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Mastitis - Inflammation of the Mammary Glands

(311) Mastitis is inflammation of one or more mammary glands caused by a variety of bacteria species or secondary to other diseases. It is a common condition that occurs sporadically in individual sows or sometimes as a herd outbreak associated with a specific infection. Disease starts at or around farrowing and becomes clinically evident up to 12 hours later. It can arise as a primary infection, that is, bacteria getting into one or more mammary glands for the first time around farrowing or it may be a flare-up of a sub-clinical latent infection, possibly present in one or more small abscesses, activated by the development of the gland and the flush of milk. It sometimes arises as a sequel to udder oedema possibly due to poor milk flow.

The route of entry of the bacteria is thought to be the teat orifice or injection into the gland by sharp piglets teeth. Very occasionally mastitis may arise from a septicaemia. Unfortunately, there has been much less research into sow mastitis than into mastitis in the dairy cows so knowledge of the disease is fragmentary and empirical.

The bacteria considered to cause mastitis in the sow can be grouped into three broad categories: coliform bacteria, staphylococci and streptococci, and miscellaneous bacteria. Limited surveys suggest that coliform mastitis is the most common and usually most serious, staphylococcal and streptococcal mastitis fairly common and usually less serious, and miscellaneous bacteria uncommon and varying in seriousness in the individual sow.

Coliform mastitis - Coliform bacteria are bacteria that are related to E. coli. The two commonest in sow mastitis appear to be E. coli itself and klebsiella species. These organisms can be responsible for severe acute necrotising mastitis. They release a toxin (endotoxin) which results in reduction in milk yield, a very ill sow and poor "doing" piglets. Marked discoloration of the skin over the udder and dark blueing of surrounding skin, ears and tail is a feature of the condition.

Major herd problems can develop because the normal habitat is the pigs intestine and faeces, and bacteria may also be present, particularly klebsiella, in sows' urine. Consequently, they are everywhere in a piggery and can survive and build up in water bowl, pipes and header tanks. They can multiply rapidly in stagnant contaminated pools or films of liquid on the farrowing room floors and in wet bedding under the sow. Coliform mastitis may thus be regarded as environmental in origin.

Staphylococcal and streptococcal mastitis - These are usually less acute and less severe than coliform mastitis. They tend to occur sporadically in individual sows in one or two or sometimes several glands and usually do not make the sow ill. The exception is an acute severe staphylococcal infection usually in a single gland which becomes swollen, hard and discoloured. In the majority of cases however the sow remains normal with a hard gland which has reduced milk supply.

Unlike coliform bacteria the source of these organisms is not usually the contaminated environment but the skin and possibly orifices of the sow herself. There is some evidence to suggest that as in the dairy cow and sheep some of these bacteria may persist sub-clinically in the udder and then flare up at or after farrowing

Miscellaneous bacteria - These include organisms such as pseudomonas which can produce a serious mastitis and toxaemia and which are often resistant to antibiotic treatment. Fortunately such infections are rare.

Clinical signs

Acute disease
The sow is inappetent at farrowing, or before if mastitis is already developing, she is obviously ill and the mucous membranes of her eyes are brick red. There may be discoloration of the ears and the whole of the udder but particularly over the affected glands. In the early stages, palpation as described earlier will identify the infected quarters but observation alone is often enough to detect swollen glands without carrying out an examination. The temperature ranges from 40 - 42ºC (104 -107ºF).

Chronic disease
This follows acute episodes at farrowing or at weaning. The mammary tissue is infiltrated with abscesses and hard lumps that are usually not painful when palpated. They may ulcerate to the surface and thereby become a potential source of infection to other sows.


The clinical signs are usually sufficient to diagnose mastitis. However if there is a herd problem with a number of sows affected, you should examine all animals clinically at farrowing and again at weaning, to determine the starting point of the mastitis. A sample of the secretions from the infected quarters should be submitted to a laboratory for examination. This is carried out by wiping the teat end with cotton wool soaked in surgical spirit, injecting the sow with 0.5ml of oxytocin and once there is a good flow squirt the milk on to a sterile swab. The swab should be immersed in a transport medium. It is very important that mastitis is diagnosed early and that prompt treatment is given.


Treatment should consist of the following:

  • Oxytocin to let milk down (0.5ml).
  • Antibiotics as prescribed by your veterinarian depending on the organism and its sensitivity.
  • The following could be used: OTC, penicillin and streptomycin, trimethoprim/sulpha, semi-synthetic penicillins such as amoxycillin; framycetin, tylosin, enrofloxacin and ceftiofur.
  • In very severe cases the sow should be injected twice daily.
  • If the sow is toxic an injection of flunixin could be given.
  • Corticosteroids may also be prescribed.
  • In severe outbreaks the sow can be injected 12 hours prior to farrowing with an appropriate long-acting injection.
  • If sawdust is used as bedding stop using it because when soaked with urine it is an ideal medium for bacterial growth.
  • Top dress sows' feed with antibiotic commencing 3 to 5 days pre-farrowing. Use OTC, trimethoprim/sulpha, amoxycillin or CTC depending on the antibiotic sensitivity.
Management control and prevention

There are two fundamental requirements for the development of mastitis. The first is the presence of the causal organism and secondly an ideal environment at the teat end for the organism to multiply and gain access to the mammary gland. Occasionally mastitis will arise from a blood borne infection associated with the farrowing process.

The following factors predispose to mastitis and require remedial action:

  • The continual use of farrowing houses.
  • Poor farrowing pen hygiene, bad drainage, inadequate bedding, poor quality bedding.
  • The use of saw dust or shavings for bedding that become soaked in water or urine.
  • A warm temperature for the organisms to multiply.
  • Worn pitted farrowing house floors.
  • Wet farrowing house floors.
  • Contaminated drinking water.
  • Adverse temperatures and ventilation in the farrowing houses that cause abnormal lying habits in the crate.
  • A build up of faeces behind the sow associated with shortage of labour or failure to carry out normal hygienic tasks. Faeces behind the sow in the crate should be removed every day.
Additional measures are as follows.
  • If a klebsiella infection is the cause of a herd outbreak it may be necessary to clean out the watering system.
  • If floor surfaces are poor these can be improved by brushing them with lime wash containing approximately 1oz to the gallon of a phenolic disinfectant. This should be allowed to dry for 48 hours or so before the sow enters the crate to farrow.
  • The udder can be sprayed daily with an iodine based dairy teat dip, commencing 24 hours before expected farrowing. This spraying should continue once a day for the first two days post-farrowing. If a specific organism is identified and its antibiotic sensitivity is known, the sows feed can be top-dressed from day of entry into the farrowing houses until three days post-farrowing with the appropriate in-feed antibiotic or injections of appropriate long-acting antibiotics at farrowing.
  • Cull chronic infected sows.
If you have a mastitis problem on your farm and have read this section now study Fig.8-20 and Fig.8-21 which summarise the various predisposing factors.

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