Mastitis: Intro and Immunity Flashcards

1
Q
  1. What is mastitis?
  2. What are is the difference between clinical and subclinical?
  3. What do grade 1-3/A/C mean?
A
  1. Mastitis is inflammation of the mammary gland
  2. Clinical- visible changes in milk, udder and cow. Subclin- infection but no visivle or clinical signs, change in SCC, quality/yield
  3. Grade 1- mild changes in milk
    Grade 2A- acute, changes in milk, udder hot, painful
    Grade 2C- chronic, changes in milk, udder hard and lumpy
    Grade 3- Changes in milk, udder, cow sick
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2
Q

What assists with infection of mastitis?

A
  • Viable pathogens on teat end- transfered, skin integrity
  • Bypass sphincter and streak canal- damaged, vaccum assisted
  • Spread into udder- damaged defences, vaccum assisted
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3
Q

What are the differetn environmental and contagious mastitis pathogens?

A

Environmental-
E.coli, Strep uberis, Klebsiella

Contagious-
Strep uberis, Strep agalactiae, strep dysgalactiae, staph aureus, Coagulase neg staphs, mycoplasma

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4
Q

What are the consequences of mastitis infection?

A
  • Clear the infection
  • Not clear the infection:
    Chronic infection- spread
    Permanent damage- reduce milk yield
    Death- toxaemia
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5
Q

How does SCC affect milk?

A

Rancid off flavour occurs a lot faster

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6
Q

What are the different innate immmunites of the mammary gland?

A
  • Teat skin
  • Teat canal
  • Resident leucocytes
  • Antimicrobial substances in milk
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7
Q
  1. What features of teat skin help immunnity of mammary gland?
  2. What are the problems?
  3. How can the problems be resolved?
A
  1. Prevent colonisation of teat skin with bacteria- stratified squamous epithelium plus bacteriostatic fatty acids
  2. Some bacteria ubiquitous, comprimised by trauma, bruising, teat lesions, deals with milking machines
  3. Post milking dips, treat teat lesions, good milking machine function
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8
Q
  1. When can bacteria enter the teat canal?
  2. What in the teat canal can trap bacteria?
  3. What forms a seal when dried off?
  4. What can cause teat canal damage?
A
  1. 20-30 minutes after milking whilst the teat sphincter is relaxed
  2. Keratin lining traps bacteria and is continuously sloughing
  3. Keratin plug forms seal over teat end when cow is dried off
  4. Milking machines, external trauma, teat lesions, teat cannulas
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9
Q

What does this image show?
What causes this?

A

Teat end hyperkeratosis
Top- rough ring
Bottom- very rough ring

Causes:
* Excessive milking vaccums
* Faulty pulsations
* Liner types
* Teat shape

Protection- genetics, machine function, loafing, teat sealants

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10
Q

What are the resident leucocytes of the mammary gland?

A

Mainly macrophages, neutrophils, T lymphocytes
Phagocytosis
Trigger the acquired immune with pro-inflammatory mediators and antigen presentation

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11
Q

What are the different antimicrobial substances in milk?

A
  • Lactoferrin iron chelating protein produced by epithelial cells/leucocytes- inhibits growth of pathogens requiring iron (E.coli)- highest in dry period
  • Lactoperoxidase- bacteriostatic agent
  • Lysozyme- bacteriocidal protein
  • Free complement- aid in opsonisation of bacteria
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12
Q

What cells and proteins are involved in the acquired immune system of the mammary gland?

A
  • Invasion of circulating neutrophils and IgG2 antibodies
  • B and T lymphocytes
  • Inflammatory cytokines
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13
Q

What are the different functions of neutrophils?

A
  • Margination
  • Migration
  • Phagocytosis
  • Respiratory burst
  • Degranulation
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14
Q

What are the functions of B lymphocytes?

A
  • Circulate through lymphatic system
  • Exposed to antigens in tissue fluids
  • Initial response produce IgM, IgG1
  • Repeated exposure produce IgG2 antibodies
  • IgG2 circulate and enter inflammed udder aiding opsonisation by neutrophils
  • Present antigen to T lymphocytes
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15
Q

What are the two functions of T lymphocytes?

A
  • T helper cells- production of cytokines following antigen recognition stimulates immune response
  • T cytotoxic cells- eliminate host cells invaded by pathogens
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16
Q

What are the different functions of the following antibodies?:
1. IgG2
2. IgM
3. IgA
4. IgG1

A
  1. IgG2 most important antibody response
  2. IgM fixates complement for opsonisation of pathogens, agglutinates bacteria, neutralise toxin
  3. IgA agglutination of bacteria and neutralise toxins
  4. IgG1 opsonisation of bacteria
17
Q

What can assist in genetic resistance to mastitis?

A
  • Complex trait, low heritability- udder types, speed of milking, neutropil function
  • Breeds- brown swiss, montbeliarde lower SCC and clinical masitis frequency than Holstein
  • Can select for low SCC, udder conformation, yield
18
Q

What stages of lactation are high risk for mastitis?

A

Dry period and early lactation

19
Q

What increases the risk of mastitis in the dry period?

A
  1. Cessation of milking- increased intra-mammary pressure and widening of teat canal
  2. Bacteria not flushed out
  3. No teat dipping
  4. Keratin plug- only 50% have adequate seal 10 days post
  5. WBC function reduced
20
Q

Why is the WBC function reduced at the early and late dry period?

A

Early- neutrophils present in high numbers in secretions but full of fat and cellular debris so function impaired

Late- peri-parturient cow-
* Increasing IgG1 for colostrogenesis may interfere with neutrophil capacity to deal with pathogens
* Neutrophil recruitment reduced by cotrisol, oestradiol
* Macrophages have reduced phagocytic function

21
Q

What nutrition can increase mastitis?

A
  • NEB- leucocytes lower activity and number
  • Vit E/Selenium- deficiency results in slow migration and weaker activity of leucocytes
  • Sub-acute rumen acidosis- poor hyigene
  • Hypocalcaemia- weaken teat sphincter mechanism
22
Q

What mastitis vaccination is available?

A

UK- Startvac
* Protects against- staph aureus, coliforms and coag-neg staphylococci
* Reduce incidence of sub-clinical mastitis
* Reduce incidence and severity of clinical mastitis

UBAC- step uberis vac- little information