L22: Mastitis (Maunsell) Flashcards

1
Q

2 categories of mastitis pathogens

A

Contagious

Environmental

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2
Q

Major contagious mastitis pathogens

A

Streptococcus agalactiae
Staph aureus
Mycoplasma bovis

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3
Q

Major environmental mastitis pathogens

A

Coliforms

Environmental strep spp.

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4
Q

Mastitis pathogen that is both environmental and contagious

A

Strep. Dysgalactiae

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5
Q

Teat canal sphincter open how long after milking?

A

2-4 hrs (high risk period for developing mastitis)

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6
Q

Teat canal lined by:

A

Squamous epithelium

  • primary means of preventing infection
  • secretes keratin (low keratin highly assoc. with mastitis)
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7
Q

IMI = intramammary infection

A

:)

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8
Q

Natural mammary defenses**

A

Cellular immune response:

-macs, neuts, and lymphos (should be

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9
Q

When is there the highest risk of IMI?

A

Beginning of the dry period

  • causes clinical mastitis in early lactation
  • another smaller peak at calving
  • can see clinical infection in early lactation as a result of subclinical infection in the dry period
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10
Q

Periparturient immune suppression period

A

About 3 wks pre to 3 wks postpartum

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11
Q

Mastitis is most common dz of dairy cattle

A

:)

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12
Q

Changes in milk production caused by mastitis

A

Subclinical: 10-30% loss; most costly aspect!
Clinical: variable losses

Effect depends on stage of lactation, duration, season, lactation #, organism

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13
Q

Costs assoc. with mastitis

A
Dec. milk yield*
Discarded milk*
Culling and death losses
Tx and vet fees
Labor
Control costs
Dec. milk quality premiums
Clinical mastitis: other periparturient dz, poor reproductive performance
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14
Q

Subclinical mastitis detection at cow level

A

SCC:

  • California mastitis test
  • Individual SCC: IMI >200,000 cells/ml
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15
Q

Detection of clinical mastitis at the milking parlor

A

1) Fore-stripping
- Goal = stimulate milk let-down and detect mastitic milk
- prevents mastitic milk entering bulk tank

2) in-line electrical conductivity (increase assoc. w/ mastitis)
3) Increase in SCC if in-line monitoring
4) monitor milk production for sudden drop

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16
Q

Detection of clinical mastitis on PE

A
  • evaluate milk for color, consistency, garget (clots)
  • observe/palpate glands for inflammation
  • perform PE to detect systemic involvement
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17
Q

Detecting what pathogens are involved with individual cow milk cultures

A
  • collect before treating
  • collect aseptically
  • proper transport and storage
  • can’t differentiate coliform and gram + mastitis clinically, so must use selective culture plates
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18
Q

Antimicrobial sensitivity testing

A
  • guides antimicrobial selection for herd protocols
  • doesn’t always translate to susceptibility in vivo
  • has limited value in individual cases
  • no benefit with coliform or chronic S. Aureus (no correlation b/w sensitivity and tx efficacy)
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19
Q

Interpreting milk cultures that don’t grow

A
  • Occurs in about 30% of clinical or high SCC samples
  • can be false negative if improperly sampled, low bacterial numbers, intermittent shedding, microbial inhibitors present, fastidious organisms, or interpreted too early
  • true negative if IMI cleared before sample collected, or due to non-infectious cause**
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20
Q

Legal limit for bulk tank SCC

A

750,000 cells/ml

  • avg. of >200,000 indicates some IMI in the herd**
  • should evaluate at least 4 samples over 4 weeks
  • strong negative correlation of annual average BTSCC and milk production
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21
Q

Standard Plate count (SPC)

A
  • performed on bulk tank milk evaluation
  • total aerobic bacterial #
  • legal limit is 100,000 cfu/ml
  • goal is
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22
Q

Bulk tank milk culture for specific pathogens

A
  • IDs the predominant bacterial groups in the herd
  • if environmental organism, assoc. with dirty udders/equipment, inadequate cooling
  • if contagious organism, assoc. with IMI
  • should take consecutive samples over 4 days
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23
Q

Properties of contagious mastitis

A
  • reservoir = infected udders*
  • spread from cow to cow at milking time via fomite, or droplet propulsion through teat canal*
  • often subclinical, chronic
  • Major pathogens: Staph aureus, strep agalactiae, Mycoplasma spp., strep dysgalactiae (also environmental)
  • minor pathogens: corynebacterium bovis
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24
Q

Strep agalactiae

A
  • usually causes chronic, subclinical mastitis**
  • lives in mammary gland, doesn’t survive well in env.
  • influx of neuts into gland –> great increase in SCC
  • shed in high #s –> increased BT SPC
  • chronic infection leads to involution of affected areas, fibrosis
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25
Staph aureus
- usually leads to chronic, subclinical mastitis** - can cause clinical mastitis but usually mild (rarely gangrenous) - recurrent cases common - bacterial toxins/enzymes --> tissue damage and fibrosis, abscesses and microabscesses - resists phagocytosis - produces beta-lactamase - inhabits mammary gland, skin (damaged teat skin)
26
Reservoirs and transmission of Staph aureus
Reservoirs: chronic subclinical cases, purchased cattle (esp. Heifers) Transmission: milking, horn flies, cross-suckling of calves
27
Mycoplasma mastitis properties
- mostly M. Bovis - highly contagious - causes chronic subclinical mastitis - often affects multiple glands** - outbreaks of clinical mastitis occur in naive herds, prepubertal heifers, dry cows - can cause arthritis, pneumonia** - causes terrible gritty, orange brown milk secretions, however cow not usually systemically sick
28
Major environmental pathogens
Streptococcus uberis Strep dysgalactiae (also contagious) Coliforms
29
Minor environmental pathogens
``` Coag-negative staphylococci Others: -Trueperella pyogenes -Prototheca -E. Faecalis -Pseudomonas aeruginosa -Nocardia species -Serratia marcescens -Fungi/yeasts ```
30
Organisms that cause coliform mastitis
E. Coli Klebsiella Enterobacter spp.
31
Percent of coliform mastitis cases that are clinical?
10% subclinical 60% mild to mod. Clinical 30% severe clinical Chronic infections uncommon
32
Pathogenesis of coliform mastitis
- infection may be cleared quickly but inflammation may persist - endotoxin release --> activation of inflammatory pathways and vasoactive mediators --> endotoxemia - high SCC may be protective - immune impairment in periparturient period, heat stress can predispose - if severe, can have high mortality
33
Most important environmental pathogens in terms of # clinical cases in US
Environmental streptococci: - Strep uberis - Strep dysgalactiae - Strep spp. - Enterococcus spp. 40-50% IMI are clinical (however usually mild to moderate)
34
Environmental streptococci
- present in skin, GI, and urogenital tract - ubiquitous in dairy environment, esp. In organic bedding (ie. Straw) - can spread once in the udder - strep dysgalactiae can colonize teat ends
35
Environmental mastitis prevention
- manage environment to decrease bacterial load - milk clean, dry teats - pre-dip - decrease exposure at high risk times - boost host defenses - manage environment to decrease teat injuries - good infusion technique
36
Contagious mastitis prevention
- milking hygiene - post-milking germicidal teat dipping - teat end condition - milking procedure machine maintenance
37
Most effective method for control of contagious pathogens
Post-dipping
38
Pre-dipping procedure
- removes environmental bacteria that have contaminated teat end since the last milking, before teat canal opened - apply to clean teats - use approved germicidal predip - allow at least 30 seconds contact - wipe dry: prevent dip residue in milk
39
Methods of minimizing exposure between milkings
- udders should be in contact with clean, dry bedding - barrier dips - fresh feed/turn out to clean lots after milking
40
Dry cow therapy
Goal = minimize new infections in the early dry period - limited efficacy against coliforms - doesn't protect against IMI in late dry period
41
Methods to boost host defense mechanisms
- adequate nutrition, esp. vit. E and selenium | - vaccination for Gram - bacteria, and to reduce severity/incidence of clinical coliform mastitis
42
Antimicrobial tx during lactation
- generally only for clinical mastitis - high cure rate for Strep. Agalactiae - moderate response for environmental Strep spp. - poor response for Staph aureus
43
Antimicrobial tx in the dry period
- high efficacy for elimination of subclinical IMI and prevention of new IMI in the early dry period - should infuse all glands of all cows at dry-off - drug should have slow release - drug choice depends on: if effective against GP spectrum, sensitivity data, and clinical efficacy in the herd
44
Abx approved for intramammary use in non-lactating dairy cattle
``` Ceftiofur Cephapirin benzathine Cloxacillin benzathine PenicillinG procaine PenicillinG procaine + Novobiocin ```
45
Antimicrobial selection based on:
-pathogen ID -milk withholding -hx of clinical efficacy in that herd (Should reassess regularly)
46
Tx of clinical mastitis with severity score of 1 or 2
1) IMM abx 2) +/- oxytocin AT MILKING if painful to milk 3) anti-inflammatories for moderate CM (ie. Banamine, aspirin, dex, isoflupredone acetate)
47
When to use abx for mild/moderate clinical mastitis (coliform, G+, mycoplasmal)
- coliform mastitis: usually NOT indicated (most infections self-resolving) - gram + mastitis: decreases time to resolution, chronic infection rate, clinical relapse rate - mycoplasmal mastitis: abx INEFFECTIVE
48
Differentiation of coliform and GP mastitis
- can't differentiate clinically - herd hx and infection patterns with frequent monitoring - on farm milk culture
49
Treating severe clinical mastitis
-decrease systemic effects of endotoxin/shock (fluids, anti-inflammatories) -abx (IMM + parenteral) +/- oxytocin at milking
50
Gangrenous mastitis: cause and CS
- uncommon - S. Aureus, Clostridium spp. (GN) bacterial toxins --> severe vasoconstriction, ischemia, necrosis - results in severe clinical mastitis, distinctive appearance of affected gland (discolored, cold, oozing serum, serosanguinous secretions)
51
Tx/prognosis of gangrenous mastitis
Tx: aggressive supportive therapy, systemic abx, +/- amputate teat to assist drainage +/- mastectomy Poor prognosis
52
Indications for teat amputation
- Severe gangrenous mastitis - severe chronic clinical mastitis w/ systemic illness or abscessed gland - better drainage is needed, and gland wouldn't have returned to normal production
53
Procedure of teat amputation
2% lidocaine ring block around base of teat (unless gangrenous) +/- teat cistern infusion with tourniquet, xylazine sedation Clamp teat distal to venous plexus, amputate below clamp, drain and flush gland
54
Chemical destruction of quarter
- cause affected gland to permanently cease milk production via infusion with chemical that destroys mammary epithelium - indications: chronic non-responding mastitis, don't want to cull the cow - do NOT use in gangrenous/toxic mastitis, or where teat already amputated
55
Procedure for chemical destruction
- strip gland, infuse with chemical (ie. Undiluted chlorhexidine, formalin) - swelling and discomfort caused at 24-48 hrs and may become systemically ill (can used NSAIDs) - gland gradually atrophies as inflammation dies down, while other quarters remain functional
56
Managing mastitis in ORGANIC herds
- mostly the same - teat dips and sealants permitted - segregate infected and clean cows - good herd mastitis monitoring program essential (BTSCC, frequent BT cultures) - segregate chronic subclinical mastitis until culling - CM: cull, treat conventionally and move to non-organic herd, or tx without abx if mild to moderate
57
Mastitis in BEEF cattle
- S. Aureus most common (also CNS, Strep, A. Pyogenes) - causes decreased weaning weight when multiple glands affected - chronic IMI --> involuted (dry) glands - should inspect udders at least once a year - ID +/- cull cows with dry quarters or with clinical mastitis in more than one gland - if there is a large outbreak, look for teat lesions that could indicate foreign dz or other teat problems
58
Dx of mastitis in small ruminants
- PE: similar to cattle, may have lameness on affected side or refuse nursing - Milk culture - SCC (direct SCC or CMT)
59
More overlap between non-infected and infected glands for goats than for cattle
:)
60
Major Pathogens for mastitis in small ruminants
S. Aureus Mannheimia haemolytica Mycoplasma spp.
61
Minor pathogens for SR mastitis
Coag-neg. staph | -very common
62
Environmental pathogens assoc. with SR mastitis
- coliforms - environmental streps - Arcanobacterium pyogenes Misc: Lentiviruses
63
Most common isolate of CM in SR
Staph aureus - can cause mild, severe, or gangrenous mastitis - chronic IMI --> involution, large fibrinous nodules, abscesses
64
Mannheimia haemolytica mastitis in SR
- causes severe or gangrenous CM in sheep - trans. By resp. Tract of suckling lambs - bacteremia and localization to joints, etc.
65
Mycoplasma spp. mastitis in SR
- highly contagious herd infection - sudden marked decrease in production - CM in BOTH glands - Chronic IMI = reservoir for the herd - doesn't respond well to tx (culling best)
66
Syndromes associated with Mycoplasma spp. Infection (besides mastitis)
- septicemia in young kids - resp. Dz in older kids - arthritis any age - conjunctivitis
67
Mastitis control in dairy sheep and goats
- similar to cattle - prevent new IMI by post-milking dips, reduce fomites, milk clean dry teats, segregate infected animals, and maintain biosecurity - eliminate existing IMI with intramammary abx (can use cow products), dry cow therapy
68
Mastitis in meat and fiber sheep/goats
- most common 2-3 wks PP and after weaning - weaning mgmt important - inspect udders at handling times prior to breeding and cull animals with chronic mastitis