Johnes Control and mastitis Flashcards
Johnes
Mycobacterium avium s. paratuberculosis
Humans
Crohne’s
Link with MAP
Source dairy
Clinical Dz
> 3 yo
After stress (calving)
Profuse D+ (bubbles)
Weight loss
Individuals bright
Importance
Poorer yield
RF - mastitis + lame
+ other GI Dz
Transmission
80% <4wks/o
In utero/ Env (faeces)
Stages
1 - silent calves
2 - sub clin shedder
3 - early clin Dz
4 - Adv Dz
Dx
Faecal culture/ PCR
ELISA
30 cow screens (herd)
- milk/ blood ab
Falce -ve avian TB test
Control strategy
Biosecurity protect and monitor
Improved management
Strat testing
Culling
Breed to terminal sire
Firebreak vax
CHeCS accreditation
Consequence of mastitis
Chr Dz -> spread of Dz in herd
Permanent damage to udder (less yield)
Death (toxaemia/ PTS)
Innate udder immunity
Leukocytes (SCC, macrophages, neutrophils, T cells)
-phagocytosis and trigger acquired immunity (pro inflammatory mediators)
AM substances in milk
-lactoferrin, lactoperoxidase, lysozymes, free complement
Mastitis acquired immune system
Invasion of circulating neutrophils and IgG2
B cells
-lymph circulation, IgM & IgG2 initially
-IgG2 enter udder, opsonisation of pathogen for neutrophils
-APC for T cells
T lymphocytes
-Helpers- cytokines
-Cytotoxic eliminate infected cells
IgM fixates complement
IgA agglutinates bacteria and neutralises toxins
IgG1 opsonises bacteria
Genetic resistance to mastitis
Low heritability
-udder type, yield, MHC
Breed variation
Select for low SCC, better udder conformation cows
-not too low SCC -> high susceptibility of infection
Vaccine- Staph aureus, coliforms and some other staph
Mastitis stage of lactation
Dry
-new Dz acquired and persistent infections
Cessation of milking -> wide teat canal (high mammary Pa)
-bacteria not flushed out
-no teat dipping
-keratin plug (often poor seal)
-early dry cows have impaired neutrophils
Periparturient
-lots IgG1 - colostrogenesis and impaired neutrophils
-phagocytosis reduced
Mastitis nutrition
NEB
-impaired leukocyte activity and less present
Vit E/ Se deficiency
-slow leukocyte migration
SARA
-less appetite-> less DMI-> NEB, D+
HypoCa
-weaken teat sphincter mechanism
Mastitis (sub) clinical
Subclinical
-Dz present
-No CS, higher SCC, milk yield and quality affected
Clinical
-1- mild, milk changes
-2a- Ac, hot, painful udder
-2c- Chr, udder hard and lumpy
-3-cow sick
Teat skin
Strat squamous epi + bacteriostatic fatty acids
Some bacteria are ubiquitous
-compromise (trauma, lesions)
Post milking teat dips emollients
Prompt lesion Tx
Teat canal
Bac enter when open (takes 30 min to close)
Keratin lining traps bacteria
Keratin plug forms in dry period
Specific teat disorders
Infectious
-papillomavirus
-pseudo cowpox
-herpes mammilitis
-impetigo
-cow pox
-black spot
Non infectious
-hyperkeratosis
-photosensitisation
-chapped teats
-teat stenosis
-blind teats
Teat end hyperkeratosis
Black spot
Hyperkeratosis
-Excessive milk vacuum
-Rough and high mastitis risk
Black spot
-common
-damage to teat
-topical AB