Mastitis Flashcards

1
Q

why is mastitis so importnat

A

number one reason for antibiotics in dairy cows

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2
Q

why do animals get mastitis

A
  • bugs get in (through teat end, hematogenous)

- failure of host-immunity (innate and adaptive)

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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
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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
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5
Q

innate immunity: cellular defense**

A
  • somatic cells (SCC)
  • normal macrophages&raquo_space; neutrophils, lymphocytes, epithelial cells
  • infection >10^6 cells/ml –> neutrophils!
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6
Q

adaptive/specific immunity

A
  • recognition of pathogen initiates response
  • augmented by repeated exposure
  • B and T cells
  • target of vaccine technology
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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)
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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
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9
Q

subclinical mastitis**

A
  • 70-75% of all mastitis cases
  • most economically significant due to milk loss
  • non-detectable changes in milk composition
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10
Q

which lags - detection or disease

A

detection

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11
Q

somatic cells**

A

-SCC 200k cells = log score 4

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12
Q

what is main driver of cheese production

A

casein

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13
Q

why is SCC an issue

A

quality issue (high count reduces quality)

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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)
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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)
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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
Q

prototheca

A
  • colorless, micro algae
  • ubiquitous in environment
  • clinical, chronic infections - high SCC, decreased milk
  • no tx –> cull
26
Q

yeast

A
  • rare, almost always iatrogenic

- non responsive to abx, some cure spontaneously

27
Q

5 point mastitis control plan**

A
  • post-milking teat disinfection
  • universal dry cow therapy
  • appropriate tx of clinical cases
  • cull chronically infected cows
  • regular milking machine maintenance
28
Q

teat dip

A
  • goal = reduce number of bacteria (reduces new infections 50%)
  • iodine, chlorhex, peroxide, etc
  • pre (environment) and post (contagious) dipping
  • 30 seconds contact time
29
Q

dry cow therapy

A
  • best chance of cure for some clinical, subclinical cases

- IMM abx, teat sealants

30
Q

goals of mastitis therapy (5)**

A
  • return cow to normal production
  • prevent mortality
  • reduce spread of infectious organisms
  • prevent new infections (dry period)
  • prevent drug residues in milk
31
Q

success of therapy**

A
  • 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
Q

practical factors in mastitis tx**

A
  • dose - 1x or 2x
  • meat or milk withold
  • cost
  • Rx vs OTC
33
Q

abx tx**

A
  • on-label IMM abx for most gram +, some gram -

- only 2 for extended tx: spectramast, pirsue (not for environmental pathogens)

34
Q

oxytocin and frequent milk-out**

A
  • 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