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TERMINOLOGY
The following is a list of terms dealing with livestock that seem to
confuse students that do not have a strong farm background. Please
note that some of these definitions will vary depending the facilities
and type of management.
Suckler:
A pig that is still nursing. Age range depends upon age at
weaning in a given management system.
Weaner:
A pig that has recently been weaned.
Nursery
pig:
Feeder
pig:
A pig that has been weaned but has not reached the grower
stage. These pigs may weigh 15 to 70 pounds or so depending
on the type of facilities. Pigs in a one stage type of
facility will be fed to around 70 pounds. Pigs in a two
stage facility will be moved out of the nursery weighing
about 40 pounds and placed in a grower unit.
A pig that is destined to be fed out and slaughtered. The
term usually refers to a young pig that has been weaned but
has not entered the finishing stage. Feeder pigs are often
thought of as being about 40 pounds or so. This can vary.
Grower:
A pig that is in the 40 to 170 pound range or so (see
definition of nursery pig).
Finisher:
A pig that is in the final stage of feeding prior to
marketing.
Fat hog:
Also called market hog. One that is ready for slaughter.
Most slaughter hogs in this country weigh about 225 to 280
pounds. Individual meat packers have different ideal
weights.
Gilt: A female pig. If the gilt is retained in the herd for breeding
purposes, she is referred to as a gilt until after she
farrows and some refer to her as a gilt until after her
first litter is weaned. Then she becomes a sow.
Barrow:
A castrated male pig. Essentially all male pigs not used
for breeding purposes are castrated.
Carcass basis (grade and yield). Slaughter hogs can be sold on the
basis of how good the carcass grades and how much it weighs
immediately following slaughter (hot weights). The hogs are killed
and eviscerated, the head, feet, tail, hair, etc. removed, and the
carcass graded on the basis of the amount of backfat, the size of the
loin eye, etc. The farmer is paid a premium for higher quality hogs
that yield a higher percentage of quality cuts of meat and less fat.
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Cattle are often sold on carcass basis also.
Live-weight basis. This is the opposite of the carcass basis. The
slaughter hogs are weighed at the point of sale and the farmer is paid
a certain amount per pound of live weight.
METHODS FOR ELIMINATION OF INFECTIOUS AGENTS FROM SWINE HERDS
CONVENTIONAL SWINE FACILITIES
These have traditionally been relatively small units on
individual farms. The farmer maintains a herd of 50 to several
hundred sows and takes care of all their needs himself with the
help of hired labor or family members. The adult breeding swine
are maintained on the farm, usually in separate facilities from
the pigs that are in the nursery or in the grower-finisher
facilities. Piglets are weaned at or after 3 weeks of age.
Diseases that are present in the sow herd are often transmitted
to the piglets as the level of colostral immunity wanes. Also,
personnel moving between the units may bring in new diseases. In
farrow-to-finish operations, all the functions take place in one
building. If infectious agents get into the piglets at or
shortly after weaning, serious disease problems can occur because
this is often the time of maximum stress and lowest levels of
immunity.
CONTINUOUS THRU-PUT
This type of operation may put pigs into barns where the pigs are
continually added to existing grower-finisher swine. The slowest
growing pigs are often the ones left behind and these are the
ones that remain when new pigs are added to the unit. They are
also the most likely to have infectious diseases.
ALL-IN-ALL-OUT
Eliminates the exposure of susceptible pigs to potential disease
carriers from other age groups.
SPECIFIC PATHOGEN FREE SWINE
Caesarian derived
Maintained separate from all other swine
Used for:
1.
Establishment of disease-free breeding stock
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2.
Preservation of valuable bloodlines that were infected with
pathogens that could not be eliminated by other means.
Limitations:
1.
Very labor intensive and expensive.
Pigs this young are difficult to rear and there tended to be
a high mortality.
2.
What happened when SPF pigs were exposed to disease agents?
3.
What happened when the SPF pigs were not really SPF (ie. had
pathogens that were not detected) and were then introduced
into herds?
MEDICATED EARLY WEANING (MEW), MODIFIED MEW and SEGREGATED EARLY
WEANING (SEW)
1.
Initial programs (1980) used high doses of tiamulin and
trimethoprim-sulfa to medicate the sows from the time of
their entry into farrowing units until the piglets were
weaned. The piglets also received the same antimicrobials
for 10 days following birth. The best doing piglets were
weaned at 5 days and maintained in isolated units to prevent
transmission of diseases from the source herds. This
regimen was used to eliminate mycoplasmal pneumonia and
Bordetella bronchiseptica. They were also trying to
eliminate Serpulina hyodysenteriae but were apparently
unsuccessful.
2.
Other antimicrobials were later tried in attempts to
eliminate other infectious diseases. The main drawbacks of
the system were the high mortality in the pigs weaned at 5
days and the labor involved.
3.
Vaccination of the sows to maximize their level of immunity
to some of the diseases was instituted. This had the effect
of increasing the level of immunity in the piglets and
allowing the weaning dates to be delayed somewhat. Piglet
mortality decreased as the age at weaning was increased.
Pigs weaned early have higher levels of maternal antibody
remaining. They can be mixed with other pigs while their
level of immunity is higher and there should be lower levels
of disease if any of the groups of pigs should be harboring
an infectious agent.
The breeding, farrowing and maintenance of the sow herd takes place
at one site. The piglets are then weaned at 10 to 21 days of age and
removed to an isolated farm where they are reared. When the pigs
weigh between 45 and 75 lb, they may be moved to another isolated
facility for growing and possibly still another unit for finishing.
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Basically, the pigs are handled much the same as in the medicated
early weaning. Specific diseases present in the breeding herd may be
targeted for elimination. This allows for specific vaccination
schemes and the utilization of specific antimicrobials if necessary.
Once the diseases are eliminated from the breeders, the use of the
antimicrobials and extensive vaccination programs can be eliminated.
Note on Immunoglobulin levels
Normal adult sow serum immunoglobulin levels are 22 mg/ml (range 18 to 27 or
so depending on the study quoted).
Sow immunoglobulin levels at parturition are approximately 14 to 18 mg/ml.
Note that the sow is apparently putting her immunoglobulin synthesis efforts
into the colostrum.
Pig immunoglobulin levels at 2 days of age: Approximately 16 to 27mg/ml or
roughly equal to a normal adult sow. A crude approximation in well-managed
pigs that receive higher levels of colostrum puts it at roughly double the
level of the sow at parturition.
By 2 weeks of age, the well managed pig will have immunoglobulin levels
roughly equal to the sow=s levels at parturition. However, the levels at
parturition are only half the normal adult sow immunoglobulin levels. The pig
is undoubtably beginning to synthesize its own immunoglobulins at this time in
response to exposure to infectious agents.
By 4 weeks of age, the well-managed pig will also have immunoglobulin levels
roughly equal to the levels seen in sows at parturition (11 to 13 mg/ml).
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Table 1. Diseases that can be theoretically eliminated using a multiple site isolated
rearing system.
Agent
Breeders and
sucklers
Wean
Age
Weaners (to 75 lb or
so)
Finishers
Pasteurella
multocida
(toxigenic)
Vaccinate sows
10-15
days
All-in, All-out by
site or unit
AIAO by site or
unit
Mycoplasma
hyopneumoniae
Vaccinate sows
10-19
days
AIAO by site or unit
AIAO by site or
unit
Actinobacillus
pleuro- pneumoniae
Vaccinate sows
21 d
AIAO by site
AIAO by site
Pseudorabies
Vaccinate sows
21 d
AIAO
AIAO
Transmissible
gastro- enteritis
Virus exposure
to whole unit
21 d
AIAO by site
AIAO by site
Brachyspira
hyodysenteriae
Medicate sows
to eradicate or
depopulate,
Sanitation
21 d
Medicate, AIAO,
extensive
disinfection and
sanitation,
Depopulate
Essentially the
same as for
weaners.
If a two or three site system is used there is a continuous supply of
pigs coming into the weaner and finisher units. If disease outbreaks
occur, one can stop the outbreak by interrupting the flow of
susceptible pigs coming into a unit. This would essentially mean a
total depopulation. The advantage of a multiple site system over a
two or three site system is that at the weaner and finisher stage,
all-in-all-out management can be substituted for the depopulation.
The flow of pigs from the farrowing unit is not interrupted and a
specific weaner or finishing unit can be closed down temporarily for
cleanup while piglets go to other units. In both types of units
however, the piglets could be sold to allow time for cleanup. The
most common type of system in use today is actually a two-site system.
The main problem with any high-health status herd is biosecurity.
Maintaining biosecurity can be difficult and even those individuals
that claim to be very careful, can have breakdowns.
What are some potential sources for breaks in biosecurity?
Potential for elimination of other disease agents using segregated
early weaning strategies.
Streptococcus suis. Some studies have found that a relatively high
percentage of SEW pigs carry this organism although the incidence of
clinical disease may be low. One study used penicillin in an MEW
program and had relatively good results. However, S. suis infections
remain an important problem in "high health status" herds. The main
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problem with elimination of this disease is the fact that it is
carried in the vagina of some sows and is transmitted to piglets at
birth. Generally it is not considered a disease that can be
eliminated from high health status herds and is usually considered to
be even more troublesome than in Aconventional@ herds.
Haemophilus parasuis. Also, generally it is not considered a disease
that can be eliminated from high health status herds. Weaning by 10
days of age has been successful in a few cases in elimination of this
organism in SEW pigs. One study indicated that to "reliably"
eliminate this organism, one has to vaccinate the sow and maintain the
pigs on one or more antibiotics. Again, however, it has been very
difficult if not impossible to eliminate this organism. When disease
breaks occur in highly susceptible populations, the economic loss can
be high.
Influenza virus. Good success following a vaccination program in the
sows. However, this disease remains a problem in many swine units in
part because it can apparently get back into such units fairly easily.
PRRS. Current thinking is that PRRS can be eliminated by SEW if the
sow herd is not undergoing an active infection in the period between
the last trimester and weaning. This is difficult or impossible in
large herds. Pigs were weaned at 10, 15, and 20 days in one study and
all remained serologically negative. Keeping the herd negative is a
problem. More recent work indicates that the virus can be kept out of
pigs with strict sanitation measures and a relatively minor barrier
between infected and non-infected groups.
PORCINE REPRODUCTIVE AND RESPIRATORY SYNDROME VIRUS (PRRS)
General Description
The disease caused by this virus was first described in the U.S.
in 1987. It subsequently spread very rapidly and by the early
1990's had become a major problem in swine. Initial descriptions
dealt mainly with the reproductive system problems but currently
the disease most often affects the respiratory system of nursery
age pigs. In addition, other disease problems are often
exacerbated by the presence of this virus.
Etiology
Arterivirus. There are two major variants, the European or
Lelystad strains and the American strains. There is a large
amount of genetic variation within the two major variants so that
there is a lot of antigenic variation and variation in virulence.
In addition, this has possibly given rise to differences in
published research results.
Epidemiology and Transmission
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Virus is carried in the lymphoid tissues and is present in the
oropharynx, milk, feces, semen, urine and other tissues. Once
excreted, the virus is not particularly resistant and will die
out within a day unless present in a moist environment. It has
been recovered for up to 11 days in water. It is readily
inactivated by disinfectants.
Persistence in the host is a major factor in epidemiology and
transmission. The virus has been recovered from sows for 157
days following infection and is present probably equally as long
in boars. Virus has been recovered from pigs infected in-utero
for up to 210 days following farrowing. However, it is essential
to note that the virus may not be shed from these animals in the
later stages of recovery. The virus may be shed for several days
or weeks during the active infection stage, but it may also be
shed only intermittently during this time. The disease may
transmit rapidly through a group of pigs or progress slowly. Up
to a 37-day lag time has been reported between introduction of
the virus and development of clinical disease. Herds may remain
infected as long as new susceptible pigs are constantly being
introduced to infected animals. It is believed that the virus
remains in the herd at least 6 months following cessation of
clinical signs. This is probably quite variable and may be
dependent on the size of the swine unit in question.
The major mode of transmission is via direct contact from pig to
pig. About 60% of outbreaks can be traced to introduction of
infected pigs. Fomites account for about 25% of the outbreaks.
In-utero transmission accounts for most of the remainder.
Airborne: Conflicting evidence. Orginally thought to transmit
long distances, then airborne was not considered to be a likely
route. More recent work indicated that airborne transmission can
be important in farm to farm transmission. Research at ISU
indicated that a one meter air space between groups was a
sufficient barrier to prevent transmission if fomite transmission
was eliminated. A solid wall works better. Can have positive and
negative pens within the same building however, it is best not to
rely on this.
Semen from boars with an acute infection contains enough virus to
transmit the disease. It has been difficult to transmit the virus
by AI but this remains a possibility. Long-term shedding in the
semen has not been demonstrated, but also remains a possibility.
Clinical signs
Pigs:
Interstitial pneumonia with a "thumping" type of
respiration.
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Mouth breathing, nasal discharge, sneezing
Listlessness, lateral recumbency, CNS-signs, paddling
Vomiting
Pre-weaning mortality may be 50% to 60% especially in
weakborn pigs that can die of starvation and crushing
Secondary infections are common with Streptococcus suis,
respiratory and enteric pathogens.
In chronically infected herds, the clinical disease often
occurs 10-14 days following weaning.
Recent studies link PRRSV to mild diarrhea in 1 to 7-day-old
pigs but the causal realtionship has not been firmly
established.
Sows:
Breeding pigs have a transient fever (104-106F), anorexia,
and listlessness that may last 4-7 days. If this occurs
during nursing, agalactia or hypogalactia may occur.
Reproductive failure:
Live-born pigs are often small and weak.
Premature farrowing (5-7days)
Increases in late-term abortions
Stillbirths (50-70%) with fetuses that are often
autolysed and edematous and have a tan-brown skin
color.
Mummies occasionally seen (these are late term
"mummies" and some people do not think they are true
mummies.
During recovery there is an poor conception rate (50%)
and slow return to heat.
Long term effects: In some herds the litter size
remains below pre-infection levels.
Diagnosis: Many different tests are available.
Serotesting: Many tests are available.
IFA was used extensively and is still available in many
diagnostic laboratories. Anti-PRRS IgM and IgG titers can be
determined in some labs. These can sometimes be used to
determine the stage of infection. If these two tests are
1:64 or higher and the serum virus neutralization (SVN) test
is negative, it generally means that the animal is
undergoing an active infection. If the SVN test is positive,
it indicates that the animal is recovering and may not be
shedding the virus.
ELISA is usually the standard test performed for detecting
the presence of the virus in a herd. It is able to detect
antibody against both the American and European strains of
the virus and has the advantage of being easily automated
and is more standardized. It is not able to differentiate
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between infection and vaccine titers.
Immunohistochemistry is performed by some labs but was initially
said to have a high rate of false negatives. More recent work
has indicated that it can be a valuable test for identifying
infected animals within a herd.
RT-PCR: Performed on boar semen and feces to detect viral RNA.
It has recently been developed for use with tissues and seems to
be very sensitive in identifying the virus.
Virus isolation: Pooled serum samples can be tested to lower the
cost. Virus can be recovered from live-born and some stillborn
pigs but not from Amummies@.
Histopath: Useful but may be complicated by secondary infections
in the respiratory form.
Control-Eradication
Depop-repop with PRRSV-negative swine is a possibility. Needs to
be done carefully and there is always a chance that the virus can
re-enter the herd.
Development/Isolation/Acclimatization: As long as PRRSV is
cycling through a breeding swine herd it would be relatively
difficult to eliminate the virus from the operation. An
essential step therefore is to make sure that none of the
breeding swine have Aactive@ infections. All replacement gilts
and sows need to be infected with the virus prior to entering the
breeding herd and be allowed to recover. If this is done, then
SEW is more likely to succeed in elimination of the virus. One
possible procedure is to obtain serum from infected animals, have
a lab determine the virus titer in the serum and use this serum
to infect (IM or orally) naïve replacement gilts.
SEW: May work if there is no active infection cycling through
the sow herd and pigs are removed to an all-in all-out facility.
Several instances of the virus spontaneously disappearing from a
farm have occurred. Elimination of the virus using SEW has been
most successful in herds with 300 or fewer sows. Gilts can then
be saved and used as replacements. Extensive serologic testing
should be done to determine that all swine in a group are
negative for PRRSV prior to introduction to the breeding herd.
Seedstock and multipliers: Need to be free of the virus so that
it is not transmitted to uninfected herds.
Semen: Transmission has occurred even when the virus could not
be detected in the semen. Boar studs should be free of the
virus.
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McRebel: Management Changes to Reduce Exposure to Bacteria to
Eliminate Losses. This is an 11 point program that was
originally designed to limit bacterial diseases but which also
helps to lessen the impact of PRRS during an acute outbreak. The
main points of McRebel are summarized as:
1.
8.
10.
11.
Cross-foster piglets only during the first 24 hr. of
life and only within the same farrowing unit.
Immediately euthanize very sick pigs.
Stop all feed-back programs of stillborn or aborted
fetuses.**
Establish AIAO nursery flow.
** Feedback programs involve the feeding of either feces of clinically
affected animals or dead fetuses or little pigs. These are sometimes
used to expose gilts and sows to the infectious agents in a herd so as
to prevent problems later (for example, stillbirths caused by
parvovirus) or boost colostral immunity for preventing disease in
offspring.
Prevention
Buy from reputable sources
Good biosecurity is essential
Vaccination. "Modified"live (B.I.-NOBL and Schering-Plough.
Vaccination should be limited to infected herds, especially with
the modified live. May inhibit eradication by complicating
testing. Also may not be completely protective. A killed
vaccine is available from Bayer and autogenous vaccines are
produced by a subsidiary of Bayer. SAMS (sow abortion mortality
syndrome) has been a problem in some vaccinated herds that
received the first MLV on the market. This is currently
considered to have been a severe form of PRRSV but SAMS has not
been a problem recently.
In infected herds, new breeding animals can be exposed to
infected animals prior to breeding. Fence to fence contact isn't
usually fast enough and you probably need to mix infected,
shedding animals with the group. Probably the best procedure is
to perform tonsil scrapings of shedding animals and administer
this material orally to all animals coming into the breeding
herd. Otherwise there are likely to be animals that do not
become infected until later and act as a source of the virus for
young pigs.
PORCINE CIRCOVIRUS-ASSOCIATED DISEASE [POST-WEANING MULTISYSTEMIC
WASTING SYNDROME (PMWS)]
Etiology
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PMWS was first described in Canada in 1991. In 1995, a
circovirus was isolated and implicated as the cause of the
syndrome. This was subsequently named a Type II circovirus (PCV2)
to distinguish it from circovirus that had been isolated
previously but not associated with disease (PCV1). Typical PMWS
has been reproduced with pure circovirus in CDCD pigs at ISU.
Another report from Ohio State indicates that minor lesions were
produced with pure circovirus infection but full-blown disease
occurred when pigs were co-infected with parvovirus. Since
circovirus seems to be so widespread in the pig population, it
appears that there needs to be some inciting cause to set off
relatively widespread viral replication in the pig. Some
adjuvants were implicated as inciting causes of PMWS,
particularly some of the adjuvants used with Mycoplasma
hyopneumoniae vaccines.
It should be emphasized that PCV2 infection doesn=t necessarily
cause PMWS. A study of sera from 28 high-health status sow herds
indicated that all the herds had antibody to PCV2 but none of
these particular herds had PMWS.
Epidemiology
PMWS most often affects pigs between 4 and 16 weeks of age and
seems to be more common in pigs around the late nursery to early
grower-finisher stage. Large quantities of virus are excreted in
the feces, urine, and nasal secretions from pigs in the acute
stages of the infection. Infected pigs have high numbers of
circovirus in their tissues. Not all of the pigs in a pen will be
affected at the same time and in most infected herds there is
only a 5-15% morbidity. However, some herds have significantly
higher morbidity rates. The disease progresses randomly through a
hog facility for a three to five week period before resolving.
Clinical signs
Initially, many pigs develop a high fever are listless and seek a
cool area of the pen. Pigs may be dyspneic, have a light cough,
and there may be diarrhea in some cases. Often the lymph nodes
are sufficiently enlarged to be palpapated on physical exam. A
small percentage of animals look pale or yellow due to jaundice
(bilirubin levels are quite high in these pigs). Pigs develop a
rough hair coat and become emaciated. Many of the affected pigs
die but it may take several weeks for them to do so. Pigs that
recover are often 50 to 100 pounds lighter than the non-affected
pigs in the same group.
Postmortem findings
Gross lesions: Enlarged inguinal, mesenteric, bronchial, and
mediastinal lymph nodes are generally observed. These have a
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white, homogeneous appearance on cut surface. Lungs are often
firm, noncollapsed, rubbery and mottled with gray nodules. The
lungs may have a patchy interstitial pneumonia that is more
characteristic of PRRSV infection. The liver may be diffusely
atrophied and mottled with yellow-orange areas. Kidneys may have
no lesions or may be grossly enlarged, waxy and contain diffuse
white foci.
Histopathology: Lymph nodes may have a loss of B-cell follicles,
infiltration of T-cell areas by histiocytic cells, and
vasculitis. Suggestive lesions also occur in the liver and
kidneys.
Culture: Culture often reveals secondary bacterial infections
with Pasteurella multocida, Actinobacillus pleuropneumoniae or
Haemophilus parasuis in animals that die.
Diagnosis
Immunohistochemistry is the standard test used in the ISU
Diagnostic Lab. It has the advantage of allowing one to
visualize virus antigen in characteristic lesions.
In-situ hybridization is used as a back-up for the IHC when
results are equivocal.
Virus isolation is relatively slow and not as sensitive
Lesions: Helpful but similar lesions can be produced by PRRSV,
salmonellosis and others.
Treatment
Good supportive care.
Otherwise none.
Prevention
Vaccination: Early indications are that the available vaccines
are highly efficacious but as of 2007, they are still in short
supply.
Good management practices such as all-in/all-out pig flow and
provision of good sanitation, air quality, and nutrition are
helpful.
Isolate PMWS-suspect pigs from the rest of the group.
Minimize cross-fostering of piglets (McRebel?). This would
decrease the chances of transmission if the disease needs to be
transmitted early in life.
Allow replacement gilts time to generate immunity to the diseases
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in a given herd.
SWINE RESPIRATORY DISEASES
As with most of the respiratory disease associated with domestic
livestock, the etiology of swine respiratory diseases is often
multifactorial. Good management practices, adequate ventilation and
good building design, prevention of crowding and stress, and
prevention of the introduction of new pathogens are extremely
important in controlling respiratory disease. Where disease does
occur, more than one pathogen may be involved.
Mycoplasmal Pneumonia
(Enzootic Pneumonia)
General description
Mycoplasma hyopneumoniae causes a chronic pneumonia characterized
by a persistent, nonproductive cough, loss of condition and
growth retardation. It is thought to be a major factor in the
development of respiratory disease in swine and its control is
key to overall respiratory disease control.
Etiology
M. hyopneumoniae is the etiologic agent but many bacterial and
viral agents usually contribute to the production of disease and
vice-versa. If these secondary (or primary) invaders are
controlled, clinical disease can be markedly decreased. A poor
environment with excessive pit gases and heavy microbial air
loads also contribute to disease.
Epidemiology and transmission
The organism is found worldwide in almost all swine herds and 30
to 80% of market-weight pigs have pneumonic lesions consistent
with infection. It is estimated that 10-20% of sows are chronic
carriers. Transmission is assumed to be primarily by droplet and
contact although movement into clean units by airborne infection
from other units is suspected. Most young pigs probably do not
become infected prior to 5 to 6 weeks of age and may not show
clinical disease until much later. Spread of disease through a
unit is generally slow. The incubation period is 10 days to 3
weeks although it can be much longer in some cases. With
boostering of colostral immunity (sow vaccination) clinical
disease may be delayed.
Clinical Signs
Clinical disease is seen mainly after 5-7 weeks of age and
persists 6 weeks or longer. There may be bouts of recrudescence
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in pigs up to market weight. Pigs have a dry, nonproductive
cough, unthrifty appearance, fever (if secondary invaders are
involved), and normal appetites. There is generally a high
morbidity. Mortality depends upon complicating factors but is
usually low to moderate. In well-managed herds the disease may
be clinically silent.
Infected pigs may have up to a 30% decrease in rate of gain and a
20% decrease in feed conversion.
Lesions
Purple to tan or gray areas of consolidation primarily in the
cranioventral portions of the lungs. These portions of the lungs
are atelectatic and appear smaller in size than surrounding lung.
The bronchi and bronchioles often have some catarrhal exudate and
bronchial lymph nodes may be swollen and edematous.
Microscopically there are collections of lymphocytes around the
airways and blood vessels and extensive destruction of tracheal
cilia. Uncomplicated lesions may resolve within 6 weeks, but may
be present 3 months after onset.
Secondary invaders are common and many lesions reflect this mixed
infection.
Diagnosis
Clinical signs:
Chronic coughing with loss of condition.
Lesions:
Gross and histologic
FA test:
Demonstrate the M. hyopneumoniae lining the airways.
Culture:
Not routine since isolation of M. hyopneumoniae is
tedious and not generally available.
Prevention
Management
All in-All out reduces the severity and seems to be the most
important factor in recent studies. Improvement of air
quality and decreased crowding are key control measures.
Vaccination of sows or gilts in combination with AIAO seemed
to give the best results. Gilts generally have higher
antibody titers in their colostrum than sows (possibly due
to more recent exposure) and vaccination for gilts may not
be needed. When combined with SEW or MEW and maintenance of
good air quality, mycoplasmal pneumonia often becomes
economically non-significant. SEW, MEW and AIAO have been
combined to Aeradicate@ the disease from some farms.
Control measures can also markedly reduce it's impact by
201
limiting secondary invaders.
Vaccination
Sixty to 80% control in some controlled studies. Mixed
reviews from practitioners but the vaccines are generally
considered to be effective. Some regard vaccination against
this organism as a cornerstone of their respiratory disease
control program and don=t believe they can do without it. It
is currently the most commonly administered vaccine in pigs.
Antibiotics
Tetracyclines suppress development of disease if started at
time of exposure. Other antibiotics can be beneficial if
Treatment
Quinolones are effective but not approved for use in the
U.S. Several others are used such as Lincomycin, Tylocin
and Tiamulin but have not been proven to have any effect on
the M. hyopneumoniae itself. These may be more effective
against some of the secondary invaders and therefore be of
value in treating the clinical disease.
SWINE INFLUENZA
Etiology
Type A influenza virus is similar to influenza A virus of humans.
About 25% of midwestern US swine have antibodies to the classical
strain (H1N1). Some studies indicate up to an 80% incidence of
serologically positive swine. Recombination of virus strains in mixed
infections is thought to play a role in the generation of new virus
types but this has not occurred in swine to the extent as that of
human influenza virus. The H3N2 virus had been a problem in Europe and
Asia but until 1998 there were no outbreaks associated with this
serotype in the U.S. Since the fall of 1998, a number of outbreaks
have occurred in the U.S. and it recent figures indicate that it is
the strain involved in a marked resurgence in clinical swine
influenza. Older surveys indicated that thirty-five percent of U.S.
swine have antibody to this virus, but it had not been seen as a
clinical problem here. Apparently, there are other genetic
differences that contribute to virulence. In addition, the H1N1 and
H3N2 viruses have undergone recombination and we now have H1N2 strains
showing up. Some H1N7 virus has also been detected. There has been
considerable antigenic drift in the swine influenza viruses.
Epidemiology
The first outbreaks reported in the US coincided with the human
pandemic of 1918. Since then influenza viruses have been
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suspected to move between avian species (turkeys harbor a similar
virus), pigs, humans, and others. The major source of the virus
for pigs is other pigs. Large numbers of viral particles are
shed in the nasal mucus of acutely infected pigs. It rapidly
moves through a group and will spread progressively through a
large facility. Apparently, some pigs in a group may shed the
virus for longer periods of time and may be responsible for
transmission to new facilities when these pigs are sold. There
is also some evidence that the virus can be wind-blown and move
to other sites.
Disease
Classically occurs in autumn or winter and is often associated
with inclement weather. Interestingly there is another peak (much
lower in severity) around May. It can infect swine of all ages.
There is a sudden onset of anorexia, depression, muscular pain,
fever, dyspnea with "thumpy or jerky" respiration, cough,
conjunctival discharge. Pigs may be very reluctant to move and
frequently will not eat. Morbidity is usually high but mortality
is usually low in uncomplicated disease. Other pathogens such as
PRRSV, Erysipelothrix, etc., that may be endemic in the herd may
become clinically apparent. Uncomplicated recovery is very rapid
and occurs at about 6 days.
May see disease in several farms in a given area at the same
time. Carrier pigs are the most likely source for some of these
outbreaks but can=t explain the majority.
"Chronic" disease is less common. Infection of pregnant sows
results in higher neonatal mortality, smaller litters with slower
growth rates. Recent anecdotal information that the virus is a
cause of abortion may not be true in the sense that the organism
has not been found in the fetus except for one case on record.
Sows that have a high fever and other problems associated with
influenza infection may abort, but it is not thought to be due to
the effects of the virus on the fetus. However, the virus may not
survive long enough in the fetus to be recovered. With the
recent H3N2 outbreak, 2-4% abortions and sow deaths of 1-4% per
week per group have been reported.
There has been an overall increase in the incidence and
importance of swine influenza in the past several years possibly
due to the effects of the PRRS virus and Mycoplasma hyopneumoniae
and definitely related to the new H3N2 strain.
Diagnosis
Clinical:
FA test:
Unique disease when a full blown outbreak occurs
Rapid and reliable.
203
Immunohistochemistry is available in VDL
Virus isolation: Inoculation of material from nasal swabs or
acutely affected lung tissue into embryonated eggs.
Hemagglutination inhibition (HI) test: Test for antibodies in
paired sera. Acute stage vs 3-4 weeks later.
Lesions: Very helpful.
bronchitis.
Necrotizing bronchiolitis and
Treatment
Supportive, antibiotics for complicated disease, expectorants,
etc.
Control and prevention
Vaccine is available commercially for both H1N1 and H3N2 virus.
They reduce clinical severity but are not completely protective.
A suggested vaccination program could include the following:
Vaccinate all sows and boars in the herd in the summer
(priming dose).
Re-vaccinate all sows 3 weeks pre-farrowing to booster
immunity. Boars should be booster vaccinated at this time as
well
Replacement gilts and boars should receive two vaccinations
3 weeks apart during the isolation/acclimatization period
and then be boostered as above.
If necessary to break the disease cycle, depopulate the
nursery after the sow herd has been stabilized by
vaccination or infection.
Vaccinate finishing pigs during late fall in high risk
situations but this is frequently not warranted on farms
with relatively low risk.
Good sanitation, prevent mixing of livestock. All-in all-out by
site is necessary to break the cycle of infection. AIAO by room
or building is not sufficient.
The possibility of the introduction of type A virus from humans,
turkeys, etc., should be considered but these appear to be minor
sources at the present time.
PASTEURELLOSIS
Etiology
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Pasteurella multocida is considered to be a common and important
secondary invader in pneumonias in swine. Initial damage to the
pulmonary defenses is caused by Mycoplasma sp., other bacterial
agents and viruses.
Type A serotype 3 (A3) P. multocida is the most common serotype
reported from pneumonic lesions, however, other serotypes are
reported.
Epidemiology
P. multocida is frequently found in the upper respiratory tract
of normal swine. It is transmitted shortly after birth to young
pigs. Type A3 organisms can be isolated from other species of
animals and these animals may serve as a source of infection for
swine.
Disease
Lesions are typically those of a purulent bronchopneumonia and
are often superimposed on the lesions of the primary disease
agent such as a mycoplasma.
In field cases, lung abscesses due
to Arcanobacterium pyogenes, Streptococcus, spp. or Haemophilus
spp. are not uncommon.
Diagnosis
Bacteriologic culture
Prevention
Control other diseases: In addition to mycoplasmal diseases,
atrophic rhinitis, influenza, inclusion body rhinitis, ascarid
larvae migration, and lungworms may serve to help initiate
disease.
Management
Treatment
Early treatment with antibiotics may be beneficial. The organism
is usually quite susceptible to antibiotics in vitro but an
antimicrobial susceptibility test is recommended because
resistant isolates are common.
Naxcel 2-3 mg/kg
Tiamulin
Tetracycline 200-400 g/ton
Tilmicosin in feed (Do not give Tilmicosin parenterally to swine
- very low margin of safety - kills pigs).
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Actinobacillus pleuropneumoniae
A. pleuropneumoniae causes acute pleuropneumonia in pigs characterized
by fever, respiratory distress and a high rate of mortality in some
outbreaks.
Etiology
A. pleuropneumoniae has 12 different capsular serotypes.
Serotypes 1, 3, 4, 5, 7, 9 and 10 are present in the U.S.
Serotypes 1, 5 and 7 are the most commonly seen. There is some
serological crossreactivity between serotypes 3, 6 and 8; 4 and
7; 1 and 9. The crossreactivity is between the LPS antigens. A.
pleuropneumoniae can be typed based on capsule, LPS and ApX
toxins.
biotype 1:
requires NAD (V Factor).
biotype 2:
Same as biotype 1 but does not require NAD.
The organism is capable of producing severe disease without the
interaction of other agents. However, P. multocida, M.
hyopneumoniae and other respiratory disease agents may influence
the severity of disease.
Epidemiology and Transmission
A. pleuropneumoniae resides in the tonsils of chronic carrier
pigs and is probably spread by droplet and contact. The organism
does not survive long outside of the host. Sows may transmit the
organism to their piglets but colostral immunity usually protects
against clinical disease in suckling pigs. In a susceptible
herd, the organism may spread subclinically until stress factors
occur which cause expression of overt disease. Overt disease
usually occurs in feeder pigs and growing and finishing pigs.
Clinical signs
The disease seen in herds where the organism has been present
for some time is usually less severe than when a completely naive
herd becomes infected. Morbidity can vary from 8 to 40% with
mortality up to 25%.
In peracute disease, pigs develop a 104 to 106F temperature,
suddenly become apathetic, anorexic, may vomit, develop severe
dyspnea with a blood-stained frothy discharge from the nose and
mouth, have a moist suppressed cough, cyanosis of the skin and
mucous membranes, and die acutely.
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An acute form is also seen where pigs may die or develop chronic
disease.
In chronic disease, pigs may have a chronic cough, reduced
appetite and a retarded growth rate. Milder cases may be hard to
recognize.
Arthritis, abortion and septicemia with CNS signs may
occasionally be observed.
Pathogenesis
The organism initially proliferates in the upper respiratory
tract but quickly spreads widely in the lung to produce a diffuse
fibrinous pleuropneumonia. There is edema, hemorrhage, and a
neutrophilic exudate with foci of coagulative necrosis. The
lesions are raised with an irregular surface and are dark red,
firm and swollen. In the chronic stages, pulmonary abscesses and
adhesions develop. Pleuritis is very common and pericarditis,
although rare, is sometimes seen. There are three RTX class
toxins produced by this organism that are apparently major
factors in the production of disease. The leukotoxin (ApX1)
causes the neutrophils to lyse and release their lysosomal
enzymes onto the pulmonary tissues helping to give rise to the
acute nature of the disease. The ApX toxins are also directly
toxic to pulmonary tissue.
Diagnosis
Differentials are Streptococcus suis, Pasteurella multocida, and
Salmonella choleraesuis.
Clinical.
Sudden deaths of fattening pigs with pneumonia.
Lesions of patchy areas of consolidated lung - raised,
distributed randomly over lung.
Bacterial culture from lesions. Use media containing NAD or
staphylococcus "nurse" culture. The organisms die quickly in
tissues and in transport. If P. multocida is present in tissues
one may need to dilute the inoculum to isolate A.
pleuropneumoniae.
Determine serotype in order to enhance chances for successful
vaccination.
Serologic tests. High percentage of pigs acquire antibody via
colostrum which persists 5-12 weeks, depending on sensitivity of
assay.
CF antibodies detectable 10 days after infection, persist
several months.
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ELISA's based on LPS or capsule are used as a good screening
test then followed with the CF test.
Treatment
Base treatment on antimicrobial susceptibility testing when
possible and treat all the pigs in a pen when extensive losses
are occurring. Commonly used antimicrobials are:
Penicillin at high dosage rates, sulfonamides, 400-500g/ton
tetracycline in feed, LA 200, Tiamulin in water and Naxel.
Control
All-in all-out production, SEW or MEW, minimize stress, improve
ventilation.
CF or ELISA to detect adult carriers.
Cull seropositive adults.
Vaccination: Autogenous and commercial vaccines are used with
mixed reports on efficacy. The presence of ApX toxin(or
toxoid)is needed for good protection but unfortunately, none of
the currrent vaccines has enough ApX to induce a titer. The
organism produces very little toxin under conditions used in
vaccine production. Need to include the common serotypes
occurring in an area. To be most effective, the vaccines need to
be in an oil-based adjuvant that may cause a high incidence of
abscesses.
A modified live vaccine has been marketed since about 1998. The
parent organism was a serotype 5 that lost the ability to produce
a capsule but which retained production of ApX1 and ApX2 toxins.
Current information from the manufacturer (B.I. Vetmedica)
indicates good efficacy especially against serotype 5 but other
serotypes as well, however some breaks in protection against
serotype 1 strains. A major problem apparently exists with
adverse reactions. In some groups of pigs, there is an immediate
adverse reaction, 10 to 30% of pigs may vomit, shudder/shake,
100% may be lethargic. The reaction disappears within a couple of
hours. This seems to be peculiar to some groups of pigs while
others may have no problems. The reaction is apparently due to
endotoxin in the vaccine strain and not due to strain virulence
or the presence of the RTX toxins. The reactions are seen with
the first dose only and are found in both infected and noninfected herds. The vaccine is not commonly used currently.
Haemophilus parasuis
Haemophilus parasuis causes septicemia and acute polyserositis,
arthritis and meningitis in young swine (Glasser's disease).
Infection of the nasal and tracheobronchial mucosa is common in young
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pigs. Infections in high health status swine units are difficult to
control and can cause significant economic losses.
Epidemiology
Haemophilus parasuis is found worldwide in swine populations. It
is carried in the upper respiratory tracts of sows although the
percentage is not known. It is readily transmitted by contact
and droplet to young pigs by 2 to 5 weeks of age and spreads
laterally through a group of pigs. Over 70% of pigs in
conventional and continuous thru-put operations are infected. In
SEW operations it is thought that many pigs do not become
infected until after being mixed with carrier pigs the same age.
SPF swine are also highly susceptible.
Stresses associated with transport, mixing, fighting, weaning and
diet changes are important factors in the onset of disease.
Viral infections such as swine influenza markedly increase the
severity of clinical disease.
Clinical disease
Glasser's disease is a polyserositis and septicemia. The
clinical appearance of the disease depends on the tissues
affected. There is usually an incubation period of 12 to 72
hours followed by a sudden onset of fever (106 to 107F). There
may be abdominal distention or tenderness, labored breathing,
coughing, lameness, orchitis, and CNS signs.
Lesions are found on any serosal surface and include peritonitis,
pleuritis, pericarditis, meningitis, arthritis, orchitis.
Hemorrhages may be found in the liver, spleen and kidneys due to
the septicemia.
The organism is extremely common in pneumonias of baby pigs and
somewhat less frequent in pneumonias of older pigs.
Diagnosis
Clinical signs. A history of acute onset following some type of
stress and the typical signs of polyserositis.
Culture. H. parasuis is readily recovered from fresh tissues
using blood agar with a staphylococcal nurse colony or media
containing NAD.
Postmortem lesions
Rule-outs
Streptococcal infection
Erysipelas
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Mycoplasma hyorhinis polyserositis and arthritis
Prevention
Minimize stress: Optimize environment and management.
Commercial bacterins are available and autogenous bacterins may
be used. Some evidence that protection is mainly type specific
but there is a lack of research information on this organism.
Expose new swine by fence contact 2-3 weeks prior to commingling
with conventional stock.
Experimental: Infecting all pigs at 5 days of age with the
strains present in the herd has been done experimentally and has
resulted in a marked decrease in incidence of disease.
Treatment
Penicillin, ampicillin, tetracyclines, sulfathiazole or
potentiated sulfonamides, where approved.
STREPTOCOCCAL DISEASES
S. equisimilis, Lancefield's group L streptococci and occasionally
other streptococci can be responsible for septicemia, arthritis,
endocarditis, and other sporadic conditions in swine.
Epidemiology
S. equisimilis, and the other organisms involved are common in
the URT, oral cavity, vaginal secretions and milk of normal
swine. They are spread to young piglets from the sow via wounds,
the umbilicus, and tonsils. Contamination of instruments for
clipping needle teeth and tail docking can result in large
numbers of pigs being infected.
Disease
Most common in piglets 1 to 3 weeks of age. One sees joint
swelling and lameness most commonly. Elevated temperatures and
unthriftiness may be observed.
Endocarditis may occur in older pigs. The pigs are usually more
severely ill, depressed, show pain on handling, and redness and
cyanosis of extremities.
Diagnosis
Bacteriologic culture: Joints may have low numbers of organisms
in advanced disease. Organisms grow readily from the vegetative
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lesions in the heart.
Control
Since the organism is widespread, good management is essential.
Disinfect equipment used for clipping needle teeth and tail
docking
Adequate colostrum
Reduced abrasiveness of flooring
Navel dipping
Vaccination of sows may be beneficial in problem herds.
Autogenous and commercial bacterins have been used and have
resulted in a reduction of infections.
Treatment
Penicillin has worked well in the past, but resistance has been
reported. Tetracyclines.
Streptococcus suis
Common cause of septicemia, meningitis, arthritis and bronchopneumonia
in pigs.
Potential human pathogen.
Etiology
About 35 serotypes of S. suis have been recognized. The
organisms are all in Lancefield's group D. Type 1 is endemic in
most herds but only sporadically affects pigs. The majority of
disease is caused by type 2. The common serotypes are 2, 3, 4,
and 7.
Disease: Three clinical forms in young pigs.
combined, but all three can be seen together.
The first two are often
Neonatal septicemia: Seen in young pigs in the absence of
colostral immunity. Pigs die in 24 h.
Suppurative meningitis: Pigs 10 days to 4 months of age. One
theory on the appearance of meningitis is that there has to be
some other agent such as Bordetella bronchiseptica present to
cause irritation of the nasal mucosa before the organism can
cause meningitis.
Bronchopneumonia:
In all ages but much more common in pigs 6 to
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12 weeks of age; more severe in young pigs. There is currently
some controversy over whether this agent is the cause of
bronchopneumonia. It has been reported that pure infections with
this agent in pigs do not cause a bronchopneumonia, however, the
bronchopneumonia is frequently present and probably requires some
type of inducing agent such as swine influenza virus.
S. suis can also cause endocarditis, arthritis, vaginitis, and
abortions in sows but the incidence is low.
Transmission
Large, intensive swine rearing operations are more commonly
affected by type 2 S. suis. Recent work indicates that the
organism can be transmitted from the sow to her piglets as they
pass through the birth canal. The organism is transmitted
between herds by carrier pigs and possibly by flies and fomites.
The organism survives long periods in feces, dust, and dead
carcasses.
Diagnosis
Bacterial culture.
Lancefield typing.
Differential Diagnosis
Pseudorabies, Haemophilus parasuis, and Streptococcus
equisimilis.
Prevention and control
Good management to minimize stress from overcrowding, poor
ventilation and mixing and moving of pigs. Temperature stress
has been identified as a major factor by some. The suggestion is
that a goal of 2 degrees fluctuation in temperature be
established. Mixing of pigs with greater than 2 weeks age
difference in the nursery is discouraged. Use all in/all out
methods with good disinfection between groups.
Treat clinically affected pigs: Penicillin or ampicillin (about
5% are resistant to penicillin).
Depopulation/repopulation with SPF or medicated early weaning
pigs has been tried but all have ultimately failed. Essentially
all herds have Streptococcus suis.
Vaccination
Commercial bacterins are available for types 1, 1.5, and 2.
Killed bacterins and autogenous bacterins for sows to boost
colostral immunity have relatively low efficacy. They have
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reduced the mortality in the piglets in some cases from about 6%
to around 2% but are generally not considered to be of
significant value. Vaccination of the piglets at weaning and 2
weeks later has given highly variable results. Vaccination seems
to be even less efficacious in PRRSV-infected herds. Recent
studies indicate that experimental modified live vaccines have
not been successful either.
Atrophic Rhinitis
Progressive Atrophic Rhinitis is a chronic disease of swine
characterized by rhinitis, atrophy of the nasal turbinates, deviation
of the nasal septum, malformation of facial bones and growth
retardation. Type D organisms have been eliminated from many high
health status swine herds but are still a problem in some continuous
thru-put facilities. Prior to the use of SEW, etc., most surveys
revealed at least 50-% of slaughter pigs had lesions.
Etiology
The main etiologic agents are Pasteurella multocida (toxigenic
capsular type D or A) and/or Bordetella bronchiseptica. Poor air
quality and noxious gases, certain other bacterial agents such as
Haemophilus parasuis, Pseudomonas aeruginosa and Fusobacterium
necrophorum, and probably some viral agents play major
contributing roles in the development of disease.
Infection
with Bordetella bronchiseptica alone may cause a non-progressive
type of disease that is considered to be much less severe.
Epidemiology
Toxigenic Pasteurella multocida and Bordetella bronchiseptica are
found worldwide in swine. Both are carried in the upper
respiratory tract. The numbers of organisms are usually much
higher in acutely affected pigs than in carrier swine.
Transmission from infected sows to piglets occurs very early in
life. Pigs that are not infected shortly after birth are readily
infected by lateral transmission. Transmission is by contact and
airborne droplets. Air in infected farrowing units may contain
several hundred toxigenic P. multocida per cubic meter.
B. bronchiseptica can be carried by other animals including rats,
rabbits, cats and dogs but these normally are not the source of
the organism for pigs.
Clinical Signs
In early or mild disease there will be sneezing and
snuffling during quiet periods that may be exacerbated when
pigs are stirred up. There is a serous nasal discharge,
excessive lacrimation and a roughened hair coat. The pigs
may cough if the trachea and bronchi are colonized (often
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with secondary invaders and pneumonia may develop. As the
disease becomes chronic in the progressive form, there is a
shortening and deviation of the snout, folding/wrinkling of
skin over snout, malapposition of teeth, epistaxis,
sneezing, pneumonia, and decreased growth rate. The degree
of these changes depends on the severity of the disease. As
far as the effect on growth rate, some investigators found
no reduction, others found 2 to 12% reductions in daily
gain. When combined with other diseases, the impact of
atrophic rhinitis could be even more significant.
Pathogenesis
Initial infection with B. bronchiseptica causes an acute
inflammation of the nasal mucosa. H. parasuis, ammonia or other
pit gases may play a role in the initial damage. The B.
bronchiseptica causes squamous metaplasia of the epithelium, loss
of cilia and inflammation of epithelium and submucosa resulting
in impairment of mucociliary clearance.
Infection with toxigenic P. multocida causes the majority of the
chronic alterations. The toxin is thought to activate mature
bone cells to release cytokines such as IL-6 that enhance bone
resorption while impairing new bone formation. The P. multocida
toxin has systemic effects among which are hepatotoxicity.
Experimentally, the toxin reduced weight gain in pigs and may be
largely responsible for the decreased growth rate that occurs.
The P. multocida toxin may also predispose to other disease, such
as sublethal pseudorabies virus infection. Depending upon the
agents involved in the disease, there may be severe alteration in
structure of turbinate, premaxillary, frontal, etc. bones. The
most severe atrophy may be seen in pigs slaughtered during the
summer months
Diagnosis
Clinical signs are characteristic.
Culture: Following the acute phase, toxigenic P. multocida may
not be detectable by culture from nasal tissues, however, it may
be present in the tonsils. Just finding P. multocida is not
generally sufficient for diagnosis since non-toxigenic strains
are often present. Toxigenic strains can be identified using a
Western immunoblot and this is the procedure that is employed at
NVSL and on a research basis at ISU. An ELISA kit for detection
of toxigenic strains has been used in Europe but is not licensed
for use in the U.S. According to the ISU Diagnostic Laboratory,
there are very few requests for testing.
Slaughter checks:
If a slaughter plant will cooperate you might be able to use
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slaughter checks to evaluate the status of atrophic rhinitis in a
herd. Use a bandsaw to cross section the snout just anterior to
second upper premolar teeth or at first premolar teeth. Changes
to look for: The inferior scroll of ventral turbinate is most
often and most severely affected. The ethmoid and dorsal
turbinates may also be involved. There may be a catarrhal
exudate on the nasal mucosa and the mucosa itself is often pale.
There is hypoplasia of the turbinates to a variable extent,
deviation of the median septum and malformation of the of the
maxillary, premaxillary and frontal bone. More frequently, the
importance of atrophic rhinitis is evaluated clinically and on
post-mortem.
Control
It is essential that control programs include monitoring atrophic
rhinitis in the herd. Disease can vary with the season and with
groups of pigs, etc.
Improve management and environment.
production and proper ventilation.
Use all-in all-out
Segregated or medicated early weaning programs can be used to
help eliminate toxigenic P. multocida from the breeding herd.
Vaccination - many products contain B. bronchiseptica and
toxigenic P. multocida. Immunization with P. multocida toxoid
appears to be the most effective. Generally, it is recommended
that sows receive 2 doses prior to farrowing and the pigs one
dose at 7 days and one at 14 -28 days of age. Vaccines usually
yield the best results when the disease is more severe and may
not be indicated if the economic loss from the disease is less
than the cost of vaccination.
Biosecurity for negative herds includes prevention of exposure to
infected swine, cats, dogs, rodents, vehicles and personnel from
infected units, and complete confinement.
Treatment
It is extremely important to improve the environment, management
and nutrition.
Tetracycline antibiotics may be useful, especially if given early
or if there is pneumonia present. The recommended dose is
20mg/kg long acting oxytetracycline at day 1, day 7, day 14 and
at weaning. Tetracyclines are more effective when used in
combination with a vaccination program.
Naxel is effective against P. multocida and is commonly used.
215
Inclusion Body Rhinitis
An acute systemic viral disease of swine causing lesions
throughout the body but especially in the nasal submucosa.
Infection with this virus was previously thought to be largely
inapparent or subclinical. Recently, however, the infection
seems to be causing disease especially in "high health status
herds". The virus is not known to cause turbinate atrophy.
Etiology: Cytomegalovirus (Herpesvirus)
Epidemiology
The virus is found worldwide and virtually all swine in
conventional herds are infected based on serological evidence.
SPF herds and segregated early weaning herds may not be infected.
Transmission is assumed to be by contact or aerosol from nasal
secretions of carriers, which probably include sows. Infections
may be more common in PRRS infected herds and the cytomegalovirus
itself is immunosuppressive.
Clinical Signs
Usually seen in 1 to 4 week-old pigs. There may be a moderate
fever, anorexia, weakness, plugging of the nasal passages with
mouth breathing. There may be coughing and piling.
Lesions
Highly inflamed and hemorrhagic nasal mucosa is almost
pathognomonic. There may be excessive mucus present. The
tubuloalveolar gland cells in the nasal submucosa are greatly
enlarged and contain large intranuclear inclusions. Inclusion
bodies are seen in various other locations such as the lungs and
kidneys.
Diagnosis
Gross lesions are almost pathognomonic.
Histopathologic exam of the turbinates (use the ventral
turbinate).
Control
One of the theories on why we may be seeing more disease is that
infection may be occurring in susceptible pigs after colostral
immunity is lost.
More attention to this disease in high health
status herds may be necessary. Control measures used for other
respiratory agents should work against this virus.
216
Treatment
None currently available.
Sanitation to minimize secondary disease
SWINE ENTERIC DISEASES
Diarrhea and enteric diseases are probably the most important
causes of economic loss to the swine industry. The approach the
differential diagnosis of swine enteric diseases is best done by age
at which the pigs are affected. Some of the enteric diseases have
very specific age ranges of pigs that they affect while others are
quite broad. The following is a listing of some of the main causes of
enteric disease broken down by age of pig and the most prominent
clinical presentations:
1-6 Days of Age
C. perfringens
Type C
Type A
1-4 days; Claret red-colored diarrhea, acute deaths,
high mortality, may have subacute and chronic forms.
increasingly recognized as a cause of watery diarrhea
in this age group (out to a week or ten days) The
diarrhea is generally mild but can be a cause of
economic loss.
C. difficile
1-7 days; Mesocolonic edema, mild diarrhea, feces with
a Acreamy@ consistency.
E. coli
1-3 days; Profuse watery diarrhea and dehydration;
gastric distention, watery contents in small
intestine.
TGE
Profuse watery greenish-gray diarrhea without blood,
vomiting is prominent, high mortality, older pigs may
be affected but not as severely.
Rotavirus
Severity depends upon antibody levels in the sow's
milk, presence of secondary invaders, and the level of
exposure. Subclinical to severe watery diarrhea.
S. choleraesuis
Rare
7-21 Days of Age
Coccidiosis
7 to 15 days of age. Yellowish to grayish diarrhea
that may progress to watery diarrhea; no blood in
feces; No response to antibiotics.
E. coli
Usually less severe than neonatal disease.
May
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respond well to antibiotics.
TGE
Pigs at the upper age range may survive.
Rotavirus
Most severe in 7 to 41-day-old pigs. Can see severe
disease, especially in early weaned pigs that get a
high infectious dose and when E. coli is also present.
Salmonella
choleraesuis
Strongyloides
Rotavirus
Others die.
Not as common as in post-weaning pigs. See more
problems as pigs near weaning. May see sporadic acute
deaths.
Diarrhea followed by progressive dehydration, death
usually occurs before 10 -14 days in heavy
infestations. Stunting and unthriftiness are more
common.
Weaners-Nursery Pigs
Combined with E. coli, it is said to be the most
common cause of postweaning diarrhea.
E. coli
Hemolytic strains, usually mild to moderate diarrhea
when uncomplicated.
TGE
Diarrhea without high mortality, depending on the age.
Salmonella
choleraesuis
Trichuris suis
Brachyspira
hyodysenteriae
Proliferative
enteropathy
Usually see occasional septicemic deaths and little to
moderate diarrhea. May have some blood in the feces.
Mucohemorrhagic diarrhea, large intestine only.
Diagnose by finding the parasites.
Bloody dysentery. May appear to have one to three
cycles of disease at about 3 week intervals.
Problems usually begin about 7 weeks of age or so.
Subclinical to pigs with anorexia, dullness, severe
diarrhea and death.
Grower-Finisher
Brachyspira
hyodysenteriae
Bloody dysentery
Trichuris suis
Mucohemorrhagic diarrhea.
Proliferative
218
enteropathy
Subclinical to severe diarrhea. May have moderate
mortality with the more severe forms. Replacement
gilts often have severe problems with the PHE form of
the disease.
COLIBACILLOSIS
Etiology
Escherichia coli associated with the production of diarrheal
diseases in pigs are characterized by the production of a number
of important virulence attributes. Listed below are those that
seem to be of some importance:
Fimbriae are essential for the attachment of E. coli in the small
intestine. E. coli that are normally found only in the distal
2/3 of the intestinal tract are not associated with diarrheal
disease. Certain fimbrial types are associated with the
attachment in the small intestine and therefore are essential for
the production of disease in neonatal pigs.
F4 (K-88) strains adhere throughout the intestinal tract.
F5 (K-99), F6 (987P), and F41 strains adhere in greater
numbers in the distal half of the small intestine.
Enterotoxins are essential in the production of diarrheal
disease. STa is produced by all strains of E. coli that produce
diarrhea in neonatal pigs. STb is associated with strains that
produce postweaning diarrhea. Some strains produce the LT toxin.
Epidemiology
Problems with E. coli enteritis in neonatal pigs increased
dramatically with the advent of swine confinement buildings.
Pathogenic strains of E. coli are maintained in the intestinal
tract of swine and to a lesser extent the environment. Baby pigs
come in contact with the organisms from the sow's feces. The
cleanliness, dryness, and design of farrowing units has been
demonstrated to have an effect on the incidence of neonatal
diarrhea in pigs. E. coli do not survive as long in dry
environments. Poorly designed farrowing crates where piglets
come in contact with feces from the sow have been shown to result
in a higher incidence of diarrhea. Drafts that result in chilling
of the baby pigs are an extremely important predisposing cause of
colibacillosis in baby pigs.
Clinical signs
E. coli usually kills pigs because of the extensive fluid loss
from the intestines and the resulting severe dehydration. Whole
litters or individual pigs may be affected within a few hours of
219
birth and up to 2 to 3 weeks later. The initial signs can vary
from acute death without signs of diarrhea to a mild diarrhea
with no evidence of dehydration. Up to 40% of body weight may be
lost. The feces may vary from an almost clear fluid to white or
brown depending on the diet. The immune status of the sow, the
age of the pig and, to some extent, the infectious dose of the
organism are important factors in determining the severity of the
clinical disease.
In post-weaning E. coli diarrhea, the clinical signs are the same
as in the pre-weaning diarrhea, but are milder and the mortality
is normally not high. Recently, cases of E. coli diarrhea have
been occurring in pigs 3 to 4 weeks following weaning.
Lesions
Distention of the small intestine and loss of tone of the
intestinal wall. On histopath, the villi are normal and there is
heavy bacterial adherence to the intestinal epithelium.
Diagnosis
It is important to recognize that more than one agent may be
contributing to a diarrhea.
Clinical signs
Bacteriologic culture of an acutely ill, untreated animal.
Strains from post-weaning diarrheas are almost always hemolytic
K88 strains.
Rule out other causes (histopath, FA)
Rule-outs
In neonatal diarrhea
Clostridium perfringens types A and C
Rotavirus
TGE
Coccidiosis
In post-weaning diarrhea
Salmonellosis
Bloody dysentery
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Rotavirus
TGE
Treatment
Temperature: Has a big effect on normal intestinal motility in
piglets; should be 32 to 34C for unweaned pigs.
Antibiotics: E. coli develops resistance readily. Base on
antimicrobial susceptibility test if possible. Probably best to
treat the whole litter.
Fluids:
Electrolytes with glucose and vitamin C are recommended.
Prevention
Sanitation and a dry warm environment.
Design of the farrowing crate: raised crates with perforated
floors that allow the fecal material to drop through have a lower
incidence.
Immunity is primarily via the blockage of adherence by antifimbrial antibodies in the sow's milk. A continuous supply of
IgA is required to protect the pigs. Just getting colostrum
isn't enough. Hypogalactia and nutritional imbalances (low
vitamin E levels) can have a dramatic effect on the incidence of
diarrhea.
Vaccination of the sows has been very beneficial in helping boost
protective antibody levels in milk. Bacterins have replaced most
of the live oral vaccines at the present time. However, it
should be noted that vaccination against one fimbrial type often
leads to an increased incidence of disease caused by other
fimbrial types.
Piglets start to produce their own antibodies
at about 10 days of age and will develop active immunity to the
various types of E. coli as the levels of protective antibodies
in the milk decline.
CLOSTRIDIUM PERFRINGENS TYPE C ENTERITIS
A severe, usually hemorrhagic enteritis that usually affects pigs
within the first week of life (usually the first 3 days). Infections
may be observed in pigs 2 to 4 weeks of age but these are not
hemorrhagic.
Epidemiology
Clostridium perfringens type C is maintained in the intestinal
tract of carrier sows and transmitted to piglets through the
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feces. Transmission probably occurs within a few hours of birth.
The intestinal tract of the young pig has not established it's
normal flora at this time and C. perfringens is able to multiply
to high numbers.
Clinical signs
May have peracute, acute, subacute and chronic manifestations of
the infection.
Peracute disease is characterized by a hemorrhagic diarrhea and
pigs may die within a few hours of onset. Occasionally, pigs may
die without showing diarrhea.
Acute cases commonly survive about 2 days and characteristically
have reddish-brown liquid feces that contain shreds of necrotic
debris.
Subacute cases survive 5 to 7 days and do not have a hemorrhagic
diarrhea. Their feces may be yellow but then change to a clear
fluid. The pigs become progressively emaciated and dehydrated
even though their appetites are relatively normal.
Chronic cases may be difficult to characterize. The pigs may
have an intermittent diarrhea and merely be stunted or die after
several weeks.
Necrosis of the intestinal mucosa usually does not occur in
either the subacute and chronic forms of the disease.
Pathogenesis
Clostridium perfringens colonizes the small intestine and but
does not invade the intestinal mucosa.
The organism produces a potent ß-toxin and antibody against this
toxin is highly protective. The toxin is susceptible to
proteolytic cleavage and is protected by the trypsin inhibitors
in the sow's milk.
The jejunum is the most consistently affected and the lesions are
generally confined to the small intestine and mesenteric lymph
nodes. They may vary in location; however, and lesions have been
observed in the colon.
Diagnosis
Gross lesions are highly suggestive. In the acute hemorrhagic
form the lesions are almost pathognomonic.
Bacterial culture-easy in the acute cases, all but impossible to
obtain a diagnosis using this in the chronic cases.
222
Mucosal scrapings--> Gram stain, should see large Gram-positive
rods, often in large numbers.
Diagnosis of subacute and chronic forms of the disease usually
requires histopathologic examination to demonstrate colonized
villi.
Mixed infections: Once secondary bacteria invade the necrotic
villi, it becomes impossible to differentially diagnose the
disease from severe coccidiosis. Therefore histopath is needed
on necrotic and non-necrotic areas of the intestine.
Treatment
Can treat with penicillin and antiserum orally and this may be of
some benefit if the infection is detected very early. Once
clinical signs become evident in the acute disease, it is
difficult to treat.
Prevention
Antitoxin. In an outbreak one can give Type C antitoxin
parenterally. This needs to be done soon after birth.
Vaccination of sows with toxoid: One dose at breeding or midgestation and a second dose 2-3 weeks before farrowing. Booster
3 weeks before each farrowing. Provides good protection for most
farms. On some farms clostridial enteritis is a difficult
disease to control, even with a good vaccination program.
CLOSTRIDIUM PERFRINGENS Type A
Produces disease in both neonatal and post-weaning swine. The type of
disease depends upon the age of the pigs and whether the infecting
strain produces an enterotoxin. The beta-2 toxin seems to be the most
important in production of disease. In neonatal pigs, disease usually
begins within 48 hr. of birth and may last up to 5 days. The feces
are usually pasty, soft and mucoid. Infections with C. perfringens
type A cause only a transient watery diarrhea. Pigs 5 to 7 weeks of
age may develop diarrhea or soft feces. The diarrhea does not result
in death but may suppress the rate of gain.
Diagnosis is based on culturing C. perfringens type A from the
affected areas of the intestine and subsequent laboratory
demonstration of the beta-2 toxin.
Vaccination. A toxoid for C. perfringens Type A is currently
being marketed with a conditional license (as of 2006).
Clostridium difficile
C. difficile is being recovered from neonatal pigs (1-7 days of
age) and is apparently a common cause of mesocolonic edema. Affected
223
pigs develop a relatively mild diarrhea with dehydration and
unthrifiness. Recent figures from the ISU VDL indicate that it is
currently one of the most common organisms associated with diarrhea in
neonatal pigs.
Epidemiology: Fecal oral transmission is assumed. There is some
indication that antimicrobial therapy may play a role in development
of disease similar to the situation seen in humans with
pseudomembraneous colitis. However, the gut of the neonatal pig
probably has not established its normal competitive microflora and
this may provide adequate opportunity for the organism to multiply.
Toxins: The organism produces two toxins, A and B that are associated
with disease production. Toxin A is an enterotoxin and B is a
cytotoxin.
Clinical signs: Usually a mild diarrhea that may have a Acreamy@
consistency.
Lesions: The most consistent finding is mesocolic edema although this
is generally considered to be a non-specific finding. This is
currently the most common cause of colitis in neonatal piglets.
Diagnosis: The toxins are apparently labile and submission of live
pigs or colonic contents that have been immediately frozen is
essential. A commercially available ELISA (TechLab Tox A/B) is used.
Culturing the organism is difficult. If colitis is seen on histopath
in this age group of pigs, the probability is about 84% that it is
associated with C. difficile.
Prevention and Treatment?
TRANSMISSIBLE GASTROENTERITIS
A highly contagious enteric disease of swine characterized by
vomiting, severe diarrhea and a high mortality in piglets under 2
weeks of age. All ages of pigs are susceptible to infection but
the mortality rate drops dramatically with increasing age. The
disease is most costly when outbreaks occur during farrowing time
and the majority of clinical disease is observed in the winter
months.
Etiology
TGE virus is a coronavirus that is antigenically related to
canine coronavirus (CCV) and FIP virus of cats. It is apparently
not antigenically related to hemagglutinating encephalomyelitis
virus (HEV) or porcine epidemic diarrhea virus (PEDV) which are
also coronaviruses infecting swine. Recently, a porcine
respiratory coronavirus (PRCV) has been described which is
antigenically related to TGEV. Initial data indicate that PRC is
224
not associated with the production of enteric disease. However,
antibody against this virus is cross-reactive with TGEV and can
lead to false positive serologic test results.
Epidemiology
The virus is transmitted readily by aerosol and also shed in the
feces. Infection occurs when the virus is swallowed. The
incubation period is 18 hours to 3 days and the virus spreads
rapidly through a group of swine.
Surveys have indicated from 19 to 54% of swine in the US and
Europe have been infected based on serologic evidence. The virus
is quite labile when exposed to sunlight, drying, heat, and
disinfectants. However, it survives for long periods of time in
frozen tissues. This has been used as an explanation for the
appearance of the disease primarily during the winter months. In
addition, reduced or fluctuating ambient temperatures predispose
pigs to infection with the virus and the resulting diarrheic
state leads to increased shedding. The virus may also be shed in
milk and possibly via a respiratory route.
The virus may also spread subclinically through a group of
susceptible swine (especially older pigs) and be maintained in a
herd. Continuous or frequent farrowing operations will maintain
the virus in this manner. Carriers have been demonstrated but
the role of the long-term carrier has not been determined. Pigs
have been shown to harbor the virus for up to 104 days but not
transmit it to sentinel pigs. TGE may also be transmitted by
other hosts. Starlings have been shown to shed the virus for up
to 32 h following experimental exposure. Cats, dogs, and foxes
may shed the virus for long periods in their feces. The virus
from the dog was found to be infectious for pigs.
Clinical signs
In young piglets one sees transient vomiting, watery and usually
profuse yellowish diarrhea, rapid dehydration and weight loss.
Growing and finishing pigs and sows have anorexia and diarrhea
for a short period (1 to a few days) and an occasional animal may
vomit.
Epizootic TGE occurs where most of the swine in a herd are
susceptible. It spreads rapidly to all ages of pigs, especially
during the winter.
Suckling pigs become very sick, dehydrated, and die rapidly with
mortality rates of almost 100%. Pigs 2-3 weeks of age have a
high mortality rate but this drops dramatically by 5 weeks of
age.
Some lactating sows become very sick, have an elevated
225
temperature, vomiting, diarrhea and agalactia which leads to
increased baby pig mortality.
Enzootic TGE results when susceptible swine are frequently or
continually introduced into a herd (such as in continuous
farrowing operations or where feeder pigs are purchased). Even
in operations that do not use a continuous farrowing system, the
infection can become enzootic. As colostral immunity wanes, pigs
become infected and show mild but typical signs of TGE.
Mortality may be as high as 10 to 20% depending upon the age when
infected. Most pigs with clinical disease are going to be
between 6 days and 2 weeks of age. A factor complicating
diagnosis is that most pigs normally scour a little when weaned.
Intermittent Enzootic TGE is caused by the re-entry of the virus
into a herd which contains immune sows. This is seen in areas of
concentrated swine production. Each winter the herd becomes reinfected and disease is seen primarily in growing and finishing
swine. If the disease is transmitted into the farrowing house,
young pigs will develop disease typical of the enzootic form.
Lesions
Dehydration and distention of the small intestine with yellow and
frequently foamy fluid with flecks of curdled milk.
Marked shortening or atrophy of the villi in the jejunum and, to
a lesser extent, the ileum. This is usually much more extensive
and severe than that seen in rotavirus diarrhea.
Diagnosis
Detection of viral antigen in frozen sections with
immunofluorescence or immunoperoxidase tests. This is best done
on pigs in the early state of diarrhea because the epithelium is
lost as the disease progresses and the peak amount of virus is
present at this time.
Serologic diagnosis can be useful if paired serum samples are
used.
Differential Diagnosis
Rotavirus
E. coli
Coccidiosis
Treatment
In very young pigs, the mortality rate is going to be almost 100
226
percent no matter what the treatment regimen.
Increase the ambient temperature (above 32C) and provide dry,
draft free environment.
Symptomatic: Water, milk replacer, and electrolyte solutions
freely available to infected pigs to alleviate dehydration,
acidosis, and starvation.
Cross-suckling pigs onto immune sows was found to be helpful.
Prevention and Control
Vaccination
Oral administration of virulent autogenous virus (feedback)
to sows at least 3 weeks before farrowing. Stimulates high
IgA levels and is relatively successful.
When confronted with an outbreak of TGE in a large farrowing
operation, it has been proposed that all sows more than 2 to
3 weeks from farrowing be exposed to the virulent virus at
the same time. The strategy is to have the whole population
of breeding swine develop immunity simultaneously and
prevent the development of enzootic TGE. This seems to work
as long as each sow or gilt is individually dosed with the
live virus so that infection can be ensured. Putting the
virus in the feed may not be sufficient.
Oral or intranasal attenuated vaccines have not been as
successful: May not survive the stomach and may not
replicate sufficiently in the gut.
Parenteral vaccination of sows with commercial vaccines
resulted in a decreased (but still high) mortality in
piglets. IM vaccines result in high IgG titers but little
or no IgA which is important for intestinal immunity. The
same was true of intramammary vaccination. However,
vaccination of infected sows resulted in an increase in IgA
and IgG in the milk.
Management
Prevent introduction into a herd. Isolate swine coming into
a clean herd. Swine recovering from an outbreak of disease
can be introduced 4 weeks after the last clinical signs
disappear. Control starlings and other birds, cats, dogs,
etc. The virus can be transmitted on boots, feed trucks,
etc. and this may constitute the major means of spread.
Control access and supply clean footwear.
After an outbreak, vaccinate all sows that have more than 2
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to 2 1/2 weeks before farrowing. Vaccination closer to
farrowing may be beneficial but there may be a high
percentage of sows that do not pass sufficient immunity to
their pigs. One can try to control the exposure of these
sows to the virus.
With enzootic TGE, vaccination with an attenuated virus may
help, but changes in management practices to eliminate the
continual influx of susceptible swine are probably
warranted. One may wish to alter the farrowing schedule,
temporarily utilize other facilities, or have smaller
farrowing units to facilitate an all-in all-out system.
COCCIDIOSIS
General description
Coccidiosis was not generally recognized as a disease problem in
swine until the middle 1970's. It generally produces a yellowish
to grayish diarrhea in 7 to 14-day-old piglets but may affect
pigs on concrete as young as 5 days of age in the summer months.
The parasite is considered to be worldwide in distribution.
Etiology
Isospora suis is by far the major cause of porcine coccidiosis.
Sows that are raised in dirt lots also carry Eimeria spp. but
these are rarely involved.
Epidemiology and Transmission
It appears that little pigs become infected from residual
organisms that build up in farrowing crates from previous litters
of pigs. The sow apparently does not play a major role in the
transmission of the parasites. Most clinical studies have been
able to demonstrate the organism in only 1% to 3% of sows. The
sporulated oocysts are very resistant to disinfectants and
survive in high numbers in the farrowing crates. When neonatal
pigs ingest the organism in high numbers, clinical disease is
produced. Diarrheic pigs amplify the dose of organisms for other
pigs.
Clinical signs
Yellowish to grayish diarrhea in usually in 7-14-day-old piglets.
Loose, pasty feces that become more fluid as the disease
progresses. Piglets may become covered with the feces and remain
wet and have a rancid odor. They continue to nurse but become
dehydrated, develop a roughened haircoat and do not gain weight
well. The severity of the disease varies among the pigs in a
given litter.
228
The severity of disease is due primarily to the infectious dose
of the parasite. Experimental inoculation of 200,000 oocysts of
Isospora suis results in a relatively severe clinical disease and
moderate to high mortality. A lesser inoculum may result in only
diarrhea or the absence of clinical disease.
Lesions
Gross: Fibrinonecrotic membrane in the jejunum and ileum in
severely affected pigs. The necrotic membrane is not seen in
pigs that are not severely affected.
****Lack of hemorrhage- even in severe disease.****
Microscopic: Villous atrophy, villous fusion, crypt hyperplasia,
necrotic enteritis and loss of enterocytes at the tips of the
villi.
Diagnosis
Main differential diagnosis is chronic clostridial enteritis.
Histopath: Most accurate method. Demonstrate the paired Type 1
merozoites. If the intestine is necrotic, one must examine both
necrotic and non-necrotic areas.
Mucosal scrapings: Better than fecal samples.
paired Type 1 merozoites.
Demonstrate the
Fecal samples: Demonstrate the oocysts on direct exam or
flotation. Hard to do unless on removes the lipid from the
sample with solvents. Sample several litters that have had
diarrhea for 2 to 3 days. This is the peak period of oocyst
production. Oocysts usually do not appear in the feces until a
day or so after onset of clinical signs.
Treatment
Supportive.
Coccidiostats have not produced good results.
Prevention
Sanitation is the key. Farrowing crates need to be steam cleaned
and thoroughly disinfected between litters. Strong bleach (50%
solution) or ammonia compounds are active against Isospora suis
but the steam cleaning seems to be the most important part.
Concrete and wood floors harbor large numbers of the organisms
and can be very difficult to deal with. One can seal surfaces
with waterseal or paint to break the cycle. Coccidiosis is the
main reason that raised, wire bottom farrowing crates were
developed. We now use coated metal for farrowing crates that is
easier to clean.
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PORCINE ROTAVIRUS
Most rotavirus infections of young pigs are either subclinical or
mild and piglets recover without treatment. However, rotaviruses have
been associated with outbreaks of severe clinical disease in the
absence of other demonstrable agents, especially in newly weaned pigs.
In addition, disease can be seen in new gilts or in very young pigs
when a new virus strain enters the herd. Other agents such as E. coli
and TGEV and adverse environmental conditions seem to enhance the
severity of the disease.
Etiology
Rotaviruses are widespread in many animal populations and the
rotaviruses of several other animals are capable of infecting
gnotobiotic piglets and causing seroconversion. The virus is
quite resistant to many normal disinfectants, heat, and adverse
environmental conditions. Rotaviruses in pigs are divided into
Groups A, B, and C and there have been at least 4 serogroups
identified within Group A alone. Groups B and C probably have
serogroups as well. Thus rotaviruses are actually a whole series
of viruses that are not cross-protective. About 75% to 80% of
pre-weaning rotavirus infections are Group A. About half of
postweaning infections are caused by Groups B and C. Pigs may
undergo multiple rotavirus infections.
Epidemiology
Porcine rotavirus is widespread in swine; most animals become
infected early in life from viruses that are circulating through
the population. Almost all pigs will shed rotavirus within 5
days after weaning. Spread of the virus is through ingestion of
fecal-contaminated material.
Clinical signs
The severity of the disease is quite variable. Concurrent
infection with rotavirus and hemolytic (usually K88) E. coli is
the most common cause of postweaning diarrhea. The incubation
period is 12 to 24 h. Depression, anorexia, and reluctance to
move are observed. Vomiting may occur immediately after feeding.
A profuse diarrhea develops and pigs become severely dehydrated
and have up to a 30% weight loss. Mortality depends upon the age
of the pigs at weaning and the amount of specific antibody in the
sow's milk. Pigs weaned at a few days of age may have a very
high mortality rate. Generally clinical signs in suckled piglets
10 to 21 days and older are mild. If infection occurs after
weaning, the disease can be quite severe in pigs up to 3 to 8
weeks of age (mortality from 3 to 10% and occasionally up to
50%). Most adult sows have antibody to rotavirus but adult gilts
230
occasionally may not.
Pathogenesis
Lesions are similar to those of TGEV but not as severe.
Desquamation of villous epithelial cells results in loss of
intestinal enzymes and interference with digestion and
malabsorption.
Diagnosis
FAT on sections from the intestine of pigs in the earliest stages
of the disease.
EM can be used
ELISA is used at ISU.
Treatment
It only detects Group A rotaviruses.
Electrolyte-glucose or sucrose solutions have been demonstrated
to be of benefit. A high quality diet following infection may
lessen the impact of the disease in the recovery phase.
Prevention and Control
Thorough disinfection and a high level of cleanliness help to
keep exposure to the virus low. It is a very difficult virus to
eliminate and it is virtually impossible to eliminate from a
whole farm.
Vaccination has been tried but the presence of multiple serotypes
and the fact that colostral immunity is not especially protective
make the vaccines questionable. Vaccination of piglets is
complicated by the presence of colostral immunity. Commercial
vaccines are available but they are usually considered to be of
little value.
Feedback of farrowing barn manure to sows can be used to booster
the level of colostral immunity.
SWINE DYSENTERY
General description
A muco-hemorrhagic enteritis that usually affects 30 to 150 lb
pigs but has been observed occasionally in all ages of pigs. It
is very rare in nursing pigs. The disease was at one time
relatively widespread in the swine population (a 1982 study
revealed that it was present in 40% of herds in Iowa, Illinois
and Missouri). It is now seen infrequently because of the severe
economic impact forced producers to either eliminate the disease
or quit raising swine. It can be a cause of serious economic
loss from mortality, poor growth performance, poor feed
231
conversion, and the cost of treatment and control.
Etiology
Brachyspira hyodysenteriae (Formerly Serpulina hyodysenteriae) is
the causative agent of swine dysentery. Other spirochaetal
agents are commonly present in the intestinal tract of pigs and
some of these have been associated with a relatively mild
disease. Recent attempts to classify many of the intestinal
Brachyspira of swine have led to the recognition of a large
number of proposed species, almost all of which have not been
incriminated in disease. The presence of these organisms as
normal flora makes diagnosis more difficult. One of the main
weakly-beta-hemolytic sprirochetes (WBHS) is Brachyspira
pilosicoli and it has been associated with relatively mild
disease in swine.
Epidemiology
Disease seems to occur most commonly in late summer or fall and
is often associated with stress. The incubation period is
variable but is usually in the range of 10 to 14 days in
naturally exposed pigs.
The organism is shed from the intestinal tract of swine for long
periods of time following infection. Introduction of the
organism into a herd is often through a carrier pig. Pigs were
found to be shedding the organism in the feces 70 days following
recovery from clinical disease. The organism can be transmitted
to suckling pigs from the sow.
B. hyodysenteriae has been shown to survive for long periods of
time in lagoon water, soil, feces, and in the intestinal tracts
of mice and dogs.
Clinical signs
Diarrhea with variable severity is the most consistent sign. The
disease progresses gradually through a group of swine.
The
initial diarrhea is characterized by a large amount of mucus
often containing flecks of blood. As the disease progresses,
watery stools containing blood, mucus, and shreds of fibrinous
exudate are seen. Abdominal pain evidenced by an arched back may
occur. Prolonged diarrhea results in dehydration and eventual
emaciation.
The disease may give the appearance of being cyclic in a group of
swine. Clinical signs will disappear and then reappear at 3-4
week intervals. This is especially true if the pigs are stressed
at these times (respiratory disease, etc.).
In peracute disease, animals may be found dead without previous
232
clinical signs but this is relatively rare. Also rare, disease
in suckling pigs may be characterized by a catarrhal colitis
without hemorrhage.
Pathogenesis
The causative organisms do not invade beyond the lamina propria.
Lesions are confined to the large intestine. The roles of
endotoxin and the hemolysin in the pathogenesis of the lesions
have not been thoroughly defined. No enterotoxins have been
described. Fluid losses appear to be the result of a failure of
the colonic mucosa to reabsorb endogenous secretions because of a
failure to actively transport sodium and chlorine from the lumen
to the blood.
Diagnosis
Clinical signs
Direct exams of colonic mucosal scrapings: Crystal violet stain.
Other spirochaetes can be quite numerous so one must be cautious
not to over-interpret direct smears.
Bacteriologic culture: Best to rely on this. The numbers of
organisms present may be low in chronically diseased or treated
pigs.
Differential diagnosis
Salmonellosis: Usually see lesions and bacteria in sites in
addition to the large intestine.
Intestinal adenomatosis: Lesions in the small intestine and
colon. Thickening of the gut wall.
Trichuriasis: Heavy infestations can look very similar to swine
dysentery. Should be able to find Trichuris suis in the large
intestine (may hide in mucus and necrotic debris). May have
mixed infections with B. hyodysenteriae.
Prevention
Herds infected with Brachyspira hyodysenteriae should be
quarantined and no animals allowed to move from them unless to
slaughter. Given the current market situations, it is
economically not viable to have a swine unit where B.
hyodesenteriae is a problem. If a herd is identified as having B.
hyodysenteriae, isolation of the herd and rigid sanitation are
essential because of the ease of transmission of the organism on
boots, equipment, etc.
Quarantine of new stock.
233
Depopulate in warm dry weather and repopulate with SPF swine.
Thorough disinfection is a must and it may be impossible to rid
some facilities of the organism. The organisms can live in small
cracks in concrete, in lagoons and in the intestinal tracts of
other animals.
Medicate the sows with Denagard (tiamulin), increase sanitation,
and early weaning may be successful in some herds but the
organisms are not completely killed by this method.
Prophylactic medication is usually too costly.
Treatment
A number of drugs were commonly used therapeutically. These
included Bacitracin, Carbadox, Mecadox, Gentamicin, Lincomycin,
Tiamulin, Tylosin, Virginiamycin and others. Resistance has been
reported with some of these.
Medication in acutely affected swine must be given in the
drinking water (the pigs aren't eating) or parenterally.
Parenteral injections in a large group of swine are time
consuming an may not be practical.
Brachyspira pilosicoli
General. Causes porcine intestinal spirochetosis, PIS and human
intestinal spirochetosis, HIS and is possibly involved in
intestinal infections in other animals.
Distribution. Worldwide in swine, humans and can be demonstrated
in other animals. It is one of the organism referred to as a
weakly beta-hemolytic intestinal spirochete. Most of these
organisms were formerly referred to as Brachyspira innocens, a
non-pathogenic spirochete, but most of these isolates were
actually B. pilosicoli.
Disease.
Swine.
Characteristically, it attaches in large numbers to
the colonic epithelium by one end of the bacterial cell.
Produces a diarrheal disease most commonly seen in the
immediate postweaning period in pigs but can occur anywhere
from 4 to 20 weeks of age. The major clinical signs include
weight loss, poor growth rate, and diarrhea with occasional
flecks of blood. Generally thought to produce a milder
disease than B. hyodystenteriae.
Humans. Human intestinal spirochetosis is also
characterized by the end-on attachment of large numbers of
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the organism. The disease is most commonly seen in people
in lesser developed countries and AIDS patients, May be
associated with a variety of intestinal disorders, but most
commonly with rectal bleeding and chronic diarrhea. There is
still some doubt in the literature as to whether this is the
same organism as seen in PIS although it has been
demonstrated experimentally that organisms isolated from
humans can cause disease in pigs.
Others. May be associated with intestinal damage in other
species of animals especially dogs. Experimentally at least,
the organism can cross species barriers and produce disease
in other animals.
Other intestinal spirochetes
Brachyspira innocens. Most of the isolations of this organism
were actually B. pilosicoli. The organism was thought to not be
significant in intestinal disease.
Many other intestinal spirochetes exist but have not currently
been associated with disease production.
SALMONELLOSIS
Etiology
The clinical disease seen in salmonellosis of swine is greatly
dependent upon the particular serotype of Salmonella involved.
The great majority of the clinically significant infections
(>90%) are caused by S. choleraesuis var. Kunzendorf. Infections
with this organism are most often characterized by a septicemia
with accompanying respiratory and systemic signs. The presence
of enteric disease is quite variable. S. typhimurium is much
more likely to produce enteric disease and is much less
frequently isolated as a cause of acute clinical illness. S.
typhisuis is relatively rare and is not usually involved in
enteric disease. Other serotypes are occasionally involved.
Since the two serotypes produce somewhat different diseases they
will be presented separately.
Salmonella choleraesuis
Epidemiology
Infected, shedding pigs are the most important source of S.
choleraesuis.
Length of carrier period
Numbers of organisms shed in feces
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Role of stress and transport in shedding
Crowding
Intestinal hypermotility
Disease
Most common in weaned pigs less than 4 months old but will
occasionally occur in market age and older swine. Infections in
suckling pigs are considered to be very rare but, recently,
infections have been recognized in very young pigs. In these
pigs, there is often a marked petechiation of the intestinal
serosa.
Septicemia (endotoxemia, DIC)
Sudden death in one or more animals
High fever:
105 to 108F
Mortality usually less than 5 to 10% of a group. In farrow-tofinish operations the mortality is commonly about 2-3% but where
feeder pigs are purchased and there is more stress, mortality can
be high. Dr. Kunesh has seen 100% mortality in highly stressed
pigs under poor housing conditions.
Enterocolitis: Diarrhea is sporadic and more frequent in nursery
age pigs.
Pneumonia:
Frequent complaint
Meningoencephalitis
Gross lesions
Cyanosis of ears, feet, tail and ventral abdominal skin.
Splenomegaly, hepatomegally, swollen lymph nodes (especially
mesenteric). Lesions are often present in the intestinal tract
in animals that have survived for a few days following the onset
of severe disease.
Diagnosis
Culture: Mesenteric lymph nodes, lungs, liver, spleen, ileocecal
junction.
Fecal cultures
Histopath
Treatment
236
Acute septicemic disease: Separate the affected animals.
Probably some benefit to antibiotic therapy. It may buy some
time. Anti-inflammatories may be indicated.
Studies have shown little effect of antimicrobial therapy on
shedding.
Prevention
Management
Sanitation
Crowding
Vaccination: Modified live vaccine is thought to be efficacious.
There are live oral and parenteral (IM) vaccines on the market.
The S. choleraesuis vaccines appear to have had a fairly major
impact on the decreasing prevalence of clinical disease.
Antibiotics? These can be useful but are probably not the answer
in the longer term.
Salmonella typhimurium
Epidemiology
Thought to be more widespread in the general swine population
than is S. choleraesuis but it is isolated from clinically
diseased pigs much less frequently. Maintained in the intestinal
tract and associated lymphoid tissues for long periods of time.
It is a common cause of salmonellosis in many other species of
animals, thus it can be transmitted to swine rather easily. It
can also be transmitted through the feed. Most recovered pigs
remain as carriers and intermittent shedders for several months.
Disease
Enterocolitis: Watery, yellow diarrhea, initially without blood
or mucus. May last 3-7 days and recur 2 or 3 times. Blood may
appear in the feces but not in profuse amounts as is seen in
swine dysentery.
Septicemia: Some outbreaks of disease may mimic infections with
S. choleraesuis.
Some pigs may remain unthrifty and develop rectal strictures.
Rectal strictures are thought to be secondary to rectal prolapse.
Some work indicates that severe enteric disease may precede the
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development of the strictures.
Lesions
Diffuse ulceration and less commonly button ulcers in the small
intestine and colon.
Mesenteric lymphadenitis
Rectal strictures?
Salmonella typhisuis
Causes a relatively specific chronic disease syndrome with
necrotic colitis, caseous lymphadenitis, and bronchopneumonia.
The organism is not often isolated (grows more slowly than other
Salmonella). Intestinal lesions may have healed leaving only the
lymphoid and pulmonary lesions.
Salmonella dublin and S. enteritidis
Both of these have been described as causes of meningitis in
suckling pigs.
PORCINE PROLIFERATIVE ENTEROPATHIES
General Description
Group of conditions that differ markedly in gross appearance but
which all involve a thickening of the mucous membrane of the
small and sometimes the large intestine. They are characterized
by proliferation and immaturity of the intestinal epithelium.
Etiology
Lawsonia intracellularis. Australian workers have also described
a different organism, Campylobacter hyoilei as a causative agent
but little work has been done on this organism since its initial
description in 1995. L. intracellularis is found intracellularly
in the apical cytoplasm of affected epithelial cells. L.
intracellularis apparently does not cause disease in germ-free
pigs and there is apparently some type of Apermissive@ role for
normal gut flora.
Epidemiology and Transmission
The condition affects swine worldwide and the organism is most
likely transmitted through the feces. Recent serologic studies in
the U.S. using NAHMS (National Health Monitoring Service) have
indicated a very high percentage of swine herds have the organism
238
present (98%) with about 20 to 30% of the swine in an infected
herd having the organism. This does not necessarily mean that
they are showing clinical disease. There is evidence that other
species of animals may be affected by an identical or similar
organism but the role of these animals in transmission of the
organism is probably minimal.
Transmission is by the fecal-oral route. PCR has detected
infection in piglets as young as 7 days of age, indicating that
vertical transmission from the sow occurs rapidly. Also, attempts
to use MEW to prevent the transmission of the agent to a group of
pigs have failed, leading one to believe that it is transmitted
from the sow to the pigs at an early age. Once in a group of pigs
lateral transmission is the most important route. Infected pigs
excrete the organism for at least 10 weeks post infection. If
sows are acting as the original source of the organism, they must
remain infected for much longer periods and perhaps for life.
Colostral antibody is at least partially protective. In infected
herds, most natural infections (as measured by seroconversion or
clinical disease) occur after 8 weeks of age suggesting that
maternal immunity may be protective for this length of time. In
infected herds, slow, progressive seroconversion occurs during the
grow-finish stage with clinical disease rates being highly
variable.
One of the major problems with this organism seems to be with
outbreaks of the disease in replacement gilts during the
acclimation/early breeding/gestation periods.
The organism may survive 1 to 2 weeks in the environment under
cool conditions. Survival under moist, warm conditions is
apparently quite good. Approximately 75% of cases of PPE occur
between May and September. The organism is susceptible to
quaternary ammonium and iodine-based disinfectants when not
protected by fecal material.
Clinical Signs and Lesions
PIA: Porcine intestinal adenomatosis. Uncomplicated
proliferation upon which NE, RI and PHE conditions may be
superimposed. Occurs most commonly in the 6 to 20 week age
range but some feel it occurs most commonly in the growfinish stage. In many cases the clinical signs may be very
slight and the swine not considered to have a problem. Most
often there is a variable percentage of a given age group
affected. In other cases the disease may result in a marked
dullness, apathy and anorexia. There may be little or no
diarrhea. Recovery from uncomplicated PIA occurs in 4 to 6
weeks and the pigs regain their appetite and rate of growth.
Lesions:
Most commonly in the terminal 50 cm of the small
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intestine and upper 1/3 of the colon. The wall is visibly
thickened, some serosal and mesenteric edema is common, deep
folds in the mucosa of the large intestine.
RI:
Regional ileitis. Occurs most commonly in the 6 to 20 week
age range with pigs about 12 weeks of age most commonly
affected. More severe clinically than PIA; severe loss of
condition and persistent diarrhea. Smoothly contracted,
almost rigid lower small intestine: "hose-pipe gut", usually
with prominent granulation tissue and a striking hypertrophy
of the outer muscle coats.
NE:
Necrotic enteritis. Occurs most commonly in younger pigs
(early nursery age) but has been reported in the 6 to 20
week age range. More severe clinically than PIA; severe
loss of condition and persistent diarrhea. Coagulative
necrosis with inflammatory exudate that appears as yellowgray cheesy masses that tightly adhere to the intestinal
wall. In chronic cases, granulation tissue may become
prominent. Many pigs never fully recover.
PHE: Proliferative hemorrhagic enteropathy. The diarrhea is
described as having the appearance of AA-1 Sauce@. Occurs
most commonly in young adults. The disease is particularly
troublesome in replacement gilts and sows. These animals
can develop a severe hemorrhagic enteritis and die acutely
in some cases. Lesions in the large intestine are rare.
The lumen of the ileum may contain a well-formed blood clot
and the colon may contain black, tarry feces. Bleeding
points, ulcers and erosions are not evident and the mucosa
may show little damage except for the adenomatous changes
and congestion. Histologically there is extensive
degeneration of the epithelium, accumulation of cellular
debris in the crypts and the formation of goblet cells in
the deep crypts.
Diagnosis
Clinical signs are suggestive but are not well correlated with
severity of lesions except in the PHE form of the disease.
Gross lesions are highly suggestive but there can be a normal
thickening of the ileum adjacent to Peyer's patches subsequent to
chronic inflammation due to other causes.
Immunohistochemistry on formalin-fixed tissues has been adopted by
the ISU VDL. The sensitivity of this method is said to be far
better than the old silver staining technique. Many labs do IHC on
fecal samples. Antimicrobial treatment apparently does not
diminish one=s ability of diagnosing the infection, especially
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with IHC.
PCR is performed on fecal samples by some labs but the feces need
to be from clinically affected animals to be reliable.
Silver stains, FA, ELISA and others if available.
Ziehl-Neelsen
Mucosal smears:
Treatment
Several antibiotics have been demonstrated to be effective in
treatment. Tylan, Tiamulin and chlortetracycline,lincomycin and
Carbadox are used for treatment. Tylan and lincomycin are
currently the only drugs approved for use against Lawsonia
intracellularis in the U.S.
Prevention
Increased attention to sanitation and biosecurity plus AIAO
strategies with thorough cleaning and disinfecting between groups
are a good idea, but are not especially valuable with PPE. This
is one disease that remains a problem even in high health status
herds.
Vaccination. Apparently the vaccines can lessen the disease by
decreasing the magnitude of colonization. Not all pigs receiving
the vaccine seroconvert. Also, the vaccine organism cannot be
differentiated from field stains and is shed from the vaccinated
animals. Animals must not be receiving antibiotics at the time of
vaccination.
Tetracyclines seem to be effective but there is some evidence for
the development of resistance. However, the information may be
compounded by poor diagnosis. Generally, intracellular organisms
related to Lawsonia have few transferable plasmids and do not
readily develop antimicrobial resistance.
NE may respond to Tylocin/sulfonamide combinations.
Continuous medication to slaughter with some antimicrobials has
been tried but the value of this is difficult to evaluate. The
method is costly and may not be wise in light of prudent
antimicrobial use. When the medication is discontinued prior to
slaughter, a large population of susceptible pigs may result.
Pulse (intermittent) medication is beneficial. The intermittent
medication allows the pigs to develop an infection and respond
immunologically.
NOTE:
A condition known as hemorrhagic bowel syndrome occurs in 120+ lb
pigs. The pigs die quite suddenly and the intestinal tracts
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cotain blood. The cause or causes of this syndrome are not
definitively known. Some feel that the bloody contents of the
bowel is the result of volvulus or some other intestinal accident.
Sometimes there is a history of the animals not having access to
feed for a time and then overeating when they get a new batch of
feed. Anecdotal evidence indicates that antibiotics may help
(BMD-bacitracin, or tylan) and these are often tried. Hemolytic
E. coli or other bacteria could possibly play a role. The disease
tends to be sporadic and there is usually a low mortality rate.
EDEMA DISEASE
A complex disease characterized by the production of a vasoactive
toxin and resultant CNS signs and edema at various body locations. The
toxin is a variant of the Shiga-like toxin II or verotoxin and is also
referred to as "edema disease principle".
Etiology
Edema disease-producing Escherichia coli usually have the
following serotypes: O138:K81, O139:K82, and O141:K85. These
three have been found to produce the vasotoxin. Other serotypes
have been implicated. Fimbrial types F18ab and F18ac are commonly
seen in E. coli from edema disease. Edema disease is apparently
Aenjoying@ a resurgence in the swine population. Strains bearing
the F18 fimbriae have recently been detected that carry genes for
both vasotoxin and enterotoxin. Some of these can produce a
combined disease.
Clinical signs
Sudden death of one or more pigs usually 1 to 2 weeks after
weaning; Often the best-doing pigs in the group.
Incoordination, staggering gait, knuckling of the forelimbs,
ataxia, paralysis, tremors, and paddling.
Edema: May be difficult to demonstrate or absent.
edema may be seen prior to the onset of CNS signs.
Palpebral
Diagnosis
Clinical signs:
CNS
Edema, when present.
more.
Rarely seen in the stomach or colon any
Large numbers of hemolytic E. coli in the small intestine and
colon. These can be serotyped if necessary.
Treatment
242
Restrict feed consumption and increase the fiber content of the
diet. Increasing the fiber content may result in a pH change in
the intestine as well as a decreased protein content and the
normal flora may be altered as a result (theory).
Antimicrobials may be useful especially in the susceptibility
pattern of the E. coli is known.
Prevention
Genetics: We now have the ability to genotype breeding swine and
eliminate those animals that possess the receptor for F18 fimbria
and are most likely to give birth to susceptible offspring. If a
producer is having serious problems with edema disease CHANGE
BOARS.
Good creep feeding program
Restricted feeding at weaning or feeding of higher fiber diets.
Vaccination with F18ab-bearing strains of E. coli has had
reasonable success but F18ac strains are increasingly causing
problems and the current vaccines do not include this fimbrial
type.
HEMAGGLUTINATING ENCEPHALOMYELITIS VIRUS
Two forms of the disease: Acute encephalomyelitis and a chronic
vomiting and wasting disease (VWD). Caused by a single serotype of a
coronavirus. The disease appears in different forms probably because
of differences in susceptibility of pigs and strain differences in the
virus.
Epizootiology
Pigs are the only known host. The virus is apparently very
widespread in the pig population with survey results varying from
0 to 98%. In one US study, the incidence of antibodies in sows at
slaughter was 98%. Disease is relatively uncommon, however.
Neonatal pigs are usually protected by colostral antibody and they
subsequently develop an age-related resistance to potential
clinical effects of the virus.
Clinical signs
Confined almost entirely to pigs less than 3 weeks of age.
Sneezing and coughing may be noticed initially. The acute
encephalomyelitic form has been described only in the US and
Canada. In the VMD form, pigs may suckle for a short time, stop,
and then vomit milk. The pigs may look listless, have an arched
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back, and huddle. Rectal temperature may be slightly elevated at
first but quickly returns to normal. Abdominal distention may be
noted in some pigs. Clinical signs may vary in severity from the
acute form to VWD. Mortality approaches 100% within a litter and
survivors remain stunted.
Pathogenesis
The virus initially replicates in the epithelial cells of the
respiratory and small intestine, spreads via the peripheral nerves
to the CNS. The vomiting is due to a disturbance in stomach
emptying.
Diagnosis
Virus isolation is the best (has to be within 2 days of developing
disease).
Serologic: Antibody is widespread in normal pigs.
is difficult to demonstrate (pigs die).
Rise in titer
Differential diagnosis
Pseudorabies
Teschen/Talfan
Streptococcal infections
All of these are usually more severe than HEV and often affect
older pigs. Pseudorabies produces respiratory signs in older pigs
and abortions in sows.
Prevention
Maintain the infection in the subclinical form so that sows pass
protective antibody to the piglets.
ERYSIPELAS
An acute to chronic disease of swine characterized in its various
forms by septicemia, arthritic and/or skin lesions.
Etiology: Erysipelothrix rhusiopathiae
Epidemiology
Distributed worldwide and of economic significance in the swine
and turkey industries in the US. It is estimated that 30 to 50%
of swine carry the organism. Pigs carry the organisms in their
tonsils and shed it in their feces. Acutely affected swine shed
the organism in most body fluids.
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The organism can survive up to 35 days in the soil and feces in a
hog lot. The organism is very widespread in a number of animal
species but the disease that we see in swine is quite serotype
specific (predominantly serotypes 1 and 2).
Incidence is highest in swine 3 months to 3 years of age.
(Passive immunity in the young and subclinical infections as
immunity wanes?)
Infection probably occurs most commonly from ingestion and
introduction through wounds.
Acute disease
Characterized by septicemia, high fever, stiffness and reluctance
to move (arthritis), depression, splenomegaly, petechial
hemorrhages, and sudden death. Sows may abort.
Diamond skin
disease is considered to be a milder form of the acute disease.
Chronic disease
Characterized by arthritis that can progress to ankylosis.
Valvular endocarditis can lead to cardiac insufficiency and sudden
death under stress.
Disease in both forms may be due to the production of neuraminidase
which cleaves neuraminic acid (sialic acid) found on host cell
surfaces.
Diagnosis
Clinical exam
Bacteriologic culture: The organism is readily cultured in the
acute disease from many organs. The organism can be recovered
from arthritic joints for up to 3 to 6 months following initial
infection.
Response to penicillin
Differential diagnosis
Acute ASF and HCV
Salmonellosis
Actinobacillus
Swine pox: Generally a mild disease seen occasionally in the US.
Prevention
245
Management, housing, etc, are very important.
better than dirt floors.
Concrete floors are
Eliminate chronically infected animals
Vaccination
Attenuated live vaccines: Strains with low virulence for
swine. Antibody and antibiotics interfere with the
vaccination.
Killed bacterins: Formalinized whole cultures of selected
strains of serotype 2 are used. These contain an important
soluble immunizing glycolipoprotein that is released into
the medium. Lysate bacterins have been widely used.
Protective in 2 to 3 weeks.
Efficacy: Adequate long-term protection is not provided by
any of the current products. Immunity wanes in 3 to 6
months. None of the products protect against the arthritic
form of the disease, although by reducing the incidence of
the acute disease, the chronic form is reduced. Vaccine
failures may be partially due to serotype differences.
Mycoplasma hyorhinis polyserositis and arthritis
General
Acute, subacute and chronic polyserositis and arthritis occurring
in swine from 3 to 10 weeks of age. Characterized by
serofibrinous inflammation of the serous membranes and joints.
Occurs occasionally in highly susceptible (SPF) young adult swine.
Etiology and transmission
Mycoplasma hyorhinis. Adult swine are carriers but the percentage
in an infected herd is probably fairly low. The organism spreads
rapidly within a litter and many pigs have a nasal and
tracheobronchial infection without clinical signs of pneumonia.
If seen, clinical disease occurs at 3-10 weeks of age and
occasionally in young adult swine. It is a frequent secondary
invader in M. hyopneumoniae pneumonia as well as other types of
respiratory and enteric disease.
Clinical signs
There is a progressive onset of disease with labored breathing,
abdominal tenderness, decreased feed intake, lameness, temperature
of 104 to 107F and sternal recumbency. Some pigs recover rapidly
while others have clinical signs of disease for several weeks.
246
There is generally a low to moderate mortality. Poor sanitation,
movement into a new herd, and other environmental and management
factors predispose to clinical disease.
Gross lesions
There is a serofibrinous inflammation of membranes lining the
pericardial, pleural and peritoneal cavities. Synovial membranes
are swollen, edematous and hyperemic. Affected joints contain a
serofibrinous to serosanguineous fluid. In chronic disease,
adhesions develop in on the serosal surfaces. A chronic arthritis
with villous hypertrophy and articular damage may be seen.
Diagnosis
Gross lesions.
Very suggestive but there are other causes
Bacteriologic culture of the joint fluid or exudate from serosal
surfaces. The organism may persist for several months in the
lesions.
Prevention
Minimize stress and control other respiratory diseases.
There is no vaccine available.
Treatment
Not very beneficial on an individual animal basis. Treatment of
the whole herd or affected group with tylosin, lincocin, or
tiamulin may be of some aid.
Mycoplasma hyosynoviae ARTHRITIS
M. hyosynoviae is the cause of acute, subacute and occasionally
chronic, non-suppurative arthritis occurring in swine from 80 lb.
to market weight. The condition occasionally affects young adult
swine.
Transmission
M. hyosynoviae is carried in the pharyngeal secretions and tonsils
of many adult swine. It is intermittently shed in nasal
secretions and usually transmitted to a few piglets in a litter
prior to weaning. The organism spreads laterally through the
group. Management and environmental factors that cause stress
predispose to disease.
Clinical signs
Many infected pigs show no disease.
In those that show signs,
247
there is a sudden onset of lameness in one or more limbs that may
shift from one limb to another. There is usually little evidence
of joint swelling. The acute stage of the disease lasts 3 to 10
days and some pigs may develop chronic lameness. There is no
mortality but morbidity can range from 5 to 50% in a group.
Heavily muscled pigs with poor leg conformation and angularity are
predisposed to joint damage and osteochondrosis and are more
commonly affected.
Lesions
Affected joints have increased synovial fluid that is
serofibrinous to serosanguineous in nature. The synovial
membranes are edematous, hyperemic and have a yellowish
coloration. As the disease becomes chronic, there may be damage
to the articular surfaces but this is most likely due to
osteochondrosis.
Diagnosis
Clinical signs are suggestive but not sufficient for etiologic
diagnosis.
Culture. Preferably submit 2 untreated pigs with typical acute
disease to a diagnostic laboratory. Samples can also be collected
from live animals or at slaughter. Synovial fluid should be
aseptically removed, frozen and submitted to a diagnostic
laboratory. The organism disappears from the joints rapidly.
Prevention
Purchase breeding stock with no history of arthritis or leg
conformation problems.
Prevent stress when the pigs are most susceptible to disease (12
to 24 weeks of age).
Treatment
Separate affected animals.
Antibiotics:
Tylosin, Lincocin, or Tiamulin
SWINE REPRODUCTIVE DISEASES
OVERVIEW
There are many documented causes of
It is wise to keep in mind that illness
septicemia and toxemia can be a cause of
performance. The following is a list of
reproductive failure in swine.
of any type including
decreased reproductive
possible causes:
248
Brucellosis
Has not been reported from Iowa since 1972 and we are a "Validated
brucellosis-free area". Regulations regarding testing of swine
have recently been relaxed. One may see abortions in all stages
of gestation, arthritis, and orchitis.
Leptospirosis
Abortions in the third trimester, stillbirths, weak piglets. When
infection enters a "clean" farm one sees acute forms of the
disease. L. pomona has traditionally been the most common cause.
Pseudorabies
Abortions in any stage of pregnancy, stillbirths, young pigs with
CNS signs, respiratory signs in others.
Influenza
Explosive febrile outbreaks affecting almost all pigs in a group.
Abortion and infertility have been described but may not have
been due to the direct effects of the virus.
Parvovirus
Fetal death and mummification depending upon the stage of
gestation (must be prior to 70 days or the fetus will develop an
immune response and survive).
SMEDI
Stillbirth, Mummification, Embryonic Death and Infertility: Caused
by a group of enteroviruses. Disease was supposedly similar to
parvovirus-caused disease. This term has fallen out of favor with
almost everyone and is no longer used.
EMC
Encephalomyocarditis virus causes acute abortions and sudden
deaths with myocarditis.
Eperythrozoonosis
Somewhat controversial as a cause of abortion.
Acute abortions
at term or chronic infertility (both are infrequent).
Campylobacter
Fifty percent of Danish abortions are isolation positive. The
strains are different from swine intestinal campylobacters.
249
HEV
Hemagglutinating encephalomyelitis virus (Coronavirus). A
prevalent virus but disease is seldom reported. Infrequent cause
of term abortions and stillbirths.
Blue eye
A paramyxovirus reported in Mexico in 1986. Stillbirths,
mummification, infertility. The main clinical presentations are
CNS signs in pigs under 30 d of age and corneal opacities in older
pigs.
Chlamydia
Abortions in any species of animal.
PRRS
Abortions, stillbirths, weakborns and occasional mummies.
Respiratory disease in nursing pigs.
Mycotoxins - Vomitoxin
Streptococcal
Beta-hemolytic streptococci are often isolated from the vagina of
both normal and infected sows and from aborted fetuses.
Streptococcal metritis is linked to abortions and piglets that
have a high incidence of streptococcal joint ill and navel ill.
Some herds can have up to a 70% mortality in baby pigs.
Antibiotics in the feed are useful in prevention. Vaccination has
not been very successful in controlling the disease.
PSEUDORABIES
General
With the advent of more intensive swine-rearing operations and
continuous thru-put, this disease became a serious problem in the
U.S. Prior to the 1960's this was a relatively sporadic disease.
We were making good progress in Iowa until 1999 when we had a
rather massive outbreak that continued into 2001. Very aggressive
eradication measures have drastically decreased the incidence of
disease in Iowa. The state was declared free of pseudorabies in
2004. The disease is basically one of reproductive failure in
breeding swine, CNS disease in suckling pigs or respiratory
disease in older swine. Once the virus has established itself in
a herd, infection may be asymptomatic or produce only respiratory
disease in finishing age swine.
250
Etiology
An alpha Herpesvirus. There is essentially only one serotype of
the virus but there are a number of minor differences between
isolates that can be demonstrated with monoclonal antibodies or
analysis of DNA.
The roles of a number of different viral proteins have been
described.
gII, gIII, and gp50 glycoproteins seem to be the most important
for induction of immunity.
The genes for gI, gIII, gX, and TK (thymidine kinase) can be
deleted and the virus remains viable although reduced in
virulence. Deletion of one or more of these proteins has been
utilized in generation of vaccines.
Transmission and Epidemiology
Herpesvirus: Latency: Stress
The primary means of transmission into a herd is through
introduction of actively shedding or latently infected pigs (95%
of cases).
Does not survive well on fomites under dry, warm conditions but
will survive up to a month under cold, moist conditions.
Dogs, cats, rodents, and raccoons are all dead-end hosts and can
play a role in transmission.
Recent evidence from our most recent outbreak indicates that the
virus can become airborne and travel at least mile or so. The
Aepidemic@ of pseudorabies that occurred in 2000 in Iowa occurred
in the areas where swine were intensively reared. Unusually
moist, warm weather in the late fall and winter months apparently
allowed the virus to remain viable an be transmitted on the
prevailing winds.
Once in a herd, the virus spreads by direct contact, inhalation,
ingestion, breeding, and transplacentally.
The virus may be spontaneously eliminated from a herd under some
types of management systems (may take 2 years or so), but will
continue to thrive under continuous thru-put systems with a
constant supply of susceptible animals.
Clinical signs
Age of the host is very important but signs also vary with the
251
particular strain of virus and the infectious dose.
Also depends greatly on prior exposure of the herd.
Neonatal pigs: High fever, CNS signs (trembling, incoordination,
dog-sitting due to posterior paralysis, head tilt, ataxia,
paddling, etc.) and sometimes vomiting and diarrhea.
When dams have varying immune status, some litters will be
affected and others will be normal. Individual litters may have
both normal and unaffected pigs.
Mortality is usually 100% in affected pigs.
Once the infection has gone through a herd and the sows are
routinely exposed, infection of the neonates and weaners does not
usually occur.
Weaners (3-9 weeks of age): CNS involvement in the younger pigs in
this age group but it becomes progressively less severe as the age
at infection increases. May have up to 50% mortality in 3-weekold pigs. Respiratory signs in older pigs become more prominent.
Often, the disease is characterized by marked depression and
sneezing. Nasal discharge and coughing are often observed.
Secondary bacterial infections are common and make the clinical
picture more complicated. Some pigs may show relatively little
long-term effect. Severely affected pigs will often be stunted
and take significantly longer to grow to market weight.
Grower-finishers: Predominantly respiratory signs in this group
and in breeder swine with only sporadic CNS signs. Pigs have
temperatures of 41 to 42C and the respiratory signs run from mild
to severe. The pigs may take a week or two longer to reach market
weight and secondary infections can lead to more severe problems.
Sows: The rate of reproductive failure is about 20% in newly
infected herds. Infection in the first trimester may result in
abortion and a return to estrus. Infection in the second or third
trimester results in abortion or stillborn or weakborn pigs (the
latter only if infection occurs close to the farrowing date).
Weakborn pigs that are infected before birth usually die. Note
that there are usually no mummies, the virus is more likely to
cause abortion although it is described as a cause of mummies in
the literature.
Other species affected
Cattle have an intense pruritus and die. They do not shed the
virus so usually the only method for them to contract the
infection is through swine. Infections tend to be sporadic unless
swine and cattle are housed together or in close approximation.
Sheep can transmit the virus to other sheep.
252
Dogs often self-mutilate.
Diagnosis:
Clinical signs and herd history:
FA test: Rapid and reliable.
Best in neonatal pigs.
CNS + Respiratory + Reproductive
Tonsil is the tissue of choice.
Virus isolation: More sensitive than FA in older swine. Brain,
spleen, lung, nasal swabs: Refrigerate samples or freeze on dry
ice. Identify the virus in cultures with an FA test.
Serodiagnosis: ELISA has been the standard. Companion
diagnostic. Latex agglutination test seems to be a little more
sensitive and detect infection earlier.
Lesions: Often minimal or not present. May see serous to
fibrinonecrotic rhinitis and tracheitis, necrotic tonsillitis,
swollen and hemorrhagic lymph nodes of the oral cavity and upper
respiratory tract. Lower respiratory tract lesions may range from
scattered "blotchy" hemorrhages to areas of necrosis.
Keratoconjunctivitis
Focal necrosis of the liver and spleen
Histopathology: Should submit tissues in formalin.
along with tissues for virus isolation.
Treatment:
Send them
Supportive.
Prevention
Vaccination: The use of vaccines had been controversial in the
face of the eradication program that was underway until the
Ablowup@in late 1999-2000. The vaccines are capable of markedly
reducing the clinical signs and resultant losses from
pseudorabies. They do not prevent infection. However, by reducing
clinical signs and shedding they are able to reduce transmission
off site. When producers stopped vaccinating, we were left with a
large population of highly susceptible swine. As of Jan. 2001,
there were 116 infected and quarantined herds in the northern 66
counties of Iowa. That was down from a high of over 800.
Vaccination in this area was required 4 times a year in the sow
herd and once or twice in finishing swine depending on the
infection status of the herd. Periodic testing of swine has been
mandatory in the 66 northern counties. In the year 2000, the ISU
VDL ran over one million serum samples for pseudorabies. By early
2002, some officials were claiming that we have eradicated
pseudorabies from Iowa, however, it was probably still present at
least for a short period of time.
Gene deletion vaccines:
Any vaccine used in the State of Iowa
253
must have a gI deletion.
The only way an animal can have
antibody against the gI glycoprotein is to have been infected with
the field virus.
Modified-live pseudorabies vaccines must be used with caution.
Although they are avirulent for swine, some of them are capable of
producing disease in other animals. Syringes and needles used for
vaccination should not be used for injection of other animals.
PORCINE PARVOVIRUS
General description
Reproductive problems are the only clinical manifestations of
parvovirus infection in swine. The virus crosses the placenta and
infects the fetus at all stages of gestation.
Etiology
All porcine parvovirus isolates are antigenically very similar or
identical. They are also antigenically similar to parvoviruses
from other species of animals but can be differentiated using very
specific serologic tests.
Epidemiology and Transmission
The virus is very stable in the environment and is difficult if
not impossible to eliminate from a swine facility. It is highly
resistant to most disinfectants and heat. The virus multiplies in
the intestine and is found in high titers in recently infected
animals. There is also considerable evidence that immunotolerant
carriers result from in-utero infection. Boars pass the virus in
their semen and it has been shown that they can infect gilts at
breeding. Essentially all swine herds are infected with this
agent and sows pass high titers of antibody through their
colostrum to their piglets. Antibody against this virus is very
long-lived (at least 3-6 months) and in some cases it prevents
replacement gilts from becoming naturally infected until after
they are bred and conceive. If infection occurs following
conception and before development of immunocompetence in the
fetus, reproductive failure results.
Clinical signs
Infection with the virus usually produces no clinical signs other
than reproductive failure even though the virus multiplies to high
titers in rapidly dividing cell types especially the lymphoid
tissues. It does not affect the intestinal crypt cells like the
parvoviruses of other animal species.
254
Maternal reproductive failure is highly dependent upon the stage
of gestation at which infection occurs. Dams may return to
estrus, fail to farrow despite being in anestrus, farrow only a
few pigs per litter, or farrow a large proportion of mummified
fetuses (see below). One may see a decrease in the abdominal
girth as the fetuses die and the associated fluids are absorbed.
Infertility, abortion, stillbirth, and neonatal death have
occasionally been associated with parvovirus infection. When
mummified fetuses are present, gestation length and farrowing
interval may be increased.
If dams are infected prior to 70 days gestation, the fetuses are
susceptible to the virus and will die and be resorbed or will
mummify. After 70 days the fetus will develop a protective immune
response to the virus. Often, only a portion of the litter will
be infected transplacentally.
The stage of gestation at which infection occurs determines the type of clinical picture seen:
Days of gestation
0
Skeletal
mineralization
30-35
a,b,c
d, e
Fetus starts to be
Immunocompetent
65-70
f
114
a=repeat breeders
b=pseudopregnancies
c=small litters
d=mummies
e=increased stillborn
f=normal litters
Diagnosis
Clinical signs: Reproductive problems in gilts but not sows is
highly suggestive. A relative lack of maternal illness, abortions,
and fetal anomalies is not seen with most other causes.
FA test: Submit several mummified fetuses (or fetal lungs) less
than 70 days of gestational age. Antibody develops in later term
fetuses that interferes with virus isolation and antigen detection.
Virus isolation: Not as reliable. The virus is widespread in swine
populations and can easily contaminate cultures. Also takes longer.
Serology: Used when fetuses are not available. Need paired or
sequential sera. Most animals have antibody. If gilts lack
antibody, a diagnosis of parvovirus is ruled out. Can test for
antibody in fetuses.
Prevention
Natural infection prior to breeding: Gilts can be exposed to
seropositive sows or placed in pens that have been recently occupied
by seropositive animals. Infection spreads rapidly in a susceptible
population.
Vaccination: Only killed products are available and are reported to
be effective; however, the vaccines apparently do not work
especially well in the face of residual maternal immunity.
PORCINE ENTEROVIRUS
Enteroviruses are ubiquitous in the swine population and usually
infection is not associated with clinical signs. However, a variety of
clinical conditions including polioencephalomyelitis, female
reproductive disorders and possibly enteritis and pneumonia have been
described. The role of the virus in the latter two is not thought to
be of great importance. Enteroviruses are commonly found in piglets
with or without diarrhea or pneumonia.
Polioencephalomyelitis
Teschen disease occurs sporadically in Europe and to a lesser extent
in Africa. This is the most severe disease and is produced by a
relatively virulent virus. The disease is characterized by CNS
signs and a high mortality.
Talfan disease is caused by a related but much less virulent virus.
This virus is essentially found worldwide. Clinical disease takes
the form of a benign enzootic paresis and rarely progresses to
paralysis.
Diagnosis of polioencephalomyelitis is usually based on isolation of
the virus or demonstration of viral antigen in pigs showing early
nervous signs.
Prevention against Teschen disease can be provided by vaccination,
but less-virulent forms of enteroviral infection are not vaccinated
against.
SMEDI
This is a term that was coined to describe a group of enteroviruses
implicated in stillbirth, mummification, embryonic death, and
infertility. These viruses have been shown to produce the clinical
signs experimentally. The exact importance of them is unknown but
they are thought to not be nearly as important as porcine
parvovirus. The ISU Diagnostic Lab doesn't look for them routinely.
Older literature discusses these as being very important but much
of what was ascribed to SMEDI was probably parvovirus and other
problems.
Diagnosis is based upon finding viral antigen in the fetus.
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Prevention of infection in gilts or sows is usually accomplished by
making sure gilts are naturally exposed prior to breeding. Gilts
should be exposed to the feces of recently weaned piglets and there
should be sufficient virus to infect. There are several serogroups
involved and this has hampered vaccine development.
LEPTOSPIROSIS
Etiology
Leptospira interrogans serovar pomona is the major cause of
leptospirosis in swine throughout the world. Other serotypes, such
as canicola, icterohemorrhagiae, grippotyphosa, and sejroe infect
swine. Only pomona and sejroe produce clinical disease. Some work
indicates that L. bratislava is involved in disease in swine but
this has not been well demonstrated.
Epidemiology
Leptospiral infections in swine are relatively common but clinical
disease is not recognized as frequently because most of the
infections are subclinical or inapparent. The epidemiology varies
somewhat with the serovar.
A large number of species of wild and domestic animals have been
shown to be capable of carrying L. pomona and spreading it to swine.
Wildlife is the major source of infection for autumnalis and
grippotyphosa. Serovar icterohemorrhagiae has the rat as its
primary host.
Transmission occurs through breaks in the skin, direct penetration
of mucous membranes, or through conjunctiva. A relatively low
infectious dose is required. The organism disseminates and grows in
many tissues but has a definite predilection for the kidney.
Antibody can be detected in the blood in 5 to 10 days and the
organisms disappear from the bloodstream at that time. The
organisms survive in the proximal convoluted tubule and are shed in
the urine of infected animals for long periods of time following the
initial septicemic phase. Leptospires are able to survive in the
undiluted urine of swine for several hours if the urine is neutral
or slightly alkaline. If the urine is diluted by water or falls in
poorly drained soil, the organisms remain viable for long periods of
time.
Transmission from infected boars into a sow herd has occurred.
However, transmission may not have occurred through breeding.
Transmission from cattle to swine and vice versa has been
demonstrated.
Oral exposure from the feed is a concern and may be a method of
introduction of the infection into a confined herd.
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Clinical signs
Most of the sows that become infected do not show marked clinical
signs. Most often, the effects are not observed. The disease
spreads gradually through the herd and only a few animals will be in
the acute phase at any given time.
Infection with leptospira during the last half of gestation may lead
to abortions, stillbirths, and neonatal deaths. Pigs may be born
prematurely and survive for a short period of time. The organisms
readily pass through the placenta to the fetal fluids and some or
all of the fetuses may be infected. Abortions and stillbirths
usually occur one to four weeks following infection of the sow and
thus most sows have antibody titers by the time of abortion.
Diagnosis
Diagnosis can present a problem because of the relatively mild
clinical disease that occurs and the low numbers of organisms that
persist following generation of specific antibody.
Culture: Definitive but difficult. Can be found in freshly aborted
fetuses but the organisms die quickly.
Serology: Microscopic agglutination test (MAT) is the standard test
for detecting antibody. Interpretation of the test is dependent
upon knowledge of the vaccination history and herd health. Some
animals develop only low, short-lived titers. It is best to use the
test on a herd basis, rather than on individual animals.
Infected swine usually develop titers of 1:100 or greater.
Vaccinated swine may develop titers but only a few may develop
titers of 1:100 or greater.
RFLP patterns (Restriction Fragment Length Polymorphism)
Prevention and Control
Maintain animals in a clean environment without standing water.
Segregate known infected animals from others: Difficult because of
the lack of clinical signs. Test any animals coming into the
breeding herd. This may not be very useful if done on an individual
basis. It is better to buy stock from herds free of the organism.
Vaccination is probably the best. Commercial bacterins containing
the most common serovars are readily available and are often
included in vaccination programs for breeding swine. Gilts should
be given 2 doses prior to breeding. Protection may last for only 6
258
months and it is best to repeat the vaccination at this interval.
Other animals and humans may be infected. As with many other
diseases, it is best to keep other animals out.
Treatment
Tetracyclines
BRUCELLOSIS
Swine brucellosis was once thought to be widespread in the U.S.
especially in areas of concentrated swine production. This was
based almost entirely upon serological testing of swine herds and to
some extent on clinical signs. In reality, the plate agglutination
test has a high rate of false positives and the true incidence may
not have been anywhere near the incidence reported in the
literature. In addition, the plate test used for diagnosis does not
differentiate between Brucella suis and Brucella abortus and the
majority of the cases of swine brucellosis may have been due to B.
abortus. The state-federal cooperative program to eliminate B.
abortus and Brucella suis has resulted in a dramatic decrease in the
numbers of infected herds in the U.S. Swine brucellosis is
esentially confined to the states that have feral swine. Iowa has
been free of brucellosis for 30 years. However, a negative
serologic test is still required for interstate shipment.
Etiology
Brucella suis biovars 1 and 3 account for the disease seen in the
U.S. Biovar 2 occurs in Europe. Biovar 4 is widespread in reindeer
and caribou but is apparently not pathogenic for swine.
Epidemiology
Swine are the most common hosts for B. suis biotypes 1 and 3 and
essentially all infections are a result of swine to swine transmission.
Feral swine are able to maintain the infection and can serve as a
source of the organism for other animals. Transmission of the organism
in swine is almost entirely by a venereal route, although it can
readily be transmitted by ingestion. The organism does not survive
long in the environment and is readily killed by sunlight and many
commonly used disinfectants. They will survive in the frozen state in
organic material for up to 2 years, however. Infected sows that abort
have shed the organism in the vaginal discharge for years but usually
the shedding only lasts 30 days or so. The organism tends to be more
persistent in boars and most of these never completely clear the
organism.
Clinical signs
The clinical signs can vary greatly.
The majority of herds may have
259
no clinical signs at all that are readily recognized. Abortion may
occur at any time in gestation with the highest rate occurring when
the sow or gilt is infected at breeding. Many of the early
abortions can easily be missed unless one looks at the breeding
records and finds a high percentage of sows returning to estrus at
30 to 45 days. Boars may have orchitis but usually the secondary
sex organs are affected. Infertility can result. Suckling and
weaning pigs may develop spondylitis and become paralyzed or lame.
This can occasionally occur in older swine.
Diagnosis
Culture: Said to be the most accurate. Routine lymph node culture
is as good as serologic testing and can serve very well as a routine
epidemiologic tool.
Serology: Used most frequently. Must be used on a herd basis.
Studies have shown up to 18% of normal swine may be serologically
positive at a low dilution (1:25). Some infected swine may be
incapable of ever forming detectable antibody against the organism
and thus test falsely negative. In addition, titers may be slow to
develop.
Prevention and Control
The organism has essentially been eliminated from most of the
intensive swine rearing areas of the U.S. The most successful method
of eliminating the disease is to depopulate known infected herds,
clean up the facilities, and then repopulate with non-infected
swine. The disease does not recur when these procedures are
followed rigorously. If there are only a few seropositive animals
in a herd, these could be removed and then the herd retested in case
these were false positives.
The cooperative state-federal-industry program utilizes routine
monitoring of sows and boars that go to slaughter. Details of the
program can be found in the Uniform Methods and Rules for
Brucellosis Eradication and from the State Veterinarian=s office.
TUBERCULOSIS
Etiology
Tuberculosis in swine can be caused by any of the three main species
of mycobacteria, M. avium, M. tuberculosis and M. bovis. The vast
majority of the infections are caused by M. avium serovars 1, 2, 4,
and 8 in the U.S. However, many other serotypes have been isolated
from tuberculous lesions in swine.
Epidemiology
260
The majority of infections in the past in the U.S. have been
associated with contact with infected poultry. Because of changes
in management and the decreased cross-species contact there has been
a decrease in the incidence of swine tuberculosis. Also, current
practices for raising poultry results in a rather short lifespan
even for laying hens and the organisms do not have as great a chance
to build up in the environment. Wild birds have also been
documented as sources of the organism for swine. Once in the
environment, the organisms can persist for long periods of time (up
to 4 years in one study). Infection is almost always by ingestion.
When M. tuberculosis is found, one needs to consider humans as the
most likely source. M. bovis can be transmitted by a number of
animals but the marked decrease in incidence of bovine tuberculosis
in this country has limited the number of swine infected with this
organism.
Lesions and Incidence
There is no routine tuberculin skin testing performed in swine
similar to the program in cattle. Swine can be skin tested on the
ear or vulva. Some infected swine will be non-reactive and the test
should be repeated especially when testing a herd with known
infected animals. Infection is detected at the time of slaughter
with routine meat inspection. The lymph nodes of swine are
carefully examined for the presence of gross lesions of
tuberculosis. Tuberculous lymph nodes are almost always cervical or
mesenteric nodes. The lesions are usually caseous and yellowish
white and vary from a few millimeters in size to involvement of the
whole node. Lesions caused by M. tuberculosis and M. bovis are more
likely to be calcified and more encapsulated. The encapsulation
makes it easier to separate the lesion from the surrounding
tissue.M. bovis tends to cause a much more disseminated infection
than the other two organisms. In some studies, a relatively high
percentage of the tuberculous lymph nodes were actually infected
with Rhodococcus equi rather than Mycobacterium sp.
There are basically four categories or dispositions that swine fall
into:
Swine with no lesions
Swine with lesions attributable to tuberculosis: These are passed
for consumption if the lesions are not disseminated.
Swine passed for cooking, PFC: These have disseminated lesions
but the carcass is not emaciated.
Swine with disseminated lesions with an emaciated carcass:
Condemned
Figures on incidence vary a little. The most recent numbers
available indicate about 3 to 4 animals per 100,000 slaughtered are
condemned, about 12 to 18 per 100,000 are PFC, and about 0.6% of all
swine slaughtered in the U.S. have lesions attributable to
261
tuberculosis. These figures represent only gross, meat inspector
interpretation of lesions and probably include swine infected with
other organisms that may cause similar lesions. These figures are
the result of a steady and somewhat dramatic decrease in the
incidence of disease from the 1970's to the 1990's.
Swine that are condemned represent an obvious loss, but the PFC
category represents a major decrease in carcass value. The carcass
is only worth about 1/3 of its normal value.
Diagnosis
Gross lesions are suggestive.
Histopathologic exam plus staining for acid fast bacteria
Bacteriologic culture
Tuberculin skin test
Prevention and control
Elimination of contact between swine and poultry and wild birds.
Thorough disinfection of premises that have had swine with
tuberculosis. Elimination of dirt floors is beneficial since the
organism is better able to survive in the soil.
Thorough cooking of garbage or meat byproducts that go into swine
feed.
CYSTITIS: Actinobaculum suis
Etiology
Actinobaculum suis (Eubacterium suis, Corynebacterium suis and
Actinomyces suis have all been used as names) has been recognized as a
cause of pyelonephritis/cystitis in sows for over 30 years. Work in
Europe has indicated that it is a major cause of death loss in sows,
especially in certain types of housing. Infections are increasingly
being recognized in this country. The organism is an obligate anaerobe
and is relatively difficult to culture.
Epidemiology
The organism is apparently widespread in the swine population and
some consider it to be a normal component of the porcine microflora.
The disease is more common in sows housed in gestation stalls, due
to the greater likelihood for spread from one sow to the next and a
reduction in activity, water intake and urination. The organism is
carried in the prepuce of the boar.
Clinical signs
The organism produces urease which splits urea into ammonia which,
262
in turn, damages the bladder mucosa. A wide range of clinical signs
may be observed. They range from sudden death to acute or chronic
renal failure.
In acute disease the sow may have hematuria and pyuria, be reluctant
to get up and appear lame in the rear. The mortality is high unless
treated aggressively. If the animal survives the acute disease, it
may show vaginal discharge, be a repeat breeder and be culled
because of poor reproductive performance.
Lesions
These consist of a thickened bladder wall with a hemorrhagic
epithelium. The bladder may contain purulent exudate and deposits
of sand-like material that are usually composed of struvite.
Diagnosis
Bacterial culture: Field isolation works best. Do not expose to
oxygen. Cut a small slit in the bladder wall and collect the sample
on a special anaerobic swab.
Treatment
Ampicillin works the best.
In chronic infections, response to therapy is disappointing.
Prevention and control
Management: Maximize water consumption, increase salt in the
ration, frequent watering and twice a day feeding to get sows on
their feet, general cleanliness and good ventilation.
Cull affected animals or isolate them from the other swine in the
unit.
EPERYTHROZOONOSIS
Historically it has been considered a cause of acute icterus and
anemia in young pigs under stress. More recently it has been
observed in a wide age range from piglets to pregnant sows.
Etiology
Mycoplasma haemosuis (formerly Eperythrozoon suis). The anemia
produced is very similar to that observed with bovine anaplasmosis
and feline Mycoplasma haemofelis infection.
Epidemiology
M. haemosuis is a pathogen only of pigs.
Experiments proving
263
arthropod transmission in swine have not been reported although
disease occurs mostly in summer. Transmission through needles and
equipment is likely. In-utero and oral transmission have been
demonstrated. The overall incidence is less than 8% seropositive by
the indirect hemagglutination test (IHA).
Clinical signs
Pigs under 5 days of age are most likely to show clinical signs of
anemia and icterus. Most pigs recover within a week but, in some,
anemia may persist after weaning especially if there are concurrent
bacterial or parasitic infections. General unthriftiness may occur
and complicate enteric or respiratory infections.
Feeder pigs are rarely observed with clinical disease although
reports used to be more common. Probably due to the use of
medicated feed.
Sows (usually those under stress immediately prepartum) may be
acutely affected and may have a high fever and anorexia for 1-3
days. Chronically infected sows show anemia, icterus and
unthriftiness. A portion of the herd may become debilitated and
some may die of secondary infections. Sows with either acute or
chronic disease show decreased conception rates.
Diagnosis
Blood smears: Used in acute cases where the organism can be
demonstrated in the blood. Organisms are easier to demonstrate in
young pigs. Diff-Quick or other stains can be used.
IHA: Indirect hemagglutination is used for diagnosis of subclinical
infections.
Treatment
Arsenicals and tetracyclines show beneficial effects.
Iron dextran in anemic piglets
Control other diseases
Prevention
Vaccines are not available
EXOTIC VIRAL DISEASES OF SWINE
Hog cholera and African swine fever are the two major exotic viral
diseases pose a threat to the swine industry of the US. Both of these
are characterized by:
264
High fever
High mortality
Lymphoid involvement
Skin erythemas to effusions
HOG CHOLERA
Classical swine fever or European swine fever
Pestivirus (enveloped) that is closely related antigenically to BVD
virus of cattle. The virus is not particularly resistant but will
survive for relatively long periods in some substrates.
Acute and chronic strains of the virus exist: Seems to be related to
virulence with acute forms being more virulent. The chronic forms are
inhibiting eradication efforts because they do not cause severe
terminal illness in a short period of time. During the US eradication
program, 55% of isolates were of low virulence during the period 1965
to 1975.
Eradication efforts
The disease was
began in 1962.
eradication was
the disease for
costing $50 million/year when US eradication efforts
The last case was reported in 1976. The cost of
about $140 million (vs. $1.1 billion to live with
the same period).
Epidemiology
Worldwide distribution but has been eliminated from the US, Canada
and several European countries. There was a significant outbreak of
disease in the United Kingdom in 2000 followed by FMD in 2001. Both
diseases have apparently been present in China and Southeast Asia.
HCV is present in Romania and Serbia.
Hosts:
Domestic swine, wild boar
Transmission: Direct contact via the oro-nasal route. Primary site
of invasion is the tonsillar crypt with viremia and spread to the
lymphoid tissues.
Garbage feeding
The virus can remain viable in pork and pork products and be
introduced into HCV-free countries by this route.
Mechanical vectors:
arthropods.
Personnel, equipment, pets, birds, and
Wild pigs. This has been the problem in Serbia where wild pigs
coming over the border from Romania have brought the disease into
the country.
265
If exposed in-utero to a HCV of low virulence, some piglets may
remain healthy for many months and shed virus continuously. They
may also have a "late onset" disease.
Clinical signs
Incubation period 2-4 days
High fever
Excitable at first followed by apathy and anorexia
Marked ocular discharge:
Severe conjunctivitis
Hind leg incoordination, huddling, diarrhea, dyspnea, recumbency
with paddling.
Morbidity and mortality 100% with survival only 10 to 20 days PI.
In subacute HC, pigs show less severe signs of disease and succumb
within 30 days. In chronic disease, pigs may survive 100 days or
more.
Congenital tremors in piglets with cerebellar hypoplasia due to
infection with strains of low virulence.
Pathogenesis
Endothelial damage including CNS cuffing
Disseminated petechiae and ecchymoses especially in the skin,
larynx, bladder, brain, and kidney (turkey-egg kidney). Multifocal
infarcts of the margin of the spleen are characteristic but
inconstant.
Button ulcers (because of infarcts) of the colon
Lymphopenia
Diagnosis:
Relatively easy in the acute form.
Reportable disease
FA on tissues (tonsil is the first tissue to become positive). This
is the standard test in many countries. Pigs can be infected with
BVDV and the FA test will not distinguish these.
SN test: Best in the chronic forms because antibody titers may be
low or absent in the acute and late onset disease. Can distinguish
BVDV infections.
VI
266
Differential diagnosis:
African swine fever: Rarely see button ulcers and spleen infarcts.
Edema of the lungs and gall bladder wall and excessive pericardial,
pleural, and peritoneal fluids not seen with HCV.
Salmonellosis
Erysipelas
AFRICAN SWINE FEVER (ASF)
An acute to chronic disease of swine and wild boars with a high
morbidity and mortality. Caused by an Iridovirus, an enveloped DNA
virus. In Africa wart hogs and possibly giant forest hogs and bush
pigs serve as reservoirs of the virus but do not show clinical signs
even when inoculated with the most virulent strains ASFV. These
animals may be persistently viremic.
The disease was initially confined to Africa, but spread to Portugal in
1957, Spain in 1960, Cuba in 1971, and Brazil, Dominican Republic and
Haiti in 1978. Periodic outbreaks have occurred in France, Italy,
Holland and Belgium but the disease was eradicated from these
countries. A 1999 outbreak in Portugal was apparently the last time the
disease occurred in Europe as of 2006.
Epidemiology
The virus survives for prolonged periods under most environmental
conditions especially when protected in meat or blood. South
American outbreaks were most likely the result of feeding improperly
processed garbage containing pork scraps (The first outbreaks were
in pigs fed garbage from international airlines). Survives 5-6
months in processed hams.
Does not survive well on premises after depopulation (3 days to 3
months)
All secretions and excretions from acutely infected domestic pigs
are infectious.
Transmission
May occur via ticks or hematophagous insects. This was important in
the outbreaks in Spain and Portugal.
Transmission commonly occurs
by introduction of infected swine or indirectly through contaminated
personnel and equipment.
Clinical signs
Incubation period of 1-4 d
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Fever:
105 - 108oF
Hyperemia of the skin
Abortions
Mortality 100% with virulent forms, but mortality drops rapidly as
the virus circulates in swine herds. The outbreaks in Spain,
France, Brazil, and the Caribbean had mortality rates of 10% with
primarily chronic respiratory forms and persistent viremia.
Surviving pigs with the chronic form are poor doers.
Pathogenesis
Enters via mouth or URT-->tonsils and spreads quickly to the
mandibular lymph nodes and throughout the body via blood and lymph.
When injected (tick bites) the virus spreads rapidly to the RES and
lymphocytes.
Lesions
In acute ASF due to highly virulent virus, the lesions are usually
marked; whereas in subclinical, mild, or chronic disease, the
lesions may be minimal or absent.
Severely hemorrhagic and edematous lymph nodes (look like hematomas,
often with little discernable lymphoid tissue.
Splenomegaly
Petechial hemorrhages throughout the body. Lungs, kidneys and lymph
nodes are often examined for characteristic lesions. Kidneys may be
very hemorrhagic.
Immune response
Antibody forms readily but is not protective.
exists.
No vaccine currently
Diagnosis
Hemadsorption (HAd) test is the standard test but some strains of
virus, especially low virulence strains, may not adsorb RBCs or will
do so only after several passages in the laboratory.
Direct FA test:
disease.
Useful but may not be positive in clinically mild
Pig inoculation with suspected tissues is one of the most sensitive
268
and reliable tests.
Once the disease has been diagnosed in an area, observation of the
clinical disease and gross lesions is reliable.
Control
Slaughter all infected and exposed swine. Cuban outbreak resulted
in slaughtering 400,000 pigs. Dominican Republic and Haiti: All
domestic and most of the feral swine were eliminated.
Restrict swine and pork movement
Thorough cooking of garbage before feeding it to swine.
VESICULAR DISEASES
Foot and Mouth Disease
General
A vesicular disease affecting cloven-hoofed animals including wild
and domestic ruminants and swine. It has the broadest host range of
the vesicular diseases affecting domestic animals and is the most
easily transmitted. In addition to cloven-hoofed animals,
elephants, hedgehogs, and even humans have been infected with the
virus. Horses are totally resistant to infection. FMD outbreaks
have occurred in the U.S. on at least nine separate occasions and
have been stamped out aggressively using total slaughter of all
affected and contact animals. There have been no outbreaks in the
U.S. since 1929. The disease is said to be one of the most
economically important worldwide when one includes the adverse
effects on trade.
Etiology
Foot and Mouth Disease virus, an Aphthovirus (picornavirus). There
is a great deal of genetic rearrangement of the various strains of
FMDV resulting in multiple antigenic variants. Some strains develop
genetic variants and a rate of 10-4 . The classic European types (A,
O, and C) are the most widespread and are the types found in South
America. South African types (SAT1, 2, and 3) are found in Africa
and the Asia 1 type is found in Asia.
Epidemiology and Transmission
269
Most of the virus particles are found in the epithelial lesions of
affected animals and the majority of transmission is thought to be
through infected saliva. During the early febrile period however,
all tissues, excretions and secretions contain the virus including
semen. The virus does not survive long in muscle tissue because of
the acidic environment but will survive in bone marrow and in organ
meats. Several outbreaks have been traced to the importation of
fresh meat or to meat scraps in uncooked garbage. The U.S.
currently has an embargo on any fresh meat, hides or offal
originating from countries infected with FMD.
Following an outbreak and total depopulation of all the animals on a
farm, the virus disappears fairly rapidly except from protected
dark, moist areas.
In countries endemic for FMD, the virus can
apparently persist in recovered animals but is not readily
transmitted by natural means. However, several outbreaks have been
observed in isolated areas and the chronic carrier state has been
implicated as a source of the virus. Cattle and sheep have been
found to harbor the virus for 1 to 5 months and, in one study in
cattle, up to 15 months. Vaccinated cattle can be subclinically
infected with virulent virus and carry the virus for long periods.
Calves from cows immunized with modified live virus have been shown
to carry the virus up to a year of age. It is theorized that the
various chronic carrier states may be important in the development
of variants of the virus. No good data exists for the role of birds
in transmission but they may act strictly as mechanical vectors.
Virus in milk has been associated with transmission through trucks
picking up milk at various farms.
Humans can inhale the virus and
carry it in their throats and nasal passages for up to 28 hours.
Humans can also become infected with the FMD virus and develop
vesicular lesions although this seems to be relatively uncommon.
Because of this, it is wise to wear protective, boots, gloves and
clothing when handling infected animals. The clothing must be
thoroughly disinfected following use.
Clinical disease and lesions
The sudden onset of lameness in a group of animals and the finding
of vesicular lesions is characteristic and warrants immediate
notification of the State Veterinarian. In cattle, the disease is
characterized by depression, elevated temperature, and the
appearance of vesicles containing a clear fluid on the epithelium of
the mouth, tongue, muzzle, interdigital space, tops of the claws,
teats and sometimes the surface of the udder. Other mucous
membranes may develop vesicles as well. The vesicles contain large
numbers of virus particles and those in the mouth are especially
prone to rupture within a few hours after formation. Following
rupture, large whitish flaps of epithelium may be found partially
covering the affected areas. In many animals, a large part of the
epithelium of the tongue may be lost. The virus is rapidly
transmitted to other animals in the herd. The incubation period
ranges from less than 48 hr to no more than 4 days.
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About 24-48 hours after the formation of vesicles, the virus enters
the blood and multiplies in various organs. The heart muscle of
calves is particularly affected by some strains of the virus and
high mortality can result from myocardial necrosis (yellowish
streaks are found in the heart muscle).
Affected cattle become lame and champ their jaws and drool because
of the mouth lesions. Most lose condition rapidly. Secondary
bacterial infection especially in the foot area complicates the
recovery. The claws may be totally undermined and eventually
sloughed. Mastitis in lactating dairy cattle can be a major cause
of economic loss.
Mortality in due to the virus infection is
generally low (1 to 3%) but has been as high as 50% in some
outbreaks.
Disease in swine is generally similar to that in cattle. Pigs
develop lameness initially as the most conspicuous sign. Large
vesicles may appear on the snout and other epithelial surfaces.
Sheep and goats also show lameness most commonly but usually are not
as severely affected as cattle.
Diagnosis
Clinical signs
Serologic tests- preferred due to rapid turnaround time. Recently
recognized that other viruses serologically cross-react with FMD and
some normal cattle have antibody.
Animal inoculation
Animal
FMD
VS
VE
Horse (intradermal-intralingual)
Cow (intradermal-intralingual)
Cow (intramuscular)
Guinea pig (intradermal-footpad)
+
+
+
+
+
+
-*
-
*Small local lesions produced without generalized disease.
Swine are not used in the above scheme because they are susceptible
to all the viruses.
Control and prevention
During an outbreak, aggressive quarantine measures need to be
instituted immediately for several miles around affected farms.
This means that sufficient personnel to enforce the quarantine need
to be immediately mobilized. No livestock should be allowed to move
within the quarantine area and of course none should be allowed to
leave. Dogs, cats, and other pets should be confined. Humans are
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also confined and allowed to move from one place to another only
with special permission and only after thorough disinfection. All
affected animals and all animals that have had contact with them are
slaughtered and buried on the farm with quick-lime.
The U.S., Canada, Japan, Australia, New Zealand, Great Britain and
Ireland have consistently dealt with FMD using aggressive total
depopulation of affected and contact animals. As a result, the
disease has never gained a firm foothold in these areas. In the
U.S., a policy of gradual restocking of a farm beginning 30 days
following total disinfection has been used. A few animals are reintroduced to the premises and inspected every other day for the
first 10 days then twice a week for the next 20 days. Additional
animals may be added to the herd at that time but it is kept under
close surveillance and quarantine for 90 days following the initial
disinfection. Because of the potential impact of FMD on the U.S.
animal industry, the U.S. currently stockpiles sufficient vaccine
for use in slowing an epidemic should one occur.
Ships and planes originating in countries where FMD is found are not
allowed to offload garbage in the U.S. Only canned or cured meat is
allowed to be imported from FMD countries.
In areas where FMD is enzootic, vaccination has been the method of
choice for controlling outbreaks. The traditional inactivated
vaccines, are generally produced in cell cultures (in monolayers or
in suspension), inactivated with first-order kinetic inactivants,
and formulated with an adjuvant. These vaccines have been successful
when applied systematically and a rigorous quality control (i.e.
efficacy or potency tests) were carried out . While most of the
control and eradication of FMD from Western Europe was based on the
use conventionally adjuvanted vaccines in cattle ( aluminum
hydroxide), significant progress has been made in South-America
through the utilization of double oil emulsion adjuvant FMD vaccines
for cattle. The oil adjuvant concept for FMD vaccines has also been
used with success in pigs in other parts of the world. Argentina
successfully eradicated FMD by 1994 using a trivalent vaccine (O, A
and C) in a single oil adjuvant. Infected herds were slaughtered
and surrounding herds were vaccinated.
Historically, problems with vaccination have arisen. The immunity
generated by many of the vaccines is relatively short lived and it
is thought that having animals partially immune to certain virus
types has provided the necessary pressure on the virus to allow
antigenic variants to arise.
Vesicular Exanthema of Swine
General
Causes vesicular lesions in swine
that are grossly
272
indistinguishable from those of foot and mouth disease. The disease
was first described in California in 1932 and was thought to be FMD
until two years later when it was determined to be a separate virus.
The virus does not spread as rapidly as FMD and the only domestic
animals routinely infected are swine which is very different from
FMD. The virus was confined to the state of California for 20 years
without the institution of any control measures.
In 1952, the
virus suddenly spread eastward and within a few months, outbreaks
had been reported in 42 states. An eradication program was
instituted and the virus was Aeradicated@ from the U.S. in 1959.
Etiology
Calicivirus.
Epidemiology and transmission
A very similar virus was isolated in 1972 from sea lions on San
Miguel Island off the coast of California. This virus produced
lesions in swine identical to those of VES and VESV produced lesions
in the sea lions identical to those of San Miguel Sea Lion virus
(SMSV). SMSV was isolated on several occasions from opaleye fish
and it has been postulated that the original outbreaks arose from
feeding raw garbage containing scraps from infected fish. The
disease was then transmitted to swine through garbage feeding.
Once established in the swine population, the disease was spread by
two routes: through the garbage and by introduction of infected
swine into a clean herd. Almost all the outbreaks occurred in
swine fed raw garbage. The virus apparently does not last long in
the environment since swine placed in pens where actively infected
pigs had recently been housed, did not develop infection. The
infection also spreads relatively slowly through a group of swine
and fully susceptible swine may not develop disease in a given
group. Lesions may take three or more weeks to completely heal,
Unlike FMD, other domestic animals are not routinely infected.
Horses and dogs have been infected with some of the four serotypes
by intralingual injection, but this is not easily done. Guinea pigs
are not affected by the virus.
Clincal disease and lesions
About 12 hours before the appearance of vesicles, swine will have a
fever and will be off feed. Vesicles of varying size appear on the
lips, tongue, snout, footpads and the skin between the claws,
coronary band, dew claws, and teats of nursing sows.
The vesicles
rupture easily, leaving a raw surface often with flaps of whitish
skin attached. The animals can become quite lame and will refuse to
rise when prodded and may walk knuckled over on their fetlocks or
knees. The lameness can persist for several weeks although the
mouth lesions heal rather quickly.
Swine experience a rapid and
extensive weight loss.
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Mortality is low in adult swine. Nursing pigs may have a high
mortality rate due to the development of lesions in the oral and
nasal cavities that may cause suffocation or from starvation because
of agalactia in the sows.
Control and Prevention
Because of the similarity of the infection to FMD, depopulation is
required. Feeding of raw garbage is prohibited. The reservoir
still exists in the sea lion and fish populations.
Swine Vesicular Disease
General
Disease was first described on two farms in Italy in 1966. The
disease was rapidly disseminated to many countries in Europe, Japan
and Taiwan. The disease produces lesions that are clinically
indistinguishable from other vesicular diseases of swine. The
disease has not been reported in the U.S.
Etiology
An enterovirus that is closely related to the Coxsackie B5 virus
that affects humans.
Epidemiology and transmission
Less is known about this virus that the other vesicular diseases.
In the outbreak in Italy, about 25 % of swine in contact with the
infected group developed lesions. No new cases were seen after
about 3 weeks. In Japan, the virus was isolated from the feces of
healthy pigs. Apparently, subclinical infections occur and carrier
pigs may be an important part of the transmission.
Disease and Lesions
Indistinguishable from other vesicular diseases.
Morbidity in
natural outbreaks has been reported at 25 to 65%. A mild nonsuppurative meningoencephalitis throughout the CNS was observed in
both natural and experimental disease.
Control and prevention
Cooking all garbage or no garbage feeding
Strict quarantine and slaughter of all affected and exposed swine
Vesicular Stomatitis
General
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Cause of fever and vesicular and ulcerative lesions primarily in
horses, cattle and swine. Lesions in cattle and swine cannot be
readily distinguished from those of FMD.
Etiology
Vesicular stomatitis virus, a Rhabdovirus. There are two main
serotypes of virus (New Jersey and Indiana). The Indiana serotype
seems to be more diverse and is divided into three subtypes but even
the New Jersey serotype possesses a lot of genetic variation. The
New Jersey serotype is thought to be the most virulent.
Epizootiology and transmission
Not as clear-cut as the other vesicular diseases. Disease occurs
only in the Western Hemisphere and is more prevalent in tropical and
subtropical areas. In some cases there appears to be an arthropod
reservoir and/or vector involved because of the occurrence of the
disease in late summer. Epidemics have occurred in winter months as
well however. A wide variety of animals can be infected with the
virus, but all of those studied did not develop sufficient viremia
to account for infection of arthropod vectors. In other outbreaks,
it seems that the virus has somehow Aseeded down@ pastures and
multiple cases occur at separate sites within a given area. In some
cases, the virus seems to move down river valleys. It seems to be
more common in areas that are shaded and moist. Direct transmission
between animals is apparently not important, because animals on
neighboring farms often are unaffected. Disease tends to recur from
year to year on certain farms and pastures.
Disease and lesions
In horses and cattle, oral lesions are more common than lesions on
the feet. The lesions may appear as blanched areas with little or
no vesiculation. Even when vesicles are present on the oral mucosa,
they rupture rapidly and leave raw denuded ulcers. Drooling, teeth
grinding, lip smacking and rubbing affected areas are most commonly
observed. Lactating cattle experience a sudden drop in milk
production and develop lesions on the teats that can be quite
extensive and severe.
Lameness characterized by hyperemia and ulceration of the coronary
band are most common in horses and swine.
The disease course is usually only 3-4 days and most animals recover
without complications. Lesions usually heal with 2-3 weeks.
Persistent lameness can occur due to damage to the coronary band.
Humans are susceptible and can develop a fever and vesicles. Most
of the human cases have involved those working with the virus in the
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laboratory or with vaccine production where large numbers of virus
particles are present.
Otherwise, most of the human infections are
subclinical. In certain areas where the incidence in animals is
high, 50% of the human population may have antibody titers.
Diagnosis
Notification of state or federal authorities is essential as with
all vesicular diseases
Demonstration of viral antigen in tissues
Paired serum samples for antibody titers.
Virus isolation and identification
Control and prevention
Complicated by lack of understanding of the epidemiology and
transmission.
Quarantine of affected premises until all clinical signs disappear.
Once diagnosed, extensive control measures are not as warranted as
with other vesicular diseases.
Vaccination can assist in control and are primarily used to protect
dairy cattle.
Vaccines were used in the 1982-83 outbreak in the
U.S.
Agalactia Syndrome of Sows (MMA)
This problem was initially termed "mastitis, metritis, agalactia
(MMA) syndrome. It had historically been a major factor in piglet
mortality but is not as common as it was 15 or 20 years ago. The
syndrome is an acute problem, occurring 12 to 72 hours after
parturition and characterized by agalactia or hypogalactia.
Etiology
Physiologic factors. Hormone imbalances have been blamed for many
cases but the exact nature of the imbalances have not been
clarified.
Coliform mastitis may be involved in some of the cases. E. coli,
Klebsiella pneumoniae or Enterobacter spp. are the most common.
Vitamin E - Selenium deficiency has a role in resistance to
infectious mastitis. Adequate supplementation has been shown to
have a beneficial effect.
Toxemia associated with retained pigs is an occasional cause.
Mycotoxins have been implicated but many believe mycotoxins to be
unlikely causes. Both ergot and zearalenone have been studied and
experimentally cause agalactia.
276
Hypocalcemia and ketosis are involved only rarely.
Clinical signs
Coliform mastitis
There is usually a high fever (105-107F) in the early acute
stages that may decline rapidly in severe disease. The sows may
be depressed and lethargic. The mammary glands are swollen,
hyperemic and have a pitting type edema. Milk flow is markedly
reduced, and may be coming only from unaffected portions of the
gland. The affected glands usually involute rapidly. Total milk
flow from the sow will be adversely affected. If the sow
recovers, milk flow will return to relatively normal levels
except in the affected glands.
Inappetence may be a contributing factor. Many sows don't eat
during the first 12-24 hours after farrowing. Sows affected with
coliform mastitis or other diseases such as TGE may not eat for
several days.
Constipation often occurs in coliform mastitis but has also been
implicated as a primary cause of agalactia in it's own right.
Metritis.
Usually not associated with the syndrome. There may be excess
vaginal discharge (lochia) but this varies a lot between normal
sows. If the discharge is purulent or bloody, there is probably
an infection.
Agalactia. Detection requires knowledge of normal nursing behavior
and careful observation of the clinical condition of the piglets.
Diarrheal diseases in the piglets and other conditions can mimic
starvation.
The behavior of the piglets is important to note. Nursing can
take place during farrowing because milk is continually
available. Normally, during the first 12-24 hours after birth
the piglets sleep and nurse at irregular intervals. After this,
nursing occurs every 40 to 60 minutes. It is important to note
that not all normal nursings result in milk letdown. Sows with
agalactia may not allow nursing this frequently, have fewer
successful nursings and may produce little milk. Glands with
mastitis may produce no milk.
There are five phases in normal piglet nursing.
1.
2.
Jostling for position on the udder.
Nosing the udder with vigorous up and down movements of
the head.
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3.
4.
5.
The quiet phase during which piglets suck on the teats
with slow mouth movements (about 1 per second).
Suckling with rapid mouth movements (about 3 per
second). Milk can be expressed only during this short
time.
A brief return to sucking with slow mouth movements and
nosing the udder.
When pigs are squealing a lot, are continuously trying to nurse
and drink water from the sows' watering cup, they are probably
not getting enough milk. The pigs progressively lose weight and
eventually become lethargic, pile up in a warm area, become
emaciated, and die. Death generally occurs between 2 and 5 days
of age due to hypoglycemia, diarrhea and being overlain by the
sow. The severity of the agalactia or hypogalactia determines
the clinical progession of starvation. Necropsy of the piglets
reveals dehydration, emaciation, empty stomachs and serous
atrophy of body fat.
The course of the disease in a sow varies with the cause of the
agalactia or hypogalactia, it's severity, continued nursing attempts
by the piglets so that the sow will resume lactation, and medication
given to the sow.
Diagnosis - Coliform mastitis
Clincal signs of agalactia based on close observation of sow and
piglet behavior during nursing attempts.
Bacteriologic culture is possible but somewhat difficult. Because
the mammary gland is segmented, milk collected from a single gland
may not contain any secretion from the infected portion of that
gland. One must collect milk from several glands during the period
of milk letdown.
Rule out other causes such as TGE, erysipelas, pseudorabies.
Prevention
It is essential to maintain good sanitation in the farrowing unit to
minimize contamination of the teats. Avoid damage to the teats from
fighting and other problems. Select sows with low incidence of
lactational problems.
Autogenous bacterins are generally of questionable value.
available on core-mutant vaccines.
Vitamin E, Selenium supplementation may be useful.
IU/kg selenium at 0.1 ppm.
No data
Vitamin E at 50
278
Treatment
Oxytocin 20-30 units several times a day to maintain milk flow.
Gently!
Antimicrobials may be of some use, especially aminoglycosides.
Banamine at 1 mg/lb - 2 doses.