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Ruminant Medicine Exam 3 (Spring 2016) > L22: Mastitis (Maunsell) > Flashcards

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
Q

Staph aureus

A
  • 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)
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26
Q

Reservoirs and transmission of Staph aureus

A

Reservoirs: chronic subclinical cases, purchased cattle (esp. Heifers)

Transmission: milking, horn flies, cross-suckling of calves

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27
Q

Mycoplasma mastitis properties

A
  • 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
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28
Q

Major environmental pathogens

A

Streptococcus uberis
Strep dysgalactiae (also contagious)
Coliforms

29
Q

Minor environmental pathogens

A 
Coag-negative staphylococci
Others:
-Trueperella pyogenes
-Prototheca
-E. Faecalis
-Pseudomonas aeruginosa
-Nocardia species
-Serratia marcescens
-Fungi/yeasts
30
Q

Organisms that cause coliform mastitis

A

E. Coli
Klebsiella
Enterobacter spp.

31
Q

Percent of coliform mastitis cases that are clinical?

A

10% subclinical
60% mild to mod. Clinical
30% severe clinical

Chronic infections uncommon

32
Q

Pathogenesis of coliform mastitis

A
  • 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
Q

Most important environmental pathogens in terms of # clinical cases in US

A

Environmental streptococci:

  • Strep uberis
  • Strep dysgalactiae
  • Strep spp.
  • Enterococcus spp.

40-50% IMI are clinical (however usually mild to moderate)

34
Q

Environmental streptococci

A
  • 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
Q

Environmental mastitis prevention

A
  • 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
Q

Contagious mastitis prevention

A
  • milking hygiene
  • post-milking germicidal teat dipping
  • teat end condition
  • milking procedure machine maintenance
37
Q

Most effective method for control of contagious pathogens

A

Post-dipping

38
Q

Pre-dipping procedure

A
  • 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
Q

Methods of minimizing exposure between milkings

A
  • udders should be in contact with clean, dry bedding
  • barrier dips
  • fresh feed/turn out to clean lots after milking
40
Q

Dry cow therapy

A

Goal = minimize new infections in the early dry period

  • limited efficacy against coliforms
  • doesn’t protect against IMI in late dry period
41
Q

Methods to boost host defense mechanisms

A
  • adequate nutrition, esp. vit. E and selenium

- vaccination for Gram - bacteria, and to reduce severity/incidence of clinical coliform mastitis

42
Q

Antimicrobial tx during lactation

A
  • generally only for clinical mastitis
  • high cure rate for Strep. Agalactiae
  • moderate response for environmental Strep spp.
  • poor response for Staph aureus
43
Q

Antimicrobial tx in the dry period

A
  • 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
Q

Abx approved for intramammary use in non-lactating dairy cattle

A 
Ceftiofur
Cephapirin benzathine
Cloxacillin benzathine
PenicillinG procaine
PenicillinG procaine + Novobiocin
45
Q

Antimicrobial selection based on:

A

-pathogen ID
-milk withholding
-hx of clinical efficacy in that herd
(Should reassess regularly)

46
Q

Tx of clinical mastitis with severity score of 1 or 2

A

1) IMM abx
2) +/- oxytocin AT MILKING if painful to milk
3) anti-inflammatories for moderate CM (ie. Banamine, aspirin, dex, isoflupredone acetate)

47
Q

When to use abx for mild/moderate clinical mastitis (coliform, G+, mycoplasmal)

A
  • 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
Q

Differentiation of coliform and GP mastitis

A
  • can’t differentiate clinically
  • herd hx and infection patterns with frequent monitoring
  • on farm milk culture
49
Q

Treating severe clinical mastitis

A

-decrease systemic effects of endotoxin/shock (fluids, anti-inflammatories)
-abx (IMM + parenteral)
+/- oxytocin at milking

50
Q

Gangrenous mastitis: cause and CS

A
  • 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
Q

Tx/prognosis of gangrenous mastitis

A

Tx: aggressive supportive therapy, systemic abx, +/- amputate teat to assist drainage +/- mastectomy

Poor prognosis

52
Q

Indications for teat amputation

A
  • 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
Q

Procedure of teat amputation

A

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
Q

Chemical destruction of quarter

A
  • 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
Q

Procedure for chemical destruction

A
  • 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
Q

Managing mastitis in ORGANIC herds

A
  • 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
Q

Mastitis in BEEF cattle

A
  • 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
Q

Dx of mastitis in small ruminants

A
  • PE: similar to cattle, may have lameness on affected side or refuse nursing
  • Milk culture
  • SCC (direct SCC or CMT)
59
Q

More overlap between non-infected and infected glands for goats than for cattle

A

:)

60
Q

Major Pathogens for mastitis in small ruminants

A

S. Aureus
Mannheimia haemolytica
Mycoplasma spp.

61
Q

Minor pathogens for SR mastitis

A

Coag-neg. staph

-very common

62
Q

Environmental pathogens assoc. with SR mastitis

A
  • coliforms
  • environmental streps
  • Arcanobacterium pyogenes

Misc: Lentiviruses

63
Q

Most common isolate of CM in SR

A

Staph aureus

  • can cause mild, severe, or gangrenous mastitis
  • chronic IMI –> involution, large fibrinous nodules, abscesses
64
Q

Mannheimia haemolytica mastitis in SR

A
  • causes severe or gangrenous CM in sheep
  • trans. By resp. Tract of suckling lambs
  • bacteremia and localization to joints, etc.
65
Q

Mycoplasma spp. mastitis in SR

A
  • 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
Q

Syndromes associated with Mycoplasma spp. Infection (besides mastitis)

A
  • septicemia in young kids
  • resp. Dz in older kids
  • arthritis any age
  • conjunctivitis
67
Q

Mastitis control in dairy sheep and goats

A
  • 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
Q

Mastitis in meat and fiber sheep/goats

A
  • 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

Ruminant Medicine Exam 3 (Spring 2016) (8 decks)

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