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Farm animal > Production diseases > Flashcards

Production diseases Flashcards

1
Q

Disbudding calves

A

Cornual nerve of lachrymal nerve local block - bony ridge halfway between eye and ear - Procaine 19 guage 1” needle 1-3cm depth and 2-3 minutes to work - check its worked by wiggling needle around horn base
Can knock down with xylazine
Hot iron - 2-3 seconds - check for copper ring - if any white do again 2-3 seconds
Antibiotic spray
NSAIDs after

Can see haemorrhage in older - grasp artery and break off below bone where it will clot

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2
Q

Mastitis

A

Diagnosis of individual
- All 4 teats and glands, milk/secretion
Look and palpate - acute and chronic inflammation
Injury/trauma
Beware cold - gangrene

Clots, watery, colour change
Conductivity
CMT - elevation in SCC
Cow SCC

Grading
1 - mild - milk changes only
2 - moderate - inflammatory signs in quarter
3 - severe - systemic signs - sub acute to toxic

Treat with intramammary antibiotics - 5-8 days
Penicillin long course

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3
Q

Environmental mastitis causes

A

Opportunistic

S. uberis
Staphylococcus (not aureus)
E.coli
Klebsiella
Pseudomonas

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4
Q

Contagious mastitis causes

A

Adaptation to mammary gland
Persistent infection
Spread at milking

Staph aureus
Streptococcus agalactiae, dysgalactiae
Mycoplasma

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5
Q

Low vs high cell count mastitis

A

High cell count likely to be contagious - penicillin
Low cell count likely to be environmental - penicillin + aminoglycoside + NSAIDs

Aseptic infusion needed

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6
Q

Subclinical mastitis during lactation

A

High SCC >200,000 likely to be G+ bacteria - spread to other cows during lactation
Best to wait until dry cow therapy at end of lactation

Could also identify quarter and dry this off
or dry off early
or cull
Or extended intra mammary 7-8 days

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7
Q

When to dry off with antibiotics

A

Individual SCC and clinical mastitis history
If <200,000 for past 3 recordings - uninfected
If >200,00 for one or more of past 3 and/or clinical mastitis in past 3 months - infected - antibiotic and teat sealant

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8
Q

Summer mastitis

A

Trueperella pyogenus
Peptococcus indolicus
Streptococcus dysgalactiae

Disease of dry cows and heifers
Can infect young calves and bulls
Transmitted by sheep head fly - Hydrotea irritans

Hot, hard, swollen, painful quarter
Characteristic foul smell
Cow often lame
Often undetected
Can lead to abortion

Prognosis poor, quarter often lost

Intramammary antibiotics useless
- Systemic penicillin
Regular stripping
Insitute drainage by removing teat/cutting vertically

Control
Fly avoidance - sprays, pour ons
Dry cow therapy
Teat sealants
Stockholm tar

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9
Q

What do we want to find out with herd level mastitis?

A

When do new infections occur?
stage of lactation
Milking or living environment
time of year
groups - age/yield

Dry period or lactating?
- Spread at milking - persistent elevation of SCC, clinical recurrance, non seasonal infection rates
Seasonal effects
Parity of cows at risk

Cows at lactogenesis/colostrogenesis - teat canal begin to open - infection risk. Wont show until lactation

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10
Q

When is dry period mastitis infection

A

Within first 30 days of lactation

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11
Q

Acute endotoxic mastitis

A

Severely sick cow - down/ataxic or very dull
Cardiovascular shock - dehydration, injected membranes, tachycardia, tachypnoea, cold extremities
Temp increases then subnormal
Eating, drinking, milking to nil

Hot, swollen, watery secretion
Can get sick cow before udder pathology is seen

DDX
- Down - hypocalcaemia, dystocia, trauma, peracute infection (metritis), neuro,toxins
- sick but standing - early hypocalcaemia, early hypomagnesaemia, ketosis, dystocia, metritis, neuro, toxins

Severe E.coli mastitis
Strip quarters and TLC
Antibiotics + systemic - oxytetracycline, TMPS, penicillin
NSAIDs
Glucocorticosteroids - only if given very very early on - high doses
IV fluid therapy - 25-35 litres in 1hour, 20 in next 24 hours. 20-50L daily
Hypertonic saline - 4-5ml/kg - 3 litres per cow

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12
Q

Acute mastitis sheep

A

Red, hot, swollen udder or udder half, painful
Lameness
Increased vocalisation
Unwilling to lie
Not allowing lambs to sick
Watery milk or pus like
Manual expression may be impossible
Pyrexic
Anorexia
Increase in SCC
Gangrenous bag - secondary infection after sloughing

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13
Q

Chronic mastitis sheep

A

Masses in udder - abscesses
Can rupture - spreading infection around udder and reform later

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14
Q

Sub clinical mastitis sheep

A

Increased SCC
Underperforming lambs - longer to reach finishing weight

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15
Q

Major causes of mastitis sheep

Risk factors

Treatment

A

Staphylococcus aureus - acute
Mannheimia haemolytica - acute
Streptococcus
E.coli - gangrenous
Coagulase negative Staphylococcus - CNS

Risk factors
Nutrition
BCS - low
Hygeine - poor hygeine at lambing time
Intramammary masses
Teat lesions - entry point - orf
Teat position and udder conformation
Cross suckling
Age
Maedi visna
Indoor lambing

Treatment
Amoxicillin/oxytetracycline 5-7 days
NSAIDs
Aim to save ewe not udder

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16
Q

Major causes of mastitis sheep

Risk factors

Treatment

A

Staphylococcus aureus - acute
Mannheimia haemolytica - acute
Streptococcus
E.coli - gangrenous
Coagulase negative Staphylococcus - CNS

Risk factors
Nutrition
BCS - low
Hygeine - poor hygeine at lambing time
Intramammary masses
Teat lesions - entry point - orf
Teat position and udder conformation
Cross suckling
Age
Maedi visna
Indoor lambing

Treatment
Amoxicillin/oxytetracycline 5-7 days
NSAIDs
Aim to save ewe not udder

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17
Q

Sub clinical ketosis can increase risk of?

A

Clinical ketosis
RFM
LDA
Metritis
Lameness
Mastitis
Culling
Death

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18
Q

What is ketosis

A

Negative energy balance
- Decreased glucose supply

Cows at biggest risk at start of lactation - type 2 ketosis - yield increasing faster than food intake
And at peak lactation - type 1 ketosis - cannot provide enough energy

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19
Q

Normal energy balance physiology

A

Some mobilisation of body fat to produce NEFAs
NEFAs oxidised in liver using glucose from proprionate and gluconeogenesis

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20
Q

Type 1 ketosis pathophysiology - underfeeding at peak lactation

A

Reduced supply of proprionate and therefore glucose
Incomplete oxidation of NEFAs in liver - ketone body production

Energy intake < energy output
“Type I” ketosis
Peak lactation
Highest energy demand
Cause and effects both normally around 20-60 DIM (days in milk, i.e. days post –calving)

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21
Q

Type 2 ketosis pathophysiology - hepatic lipidosis, early lactation

A

Excessive mobilisation of fat, increased NEFAs
Incomplete oxidation of NEFA (ketones) and excessive fat accumulation in liver
Reduced gluconeogenesis and liver function

Fat infiltration of liver
“Type II” ketosis
Not just fat cows!
Around calving
Diet/intake in late dry period critical
Effects normally seen <20 DIM

Under or over supply of energy in dry period (under as will mobilise pre calving, over as will lay down fat in liver)

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22
Q

Clinical signs of ketosis

A

Off food
Milk drop
Can smell ketones
Nervous ketosis

Hepatic lipidosis
Off food
Milk drop
Immunosuppression
Collapse, liver failure

Diagnosis
Blood -cow side ketone meter or laboratory
Urine -ketone dipstick
Milk -Rothera’s reagent

Hepatic lipidosis:
*Look for ketones
*Blood NEFA
*Evidence of liver damage, e.g. biochemistry of liver enzymes (AST, GGT)
*Assess fat in liver (biopsy, necropsy)

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23
Q

Nervous ketosis

A

Unusual complication
CNS signs
- Caused by hypoglycaemia
- Ketones
- Other circulating chemicals

Can be aggressive
Furious licking

24
Q

Treating ketosis

A

Same for type 1 and 2, and hepatic lipidosis
Provide an energy source
The more fatty the liver is the harder it is to treat - no treatment for bad liver damage
Insulin resistance can be slow to recover

Glucose precursor - propylene glycol - creates insulin peak - should resensitise

Glucocorticoid - promote gluconeogenesis, might increase appetite

Glucose
Supply IV
Rapid peak and decline - metabolised within minutes - no evidence
Use in nervous ketosis

25
Q

Pregnancy toxaemia in sheep - twin lamb

A

Pregnancy ketosis
Usually occurs before lambing
Can occur in beef

Sheep peak energy demand is producing the lamb and colostrum at end of pregnancy not peak lactation - energy demands exceed supply

Clinically indistinguishable from hypoCa - often one will precipitate other
Off feed, dull, depressed, nervous (blindness), death
Can be caused by teeth/lameness in sporadic cases
Outbreaks - change in management - reduced DMI

26
Q

What acts on calcium in blood?

A

Calcitonin = deals with blood calcium that’s too high

Parathyroid hormone and vitamin D increase blood calcium
Vitamin D and parathyroid hormone increases calcium uptake from the gut
Parathyroid increases calcium release from bone and activates vitamin D

Takes 1-2 days for parathyroid hormone effects to kick in

27
Q

When does risk of hypoCa increase

A

Increased with parity
Less parathyroid receptors and less calcium stores
Almost never see hypoCa in heifers as good calcium supplies and PTH receptors

28
Q

Ddx for hypoCa

A

Thrashing limbs and hyperaesthesia = hypomagnesemia

Constipation and ruminal bloat = hypocalcaemia (muscles of rumen and GIT stop working)

Sunken eyes and diarrhoea = toxic mastitis (toxins cause vasodilation and fluid leakage into the gut = dehydration); pyrexic initially then hypothermia

Unable to weight-bear on one leg = nerve paralysis, broken leg -traumatic condition (can be secondary to milk fever but this is normally a generalised weakness, but milk fever could predispose/cause trauma)

29
Q

Botulism clinical signs

A

Toxin causes flacid paralysis
Looks like milk fever - down, constipated, rumen stops working
Toxins produced by clostridia botulin growing in rotting organic matter
Antibiotics dont help as toxin causes illness not bacteria
Need to euthanase if nursing hasnt stopped progression
No treatment

30
Q

HypoCa clinical signs

A

Skeletal muscle -weakness and S bend in neck
Smooth muscle -GIT stasis and poor uterine involution
Cardiac muscle -poor contractility and slightly increased heart rate (very increased in toxic mastitis)

31
Q

HypoCa treatment

A

400ml 40% calcium borogluconate slowly IV

Monitor heart rate and rhythm
Can cause dysrhythmias - slow down rate of calcium infusion if slight dysrhythmias
Needs calcium so just hope it’s not a cow who’s heart will be affected
Consider blood sample in case no response

Take bloods initially and maybe don’t run them unless treatment hasn’t worked

Outcome of treatment
Eructation, defecation, standing
If no response, consider alternatives and complications (e.g. “downer cow”)
Should respond quite quickly

Muscle, nerve or bone damage not uncommon if large cow has been down for a while

32
Q

Additional treatments for HypoCa

A

Calcium orally
Well absorbed
Required GI uptake
Relatively easy
Becoming more common

Calcium subcutaneously
Poor absorption due to peripheral vasoconstriction
Not as effective as boluses and probably don’t last as long
Easy
Negative feedback
Relatively common

NSAID
700kg down cow is predisposed to secondary trauma complications
Won’t do any harm and might help make it more comfortable and get up quicker

Phosphorus
If calcium is low then phosphorus is also often low - can mix in with calcium
Common preparation of phosphorus isn’t biologically active so is just excreted
Probably doesn’t have an effect
*Phosphorus should recover anyway as calcium recovers if you just give calcium

33
Q

How to prevent HypoCa

A

Feed less calcium in the dry period so at the point they calve they have lots of parathyroid in their system
Then switch quickly to a high calcium diet on the day they calve, allowing their bodies to utilise all available calcium

Giving less sodium and potassium in the dry period reduces blood pH, which increases the efficacy of parathyroid hormone, but do have to feed calcium at the same time
Pouring loads of salt onto their diet -taste disgusting so reduces feed intake and predisposes to ketosis

34
Q

5 iceburg diseases of sheep

A

Maedi visna - lentivirus
- Wasting, respiratory, neuro signs

Ovine pulmonary adenocarcinoma (OPA)
- Retrovirus
- Weight loss, respiratory, sudden death

Caseous lymphadenitis (CLA)
- Corynebacterium pseudotuberculosis
- Lymph node abscesses

Ovine Johne’s disease (OJD)
- Mycobacterium avium paratuberculosis
- Reduced ferility and weight loss

Border disease (BD)
- Pestivirus
- Poor ewe fertility, hairy shaker/weak lambs and abortions

35
Q

Maedi visna

A

*Lentivirus– long incubation period (months to years)

  • Presentation variable, often chronic wasting and laboured breathing

*Oronasal is the main route of transmission, but can also be spread through colostrum/milk and by fomites

*Regional variation in prevalence (Leicestershire and Gloucestershire high)

*Serological diagnosis (antibodies produced within weeks to months but tend to wax and wane)

*No treatment or vaccine: control methods include purchasing from accredited flocks (or isolate and test), monitoring and culling positive animals (if practical) and reducing stocking density, preventing contact with neighbouring flocks.

If high level of infection:
1. Cullflock & restock with accredited sheep
2. Try and reduce losses through management:
a) Keep flock young
b) Split into older & younger sheep for management
c) Cull thin/suspect cases
d) Run a less intensive system to reduce spread

36
Q

Ovine pulmonary adenocarcinoma - OPA

A

*Retrovirus
* Causes neoplastic proliferation of lung cells = adenocarcinoma, resulting in laboured breathing, increased respiratory rate, ill thrift and sudden death

  • Transmission mainly aerosol, but can be spread through milk and colostrum

*Long incubation period – 6 months to several years
No blood test commercially available for diagnosis; lung ultrasonography has been used but should be interpreted with caution; post-mortem the only definitive way to diagnose

*No treatment or vaccine

*Identify & cull infected & offspring – very difficult without test.
Need to PM any sudden deaths/those showing ill thrift.
* Manage in single age groups – keep young separate from adults
*Reduce close contact – housing, stocking density, trough feeding. Need good hygiene
*Snatch lambing & rear artificiall

37
Q

Caseous lymphadenitis - CLA

A

*Corynebacterium pseudotuberculosis

  • Transmission through skin abrasion, inhalation or ingestion –often when sheep are grouped
  • Forms abscesses in lymph nodes with characteristic green pus, typically around head and neck (inguinal/scrotal in tups)
  • Diagnosis by bacteriology/serology
    *Bacteriology requires draining abscess
    *Serology has high specificity but low sensitivity
    Antibodies tend to wax and wane and presence of antibody doesn’t necessarily lead to disease.
  • Control methods include buying from trusted sources, boundary biosecurity and separating infected animals
  • Treatment with antibiotics not effective; vaccine not available in UK but can be imported on special licence (efficacy variable)

*Zoonotic(although rarely reported in people)

38
Q

Ovine Johne’s disease

A

*Mycobacterium avium spp. Paratuberculosis (MAP)

  • Causes inflammation in the gut and reduces metabolic efficiency, leading to reduced fertility and weight loss; don’t see scouring, but thin sheep/high flock culling rates/poor lamb performance

*Cattle and sheep strains (C and S) – sheep susceptible to both (cattle fairly resistant to S strain)

  • Transmission mainly faeco-oral, but can be passed via milk/colostrum; lambs are infected early on in life (first 3-4m usually), but clinical signs are usually seen in animals over 2-3y
  • Diagnosis can be by serology, but antibody levels often remain low until clinical disease; faecal PCR – unclear how much bacteria correlates with disease; PME most definitive

OJD control challenges
- Low sensitivity of diagnostic tests
- Inability to detect sub-clinical animals
- Practicalities of testing entire flocks
- Snatch lambing not practical
- Contact between sheep and cattle - cograzing, slurry spraeding

OJD control solutions
- Lamb old/thin/high risk ewes away from rest of flock
- Select replacements from younger ewes - younger less likely to be shedding
- Cull low BCS
- Maintain good hygiene and clean bedding
- Vaccination - reduced shedding and clinical signs - not infection

39
Q

Border disease - BD

A
  • Caused by virus very similar to BVD in cattle (pestivirus); see hairy shaker lambs, poor ewe fertility, high levels of abortions or weak lambs
  • Proportion of UK flocks infected estimated to be between 30-38%
  • Transmission via respiratory secretions, transplacental, from dam to offspring during peri-parturient period, or via semen of PI rams
  • Intensive flocks at increased risk - transmission in extensive flocks appears to be moderate
  • Diagnosis by detection of antibody or antigen; as in cattle, PI animals will be negative for antibody (persistently), but will be positive for antigen

Control
- PI hunt not as practical as in cattle
- BVD tag and test not valid for BD
- Natural immunity through exposure of non pregnant animal to PI - but transmission can be slow
- BVD vaccine - no evidence
- Dont retain breeding females from lamb crops with affected cases/test all ewes to be retained (antigen test)
- Optimise nutrition and parasite control

40
Q

General iceburg control strategies

A

Biosecurity - most risk from animal movement
Testing/accreditation
Screen cull ewes and fallen stock
- BD is exception - screening lambs more useful
Screen bought in animals - ideally pre-purchase
Quarantine - seperate from pregnant ones until after lambing - also for chlamydia

41
Q

Effects of subclinical ketosis / NEB

A

Reduced milk quality
Decreased fertility
Impaired immune function - metritis/RFM
Role in other diseases - LDA

42
Q

BCS targets

A

No change over dry period
Max decrease of 0.5 between calving and peak lactation
Aim for 2.5-3 at calving
Avoid >3

43
Q

Metabolic profiles for NEB

A

Blood sample random selection at specific stages
Usually transition (21-7d pre calving) and fresh calvers (10-25 DIM)

BHB - ketone body, current energy supply demand, esp useful in fresh calvers

NEFA - non esterified fatty acids - transport of fat, indicator of fat mobilisation
Esp useful for transition

8-12 samples/group
Target prevelance of high BHB/NEFA <10-20%
Usually means any abnormal result suggests a problem
>= 3/12 abnormal results taken to indicate herd problem

44
Q

NEB in transition/calving

A

Poor DMI
Excess BCS/overfeeding

45
Q

BEN in early/peak lactation

A

Poor DMI
Low ration energy density

46
Q

How to improve DMI

A

Easy access trough space per cow
Minimise impact of group changes
Avoid overconditioned cows - esp at calving
Maximise ration palatability
Manage environment appropriately - temp, humidity, comfort

47
Q

DCAB and hypoCa

A

Dietary cation-anion balance

Difference between concentrations of major cations (Na+, K+) and major anions (Cl-, S2-) in the diet

I.e. it’s just a chemical property of a feedstuff or diet

DCAB = ([Na+] + [K+]) – ([Cl+] + [S2-])
(all in mEq/kg DM)

Diets with low DCAB (<0 mEq/kg DM) induce mild metabolic acidosis…

Metabolic acidosis means…
Enhanced uptake of Ca from the GI tract
Ca mobilisation from bone
Higher rate of vitamin D3 activation per unit PTH
Increased target tissue sensitivity to PTH and activated vit D3
So the cow is able to mobilise Ca from body reserves more quickly

True/full DCAB
Aim for diet DCAB around 0 to -50 mEq/kg DM
Often just by choosing lower DCAB feeds, may also use salts
Usually doesn’t require Ca supplementation
More common in lower yielding herds

“Partial” DCAB
Aim for diet DCAB around -100 mEq/kg DM
Likely to require use of anionic salts (e.g. MgCl2, MgSO4)
Usually needs Ca supplementation too
Effective but more involved/ expensive

48
Q

Mineral supplements for beef cattle

A

Calcium – requirements change depending on animal age and production status; nonlactating pregnant cows need 0.18% Ca of total DMI, and growing and finishing cattle need 0.31% Ca

Phosphorus – works with calcium to form bone and used in DNA and energy metabolism; deficiencies involve decreased milk production, reduced weight gain, poor reproductive efficiency, etc.; calcium to phorphorus ratio should be 2:1 to 1.2:1

Magnesium – activates metabolic enzymes; low levels (e.g. lush grass in early Spring) cause grass tetany (urination, erratic behaviour, convulsions); need Magnesium to make up 0.04-0.1% of DMI

Sodium and Chlorine – maintain volume, pH and osmolarity of body fluids; sodium used in muscle and nerve function; chlorine used for HCl in abomasum and CO2 transport; Na should be maximum 0.08% of DMI for dry cows and 0.1% for lactating cows; no known Cl deficiencies seen in cattle

Potassium – deficiency causes nonspecific clinical signs of poor appetite, weight loss, performance drop and stiffness; need potassium levels of 0.6-0.7% of DMI; normally found in high enough quantities if plenty of roughage/silage fed

Sulphur – in protein, some vitamins, enzymes, etc.; growing and finishing cattle should have 0.15% of DMI as sulphur; DMI sulphur over 0.4% is potentially toxic; excess sulphur interferes with selenium, copper, molybdenum and thamin metabolism; sulphur deficiency signs include increased feed uptake, unthrifty appearance, dull har and alopecia; excess sulphur signs include aimless wandering, blindness, muscle tremors and convulsions

Cobalt – needed by ruminal bacteria to make vitamin B12; essential mineral; beef cattle need 0.00001% of total DMI; deficiency signs include loss of appetite, muscle wasting and anaemia

Copper – deficiency signs include unthriftiness, bleaching of hair coat (spectacled eyes) and anaemia; need to be 0.001% of DMI in beef cattle; toxicity signs include haemolysis, haemoglobinuria and jaundice

Fluoride – toxicity is the main issue and signs include abnormal bone structure and softening and irregular wear of teeth; safe levels for finishing cattle are no more than 0.01% of DMI and 0.004% of DMI for the breeding herd

Iodine – essential to produce thyroxin; deficiency signs include a goiter, weak or hairless calves, reduced reproductive performance and retained placentas; needs to be 0.00005% of DMI

Iron – used in oxidative enzyme systems and haemoglobin; needs to be 0.0005% of DMI; iron deficiency can occur in calves fed an exclusive milk diet, unless out at pasture; deficiency signs include reduced feed intake and pale mucous membranes; not really seen in adult cattle, but can be caused by extremely high levels of external parasites drinking blood

Manganese – used in many enzyme systems; needs to be 0.0002% of DMI in growing cattle and 0.0004% of DMI in breeding cattle; high calcium and phosphorus levels interfere with manganese metabolism; deficiency signs include reduced fertility in cows and crooked calf syndrome in young calves

Selenium – deficiency signs include white muscle disease (degeneration) and retained placentas; has similar metabolic activities to Vitamin E, so selenium requirement in diet depends on Vitamin E levels; beef cattle need about 0.00001% selenium of DMI

Zinc – needed in enzymes for protein and carbohydrate metabolism and for immune function; maintenance requirement is 0.003% of DMI; lactation and reproduction requirements not known; deficiency signs include unthriftiness, excessive salivation, scabby skin on legs, slow wound healing, alopecia and dermatitis over the whole body; zinc supplementation not consistently beneficial

49
Q

Mineral deficiency - poor growth, illthrift, loss of condition

A

Copper
Selenium
Cobalt

50
Q

Mineral deficiency - decreased repro performance

A

Iodine
Zinc
Phosphorus
Selenium
Copper

51
Q

Mineral toxicities in UK

A

Lead poisoning: neurological signs, commonly associated with access to a fairly obvious lead source (e.g. car batteries, old paint)

· Copper poisoning: almost exclusively related to inappropriate or excessive supplementation - sheep are especially sensitive. Pig concentrate feeds can have high copper levels and can be a cause of toxicity in ruminants. Long-term exposure tends to accumulate within the animal (esp liver), followed by an acute haemolytic crisis - as this is often a group problem, one or two clinically severely affected animals may present initially but the rest of the group may be earlier in the “accumulation” phase.

52
Q

Prognosis for teat laceration

A

<4 hours ideal
More proximal better prog
Vertical better prog
Streak canal ideally not involved
Superficial

53
Q

Teat granulomas - teat peas

A

Basal
- Congenital in heifers
- Chronic inflammation from infection in the dry period

Mid teat
- Chronic inflammation
- Milk calculi - teat peas
- Neoplasia - bovine papillomatosis
- Congenital obstruction

Apical
- Fibrosis and stenosis of the streak canal due to chronic inflammation in heavy milkers

Tight teat sphincter
- Trauma to teat end creates scar tissue - leads to mastitis

54
Q

Local anaesthetic for teat surgery

A

Teat cistern infusion
Infuse local anaesthetic via a teat cannula or syringe into the teat cistern

Ring block
Local anaesthetic into the full thickness of the teat in 4-6 sites around the teat base, with or without a torniquet; avoid entering teat canal and vessels

Inverted V block
Full thickness line block given over and adjacent to the affected tissue/incision

Intravenous regional anaesthesia
Torniquet around the teat and inject 5-7ml of local anaesthetic into any superficial vessel

Line block
Multiple subcutaneous injections of local anaesthetic 0.5-1cm apart

Topical splash application
Dripping or splashing local anaesthetic onto a wound and waiting 20 mins

Paravertebral anaesthesia
Anaesthesia to cranial udder and teats for standing surgery

Lumbosacral epidural
Anaesthesia of caudal abdominal wall up to the level of the umbilicus; temporary dysfunction of the hindlimbs, so need sedation and lateral recumbency

55
Q

3 layers in teat and what suture material and pattern to use

A

Mucosa
Continuous sutures with vicryl

Submucosa
Continuous sutures with vicryl

Skin
Simple interrupted or horizontal mattress sutures with prolene

56
Q

Infectious causes of teat lesions

A

Bovine herpes mamillitis
Mastitis - various organisms

57
Q

Non-infectious causes of teat lesions

A

Lacerations
Photosensitisation
Hyperkeratosis
Udder oedema
Ischaemic necrosis

Farm animal (8 decks)

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