
- blindness
- stiff gait
- convulsions with opisthotonus
- pupil dilation
Subacute - adult cattle and sheep, survive few few days, neuro signs:
- dullness
- anorexia
- salivation
- blindness
- incoordination
- staggering
- circling
- muscle tremors
- colic
- luminal atony
- recumbency
Chronic - typical in lambs with access to soils high in leads
- nephrosis common
- ill thrift with gait abnormalities or lameness and paralysis due to fractures (osteoporosis)
- abortion and poor fertility in pregnant animals
Subclinical - chronic exposure at low levels, may have no clinical signs

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12
Q

Diagnosis of lead poisoning in farm animals?

A

Clinical signs
Heparin - levels in blood >0.48
Kidney lead levels = diagnostic gold standard
Liver biopsy can also be used >0.5ppm

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13
Q

Treatment for lead poisoning in farm animals?

A

Chelation therapy
Thiamine hydrochloride
Supportive therapy
Rumenotomy

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14
Q

Prevention of lead poisoning in farm animals?

A 
Remove animals from source
Good waste management on farm
Check old buildings for paint etc
More difficult if soil contamination
Obliged to avoid contamination of food chain - 16 week voluntary withdrawal
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15
Q

When is copper poisoning most commonly seen in cattle?

A

If access to pig feed or graze pastures fertilised with pig manure

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16
Q

Copper poisoning clinical signs in farm animals?

A 
Sudden onset
Depressed
Anaemia
Jaundice and haemoglobinuria
Ataxia
Recumbency and eventually death
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17
Q

PME for copper poisoning in farm animals?

A 
Pale or jaundiced carcass
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

Diagnosis of copper poisoning in farm animals?

A

History, clinical signs and PME
Kidney coper concentrations confirms diagnosis
Can check subclinical liver damage using AST

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19
Q

Treatment of copper poisoning in farm animals?

A

Supportive therapy

Copper antagonists - molybdenum or sulphur (care to monitor and avoid deficiency)

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20
Q

When is selenium poisoning usually seen?

A

Oversupplementation

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21
Q

Clinical signs of selenium poisoning in farm animals?

A

Toxic damage to cardiovascular, respiratory and urinary systems and damage to secondary lymphoid tissue
Non specific - staggering gait, dyspnoea, tympani, colic, diarrhoea, recumbency, cyanosis, death

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22
Q

PME of selenium poisoning in farm animals?

A 
SC haemorrhages
Straw coloured fluids in pericardium
Severe pulmonary oedema
abomasitis
Intestinal and hepatica congestion
Brainstem haemorrhages
Destruction of renal cortices
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23
Q

Diagnosis, treatment and prevention of selenium poisoning in farm animals?

A

Diagnosis - elevated levels in liver, heart kidneys
No treatment
Prevention - ensure correct doses when giving selenium supplements, ensure proper mixing of drenches or wormers containing selenium

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24
Q

Clinical signs of anticoagulant rodenticide poisoning in farm animals?

A 
Mostly seen in pigs
Anaemia
Non pyrexic
Weak
Haemorrhages
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25
Q

What is the problem with nitrate poisoning in ruminants?

A

Nitrate -> nitrite -> ammonia -> bacterial protein
But if ruminants consume lots, get accumulation of nitrite which is then absorbed into bloodstream and converted to haemoglobin to methaemoglobin which cannot transport oxygen

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26
Q

Clinical signs of nitrate poisoning in ruminants?

A 
Due to lack of oxygen:
- anoxia
- cyanotic mm
- tachypnoea
- weak and rapid pulse
Can get subacute or chronic forms with more vague signs
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27
Q

Diagnosis and treatment of nitrate poisoning in ruminants?

A

Clinical signs/history
Blood - plasma protein bound nitrite
Chocolate brown discolouration of blood
Treat with methylene blue IV

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28
Q

Prevention of nitrate poisoning in ruminants?

A

Usually occurs accidentally
Spilt fertiliser on pasture that animals turned out on to graze
Run off entering cattle accommodation
Carry over to bowsers and equipment used to carry water previously used for fertiliser are not properly washed out

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29
Q

When is plant poisoning seen?

A 
Poor pasture availability ie heavy snow
Overgrazing
Incorporation into conserved forages
Use of herbicides
Increased accessibility e.g. dumping of hedge cuttings
Transportation - hungry on arrival
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30
Q

Diagnosis of plant poisoning in farm animals?

A

Evidence of potential exposure
Believable time frame
Risk factors e.g. overgrazing
Clinical signs

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31
Q

Treatment for plant poisoning in farm animals?

A

Remove stock from suspected source
Give access to good quality forage
Eliminate poison - rumenotomy or adsorption with activated charcoal
Treat symptomatically

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32
Q

Ragwort poisoning clinical signs in farm animals?

A

Weight loss, oedema, straining diarrhoea
Photosensitisation
Pigs quite resistant to toxicity

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33
Q

Aetiology and diagnosis of ragwort poisoning?

A

Pyrrolizidine alkaloids - hepatotoxic

Liver biopsy - fibrosis, vein occlusion, bile duct proliferation

34
Q

Clinical signs of yew poisoning in farm animals?

A 
Sudden death
Cardiac depression
Dyspnoea
Abdominal pain
Muscle tremor
Weakness
35
Q

Aetiology and diagnosis of yew poisoning in farm animals?

A

Taxine - very acute ingestion of yew

Diagnosis - presence of plant in rumen or mouth

36
Q

Clinical signs of rhododendron poisoning in farm animals?

A 
Projectile vomiting (pathognomic)
Abdominal pain
Tremors
Staggering
Recumbency
Paddling 
Death
37
Q

Aetiology and diagnosis of rhododendron poisoning in farm animals?

A

Ingestion of polycyclic diterpenes - access to woodland or ornamental shrubs
Diagnosis - clinical signs and presence of plant in rumen

38
Q

Aetiology and diagnosis of brassica poisoning in farm animals?

Clinical signs?

A

SMCO, nitrate/nitrite, goitrogens, oxalates in common feed plants (fodder beets, rape, turnips)
Poss inherited predisposition e.g. Zwarbles to oxalate deposition
Diagnosis - bloods (nitrate levels, haematology - RBC inclusions on smear)

SMCO - haemolytic anaemia, haemoglobinuria, pallor, jaundice, tachycardia

Nitrates - hypothyroidism, goitre and hypocalcaemia

39
Q

Aetiology and diagnosis of St John’s Wort poisoning?

A

Hypericin

Diagnosis - clinical signs and history

40
Q

Clinical signs of St John’s Wort poisoning?

A

Photosensitisation - erythema, swelling, skin necrosis in white areas (sunburn on hairless and unpigmented skin especially on dorsal aspect)

41
Q

Treatment and management of St John’s Wort poisoning?

A

Move affected animals into shade
Anit-inflammatories and antibiotics if required
Supportive therapy for liver

42
Q

Prevention/control measures of mycotoxicosis in farm animals?

A

Prevent production of mycotoxins - influenced by temperature, CO2 and water levels (more likely problem in warm wet conditions)
Ensure grain is dried to correct moisture content
Prevent exposure of silage to oxygen by ensuring adequately compacting and covering
With big bale silage, handle 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 mycotoxin binder to ration

43
Q

Aetiology of Aflatoxins?

Clinical signs? Treatment?

A

Aspergillus fungi
Occur in field prior to harvest or post harvest if drying delayed, insect or rodent infestation
Highest risk of contamination - corn

Primarily a hepatic disease
Decreased feed intake
Decreased milk yields
Recurrent infections - immune suppression
No treatment - remove source
44
Q

Aetiology of Deoxynivalenol mycotoxicosis (DON)?

Clinical signs and treatment?

A

High prevalence in UK cereals
Fusarium fungi

Lower feed intake
Lower milk yields
Diarrhoea
Immune alterations
No treatment - remove source
45
Q

Aetiology, diagnosis and treatment of zearalenone mycotoxicosis in farm animals?

Clinical signs of zearalenone mycotoxicosis in farm animals?

A 
Fusarium fungi
Production enhanced by high temperatures
Pigs more susceptible
Diagnosis - clinical signs and history
Treatment - none, remove source

Signs of hyperoestrogenism
Hyperaemia and swelling of vulva and mammary glands
Nymphomania
Other signs - rectal and vaginal prolapses, poor libido in boars

46
Q

Aetiology of facial eczema (mycotoxicosis) in farm animals?

Clinical signs of facial eczema (mycotoxicosis) in farm animals?

Diagnosis and treatment of facial eczema (mycotoxicosis) in farm animals?

Prevention/Control?

A

Ingestion of sporidesmin - produced by 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

Ill thrift, reduced fertility
Severely affected animals develop photosensitisation - photophobia, swelling of face and ears

Serum GGT concentration can be used to diagnose subclinical disease
Can measure pasture spore counts
No specific treatment available

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

47
Q

Ryegrass staggers - aetiology? Clinical signs?

A

Ingestion of mycotoxin Lolittrem produced by Acremonium loliae found on perennial ryegrasses

Neurological signs 1-2 weeks after introduction to toxic pasture:

  • fine tremors of head and neck at rest
  • head nodding
  • jerky movements of neck and limbs
  • alteration in stance
  • severely affected animals can collapse head first before rolling into lateral recumbency with necks arched back and limbs extended - tetanic spasma can persist for several minutes before apparent recovery

No specific treatment
Remove from affected pasture
Avoid close grazing
Consider feeding supplementary hay/reseeding

48
Q

Ergotism - aetiology? Clinical signs? Diagnosis? Treatment?

A

Ingestion of ergot alkaloids produced by Claviceps purpurea (parasitic fungus of rye and other small grain crops)
Ergots = resting stage, seen as dark horn like structures which replace grass seeds

Capillary damage
- painful, inflamed extremities
- then cold with numbnesss and development of dry gangrenous lesions
Weight loss
Reduced milk yield
Painful udders
Irritation of digestive tract - abdominal pain and vomiting

Diagnosis - history and clinical signs
No specific treatment available
Remove from affected pasture

49
Q

What skin lesions can cows get due to poor management?

A

Hock scuffs and hygromas
Stifle/pelvic/upper hindlimb injuries
‘Neck rub’ - hair loss and skin thickening (cubicle design of neck rail, feed barrier position)
Dirty

50
Q

Which lice do cows get? Treatment?

A

Sucking - Damalinia bovis
Chewing - Haematopinus eurysternus, Lignognathus vituli, Solenopotes capillatus
Treat with ivermectin, permethrins

51
Q

Chorioptic mange of cattle - When seen? Where affected? Signs? Treatment?

A

Seen in winter - housed cattle
Tail head lesions and udder
Mild pruritus - erythema, rubbing, crusts
Treatment - Ivermectins
(any in cattle, only Eprinex licensed for dairy cattle with a milk withhold)
Often left untreated, goes away in summer

52
Q

Sarcoptic mange of cows - Signs? Where affected?

A

Intense pruritus
Alopecia, crusting, thickening of skin
Head, neck and shoulders
Zoonotic

53
Q

Psoroptic mange in cows - signs?

A

Intensely pruritic
Bloody, crusty lesions - tail head, shoulders
Weight loss, death
Don’t treat with ivermectin (variable results)
Use 4% permethrin pour on
If unresponsive, use amitraz

54
Q

Which is the main organism causing ringworm in cattle? When seen? Treatment?

A 
Trichophyton verrucosum
Housed animals (UV light kills it)
Rectify underlying husbandry/disease e.g. pneumonia
Antiseptics, iodine
Enilconazole
Griseofulvin is illegal!!
55
Q

Dermatophilus congolensis in cattle - When seen? Signs? Diagnosis? Treatment?

A

Uncommon - associated with wet conditions
Seen on back and udder - crusty
Diagnosis - smear and methylene blue stain
Associated with milk scald in calves
Treat with penicillin, oxytetracycline

56
Q

What causes wooden tongue? Skin lesions seen? Treatment?

A 
Actinobacillus lignieresi
Abscesses and fistulation
Granulomatous lesions
Especially of head and LN
Treatment: antibiotics (pen/strep, oxytet), potassium iodide (not licensed)
57
Q

Cellulitis in cows?

A 
Peracute/acute
High mortality
Head and neck
Gross swelling
Pyrexic often
Treat with antibiotics Staphs and Clostridia associated
58
Q

Photosensitisation in cows - Causes? Signs?

A 
Primary - photodynamic agents in diet
Secondary - hepatic damage (phyloerythrin accumulation)
Lesions of white/unpigmented areas 
Erythema, pruritus, crusting, fissures
Also in congenital porphyria
59
Q

Papilloma warts in cows?

A 
Viral
Young animals
Resolve spontaneously
Can be problem if on penis/teats
Autogenous vaccine
60
Q

Haematomas in cows - Where seen? What to do?

A 
Common in dairy cows
Flank, hindlimbs - large swellings
Resolve spontaneously 
Don't open!
Care with needle centesis (can introduce infection)
61
Q

Bovine neonatal pancytopenia?

A

‘Blood sweating disease’
Due to Ab transmission via colostrum
Newborn - 4wo
Dairy and beef calves
Bleed from orifices, injection sites, skin, internal haemorrhages
Bone marrow & blood changes - Granulocytopaenia, thrombocytopaenia, anaemia, aplastic anaemia
Possible causes:
- Infectious
- Toxic
- Vaccine associated “Pregsure” (now off the market but cases still occurring)

62
Q

Lumpy skin disease - Cause? Transmission? Signs?

A 
Capripoxvirus
Closely related to sheep & goat pox
Transmission:
- biting flies, ticks, needles
- cattle movement
Fever 10 -14 days
Skin nodules (can persist), erosions
Lymph nodes enlarged, nasal discharge
Mastitis
Emaciation
Control:
- biosecurity (national & local)
- vaccine
63
Q

Besnoitiosis in cattle and horses - Cause? Signs? Transmission?

A 
Besnoitia besnoiti (toxo-like group)
Forms cysts - eye & skin
Chronic, debilitating disease
Arthropod transmission
Wildlife reservoir ?
64
Q

Features of Clostridium perfringens? Types?

A

Gram positive, rod shaped, anaerobic spore former
Widespread in environment and GI tracts
Disease associated with injury/wounds, diet changes, over eating, co-infection or ingestion of preformed toxin
Major toxins - alpha, beta, epsilon, iota, enterotoxin (CPE), beta-2, NetB
Minor toxins - theta, delta, gamma, kappa, lambda, Mu, Nu, sialidase
Type A: necrotic enteritis in chickens, gas gangrene, enterotoxaemia, colitis in horses - alpha toxin
Type B: lamb dysentery, bovine enterotoxaemia, bovine and equine haemorrhage enteritis - a, b, epsilon
Type C:necrotic enteritis in piglets - a, b
Type D: pulpy kidney disease in lambs, enterotoxaemia in sheep, goats and cattle - a, epsilon
Type E: rabbit enterotoxaemia - a, iota

65
Q

Features of C perfringen alpha, beta and epsilon toxins?

A 
Alpha:
- Membrane damaging toxin
- Essential with theta toxin for causing gas gangrene
- Associated with type A
- Sudden broiler flock mortality
- Immunisation with a-toxoid protects against necrotic enteritis
Beta:
- heat labile pore forming toxin
- increases capillary permeability
- dermonecrotic and cytotoxic
- sensitive to trypsin 
- lamb dysentery (type B) and Pig-bel (type C)
Epsilon:
- pore forming toxin
- activated by trypsin
- vascular permeability in organs
- affinity for kidneys
- type D: enterotoxaemia in sheep and goats, pulpy kidney disease
66
Q

What are the clostridial diseases?

A 
C chauvoei - blackleg
C septum - malignant oedema, braxy
C novyi type A - big head
C novyi type B - black disease (necrotic hepatitis)
C haemolyticum (novyi type D) - bacillary haemoglobinuria
C sordelli - gas gangrene, abomasitis
C tetani - tetanus
C botulinum - botulism (A-G)
67
Q

What is a vector borne disease?

A

A disease caused by a pathogen spread by an arthropod host (not a disease caused by an arthropod itself e.g. scabies)

68
Q

Lyme disease: Transmission? Human disease?

A 
Spread by Ixodes ricinus
Human disease:
- rash
- flu
- joint pain
- fatigue
- neuroborreliosis
69
Q

Bluetongue: Aetiology? What does it cause? Spread?

A

Bluetongue virus = orbivirus
25 serotypes
Causes severe disease in sheep and mild disease in cattle
Spread by culicoides

70
Q

Drivers of emergence of bluetongue and schmallenberg?

A

Climate change - causing midges to spread, increasing their vector competence
Global movements of animals/goods - bringing the viruses into Europe
Virus evolution

71
Q

Why is hard to make vaccines for parasitic protozoa and helminths?

A

Complex life cycles and immune evasion

72
Q

What is an autogenous vaccine? When used?

A

Produced from a pathogen isolated from infected animals in a flock/herd during a disease outbreak
Can be used/licensed by VMD as an emergency vaccine, usually when no effective commercial vaccine available
Usually simple inactivated vaccine

73
Q

What are adjuvants in vaccines?

A

Compounds delivered with the Ag in a vaccine that help develop the immune response
Aluminium salts most common
Most work by stimulating APC

74
Q

What is the microbiome?

A

The microbiome is the genetic material of all the microbes - bacteria, fungi, protozoa and viruses - that live on and inside an animal

75
Q

TSEs that affect cattle and sheep?

A

BSE

Scrapie

76
Q

What causes TSE disease?

A

PRP = a gene with 5+ alleles
Sc and C = 2 physical forms of protein
PrPc and PrPSc have an identical amino acid sequence (primary structure) but a different tertiary structure
PrPSc converts PrPc to itself
In a normal cell, PrPc is constantly made and digested
PrPSc is partially resistant to digestion so it accumulates and leads to disease

77
Q

Characteristic of TSE diseases?

A 
Long incubation period
Progressive and invariably fatal
Holes in brain give spongiform texture
No signs of fever
No signs of inflammation
No antibody response
No signs of a pathogen with a genome
No sign of infection!
78
Q

Chronic wasting disease: What is it? Which animals affected? Clinical signs? Transmission?

A 
Only TSE of wild populations
Only naturally spreading TSE
Limited genetic control of susceptibility
Affects deer
Incubation period: 16 months
Clinical signs:
- loss of condition
- standing away from herd
- listless
- ataxia
- nervousness
- excessive drinking and urination
- aspiration pneumonia common cause of death
Transmission:
- faeces, urine, saliva
- shed infectious prions into environment, contaminated herbage 
- also direct animal-animal
79
Q

Cascade for drugs?

A

Responsible antibiotic use under the cascade requires vets to take into consideration not only the most appropriate active substance(s) but also:

  • the most appropriate formulation
  • the posology (dosage)
  • the current pattern of resistance in their locality
  • an awareness of how to reduce selection pressure
  • and related factors eg good biosecurity and husbandry/hygiene, avoiding surgical sepsis etc

If a vet can demonstrate that these steps have been taken, then cascade use of antibiotics is supported

80
Q

Dutch formulary for cattle antibiotics?

A 
First Choice (not induce ESBL or AmpC):
- Pencillins
- Tetracyclines
- Phenicols
- Sulphonamides
- Licosamides
- Macrolides
Second choice:
- need justification due to natural or acquired resistance of bacteria AND bacteriology cannot be done
- Amino-penicillins
- 1st and 2nd generation Cephalosporins
- Aminoglycosides
Third line:
- only after individual bacteriology has been performed and NO alternatives was available
- 3rd/ 4th generation Cephalosporins
- Fluoroquinolones
81
Q

Success rates for treatment of endometritis with oxytet, prostaglandin and estradiol?

A

Oxytet: 73%
Prostaglandin: 67%
Oestradiol: 63\5

82
Q

Antibiotic choices for calf pnueumonia?

A

Florfenicol - licensed
Macrolides
Oxytetracycline

4th year (44 decks)

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