Mastitis - Inflammation of the Mammary Glands (Bacteria)

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 septicemia. 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.
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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 necrotizing
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 bluing 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 feces, 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 discolored. In the
majority of cases however the sow remains normal with a hard gland which
has reduced milk supply.
Unlike coliform bacteria the source
contaminated environment but the
herself. There is some evidence to
sheep some of these bacteria may
then flare up at or after farrowing

of these organisms is not usually the

skin and possibly orifices of the sow
suggest that as in the dairy cow and
persist sub-clinically in the udder and

Miscellaneous bacteria - These include organisms such as pseudomonas

which can produce a serious mastitis and toxemia and which are often
resistant to antibiotic treatment. Fortunately such infections are rare.

Causes / Contributing factors

The continual use of farrowing houses.

Poor farrowing pen hygiene, bad drainage, inadequate and poor quality
bedding.

The use of saw dust or shavings for bedding that becomes soaked in
water or urine.

A warm temperature for the organisms to multiply.

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Worn pitted farrowing house floors.

Wet farrowing house floors.

Contaminated drinking water.

Adverse temperatures, draughts and poor ventilation in the farrowing

houses.

A buildup of feces behind the sows.

Klebsiella in the water system.

Clinical signs
Acute disease
The sow is in appetent 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 - 42C (104 -107F).

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.

Diagnosis
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
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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
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 prefarrowing. 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 ends 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 becomes 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 buildup of feces behind the sow associated with shortage of labor or

failure to carry out normal hygienic tasks. Faces 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, study the following figures
which summarize the various predisposing factors.

Salmonellosis (Bacteria)

Salmonella bacteria are widespread in

human and animal populations. Some
of them can cause disease in pigs.
They multiply mainly in the intestines
of young growing pigs but also in some
sows. They may be shed in faeces for
several weeks or months with no
clinical disease. Salmonella in the gut
of the pig can contaminate carcasses
during the slaughter process and their
presence creates potential public health risks from food poisoning.
Of the many serotypes of salmonella that exist, the ones that are most likely
to cause clinical disease in pigs are Salmonella choleraesuis, and Salmonella
typhimurium and to a lesser extent Salmonella derby. Other "exotic"
salmonella serotypes may infect pigs and be shed in the faeces for limited
periods but they usually remain sub-clinical. S. choleraesuis and S. derby are
host-adapted to the pig and may be carried for long periods by sows, the
former sometimes causing clinical disease in sows (fever, depression,
septicaemia, pneumonia, meningitis arthritis and diarrhoea) but rarely in
people.
Pigs may become long-term sub-clinical carriers of S. choleraesuis and S.
derby, the organisms surviving in the mesenteric lymph nodes draining the
intestine. Many such carriers do not shed the bacteria in faeces unless they
are stressed. Pigs may be intermittent or continuous faecal shedders of other
serotypes but the carrier state is usually short, weeks or a few months and is
self limiting.
S. typhimurium and S. derby are more likely to cause milder disease, the
main sign of which is usually diarrhoea. The serotype most commonly found
in pigs, however, is Salmonella typhimurium which sometimes is associated
with diarrhoea in young pigs but which is also a major cause of food
poisoning in people. Some strains have multiple medicine resistance. If it is
diagnosed in your pigs you should take hygienic precautions not to become
infected yourself. Many other so called exotic types may also be detected in
pigs without causing disease.
Remember that S. typhimurium, which occasionally can be isolated from
pigs, are common causes of food poisoning in people.

Salmonellosis can occur at any age but is most common in growing pigs over
eight weeks of age. Severe S. choleraesuis infection occurs typically at
around 12 to 14 weeks.
Disease is dose dependent, that is, a relatively large number of organisms
are required before clinical signs occur.

Causes / Contributing factors

Poor hygiene.

Overcrowding.

Stress by moving and mixing.

Permanently populated houses.

Contaminated boots and clothing.

Mechanical means via faeces and the movement of contaminated

equipment.

Vermin and flies.

Contamination of feed by birds, rats and mice

Contamination of raw feed ingredients and thus the final product.

Clinical signs
Weaners & Growers

The acute septicaemia and pneumonia which may occur with S.

choleraesuis may result in fever, inappetence, respiratory distress,
depression, coughing, red skin and poor doing pigs.

The skin of the extremities (i.e. tail, ears, nose and feet) become blue.

Foul-smelling watery diarrhoea which may be blood stained, is a

common feature.

Yellow jaundice may result from liver damage and lameness from
arthritis.
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Nervous signs resulting from meningitis.

If untreated, mortality may be high.

Infections with S. typhimurium usually are manifest by diarrhoea.

Piglets

Disease would be uncommon in the piglet and due to passive immunity

provided via colostrum.

Sows
Clinical signs of Salmonella choleraesuis and occasionally Salmonella
typhimurium infection may include any combination of the following:

A high temperature.

Depression.

Loss of appetite.

Congestion of the ears, snout and tail.

Pneumonia.

Coughing.

Nervous signs.

A smelly sometimes bloody diarrhoea.

Death may occur in the acute phase of the disease.

Acute septicemia and pneumonia result in fever, in appetence, respiratory

distress and depression. The skin of the extremities (i.e. tail, ears, nose and
feet) becomes blue. On the ears, in S. choleraesuis infection, there is often a
clear line of demarcation between the blue and normal skin. Foul-smelling
diarrhea which may be blood stained, is a common feature. Jaundice
(yellowing) may result from liver damage and lameness from arthritis.
Meningitis results in nervous signs. If untreated, mortality may be high.

Diagnosis

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The post-mortem lesions are strongly suggestive of S. choleraesuis,

particularly the generalised pneumonia, the appearance of the lining of the
small and large intestine, the congested spleen and multiple small
haemorrhages. However, to make a specific diagnosis it is necessary to
submit to the laboratory either fresh faecal samples from untreated pigs or
where available a dead or live untreated pig.
Severe salmonellosis caused by S. choleraesuis can occur alone but it also
commonly occurs with classical swine fever (hog cholera) in those countries
in which this disease still occurs. In such countries it is important to ensure
by serology and laboratory tests that swine fever is not the primary cause
(NB. swine fever usually also affects sows and sucking piglets and also
causes mummified litters and abortions).
Severe PRRS in herds with endemic EP may give the appearance of
salmonellosis, however PRRS also causes abortions, stillbirths and
precipitates scouring in piglets.

Similar diseases
Severe salmonellosis caused by S. choleraesuis can occur alone but it also
commonly occurs at the same time as classical swine fever (hog cholera) in
those countries in which this disease still occurs. In such countries it is
important to ensure by serology and laboratory tests that swine fever is not
the primary cause (NB. swine fever usually also affects sows and sucking
piglets and also causes mummified litters and abortions).
Severe PRRS in herds with endemic EP may give the appearance of
salmonellosis; however PRRS also causes abortions, stillbirths and
precipitates scouring in piglets.

Treatment

The response to the treatment of salmonella infections is often poor. It

is necessary to determine the serotype, the antibiotic sensitivity and
treat individual pigs at a very early stage.

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Preventive medication or strategic medication both in-feed or in the

water are important and the medicines used are dependent on the
bacterial sensitivity.

Management control and prevention

It is most important point to realize that the severity of clinical salmonellosis
is dose dependent. This is true to a greater or lesser extent of all infectious
diseases but is particularly so of salmonellosis. The overall aim, therefore, is
to get the levels in the environment down to below the disease-producing
threshold. The second aim is to reduce the spread of infection.

Improve hygiene by frequent and thorough removal of waste.

Optimize stocking density. Overcrowding predisposes.

Reduce stress by reducing moving and mixing.

Develop an all-in all-out system with cleaning and disinfection between

batches.

Avoid the movement of pig feces between one batch and another.

Vaccines against S. choleraesuis are available in some countries and

can be used to help in elimination programs if this type is present. The
principle is to vaccinate the sow to produce high maternal antibody
and then carry out segregated early weaning or segregated disease
control programs.

Disinfect boots between houses.

Control vermin and flies.

Prevent contamination of feed by birds, rats and mice.

Monitor raw feed ingredients and final product.

Cleanliness and hygiene are important.

Organic acids added to feed also help.

In some countries formalin is added instead.

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Oedema Disease (OD) - Bowel Oedema(Bacteria)

This is also called bowel disease or gut oedema. It is caused by certain

serotypes of E. coli bacteria that produce a powerful toxin (Vero toxin). These
toxins damage the walls of small blood vessels including those in the brain
and cause fluid or oedema to accumulate in the tissues of the stomach and
the large bowel. Damage to the blood vessels in the brain results in some of
the characteristic signs. The specific E. coli are described as O138, O139 and
O141. Disease is generally seen 1 to 4 weeks after weaning, the peak being
at 10 days. It was very common when pigs were weaned at 5 to 8 weeks of
age. Since weaning ages have reduced to 17 to 26 days and starter diets
have been improved the disease in its classical form is rarely seen. The E.
coli bacteria attach themselves to the finger-like villi in the anterior small
intestine and produce the toxins. This mechanism is similar to that which
occurs in post-weaning diarrhea associated with different strains of E. coli.
During sucking the secretory IgA immunoglobulin component in milk
prevents the bacteria adhering. After weaning when the IgA has disappeared
the pigs becomes susceptible to disease.

Causes / Contributing factors

Associated with weaning and changes of diet.

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Clinical signs
Acute disease
Sometimes the only sign is a good pig found dead 1 to 4 weeks post
weaning. A typical live affected pig will show a staggering gate, puffy eyelids
giving a sleepy appearance and an abnormal high pitched squeak. Pigs stop
eating and in the later stages become partially paralyzed and go off their
legs, sometimes with nervous symptoms. Diarrhea is not a consistent feature
but breathing difficulties become evident. The damage to the brain is
irreversible and most pigs die. Recovery in the few pigs that do not die takes
up to 2 to 3 weeks. Certain breeds of pigs may be associated with disease
suggesting a genetic predisposition. The temperature is usually normal.

Diagnosis
This is made from the typical clinical signs, the sudden appearance of
disease after weaning, post-mortem examinations showing oedema of the
greater curvature of the stomach wall, coiled colon, and eyelids and isolation
of the hemolytic E. coli serotypes from the duodenum (anterior small
intestine).

Treatment
By the time the clinical signs are seen it is often too late and most pigs die.
Treatment routines are aimed at preventing the organism establishing itself
and also reducing the weight of infection. The general principles of
controlling coliform infections and post-weaning diarrhea should be followed.

Isolate the organism and determine the antibiotic sensitivity.

Identify the stage (e.g. 10 days post-weaning) when disease first

appears and apply either in-feed or water medication 3 to 5 days
before this.

In-feed antibiotics of value include apramycin 100g/tonne, framycetin

100g/tonne, neomycin 163g/tonne. Alternatively apramycin, neomycin
or trimethoprim/sulpha can be used in the water.

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Individual treatments give a poor response but flunixin will help to

reduce the effects of toxins and diuretics can be used to remove fluid.

It must be admitted however that the disease is most difficult to deal with
and often preventative medication and treatment are unsuccessful.

Management control and prevention

This can be difficult and unrewarding.

Certain types of breeding animals may be more susceptible and

mortalities in such cases may rise to 25% or more.

Reduce piglet exposure to the E. coli during sucking. Adopt all the
procedures in the farrowing house for the control of scour in the
sucking pig.

Consider the use of an autogenous vaccine in sows to raise colostral

antibodies and block out infection in the sucking pig. This has been
effective on a few farms.

Assess the effects of no creep feeding pre-weaning.

Restrict feed intake post-weaning.

Assess the effects of different diets and feeding routines.

Reduce the nutrient composition of the diet by increasing the fiber

content by 10 to 15%.

If the problem is a major one and it continues, consider a change of

genotype. Some strains of pig are more resistant than others.

Lower or alter the age of weaning.

Alter the environment at weaning time.

Asses the effects of adding 3% of milk powder to the diet.

Assess the effects of zinc oxide to the diet at a level of 2500ppm zinc.

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Eperythrozoonosis (Epe) Bacteria

This is a disease caused by a bacterium called Mycoplasma suis which
attaches to the surface of red blood cells and sometimes destroys them. The
pig then may become anemic and the products left after the destruction of
the cells may cause jaundice. Clinical disease is more commonly seen in the
young growing pigs. However it can also cause reproductive problems in the
breeding herd. A sow may carry Epe and yet remain quite healthy; however,
it can cross the placenta and infect pigs in utero causing weak piglets at
birth. The disease can be transmitted by direct inoculation, through pig lice,
biting house flies, mange mites and perhaps more importantly the needles
that are used to inject pigs. It is also thought that Epe may enter through the
mouth to the stomach and intestine and be transferred into the body this
way. This is one reason why the practice of feed-back using placenta is not
advised.
Epe is present in most if not all herds but the mechanisms which allow it to
become pathogenic and produce disease in some populations and not in
others are unknown. The incidence of disease is low.

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Causes / Contributing factors

Biting insects.

Internal parasites

Lice or mange mites.

Cannibalism / vice (Abnormal behavior).

Sows method of spread:

Vaccinating sows with the same needle.

Tagging gilts.

Feeding placenta or farrowing house material.

Fighting.

Vulva and tail biting etc.

Piglets - method of spread:

Tailing, tooth clipping and iron injections.

Weaners & Growers method of spread

Fighting.

Tail biting and other vices.

Clinical signs
Acute disease
Affected sows are in appetent with fever 40-42C (105-107F) when high
numbers of organisms are present in the blood. This clinical picture is seen
after farrowing and anemia is a common symptom. Similar acute infections
occur in sows at weaning time together with anestrus.
Chronic disease
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Sows become debilitated and pale with jaundice, poor conception, repeat
matings and anestrus. Signs of infertility that have been attributed to Epe
include:

Delayed returns to estrus.

Anemia.

Jaundice.

Bleeding into tissues.

Abortion.

Reduced conception rates.

The carrier state

This is common and blood provides a constant source of transmission
throughout the herd, particularly when females are vaccinated using
common needles.

Diagnosis
This is carried out by making a blood smear on a glass
special stain (Wright's stain) and looking for the
microscope. The presence of Epe in a smear need
disease and there is still controversy over the actual
and its capacity to cause disease.

slide, staining it with a

organism under the
not necessarily imply
role of this bacterium

Treatment

Arsenic acid at a level of 90 grams to the tonne has been used to

provide a dose of approximately 250mg per day to each female.

If the herd is infected with mange it is important to adopt a control

program.

Oxytetracycline at a level of 400g to the tonne for four weeks is

claimed to have some effect but generally the response to treatment is
only moderate.

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Management control and prevention

There are no known methods for preventing this disease other than reducing
its movement around the herd by changing needles very frequently. It is
possible that infection with PRRS initiates disease.

Take precautions when vaccinating large numbers of sows. Change

needles every 2 to 3 sows and gilts.

Wipe the needle between each animal with cotton wool and surgical
spirit.

Reduce fighting episodes.

Take precautions to keep vice at a minimum.

Do not carry out feedback using placenta or farrowing liquids.

Keep stress and immuno-suppression to a minimum.

Control mange and lice if they are present.

Control biting insects.

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Porcine Epidemic Diarrhea (PED) (Virus)

Porcine epidemic diarrhea is caused by a
coronavirus somewhat similar to that which
causes TGE. This virus is widespread in
Europe. The virus damages the villi in the
gut thus reducing the absorptive surface,
with loss of fluid and dehydration. After
introduction of the virus into a susceptible
breeding herd, a strong immunity develops
over two to three weeks. The colostral
immunity then protects the piglets. The
virus usually disappears spontaneously from
breeding herds particularly small ones (<
300 sows).
Acute outbreaks of diarrhea occur when the
virus is first introduced into a susceptible
population. In such cases up to 100% of sows may be affected, showing a
mild to very watery diarrhea. Two clinical pictures are recognized: PED Type I
only affects growing pigs whereas PED Type II affects all ages including
sucking pigs and mature sows. The incubation period is approximately 2 days
and diarrhea lasts for 7 to 14 days. In sucking pigs the disease can be mild or
severe with mortalities up to 40%.
In large breeding herds, particularly if kept extensively, not all the females
may become infected first time round and there may be recrudescence. This
only occurs in piglets suckling from sows with no maternal antibodies and is
therefore sporadic.

Causes / Contributing factors

The immunological status of the herd i.e. no immunity.

Disease may be perpetuated as susceptible pigs enter the finishing

herd.

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Disease normally only seen when virus first enters the herd.

Clinical signs
There is an acute watery diarrhea and no evidence of blood or mucus. In
breeding finishing farms disease is usually sporadic; however PED is common
where weaners are continually entering finishing only operations. Groups of
pigs become infected when they reach a certain age and as they enter a
building where infection is endemic. Mortality is usually low but morbidity
can be high.

Diagnosis
This is based on the history, clinical symptoms and examinations of feces
samples for evidence of porcine epidemic diarrhea virus by ELISA tests or
electron microscopy.
Post-mortem examination of dead pigs and laboratory tests on the small
intestine may be necessary to confirm the diagnosis.

Similar diseases
TGE could give a similar picture and live affected pigs are best submitted to
a laboratory for differential tests.

Treatment

The growing pig normally recovers without treatment unless there are
secondary infections. In such cases antibiotics in the water or
preventative medication in-feed maybe required.

Use neomycin, apramycin, framycetin or trimethoprim/sulpha.

Sometimes a good response is obtained with either lincomycin or
tiamulin depending on the secondary bacteria present.

Specific treatment is of no value since this is a virus infection.

Management control and prevention

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The disease may occasionally become endemic in finishing units as

new weaners are introduced onto the farm. Under such circumstances
it is necessary to break the cycle by stopping purchasing for three
weeks or utilizing segregated disease control methods. (See chapter
3).

All-in all-out procedures with disinfection will often break the cycle.

The virus is easily killed by phenolic, chlorine or iodine based

disinfectants or peroxides.

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