1
Q
why is mastitis so importnat
A
number one reason for antibiotics in dairy cows
2
Q
why do animals get mastitis
A
- bugs get in (through teat end, hematogenous)
- failure of host-immunity (innate and adaptive)
3
Q
innate immunity in mammary gland
A
- major role
- non-specific, present in mammary gland all the time, activated quickly
- not augmented by repeat exposure
- physical barrier, macrophages, neutrophils, NK cells, soluble factors
4
Q
innate immunity: teat end**
A
- first line of defense, physical barrier
- sphincter muscles that maintain closure between milking
- canal lined with keratin - waxy, antimicrobial properties, physical barrier
5
Q
innate immunity: cellular defense**
A
- somatic cells (SCC)
- normal macrophages»_space; neutrophils, lymphocytes, epithelial cells
- infection >10^6 cells/ml –> neutrophils!
6
Q
adaptive/specific immunity
A
- recognition of pathogen initiates response
- augmented by repeated exposure
- B and T cells
- target of vaccine technology
7
Q
grading of mastitis**
A
- grade 1: mild - abnormal milk
- grade 2: moderate - abnormal milk, abnormal quarter (red, hot, swollen)
- grade 3: severe - abnormal milk, abnormal quarter, sick cow (fever, depression, dehydration, off feed, weak, shocky)
8
Q
3 forms of mastitis
A
- peracute: sudden onset, systemic signs
- acute: abnormal milk, udder inflammation to mild systemic signs
- subacute: minimal udder inflammation, no systemic signs
9
Q
subclinical mastitis**
A
- 70-75% of all mastitis cases
- most economically significant due to milk loss
- non-detectable changes in milk composition
10
Q
which lags - detection or disease
A
detection
11
Q
somatic cells**
A
-SCC 200k cells = log score 4
12
Q
what is main driver of cheese production
A
casein
13
Q
why is SCC an issue
A
quality issue (high count reduces quality)
14
Q
california mastitis test**
A
- test for subclinical mastits only (abnormal milk = posititive test)
- CMT reagent lyses cells in milk –> forms “snot” (clumping/gelling = pos test)
15
Q
contagious pathogens**
A
- transmitted when teats exposed to bacteria that originated in infected udders (cow to cow, during milking, contaminated equipment/hands)
- staph aureus, strep ag, mycoplasma, prototheca)
16
Q
environmental pathogens**
A
- transmitted when teats exposed to bacteria that originate in environment
- coliforms (e coli, klebsiella, enterobacter, citrobacter), environmental streps, environmental staphs
17
Q
contagious v environmental pathogens infectious characteristics**
A
- contagious: gram +, mild/mod clinicals may resolve without tx, likely to revert to subclinical
- environmental: gram + may be clinical/subclinical, gram - usually opportunistic, short duration, mild to severe
18
Q
gram - v gram +**
A
- gram -: rapid, robust host immune response, high spontaneous cure rate
- gram +: less robust immune response, low rate of spontaneous cure
19
Q
staph aureus**
A
- gram +, catalase +, coagulase + cocci
- major contagious mastitis pathogen, variable prevalence
- very low cure rates
- chronic with acute flare-ups
- gangrenous mastitis (blue bag) –> alpha toxin causes vasoconstriction
20
Q
strep agalactiae**
A
- gram +, catalase - cocci
- contagious, obligate udder pathogen
- easily cured with IMM abx, no penicillin resistance
- prevalence has declined due to dry cow therapy
- chronic, subclinical infection
21
Q
e coli
A
- gram - most common coliform
- mild to severe
- systemic and supportive therapy may be needed for severe cases
22
Q
klebsiella
A
- gram -, second most common
- mild, moderate, severe (death) cases
- no treatment
23
Q
common gram negative control**
A
- control of coliform mastitis: reduce exposure to pathogens in environment
- J-5 antigen vaccine! reduces clinical cases and severity of them (3 doses)
24
Q
mycoplasma**
A
- bacteria with no cell wall (no abx targert)
- most commonly m bovis
- contagious aerosol/blood/milk transmission
- multiple quarters affected, decreased milk production, cow not sick, normal to abnormal milk increased SCC
- no tx –> cull
25
prototheca
- colorless, micro algae
- ubiquitous in environment
- clinical, chronic infections - high SCC, decreased milk
- no tx --> cull
26
yeast
- rare, almost always iatrogenic
| - non responsive to abx, some cure spontaneously
27
5 point mastitis control plan**
- post-milking teat disinfection
- universal dry cow therapy
- appropriate tx of clinical cases
- cull chronically infected cows
- regular milking machine maintenance
28
teat dip
- goal = reduce number of bacteria (reduces new infections 50%)
- iodine, chlorhex, peroxide, etc
- pre (environment) and post (contagious) dipping
- 30 seconds contact time
29
dry cow therapy
- best chance of cure for some clinical, subclinical cases
| - IMM abx, teat sealants
30
goals of mastitis therapy (5)**
- return cow to normal production
- prevent mortality
- reduce spread of infectious organisms
- prevent new infections (dry period)
- prevent drug residues in milk
31
success of therapy**
- pathogen factors (gram pos v neg, host adaptation/contagious organisms, virulence factors/abx resistance)
- cow factors (age, lactation stage, immunity, hx, duration of infection)
- therapy factors (duration, efficacy)
32
practical factors in mastitis tx**
- dose - 1x or 2x
- meat or milk withold
- cost
- Rx vs OTC
33
abx tx**
- on-label IMM abx for most gram +, some gram -
| - only 2 for extended tx: spectramast, pirsue (not for environmental pathogens)
34
oxytocin and frequent milk-out**
- theory: increased milk let-down and milk removal gets rid of abnormal milk, any viable pathogens, microbian toxins, inflammatory mediators
- no evidence to support improved outcomes
Repro Bio 3
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