Flashcards in Pathogenesis/Pathology of Mastitis Deck (24):
Which pathogen can cause disease in the non-lactating cow or immatrure glands?
What 3 routes of entry into the mammary gland are possible?
- galactogenic (most common) via teat canal
- haematogenous eg TB, brucellosis
- percutaneous due to wounds
Should normal milk be sterile? How does the udder resist infection?
- teat sm mm sphincter secretes bacteriocidal fatty acids, desquamates, desiccates
-Furstenburgs Rosette - fatty acids and cationic proteins, subepithelial plasma cells produce IG
- fulshing action of milk
- lactoferrin (Fe binding, more effective in non-lactating gland)
- lysozymes, complement, cytokines
- neutrophils, macrophages, NKCs (ineffective in milk cf. blood)
- IgG, IgM and IgA
> mostly aimed at preventing infection - if pathogens injected into cisterm WILL CAUSE MASTITIS
What are the 3 clinical presentations of mastitis?
1. peracute potentially life threatening (particularly around parturition)
2. acute (±systemic signs) may progress to chronic
3. sublicincal chronic - progressive loss of secretroty ability
WHat may peracutue mastitis also be known as?
- Toxic with coliforms
- Gangrenous esp. S. aureus
How does peracute mastitis present grossly?
- swollen, painful
- rapid progrssion to moist gangrene
- darkblue/black, oozing serum
- dark haemorrhagic lobules on cut surface
- ventral oedema
- comatose due to toxaemia possible
How may acute mastitis appear microscopically?
- initially extensive oedema with neutrophilic infiltration of both interstitiium and glandular acini
- vacuolation and desquamation of acinar and ductal epithelium
How may chronic mastitis appear microscopically?
- fibrosis with obliteration of acini
- obstrustion of ducts by polyps
- subsequent retention cysts anterior to blocked ducts
- involution (temporary loss of secretory fucntion due to obstruction)
- fibrosis (permentant loss of secretory tissue due to progressive destructive)
How prevalent is subclinical v clincial mastitis?
10 - 40 times
How can subclinical mastitis be identified?
no gross inflammation or changes in milk
- SCC only
< 200,000 cells/ml in whole udder = no infection (normal epithelial cells and inflam cells always present)
How may chronic subclinical mastitis be identified?
Gross - fibrosed and atrophied gland
- involution due to blockage of secretion and acinar stagnation
Microscopy - similar to chronic mastitis following acute
- permenant loss of secretory function
What may occour after an initial subclinical mastitis flare up?
further flare ups - ??botromycosis, s aureus, no effective ABx, granulomatous /? LOOK UP!
Should udder tissue be sterile?
At what stage in the udder does milk become colonised? By which bacteria?
- Lactobacillus ap
- Lactic strep
> in the duct - normal, hamrless (protective) bacteria
WHat are the 5 main pathogens associated with mastitis?
- Strep agalactiae
- Strep dysgalactiae
- Strep uberis
- Staph aureus
- E. Coli
What are coliforms
G- rods similar to E. Coli
Which pathogens cause contagious mastitis?
Staph aureus, strep agalactiae (associated with mammary gland)
- although s. aureus lives in nasal passages so may get onto bedding -> environmental?
Which pathogens cause environmental mastitis?
(although still come from GIT of animals so dont truely come from environment)
What is another term for dry cow mastitis and which pathogens are associated with this? How is it spread?
- strep dysgalactiae
- arcanobacterium pyogenes
- G+ coccus
> spread by flies
Which pathogen is spread heamatogenously? How severe is the disease this pathogen causes?
- milk disease
Give egs. of pathogens causing subclinical infection and ^ SCC
CNS (coag - staph) and G+ corynebacterium bovis
What are the most common pathogens seen in mastitis of EWES
Mainheimia haemolytica, S. Aureus, E. Coli, Strep
Which pathogen may colonise when ABx are used to treat mastitis?
Pseudomonas - massive levels of resistence mean may colonise when other species are wiped out