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PMVPH > Microbiology and pathology of the mammary gland > Flashcards

Microbiology and pathology of the mammary gland Flashcards

1
Q

What are the high costs of mastitis associated with?

A

direct and indirect costs

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2
Q

When do most cases of mastitis occur?

A

In the lactating gland although Trueperella pyogenes also causes disease in the non-lactating/dry cow and immature glands

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3
Q

How might microorganisms enter the mammary gland? 3

A

GALACTOGENIC route - organisms gain entry via teat canal
HAEMATOGENOUS - e.g. Tb and Brucellosis
Percutaneous - due to wounds

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4
Q

How is the udder adapted to resist infection? 3

A

Teat canal has the PRIMARY role:
1.) Smooth muscle sphincter
2.) Keratin from epithelium containign FAs (bactericidal, absorbing bacteria, desquamating when coated with bacteria, dessicating)
3.) Furstenberg’s Rosette (prevents physical entry of organisms to canal, FAs and cationic proteins e.g. ubiquitin., subepithelial plasma cells producing immunoglobulin).
ALSO
INNATE IMMUNITY - physical factors, soluble factors, cellular factors
ADAPTIVE IMMUNITY - lymphocytes and immunoglobulins

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5
Q

What are the physical aspects of innate immunity?

A

sphincter and keratin of teat, flushing action of milk

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6
Q

What are the soluble factors of innate immunity? 4

A

Lactoferrin (from secretory epithelium and in neutrophil granules - an iron binding prtein which inhibits bacteria but is more effective in the non-lactating gland.
Lysozyme
Complement
Cytokines

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7
Q

What cellular factors make up innate immunity 3

A 
Mainly blood derived in an infection:
neutrophils - acute inflammation
macrophages - later, ingest bacteria 
BOTH of ABOVE detected by CMT
Also Natural Killer Cells
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8
Q

what are the 2 aspects of adaptive immunity?

A

lymphocytes

immunoglobulins (IgG mainly, also IgM and IgA)

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9
Q

What are the 3 clinical pathological presentations of mastitis?

A

PERACUTE - potentially life-threatening (especially around parturition)
ACUTE - with or without accompanying systemic signs - if unchecked may lead to chronic mastitis
SUBCLINICAL CHRONIC - progressive loss of secretory ability

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10
Q

What is another name for peracute masittis?

A

toxic mastitsi

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11
Q

What can cause peracute mastitis?

A

Coliforms
Gangrenous mastitis - especially S. aureus
Mostly occur around parturition and death can occur within hours

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12
Q

Gross appearance of peracute masitis

A 
swollen painful quarter
rapid progression to moist gangrene
dark-blue to black
blistering and oozing serum
becomes cold to the touch
on cut surface, a variable number of dark haemorrhagic lobules
ventral abdominal oedema
animal may be comatose due to TOXAEMIA
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13
Q

Microscopy of acute mastitis

A

initially extensive interstitial oedema with neutrophilic infiltration of both interstitium and glandular acini. Vacuolation and desquamation of acinar and ductal epithelium.

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14
Q

Describe what happens in chronic mastitis

A

fibrosis with obliteration of acini
obstruction of ducts by polyps
subsequent retention cysts anterior to the blocked ducts
all stages of above may be present simultaneously
also abscess formation depending on pathogen

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15
Q

What is the sequel to chronic mastitis? 2

A

INVOLUTION - temporary loss of secretory function due to obstruction
FIBROSIS - permanent loss of secretory tissue due to progressive destruction

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16
Q

What is botryomycosis?

A

An infection of the skin caused by S.aureus usually or a few other spp too. The pathology has a granulomatous-like structure and the lesion is similar to actinomyces and mycetoma.

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17
Q

Describe a botryomycosis lesion

A
  1. ) neutrolphils and bacteria int eh centre

2. ) thick layer of fibrous tissue around the above (ABs won’t penetrate)

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18
Q

How common is subclinical mastitis?

A

10-40 times more prevalent than clinical mastitis

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19
Q

Describe features of subclinical mastitis

A

no gross inflammation or changes in milk

detection of subclinical mastitis by estimating SCC (<200,000 cell/mL for whole udder denotes absence of infection).

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20
Q

What are the 4 phases of subclinical mastitis?

A

Initial flare up –> repair by fibrosis –> further flare-ups –> progressive fibrosis

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21
Q

Describe gross appearance of chronic subclinical mastitis

A

in chronic stages, the gland is hard (fibrosed) and atrophic (undergoes involution due to bloackage of secretion and acinar stagnation)

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22
Q

Describe the microscopy of chronic subclinical mastitis.

A

similar to chronic mastitis following acute mastitis. permanent loss of secretory tissue due to progressive destruction

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23
Q

What are normal colonising bacteria of the milk/udder?

A

Lactobacillus spp and lactic streptococci

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24
Q

Is the udder normally a sterile tissue?

A

Yes

25
Q

True/false - mastitis is the commonest infection of dairy cattle

A

True

26
Q

What are the 5 main pathogens causing mastitis?

A 
S.agalactiae
S.dysgalactiae
S.uberis
S.aureus
E.coli
27
Q

Other than environmental/contagious, how can bovine mastitis be classified?

A

Lactating cow or or dry cow/summer mastitis

28
Q

2 causes of contagious mastitis

A

S.aureus

S.agalactiae

29
Q

Environmental mastitis pathogens - 2

A

E. coli

S. uberis

30
Q

Give examples of where the contagious/environmental definition is blurry.

A

S.aureus will live in the nasal passages and wounds and so gets onto bedding (environment)
E.coli and S.uberis come from the GIT of animals (contagious???)

31
Q

Which (different) pathogens are associated with summer mastitis in dry cows and heifers? 3

A

Arcanobacterium pyogenes
Streptococcus dysgalactiae
Peptostreptococcus indolicus (anaerobic gram positive coccus)

32
Q

How is summer mastitis thought to be spread?

A

by flies

33
Q

When does most lactating mastitis begin?

A

During the dry period

34
Q

What can be highly effective in controlling lactating mastitis?

A

Dry cow mastitis prevention

35
Q

Can M.bovis causes mastitis?

A

Yes but unlike other pathogens this may arrive in the udder via the bloodstream rather than ascending through the teat canal.

36
Q

What pathogens are of minor importance and why? 2

A

COAGULASE negative staphylococci (CNS) and Corynebacterium bovis because they are much less pathogenic but can cause subclinical intramammary infection and raise the SCC

37
Q

Which pathogens are seen in milking ewes? 4

A

Mannheimia haemolytica
S. aureus
E.coli
Streptococci

38
Q

Where are S.aureus found?

A

Skin and mucous membranes –> enter through teat canal where phagocytosis and killing in milk is insufficient

39
Q

Describe the different presentations of S.aureus mastitis.

A

SUBCLINICAL –> severely gangrenous
PERACUTE - rare
ACUTE –> progresses to chronic and increased SCC

40
Q

True/false: 70% of S.aureus strain are b-lactamase positive

A

True

41
Q

How does S.aureus avoid the immune system?

A

Intracellular location

42
Q

Does S.aureus always invade the udder tissue?

A

No - inflammation may be due to an immune response to S.aureus organisms adherent to the internal duct and sinus epithelium ==> hypersensitivity

43
Q

List pathogenicity factors produced by S.aureus

A 
alpha toxin (potent necrotising toxin)
beta toxin (sphingomyelinase)
TSST-1 (superAg)
polysaccharide capsule (in vivo)
Protein A
enzymes (hyaluronidase, lipase)
fibronectin binding protein --> adherence
44
Q

In which lancefield group is S.agalactiae?

A

Lancefield group B (referred to by medical profession as GBS - group B streptococcus)

45
Q

What is the natural habitat of S.agalactiae?

A

Teat canal of the udder

46
Q

List 4 S.uberis pathogenicity factors

A

Steptolysin S
STST-1 (superAg)
Enzymes (hyaluronidase, lipase)
Polysaccharide capsule

47
Q

Why is S.uberis no longer the major cause of mastitis in the UK?

A

Those animals suffering from this infection have been culled

48
Q

Is S.agalactiae host adapted?

A

Yes –> slow, progressive and chronic infections

49
Q

Which lancefield group does S. dysgalactiae belong to?

A

Lancefield group C

50
Q

What is the natural habitat of S.dysgalactiae?

A

Outside udder teat (not so host adapted as S.agalactiae - more acute and inflammatory responses are seen) It requires trauma or a wound to initiate infection

51
Q

Outline S.dysgalactiae features. 2

A

Hippurate negative

CAMP negative

52
Q

List 3 pathogenicity factors of S. dysgalactiae

A

STST-1 (superAg)
enzymes (hypaluronidase, lipase)
polysachharide capsule

53
Q

Does S.uberis belong to a lancefield group?

A

No

54
Q

Natural habitat of S.uberis

A

In environment, possibly in faeces. Requires trauma or wound to initiate invasion

55
Q

What does it mean that S.uberis is aesculin-positive?

A

that this bacteria can hydrolse aesculin (a common glucoside)

56
Q

Is E.coli of increasing or decreasing importance in UK bovine mastitis?

A

increasing (usually acute but relatively mild in most cases). increasing number of cases that are antimicrobially resistant

57
Q

List some pathogenicity factors of E.coli

A 
alpha-haemolysin
CNF-1
Endotoxin
Fe-acquisition
different K types 
pili and fimbriae
58
Q

Is there a vaccine for S.dysgalactiae?

A

No, not yet

59
Q

Is there a vaccine for E.coli?

A

Yes - killed J5 (this is a bacterin vaccine which contains whole killed bacteria and they are a mutant which has no LPS - i.e. the E.coli is missing the o-side chain and therefore has core oligosaccharide structure without chains

PMVPH (33 decks)

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