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Contagious pathogens
Staph. aureus
Strep. agalactiae
Mycoplasma
C. bovis
all spread during milking
Environmental pathogens
coliforms: E. coli, Klebsiella, Enterobacter
environmental Streps (uberis, dysgalactiae, enterococcus)
non-aureus Staphs
others: Pseudomonas, C. perfringens, T, pyogenes, etc.
Opportunistic pathogens
part of the normal flora of the animal that can infect the udder if compromised
Klebsiella, non-aureus Staphs, T. pyogenes (abscesses), Psuedomonas
Staph. aureus mastitis
gram + cocci (bundle of grapes)
catalase & coagulase +
high prevalence, low cure rate, often subclinical + chronic
infects deep in udder parenchyma
Strep. agalactiae mastitis
gram + cocci (chains)
CAMP + (blood agar lysis), catalase -
rare since dry cow therapy, less severe Dz
Mycoplasma mastitis
bacteria w/out cell wall
Dx via microaerobic culture or PCR
very contagious, lasts well in environment, & no treatment
most commonly affects cows that just calved
part of normal resp + repro flora
C. bovis mastitis
gram + curved rods
catalase +, CAMP -
colonizes teat canal w/lack of proper teat dipping
E. coli mastitis
gram - bacteria
Dx via culture plate
occurs at dry off or during calving (early lactation)
bacteria cleared easily, LPS toxins absorbed into blood & cause mod-severe acute illness
Klebsiella mastitis
gram - bacteria
occurs from sawdust/recycle manure bedding or during milking
environmental → contagious, also opportunistic
invades deep into secretory tissue & causes persistent subclinical infections
harder to treat than other coliforms
Environmental Strep mastitis
gram + cocci (chains)
Dx via isolation from clinical cows in early lactation
occurs from dirty living environment or during milking
normal in GI/manure flora
most common Strep isolated from bovine mammary gland
Non-aureus Staph mastitis
gram + cocci (bundle of grapes)
catalase & coagulase -
occurs from poor udder prep or improper vacuum suction
mostly subclinical & mild-mod
come from normal skin flora
Psuedomonas mastitis
comes from dirty water
non treatable
T. pyogenes mastitis
comes from abscesses
non-treatable
C. perfringens mastitis
occurs from sepsis or primary infection
causes gangrenous mastitis
non-treatable
Clinical vs subclinical mastitis
visible changes to milk (chunky/flaky, off-color, may contain pus/blood/gas)
vs
increase in SCC in grossly normal milk (>200k cells/mL)
Severity of mastitis
mild: changes to the milk only
moderate: changes to the milk & udder (inflamed, edematous, firm, abnormal temperature)
severe: changes to the milk, udder, & cow (fever, dehydration, off-feed, D+)
Mastitis testing
clinical: collect aseptic milk for culture**
subclinical:
herd-wide somatic cell count (bulk tank)
electro-conductivity (received signal = increased SCC)
California mastitis test (agglutination)
Maldi-TOF/PCR for pathogen ID
Mastitis in a herd
legal bulk tank SCC limit in US = 750k cells/mL, most farms stay under 400k (European limit)
tracked by # of clinical cases & SCC count
individuals w/SCC>200k should be checked
clinical cases should be cultured pre-treatment
clinical rate should be <10%
Who to sample for mastitis
every clinical cow (culture)
fresh cows (calved w/in 30 days)
cows w/high SCC (culture or milk PCR)
Mastitis in other species (horses, SR, SA)
equine: can affect all ages of horses, + C. psuedotuberculosis
SR: similar pathogens (+ Mannhaemia) & clinical signs to cows, can get more severe Dz more commonly
SA: +Psuedomonas
all: coliforms, Clostridium, Strep, Staph
Mastitis risk factors (herd)
high prevalence of infection
poor milking hygiene/dipping
poor bedding mgmt
improper/no dry cow therapy
overcrowding/poor ventilation
Mastitis risk factors (individual)
early (first 30 days) lactation
parity/higher number of lactations
abrupt dry-off (<2wks)
immunosuppression (stress/nutrition)
previous mastitis Hx
high production
teat injury/poor conformation
poor environmental hygiene