Bovine Udder Health 3 Flashcards
- When do environmental pathogens normally enter?
- Where on farm can the pathogens be picked up? – as such what needs to be identified?
- Between milkings.
- Cubicles, sheds, bedding, paddock and pasture. – weaknesses in design and management to help combat new infections and other health/welfare issues.
- What is development of an IMI from an opportunistic / environmental pathogen a function of?
- When is a cow most susceptible to mastitis?
- Exposure of the teat ends to pathogens.
- Resistance of cows to infection.
- Exposure of the teat ends to pathogens.
- After drying off and just before calving.
- Major environmental pathogens.
- Minor environmental pathogens.
- E. coli.
- Strep. uberis.
- Klebsiella.
- Enterobacter spp.
- E. coli.
- Strep. dysgalactiae.
- Pseudomonas aeruginosa.
- Nocardia spp.
- Serratia marcescens.
- Yeasts.
- Algae.
- Strep. dysgalactiae.
Coliforms.
- E. coli, Klebsiella, Enterobacter spp.
– Always present.
– Respond to environmental conditions.
–> Increase w/ high humidity, warm temps.
– Bedding factors.
–> Often found in sawdust.
– 70-90% IMI result in clinical signs.
– High self-cure rate.
–> ABX therapy can be effective (but is it wise?)
- Is E. coli gram positive or gram negative?
- Key component of E. coli infection.
- Gram negative.
- Endotoxin release.
- Classically severe mastitis, but often starts mild and progresses.
- Bacteria multiply to peak in 12-24hrs.
- LPS released from proliferating and phagocytosed organisms.
- Excessive inflammation and systemic signs result (toxicity).
Strep. Uberis.
- Gram positive.
- More persistent infection than coliforms.
– Udder becomes reservoir. - May case high bacteria counts, +/- high SCC.
- Bedding factors.
– Often found in straw, out on pasture. - Dry period can be major risk time.
– >50% of new environmental Strep. infections.
Strep. dysgalactiae.
- Environmental vs contagious.
- Associated w/ teat end lesions.
- Spread by indirect contact e.g. hands or cloths at milking.
Which environmental pathogens cause most clinical and subclinical mastitis?
Strep. uberis and E. coli.
Herd signs of environmental mastitis.
Increase in clinical mastitis:
- Mildly clinical.
- May include rise in toxic mastitis.
- Often early dry period or early lactation.
Elevated SCC.
- In bulk tank and individuals.
- High rate of volatility / variability in records.
- Seasonal changes.
Positive bulk tank cultures for environmental pathogens.
Control of environmental pathogens.
- Reduce new infection rate.
- Reduce duration of infection.
Factors in the control of environmental mastitis by reducing the new infection rate.
- Milking routine.
- Hygiene.
- Vac.
- DCT.
Reducing new IMIs in milking routine.
Pre milking teat dip / teat cleaning.
- Reduce environmental bacteria entering udder during milking process.
- Approved product.
- Contact time.
Post milking teat dip.
- Mainly for contagious.
- Can provide some barrier.
Keep cows standing.
- Decreases teat end exposure.
- 30 mins +.
- Feed and water.
Reducing new IMIs w/ general hygiene.
Keep environment clean and dry.
Cubicle v yard.
- Based on individual farm.
– stocking density and space allowances to be considered to make decision.
Bedding type.
- Mattress and top layer vs deep bed.
- Sawdust (Klebsiella), straw (Streps).
- “Green bedding” – manure – risky.
- Inorganic substrate…sand!
Bedding management.
- Clean backs of cubicles.
- Frequent top-ups.
- Frequent changes.
- Add lime to raise pH – not good environment for bacteria.
Passageways.
- Scrape frequently.
- Areas of pooling?
Collecting yard.
- Cleanliness / scraping frequency.
Ventilation.
Feed and water spaces - sufficient?
Pasture.
- Stocking density.
- Rotation.
- “Poaching” – leaves wet/boggy areas.
Can assess cow cleanliness subjectively or objectively by scoring.
- Target for cow cleanliness?
- Reduction of new IMIs by environmental pathogen by vac.
- <5% cows with dirty udders.
- Common in coliforms.
- In large herds.
- Little impact on new IMI rate but decreases severity.
Strep. Uberis – newly released product.
The problem of pathogens in the dry period.
Dry cows normally the most forgotten about animals on the farm.
No pathogen flush-out as no milking so more time for the pathogens to establish infection.
- Extent of risk increase of IMI in dry period compared to in lactation.
- Periods of dry period and levels of risk.
- Issue of new IMI in dry period?
- 10X higher DESPITE ABX therapy.
- During involution – high.
Steady state (involuted) – low.
Transition (colostrogenesis) – high. - Can persist into the subsequent lactation (first 30 days).
Classic dry cow therapy.
- Treats existing IMIs and prevents new IMIs.
- Dry cows off abruptly.
- Dry treat each quarter immediately following the last milking.
- Treat all quarters of all cows – “blanket dry cow therapy”.
– Commercially available, approved, long-acting IMM antibiotic product.
– A lot antimicrobial use –> blanket treatments —> irresponsible use.
What do teat sealants replicate and how to use.
Replicate keratin plug to prevent bacteria entering teat streak canal but variable time to form.
Administer at drying off by inserting into teat end (not massage up).
Highly viscous paste (bismuth subnitrate).
Remove at calving by stripping/suckling.
V effective.
MUST be done hygienically as to avoid introducing and trapping the pathogens in the teat.
- When would blanket dry cow therapy be done?
- Selective dry cow therapy.
- When the herd has BTSCC >250K.
All cows have an antibiotic dry cow tube. - Consider which cows need antibiotics, not which cows do not.
- High SCC cows or those w/ clinical mastitis = ABX.
- Low SCC cows or those w/o clinical mastitis in last 3mths = sealant.
Requires decision making at individual animal level.
A requirement of most farm assurance schemes.
What info is used when making decisions on selective dry cow therapy?
- BMSCC.
- BactoScan.
- Milk recording records.
- Clinical mastitis data (dairy etc.)
- Bacteriology.
- Aims for high SCC cows in selective dry cow therapy.
- Aims for low SCC cows in selective dry cow therapy.
- Treat existent gram + infection.
- Prevent gram neg infection.
- Treatment of coliforms.
- Treatment of environmental streps.
- High self-cure rates so questioned if necessary.
Disease ranges from subclinical to peracute so treat according to clinical signs.
Short duration of treatment should cure disease. - Moderate self-cure rates w/ high recurrence if untreated.
– Persistent.
– ABX therapy may be considered more than it is for coliforms.
- How can we establish what pathogen is present at time of dx? – treatment based on result?
- On farm culture w/ triplate.
- Helps establish if organism Gram + or Gram neg.
– If Gram neg or no growth –> no treatment (little efficacy against coliforms and coliforms have high self-cure rate).
– If Gram+ –> IMM protocol.
Responsible use of antibiotics and lower costs
Pseudomonas aeruginosa.
- Minor.
- Can cause acute clinical mastitis but more often chronic high SCC and intermittent flare-ups.
- Treatment ineffective – usually leads to culling.
- May be associated with contaminated water, soil, milking systems.
– Examine wash water, infusion technique, “home-made” treatments, diluted teat dips.
Other pathogens that are difficult to cure and usually result in culling.
Serratia (water and teat dip), Nocardia (soil, poor infusion technique, contaminated products), Yeasts (Candida, infusion technique, teat injuries, multi-dose products), Algae (Prototheca, standing water, contaminated drinking systems, poor parlour hygiene).
