Mastitis 1&2 Flashcards by Madeleine Gauthier

When is mastitis most likely to occur?

just after dry-off (involution)

just before calving (colostrogenesis)

basically, within the first 90 days after calving

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why is mastitis risk increased just after dry off?

increase of P bc milk secretion continues (slowly) for first few days
autophagocytosis of secretory epithelium impacts blood-milk barrier
changing in conc of serum and milk components (increase in albumin and immunoglobulins)
increase in lactoferrin, which is bacteriostatic and immunomodulating

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why is mastitis risk increased just before calving?

active cell differentiation
increase P from milk
decrease of lactoferrin and lymphocytes
colostrum components impair phagocyte activity
dry cow therapies not at MIC at this time
immune suppression

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why does mastitis occur?

failure of host immunity
overwhelming exposure (at teat end)

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what is the innate immunity of the mammary gland like?

teat sphincter, keratin lining + plug, WBCs, natural killer cells, soluble factors

not augmented by repeated exposure

non-specific, present always, activated quickly

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what is the cell population of the mammary gland like normally? what is it like during infection?

normal: <105 cells/mL, mostly macrophages

infection: >106 cells/mL, mostly neutrophils

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what impairs innate immunity of the mammary gland?

damage to teat end –> immune suppression
teat conformation
“the black spot”
BHV4
pseudo cowpox

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why does teat end damage impair innate immunity?

leads to teat end hyperkeratosis, which predisposed to bac t colonization

caused by over milking (and other milking mgmt factors)

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tell me about teat conformation scoring

1-4, with 3 and 4 being the worst

ideal: <5% score 4, <15% score 3

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what is “the black spot”?

necrotic area at teat orifice that has a secondary infection (usually S. aureus)

primarily caused by poor milking conditions (typically several in herd affected)

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why does BHV4 impair innate immunity?

bovine herpes virus 4 = bovine herpes mammilitis

vesicles –> ulceration –> thick dark red scab + painful swelling

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what should you do if you have BHV4 in your herd?

milk affected cows last, disinfect clusters

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what part of the milking machine matters the most? why?

teat-end vacuum

must be within a narrow range, must be stable, not above 12.5mmHg for more than 30 seconds, pulsation rate/ratio must be appropriate

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why are pre and post milking teat disinfections important?

major control point for prevention of new infections

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what are the broad steps of milking?

fore stripping
prep (pre-dip, wiping), and milk let down
attach milking unit —> milk
detach
post-dip

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what is the most meaningful way to provide stimulation of milk let down? why else is it important?

fore stripping

also allows observation of milk and udder

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what is bimodal let down and why does it happen?

not fore stripping and applying milking cluster to teats before she’s ready, results in release of cisternal milk only, then a pause, then oxytocin comes in and milk comes back

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why is bimodal let down bad?

exposure to teat end to high vacuum levels (discomfort, teat end hyperkeratosis), less milk total

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what is the single most important step of the milking routine to prevent new intramammary infections?

post dipping

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does post dip get wiped off? what about pre dip?

post: no
pre: yes

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what are the contagious mastitis pathogens?

Staphylococcus aureus

Streptococcus agalactiae

Mycoplasma bovis

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staphylococcus aureus mastitis:
1. what does infection look like?
2. how to treat?

mostly subclinical, can be clinical, cyclical cycles, invasive of deeper tissues, likely to form abscesses
extended therapy intramammary Abx (most effective in dry period)

Streptococcus agalactiae mastitis:
1. what does infection look like?
2. how to treat?

more uncommon, but outbreaks can be like wildfire
short term intrammaary Abx

Mycoplasma bovis mastitis:
1. what does infection look like?
2. how to treat?

clinical, multiple quarters, often w/ septic arthritis and pneumonia (hematogenous)
strict biosecurity! non-responsive to Abx

what are the environmental mastitis pathogens?

E. coli Klebsiella pneumoniae Streptococcus uberis Prototheca

what are the opportunist mastitis pathogens?

Non-aureus staphylococcus

E. coli mastitis: 1. what does infection look like? 2. how to treat?

1. acute (endotoxin), septicemia/bacteremia/systemic signs, large swollen quarter w/ watery milk, often by the time they become sick the infection is cleared from udder but they're still sick systemically 2. systemic tx --> Abx, NSAIDs, fluids

Klebsiella pneumoniae mastitis: 1. what does infection look like? 2. how to treat?

1. acute, systemic but not as severe as E. coli (1/3 mild, 1/3 mod, 1/3 severe systemic) 2. systemic tx --> Abx, NSAIDs, fluids

Streptococcus uberis mastitis: 1. what does infection look like? 2. how to treat?

1. mod clinical, 4-6 weeks, invade deeper into tissue 2. intrammamary abx, extended duration

Non-aureus Staphylococcus mastitis 1. what does infection look like? 2. how to treat?

1. mild clinical or subclinical only, seen in heifers esp!, superficial mucosa 2. self-cure or short duration intramammary Abx

tell me about bedding and how it impacts mastitis

dry + inorganic = low bac t counts fresh + clean no matter what type = low bac t counts best to worst bedding: new sand, organics (straw, shavings), recycled manure solids used bedding high in E. coli and Klebsiella

tell me about udder hygiene scoring

1-4, scores of 3 and 4 more likely to have infection

what is linear score and how does it relate to somatic cell count?

LS: measure milk prod losses from subclinical mastitis as SCC goes up, LS goes up (more losses)

what are the 2 main testing methods for mastitis pathogen ID?

milk culture = gold standard PCR

if bac t grow on a staph-specific plate, what could we use to determine type of staph?

coagulase test --> positive = S. aureus staph chromogenes --> positive = S. aureus

gram _____ grows on blood agar and MacConkey agar

blood: + and - McConkey: -

what is the 1/3, 1/3, 1/3 rule in AB?

1/3 no bac t growth 1/3 no tx 1/3 tx

should you send for culture before starting Abx? why or why not?

yes, for non-severe cases. it reduces the use of IMM Abx for clinical mastitis for non-severe cases, there is no difference in clinical outcome waiting up to 24hours use meloxicam at time of onset before results come back

composite samples increase/decrease/have no effect on getting back contaminated samples

increase

what is the preferred route of Abx admin for mastitis?

intramammary good evidence against gram +, not so much for gram -

bac t that have deeper tissue invasion require what type of Abx?

longer duration (5-8 days)

what are your Abx options for treating mastitis in **lactating** cows? what do these Abx treat? why are these not super good?

- cephapirin (Cefa-lak) --> S. agalactiae, S. aureus - Ceftiofur (Spectramast) --> E. coli, S. dysgalactiae, NAS Cephapirin is Category 2 and Ceftiofur is Category 1

**Make sure to help control pain while treating mastitis and to make the cows comfortable!!!**

intra-mammary medications work better in ____ mammary glands.

involuted/dry

what is the largest use of prophylactic Abx in dairy industry? do we like this or not?

Blanket dry cow therapy = every dry cow gets IMM Abx extremely effective!

the Abx for IMM abx for dry cows are the same as lactating cows, except what?

they use 2-3x the drug concentration

what are teat sealants and when are they used?

forms physical barrier in teat canal, should be applied whether dry cow therapy is used or not

is there an E. coli vaccine? does Betty Jo like it?

yes and yes (don't admin more than two bacterin vaccines at a time)

what grouping of **beef** cows is most at risk for mastitis?

olders cows with poor udder conformation

how do you tx mastitis in beef cows?

mostly gram +, so IMM abx

what types of teat lacerations are heal the best?

longitudinal (vs horizontal) base of teat (vs apex)

how do you treat a teat laceration that does not have to be amputated?

- restraint! - ring block at base of teat with lidocaine WITHOUT epinephrine (bc causes vasoconstriction) - wound mgmt (clean, lavage, etc) - suture closed in 3 layers (submucosa, intermediate layer, skin) with 4-0 or 3-0, interrupted suture

when can you suture a teat laceration closed? what do you do if you can't suture closed?

<12 hours old, longitudinal, teat canal intact, base of teat teat amputation

how do you perform a teat amputation?

- drain of all milk - infuse IMM Abx - ring block - place clamp at base of teat - cut that thang off - appose submucosa and intermediate layers w/ 1 non-perforating continuous horizontal mattress (4-0 monofilament) - close skin with interrupted sutures, 3-0 or 4-0 monofilament reverse cutting