What are the barriers faced by invading pathogens? TYPES OF IMMUNE SYSTEM:
Innate immune system > first line defence (teat skin and canal, resident leucocytes- can be impacted by ABs in the milk).
Acquired immune system > humoral and cellular memory
Teat skin > present to prevent the colonisation of teat skin with bacteria = stratified squamous epithelium + bacteriostatic FAs.
Can be compromised by bruising, chapping, trauma, lesions and problems with the milking machine. This can allow colonisation with ubiquitous skin bacteria.
Therefore best to treat lesions promptly and use post-milking teat dip emollients.
Teat canal > bacteria can enter when the canal is open after milking, teat sphincter muscle acts as a barrier- but takes 30 mins to close.
What are the components of the innate IS in the udder? Inside the udder there macrophages, neutrophils and T lymphocytes = phagocytose the invading pathogen + release pro-inflammatory mediators & antigen presentation.
When there is an infection, a high increase in these will be noticed= high SCC.
Also release:
- Lactoferrin > Iron binding protein produced by epithelial cells + leucocytes. High concs found in dry periods and prevents the growth of pathogens which require iron = E.coli
What are the components of the acquired IS in the udder? - Neutrophils
- B lymphocytes > present in the lymph fluid and produce IgM, IgG1 and IgG2 (on repeated exposure) > circulate to enter the inflamed udder and help the neutrophils. Can be utilised for vaccines= only able to minimise the severity of mastitis infections.
- T lymphocytes > T helper cells produce cytokines and stimulate IR. cytotoxic T cells are present to kill host cells invaded by pathogens.
- Antibodies > IgG2 is the most important. Abs present pathogens + neutralise toxins + agglutinate bacteria.
What are the factors influencing mammary glandimmunity? 1. Genetics (immunity and conformation) > hard to select as low heritability, also problems with speed of milking and yield size.
2. Stage of lactation > dry period is high risk for new infections and existing infections to persist (despite long term AB use).
Highest risk at:
- Early dry period > high levels of neutrophils but lots of fat and cellular debris.
- Peri-parturient > colostrgogenesis can interfere with neutrophil capacity and recruitment + phagocytic ability is reduced. There are also hormone changes.
3. Nutrition > NEB results in low leukocyte counts, also low Vit E and Selenium levels can interfere with leukocyte function.
Hypocalcaemia = weakened teat sphincter mechanism + lying down in a contaminated environment.
Also sub-acute rumen acidosis is at risk (reduced appetite> reduced DMI > NE > diarrhoea >poor hygiene and not eating enough > high risk of infection and NEB.
4. Vaccination > only one, and against S.aureus and coagulase-negative staphylococci. Reduces incidence and severity of clinical mastitis. Takes a lot of effort = repeated every gestation.
5. Stress
** Dry period management is key to udder health. Make sure they get correct ABs and clean up any infections.
What to consider with teat injury? Teats are vulnerable to trauma (being trodden on), damage > allows bacterial colonisation > mastitis.
Often lesions are painful and will prevent calves from suckling.
**Can be a sign of systemic disease= FMD, MCF, photosensitisation, milking machine error.
Ensure good breeding genetics, loafing time post milking, teat sealants at drying off and a good quality milking machine. Care as loafing time can exacerbate lameness problems
Udder / teatimpetigo: Pustular lesions on the teat and udder skin. Usually S. aureus and can spread to the milkers. Control with PMTD + antiseptic udder creams.
Photosensitisation: Can occur as part of generalised skin photosensitisation disorder in which non-pigmented skin is affected = underlying hepatic injury.
Treat with general supportive care (keep in shade, NSAIDs, sunblocks).
Teat pea: Pedunculated granuloma attached to the wall of the teat canal = blocks the flow of milk.
Remove with Hudsons spiral > inserted by rotating up the teat canal and then jerk upwards to tear the granuloma off > can then be milked out. OR mosquito forceps up canal to tear granuloma off. OR treat like surgical lump removal.
Can distort the canal + allow bacterial growth.
Give prophylactic ABs to prevent mastitis + sedate, cannulate, open teat wall and suture.
What do you need to remember? Damage to teat skin > bacteria allowed to colonise.
Blue, oedematous petechians or chapped teats.
Often due to hard / worn linters or inadequate rate phase in pulsators = poor circulation.
Also can be due to excessive vacuum in milking cluster or inadequate emollient use in post milking teat dip.
It is better to leave residual milk in the teats and not leave her completely dry as this can cause damage / increase risk of infection / reduce milk yield in future.
What happens when the milking machine goes wrong? For milk release = apply vacuum to whole cluster > end of cow teat > liner closes on the teat to draw milk out..
Not continuous as can do damage and limit BS = pulsator linter which opens and closes intermittently.
Vacuum on to off is 2:1, and the claw piece collects milk > long tube > bulk tank.
Need good hygiene to prevent introduction and spread of infection. Also to ensure no damage to teats and teat ends, and des not act as a vector for spread of infection.
Milking parlours hold risk of spready mastitispathogens from cow to cow.
- Contagious pathogens from cow to cow in milk (esp. S aureus)
- Environmental pathogens on the teat ends / cluster
Best to flush clusters between each cow and keep parlour as clean as possible at all times.
Essential hygiene: gloves, pre-milking teat preparation (kills coliforms), post milkingteat dipping, loafing time, parlour management of those clinically / subclinically infected.
Assess milking order and cluster disinfection, also observe the parlour wash up routine.
Dysfunction:
- Contamination of liners > transfer of pathogens on teat skin
- Wet milking > milk flushed up into the teat canal + pathogens > due to inadequate vacuums, fluctuating vacuums or a blocked air bleed.
What are some common problems with milking clusters? 1. Vacuum > can be too high (incorrect setting or the regulator is not working), or fluctuating / inadequate (poor pump, holes in tubing, liner slip with clusters flailing off, inadequate vacuum reserve)
2. Blocked air bleed on cluster unit with flooding into the claw piece > milk will not drain away properly
3. Faulty pulsation > set too fast can result in poor circulation with inadequate rest phase + holes in tubing.
Can develop teat end sphincter hyperkeratosis = increased risk of mastitis, due to XS vacuum or overmilking or faulty liners or poor pre-milking teat preparation.
How to assess milking machine? Examine cluster > blocked air bleeds, cleanliness of liners, wear of liners, holes in tubing.
- Liner slipping = hear shhh sound
- Note vacuum gauge in parlour and watch while milking to observe for fluctuations
- Look at teats > those that are a bit blue or swollen = dodgy vacuum
- Look at cows > kicking, over milking at the end, hard liners, excess vacuum
- Teat score
- Assess the wash up routine and look at service invoice.
Milking parlour machinery needs a check up at least once a year, better to do it more often. Also need to replace rubber / silicone liners after a couple of months (depends on number of cows).
Which refelex is involved? It is a legal requirement.
Done to detect early mastitis and stimulate milk let down reflex > for more rapid milking overall.
Can then clean / disinfect the teats depending on how clean the environment is.
Aim is to decrease environmental bacterial contamination to improve public health and reduce mastitis cases- esp. the environmental pathogens= E.coli and Strep uberis.
If the teat is being washed it must be dried before milking. Also can use cup with disinfectant / foaming products.
Milk ejection reflex > teat stimulation results in stimulation of the hypothalamus > oxytocin is released from the posterior pituitary > results in contraction of myoepithelial cells in mammary gland.
The stimulation to secretion delay determines milking routine.
What disinfectants can be used? Pre-milking teat dipping is done to remove organisms from the teat skin which may enter the udder via teat during milking = environmental mastitis pathogens
Post-milking is done to kill bacteria on the teat after milking and protect the teat from new infection from environment = contagious mastitis pathogens and teat skin pathogens.
Can also condition teat skin to withstand disinfectants and milking machine.
Loose housing with straw VS cubicalbedding: LOOSE HOUSING: mostly dry cows / calving area. Comfortable so can be good in lameness cases.
Hygiene can be limited = warm, wet straw can encourage bacterial growth > increased environmental mastitis risk.
70:30 of bed:loafing, needs good drainage layer under bed, and store the dry bedding under cover.
Scrape out daily and totally clean out at least every 2 weeks.
Have clearly divided sections with bedding kept back by sleepers.
CUBICAL BEDDING: each cubical needs concrete base with protective mattress. Also division + brisket barrier board + head rail to aid cow position.
Good practice is 5% more cubicles than cows.
Aims of cubicle design > comfortable when both lying / standing, 2% slope upwards, dung passed over the kerb with minimum deposited on cubicle rear. Whilst also minimising pathogen growth.
Dimensions are recommended based on BW.
Can assess CCQ (cow comfort quotient= <50% is poor, >80% is okay), SUI (stall use index) and SSI (stall standing index)