PRRS (PORCINE REPRODUCTIVE AND Gijapon

RESPIRATORY SYNDROME)
ETIOLOGY
The PRRS virus is an enveloped RNA virus in the genus Arterivirus,
classified in the virus family, Arteriviridae.
The PRRS virus is only moderately resistant to environmental
degradation. The virus is easily inactivated by phenol,
formaldehyde, and most common disinfectants. The virus has a
predilection for cells of the immune system, including pulmonary
intravascular macrophages (PIM) and pulmonary alveolar
macrophages (PAM); in the latter it replicates extensively.
The virus often appears to interact with other pathogenic viruses,
bacteria and Mycoplasma hyopneumoniae to magnify severity of
diseases.
TRANSMISSION
An important feature of the virus is its ability to persist in long-term
carrier pigs (greater than 200 days). However, field observation
suggests that most infected pigs eventually become immune, then cease
to shed virus by 60 days post-infection.
Shedding carriers probably are the most common means of virus
introduction to a herd or population of pigs.
It is present in nasal secretions, urine, semen, mammary secretions
and feces.
With the advent of artificial insemination, semen became a major
source of viral introduction. The virus spreads readily by direct
contact.
SOWS
Sows infected while pregnant may deliver viremic, persistently
infected piglets as a congenital PRRS virus infection. Virus can
transmit from infected piglets or dams to other piglets.
The cycle of shedding and infection can continue well into the
nursery phase in situations where the sow herd is actively infected.
Older infected pigs held back in nurseries or cross-fostered in the
farrowing house often are a source of virus for younger pigs.
Likewise, older pigs and their secretions can be a source of
infection to younger pigs on premises where biosecurity between
groups is lacking.
BOAR
Boars are known to shed PRRS virus in semen for up to 92 days
post-infection and can infect dams during breeding.
Infection of sows occurs through natural breeding or artificial
insemination. The advent of artificial insemination and boar studs
has created a need for strict biosecurity and monitoring of PRRS
virus in these facilities.
Research suggests that the virus is unlikely to be spread to pigs by
birds or rodents. There are no known replication-competent insect
vectors but mosquitoes and house flies are capable of acting as
fomites with the potential to spread the virus mechanically.
INCUBATION PERIOD
14 days

-For the purposes of the Terrestrial Code, the incubation

period for PRRS is 14 days. Pigs are usually infective between
days 3 and 40 post-infection, but can remain so for several months.
PATHOGENESIS
Once transmission of virus to the tonsil or upper respiratory system
has occurred, primary replication occurs in lymphoid tissues.
Viremia follows and may persist for several weeks. The virus has
a predilection for lymphoid tissues (spleen, thymus, tonsils, lymph
nodes, Peyer’s patches).
It infects and compromises the function of pulmonary alveolar
and intravascular macrophages resulting in interstitial
pneumonia. PRRS appears to increase susceptibility of the lungs to
other pathogens.
PRRS virus is known to cross the placenta in late gestation (after
the 72nd day) and may reach a high titer in fetuses. It may kill all,
part or none of the fetuses.
It is suggested that fetuses are killed by hypoxia that occurs as a
result of the arteritis that may develop in umbilical vessels.
Abortions are common, the result of either the effects of acute
disease and fever in sows or infection and death of fetuses.
Recovered sows are resistant to re-infection when exposed to a
homologous strain of the virus but are likely to show clinical signs if
a heterologous strain is encountered.
DIAGNOSIS, CLINICAL SIGNS AND
LESIONS
CLINICAL SIGNS
BREEDING AGE GILTS, SOWS, AND BOARS
Period of anorexia Mild cyanosis of the ears, abdomen and
vulva has been reported in some outbreaks.
Fever
Lethargy
Depression
Respiratory distress
vomiting
REPRODUCTIVE PROBLEMS
Include a decrease in the number of dams that conceive or farrow.
There is usually an increase in premature farrowing, late term
abortions, stillborn or weak piglets and mummified fetuses.
Preweaning mortality is high. Nursing pigs may have dyspnea
(“thumping”). The period for reproductive signs varies with herd
size but is usually two to three months in duration. A slow
improvement in reproductive performance then begins. In larger
operations, signs may be cyclical, especially if naïve gilts or sows
continue to be introduced into the herd.
BOARS
Clinical signs are similar to sows and are accompanied by
a decrease in semen quality.
YOUNG, GROWING AND FINISHING PIGS
Primary clinical signs among young pigs are fever, depression,
lethargy, stunting due to systemic disease, and pneumonia.
Sneezing, fever and lethargy are followed by expiratory dyspnea
and stunting. Peak age for respiratory disease is four to ten weeks.
Post weaning mortality often is markedly increased, especially with
more virulent strains and the occurrence of ever-present concurrent
and secondary infections.
LESIONS
PRRS virus infection generally results in mild to severe lesions in
lungs and lymph nodes.
The interstitial pneumonia varies from multifocal to lobular to
diffuse in distribution. Lungs appear mottled and tan but are highly
variable in extent. Lymph nodes are generally swollen, tan and
edematous or cystic.
Microscopic lesions may include nonsuppurative interstitial
pneumonia, mild nonsuppurative encephalitis, myocarditis, rhinitis,
and perhaps depletion of germinal centers of lymph nodes.
LUNGS WITH HEMORRHAGES OF A PIG INFECTED
Most fetuses and stillborn pigs with uncomplicated PRRS have no
discernible lesions but some may have umbilical cord arteritis and
hemorrhage; patchy distribution of slightly firm lungs (interstitial
pneumonia); enlargement of lymph nodes; hemorrhages in the
skin; edema of the eyelids, periorbital tissues, colonic mesentery
and various body cavities; and dehydration with prominence of
the vertebral column.
Sows with acute PRRS virus infection have typical lung and systemic
lesions.
Endometritis, myometritis and placental lesions have been reported.
PRRS WEAK PIGLETS AND ABORTION
DIAGNOSIS
Clinical signs and history often suggest PRRS, especially in acute
outbreaks. Characteristic microscopic lesions in lungs and several
other tissues also are suggestive but not pathognomonic.
Any tentative clinical diagnosis should be confirmed by detection
of the PRRS virus. This can be by virus isolation (VI), detection of
PRRS antigen by fluorescent antibody tests (FAT) or
immunohistochemistry (IHC), or detection of PRRS virus genome
by polymerase chain reaction (PCR) and be coupled with
presence of typical lesions.
Serology provides indirect evidence of infection but does not
determine if there is actual disease caused by PRRS virus.
Detection of PRRS virus is best performed in affected pigs during the
early stages of PRRS infection.
Suitable specimens are obtained from weak-born neonates that have not
nursed, or clinically affected (thumping, febrile) nursing pigs, and from
febrile, anorectic post weaned pigs and sows. Probably the best tissues
for virus detection methods include bronchoalveolar lavage (BAL),
serum, lung, lymph nodes, tonsil and spleen.
Aborted, mummified, or stillborn pigs are sometimes (50% positive) useful
for diagnosis by performing PCR on fluids and also for ruling out other
infections. Sows that are not sick at the time of abortion are usually not
viremic but should have high antibody levels in serum. Sows that are
acutely ill should have virus in serum that can be detected by PCR or virus
isolation.
CONTROL
There is no single successful strategy for control of PRRS, largely
because of virus variation, large swine populations, and
unresolved issues of transmission.
In some smaller herds, immunity may be sufficient so that infection is
not causing significant economic losses, in which case no intervention
is necessary.
Often, there are sufficient losses to consider some or all of the
following points for control. A control program should be tailored to
fit the individual farm situation.
 ONCE THE DISEASE IS DEFINED, A STRATEGY CAN BE DEVELOPED TO
ACHIEVE ONE OF TWO GENERAL GOALS, EITHER TO ELIMINATE PRRS OR
TO CONTROL (“LIVE WITH”) PRRS.
The goal of many herds is to “stabilize” the infection in the sow herd by
assuring immunity in all breeding stock.
This “herd immunity” prevents the reproductive failure and can decrease the
likelihood of transmission of virus from dams to fetuses and offspring. When
coupled with segregated rearing of offspring, clinical effects of infection can
be minimized.
Breeding herd stabilization can sometimes be accomplished by vaccination,
intentional whole-herd infection, aggressive acclimatization of replacement
breeding stock, or combinations of these strategies.
Two major, generally recognized as essential, components are to limit the
frequency of seed stock introductions to the sow herd and to assure that
the replacement gilts be well-acclimatized to the PRRS virus present in
the sow herd.
Seed stock introductions to sow herds should not be more frequent than
monthly, with quarterly or semiannual introductions preferred.
Assuring infection of replacement gilts, followed by at least 60 days
recovery (cool-down) before they enter the sow herd is strongly
recommended. Ideally, replacement gilts should originate from a single,
PRRS-negative source and be infected only with the PRRS strain(s) present
in a particular sow herd.
 OR…
..it may be economically feasible to depopulate, clean and
disinfect the facilities and, after a few weeks, repopulate with
stock free of PRRS and other major diseases. Herd closure for at
least 200 days has also been used as another means to stabilize
a breeding herd without having to depopulate.
 TREATMENT
There is no specific treatment for PRRS. Broad-spectrum antibiotics
may be useful in controlling secondary infections. Anti-inflammatory
products (e.g. aspirin) are commonly administered during acute
disease.
Other helpful techniques include early weaning and isolation of
piglets, various PRRS vaccination protocols, regular serologic
monitoring, testing (ELISA, PCR and IFA) and removal of persistent
carriers in herds with <10% infection, and improving biosecurity.
POST-WEANING MULTISYSTEMIC Gijapon again
WASTING SYNDROME (PMWS)
ETIOLOGY
The disease is associated in part with a porcine circovirus (PCV), so called
because its DNA is in the form of a ring. It is extremely small and hardy.
There are two serotypes, Type 1 causes no known disease. Type 2 can be
found in the lesions and can be isolated in pure culture. There are several
different strains (biotypes and genotypes). Antibodies to circovirus type 2
have been detected in pig sera collected in Belgium in 1985 but the clinical
disease was not described until 1991 in Western Canada. It has since become
widespread in North America and Europe.
TRANSMISSION
Transmission may be by direct contact with infected pigs. PCV2 has been
detected in almost all potential excretion routes such as nasal, ocular, and
bronchial secretions; saliva; urine and feces. The virus can be found in semen,
but the practical importance of this is probably negligible.

Although not demonstrated, it is assumed that contact with contaminated

fomites, exposure to contaminated feeds or biologic products, multiple use of
hypodermic needles, or biting insects may play a role in transmission.
INCUBATION PERIOD
Under field conditions, the incubation period of PMWS is two to three weeks,
and PCV2 can be detected in serum for up to 100 days after infection.
 CLINICAL SIGNS
PMWS tends to be a slow and progressive disease with a high fatality rate in affected pigs.
Starting usually at about 6 - 8 weeks of age, weaned pigs lose weight and gradually become emaciated. Their
hair becomes rough, their skins become pale and sometimes jaundiced.
Sudden death.
Enlarged peripheral lymph nodes.
May show diarrhea.
May show respiratory distress caused by interstitial pneumonia.
Incoordination.
Post weaning mortality is likely to rise to 6 - 10% but is sometimes much higher.
Clinical cases may keep occurring in a herd over many months. They usually reach a peak after 6 - 12 months
and then gradually decline.
DIAGNOSIS
Since most herds have antibodies to PCV, blood testing a herd usually does not
help.
The clinical signs are not specific (although the picture may be highly
suggestive) and to make a diagnosis it is often necessary to post mortem
several pigs.
Diagnosis is based upon the presence of PCV type 2 histological lesions in
lung, tonsil, spleen, liver and kidney tissues. Immunohistochemistry is used to
demonstrate PCV in tissues. Probably many small mild outbreaks go
undiagnosed.
TWO INFECTED PIGS WITH A HEALTHY ONE
PCV2-SD‐affected pig (left) compared with an age‐ matched healthy pig (right). Note the severe growth
retardation and the marked spinal cord of the affected animal.
 POST MORTEM
The gross post-mortem lesions are variable.
The carcass is emaciated and may be jaundiced.
The spleen and many lymph nodes are usually very enlarged, however, the clinical picture with
enlarged lymph glands is highly suspicious.
Kidneys may be swollen with white spots visible from the surface.
The lungs may be rubbery and mottled with edema. Microscopically these lesions are characteristic
and diagnostic particularly if the circovirus is demonstrated in them. If affected pigs are suspended
by their back legs the inguinal lymph nodes appear enlarged often the size of large grapes.
Edema or fluid may be seen in the chest and abdominal organs and tissues.
LESIONS
Lesions are primarily found in lymphoid tissues, and enlargement of lymph nodes is
the most prominent feature of the early clinical phase.
Cytoplasmic viral inclusion may be found in histiocytes or dendritic cells.
Lungs may be enlarged, non-collapsed, and rubbery in consistency, in a diffuse or
patchy distribution, with fluid-distended interlobular septa. These findings correspond
microscopically to interstitial pneumonia, with thickening of alveolar septa,
pneumocyte type II hyperplasia, and the presence of macrophages and few
neutrophils in alveolar spaces.
Peribronchial fibrosis and fibrinous bronchiolitis occur in advanced cases.
Histological appearance of a mesenteric lymph node from a PCV2-SD‐affected pig. Note the lack of
lymphoid follicles together with a change in cell subpopulations, which are dominated by macrophages and
multinucleate giant cells with a marked loss of lymphoid cells. Hematoxylin and eosin stain.
Inguinal superficial lymph node. Presence of various intracytoplasmic rounded inclusion bodies characteristics
of porcine circovirus type 2 infection in a PCV2-SD‐affected pig. Hematoxylin and eosin stain.

Inclusion bodies , sometimes called elementary bodies, are nuclear or cytoplasmic aggregates of stable
substances, usually proteins. They typically represent sites of viral multiplication in a bacterium or a
eukaryotic cell and usually consist of viral capsid proteins.
 CONTROL AND PREVENTION
Control of the disease is based on pig flow, particularly all-in, all-out systems. Do not move pigs from one
batch to another.
Virkon S has been shown to be effective in killing the virus. PCV is a very persistent virus in the
environment.
Pay attention to good husbandry, ventilation and temperature.
Avoid high stocking density and reduce mixing of pigs.
Avoid fostering pigs after 48 hours of age.
Early recognition of sick pigs and segregation is essential.
If other diseases are present treatment and control of them may help overall.
Closure of the herd to build up a herd immunity has been tried but without much success. The suggestion
has been made that, since the virus cycles in the nurseries their temporary emptying may break the cycle.
It has been shown that groups of young pigs that are removed from the farm and reared elsewhere do
much better than those left in the herd.
Keep similar age groups of pigs segregated to separate buildings or sections
and reduce faecal transfers as far as is practicable.
Use solid partitions between pens.
Vaccinate for parvovirus (PPV) and control PRRS.
Only purchase breeding stock from herds with no history of the disease or close
the herd and use AI only.
Only use semen from AI studs where all the boar sources have no history of
disease.
 TREATMENT
Antibacterial medication is usually ineffective unless given preventively for a long time
in advance of when the start of the disease is anticipated. However, recent reports
from Eastern England report good responses to controlling secondary infections using
stabilized amoxycillin in feed. (Not a cure).
There is no vaccine but if a Pasteurella is isolated it would be possible to produce an
autogenous vaccine.
Recent reports have indicated that where secondary enteric infections occur the use of
tiamulin by both injection and in feed may be useful.
Pigs are also reported to respond well to injections of corticosteroids (2mg/kg) with
improved growth rates and reduced mortalities.