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Corynebacterium bovis

Inflammatory disease of the mammary gland - mastitis

In general, the production species are prone to inflammation rather then neoplasia (cf. carnivores).

  • Mastitis may be sterile or infective.
  • Clinical cases of mastitis in domestic species are usually the result of establishment of an unusual, resistant or highly virulent pathogen - usually bacteria - in the udder.
  • The presence of bacteria in the udder does not invariably invoke inflammatory disease.
  • The terms acute, subacute and chronic can be used in a clinical or pathological sense with differing implications.

Basic model of mastitis

  • STERILE MASTITIS: damage by trauma without infection. Seldom clinical but small localised lesions are the gateway to infective mastitis. Blockage of ducts by milk clots and exudate leads to spread of inflammation as a ripple effect through the gland. Where the reaction is long standing acinar chronic inflammation followed by fibrous scarring may ensue, paralleled by squamous metaplasia and blockage of ducts.
  • INFECTIVE MASTITIS: seldom the result merely of the host meets organism but rather the organism gains access and established itself when the host's internal environment becomes favorable. This depends on three factors;
  1. Microorganism considerations = species, virulence and prevalence in the environment.
  2. Establishment of infection = invasion of the udder and bacterial proliferation
  3. Udder reaction = level of tissue penetration and type of inflammatory reaction plus sequelae.

The type of host reaction to the establishment of infection and tissue damage results in a series of patterns of mastitis. The differing patterns of tissue reaction partially explains why the differnet serotypes of the same pathogen produce more resistant or severe forms of mastitis.

  1. Acute catarrhal = essentially similar to sterile. Often subclinical. Usually eliminated by simple hygiene e.g. Streptococci spp
  2. Acute suppurative = organism survives in ducts and acini and penetrates to connective tissue. Charcteristically there is pus production. May become chronic. E.g. Staphylococci and Arcanobacterium pyogenes
  3. Necrosis = organism/toxin penetrate and cause necrosis before a host response occurs. Death results from toxaemia e.g. Arcanobacterium pyogenes and Staphylococci spp. This pattern may become complicated by Clostridial infection i.e. becomes gangrenous.
  4. Granulomatous = a balance between host defense and bacterial attack e.g. Staphylococci, Arcanobacterium, Actinobacillus. This pattern may become complicated by yeasts, classically mycobacterial infection.
  5. Allergic = necrotising vascular damage associated with endotoxic shock syndrome (not purulent) e.g. Coliform. May be complicated by other infective agents such as Mycoplasma.

Bovine mastitis

  • Streptoccocal spp. and Arcanobacterium pyogenes used to be major problems but these infections are relatively easily controlled by farm hygiene.
  • Arcanobacterium pyogenes can cause an acute suppurative/necrotising mastitis in dry cows. This is summer mastitis.
  • Staphylococcus spp. are still major problems because of the lage number of serotypes and varying virulence. The chronic 'carrier cow' is also an important factor in high incidence herds.
  • Complex mastitis patterns are associated with unusual pathogens (Pseudomonas, Klebsiella and Mycoplasmas) but Staphylococcus, Coliform and summer mastitis present major clinical problems
  • Resistant strains of bacteria can cause serious herd problems even where hygiene methods are of a high standard.

Mastits in Ewes

  • More common in lowland flocks than in upland or hill sheep. Causal/contributory factors:
Teat injuries and udder damage (trauma)
Udder chilling in wet and cold condotions
Lamb sick fields where there is a high reservoir of bacteria with increases virulence.
  • Causal organisms is most commonly Staphylococcus aureus which produces a a-haemolysin.
  • The severe situation arises as a per-acute or acute necrotising disease:
  1. Per-acute = death in 12-48 hours as a result of toxaemia
  2. Acute = seen as hot inflammed red and oedematous udder initially and can produce death in 7 - 10 days, at this stage the udder is cold and necrotic.

Sequele The affected udder may slough over 3-4 weeks as a result of vascular thrombosis and tissue necrosis and the ewe survive OR the vascular supply is maintained or re-established and the surviving tissue heals or a chronic abscess develops which may periodically discharge.
Less commonly, the Staphylococcal infection may produce only chronic abscesses. Other organisms such as A.pyogenes may be the cause of similar chronic mastitis but not the acute necrotising reaction.

Mastitis in Sows

  • A disease of intensive breeding sow units with sporadic occurrences.
  • Causal factors include hygiene and husnamdary levels and teat injuries.

Agalactia sundrome

  • Mastitis combined with metritis and agalactia
  • Causal agents may include E.coli and Mycoplasma hyogenitalium and possibly involving Klebsiella
  • This results in agalactia and necroses of udder tissue
  • 68-70% of cases occur in the first 24-48 hours post-farrowing
  • There is a 50% recovery rate if agalactia is treated successfully

Granulomatous mastitis

  • Caused by Staphylococcal infection or Arcanobacterium spp, often complicated by A.pyogenes
  • Results in a firm granulomas or acute abscesses which erupt from skin surface

Mastitis in Mares

Unusual but caused by Streptococcal infection

Mastitis in bitches/queens

  • Unusual. Neoplasia of the mammary gland is more common than mastitis in these species.
  • Staphylococcal and Streptococcal and more rarely Proteus and Coliform agents may cause the suppurative type.

Information by permission of Professor RW Else

Pages in category "Mastitis"

The following 6 pages are in this category, out of 6 total.