Production diseases Flashcards
Name some environmental mastitis pathogens
- Strep. uberis, Staphylococcus species (not Staph. aureus), coliforms like E. coli
Name some contagious mastitis pathogens
- Staphylococcus aureus, Strep. agalactiae, Strep. dysgalactiae
What is summer mastitis complex
Signs
Tx
Bacterial infection spread by head flies (Hydrotea irritans)
Signs: Hot, hard, swollen, painful quarter +/- foul smell and lameness
Tx: Systemic penicillin
Cow presenting with mastitis under 30 days in milk
Origin:
Dry period origin
Enviromental
Cow presenting with mastitis over 30 days in milk
Origin:
Lactation origing
Environmental or contagious
Signs of mastitis in the fore milking
Clotted, watery, grey/yellow/red
What should SCC be under
200,000
Grading of clinical mastitis
- Grade 1: milk changes only
- Grade 2: milk changes and swollen udder
- Grade 3: above…+ cow is ill
Implications of a high herd bulk SCC
Tx
contagious more likely
Penicillin for 5 days
Implications of a low herd bulk SCC
Tx
Likely environmental
Penicillin & aminoglycoside daily 3 days
How to prevent contagious mastitis
5 point plan:
Post-milking teat disinfection,
blanket dry cow therapy,
culling problem cows,
milking machine maintenance,
treatment of clinical cases
How to prevent environmental mastitis
Improved cleanliness: scrape more, muck out more
Prevent faecal contamination of sleeping areas
Stop over stocking
Treatment protocol when drying off cows
- High SCC= Treat with IM antibiotic + sealant to treat existing infections (Over 200,000 for 1+ of last 3 recordings before drying off)
- Low SCC = Treat with sealant ONLY
Differences with sheep mastitis
Mannheimia haemolytica can be implicated
Reduced milk yield may show as poorly growing lambs
More likely to turn into black back from toxin secretion
How does low glucose lead to ketone bodies
Glucose converts NEFA to VF
Low glucose = less NEFA converted
Excess NEFA become ketone bodies
How does hepatic lipidosis occur
Need more energy as can’t keep up with increasing yield
Fat is mobilised to provide energy
Excess NEFA
Can’t all be oxidised to VFAs
Fat accumulation in the liver
When and how does Type 2 ketosis occur
Start of lactation
Due to poor DMI and excess body condition
hepatic lipidosis seen here
When and how does Type 1 ketosis occur
Peak lactation
Due to underfeeding
Pathogenesis of T2 V T1 ketosis
T2: Feed intake cannot keep up with increasing yield ==> fat mobilised ==> accumulates in liver ==> liver function impaired
Less NEFA oxidation, less gluconeogensis
More ketones
T1: NEB ==> less glucose ==> less NEFA oxidation to VFA ==> more ketones
diagnostics for T2 v T1
T2:
Monitor transition cows and cows under 30 days calved
Look for ketones (BHB in blood, urine, milk)
Look fro NEFA (blood)
evidence of liver damage (enzymes, biopsy)
T1:
Look for ketones (BHB in blood, urine, milk)
Tx of ketosis
Propylene glycol
monitoring
of ketosis
Monitor BCS: Aim for 2.5-3 (3 max)
Max 0.5 decrease between calving and peak location
Monitor Butter fat: protein in milk
Cow in NEB = milk protein goes down and BF up
Ration analysis
Differences with sheep ketosis
- Called Pregnancy Toxaemia (Twin lamb disease)
- Difference is peak energy demand is in pregnancy, usually before lambing
- Clinically indistinguishable from HypoCa
- Treat with glucose and calcium
Cows at risk of hypocalcaemia
Older cows
First few days calved
