L22: Mastitis (Maunsell) Flashcards
2 categories of mastitis pathogens
Contagious
Environmental
Major contagious mastitis pathogens
Streptococcus agalactiae
Staph aureus
Mycoplasma bovis
Major environmental mastitis pathogens
Coliforms
Environmental strep spp.
Mastitis pathogen that is both environmental and contagious
Strep. Dysgalactiae
Teat canal sphincter open how long after milking?
2-4 hrs (high risk period for developing mastitis)
Teat canal lined by:
Squamous epithelium
- primary means of preventing infection
- secretes keratin (low keratin highly assoc. with mastitis)
IMI = intramammary infection
:)
Natural mammary defenses**
Cellular immune response:
-macs, neuts, and lymphos (should be
When is there the highest risk of IMI?
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
Periparturient immune suppression period
About 3 wks pre to 3 wks postpartum
Mastitis is most common dz of dairy cattle
:)
Changes in milk production caused by mastitis
Subclinical: 10-30% loss; most costly aspect!
Clinical: variable losses
Effect depends on stage of lactation, duration, season, lactation #, organism
Costs assoc. with mastitis
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
Subclinical mastitis detection at cow level
SCC:
- California mastitis test
- Individual SCC: IMI >200,000 cells/ml
Detection of clinical mastitis at the milking parlor
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
Detection of clinical mastitis on PE
- evaluate milk for color, consistency, garget (clots)
- observe/palpate glands for inflammation
- perform PE to detect systemic involvement
Detecting what pathogens are involved with individual cow milk cultures
- collect before treating
- collect aseptically
- proper transport and storage
- can’t differentiate coliform and gram + mastitis clinically, so must use selective culture plates
Antimicrobial sensitivity testing
- 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)
Interpreting milk cultures that don’t grow
- 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**
Legal limit for bulk tank SCC
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
Standard Plate count (SPC)
- performed on bulk tank milk evaluation
- total aerobic bacterial #
- legal limit is 100,000 cfu/ml
- goal is
Bulk tank milk culture for specific pathogens
- 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
Properties of contagious mastitis
- 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
Strep agalactiae
- 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
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)
Reservoirs and transmission of Staph aureus
Reservoirs: chronic subclinical cases, purchased cattle (esp. Heifers)
Transmission: milking, horn flies, cross-suckling of calves
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
Major environmental pathogens
Streptococcus uberis
Strep dysgalactiae (also contagious)
Coliforms
Minor environmental pathogens
Coag-negative staphylococci Others: -Trueperella pyogenes -Prototheca -E. Faecalis -Pseudomonas aeruginosa -Nocardia species -Serratia marcescens -Fungi/yeasts
Organisms that cause coliform mastitis
E. Coli
Klebsiella
Enterobacter spp.
Percent of coliform mastitis cases that are clinical?
10% subclinical
60% mild to mod. Clinical
30% severe clinical
Chronic infections uncommon
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
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)
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
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
Contagious mastitis prevention
- milking hygiene
- post-milking germicidal teat dipping
- teat end condition
- milking procedure machine maintenance
Most effective method for control of contagious pathogens
Post-dipping
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
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
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
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
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
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
Abx approved for intramammary use in non-lactating dairy cattle
Ceftiofur Cephapirin benzathine Cloxacillin benzathine PenicillinG procaine PenicillinG procaine + Novobiocin
Antimicrobial selection based on:
-pathogen ID
-milk withholding
-hx of clinical efficacy in that herd
(Should reassess regularly)
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)
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
Differentiation of coliform and GP mastitis
- can’t differentiate clinically
- herd hx and infection patterns with frequent monitoring
- on farm milk culture
Treating severe clinical mastitis
-decrease systemic effects of endotoxin/shock (fluids, anti-inflammatories)
-abx (IMM + parenteral)
+/- oxytocin at milking
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)
Tx/prognosis of gangrenous mastitis
Tx: aggressive supportive therapy, systemic abx, +/- amputate teat to assist drainage +/- mastectomy
Poor prognosis
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
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
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
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
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
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
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)
More overlap between non-infected and infected glands for goats than for cattle
:)
Major Pathogens for mastitis in small ruminants
S. Aureus
Mannheimia haemolytica
Mycoplasma spp.
Minor pathogens for SR mastitis
Coag-neg. staph
-very common
Environmental pathogens assoc. with SR mastitis
- coliforms
- environmental streps
- Arcanobacterium pyogenes
Misc: Lentiviruses
Most common isolate of CM in SR
Staph aureus
- can cause mild, severe, or gangrenous mastitis
- chronic IMI –> involution, large fibrinous nodules, abscesses
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.
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)
Syndromes associated with Mycoplasma spp. Infection (besides mastitis)
- septicemia in young kids
- resp. Dz in older kids
- arthritis any age
- conjunctivitis
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
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
