Porcine Reproductive and
Respiratory Syndrome (PRRS)
PRRS is an
acronym (porcine reproductive and respiratory syndrome) for
a relatively new viral disease of pigs that is characterized
by two overlapping clinical presentations - reproductive
impairment or failure in breeding animals, and respiratory
disease in pigs of any age.
The causative agent
The causative agent of PRRS is the PRRS virus, which is an
RNA virus classified under the order Nidovirales,
family Arteriviridae and genus Arterivirus.
There are two related but antigenically and genetically
distinguishable strains: genotype 1, with the prototype
Lelystad virus representing the viruses predominating in
Europe and genotype 2, represented by VR 2332, the prototype
of strains originally mostly found in North America.
In 2006, a clinical outbreak characterized by high body
temperature, rubefaction on the skin, respiratory disorder,
and high mortality and morbidity in the affected pig herds
attacked on the pig-producing areas of China. It has been
proven that this outbreak of atypical PRRS occurred in China
in 2006 was caused by a highly pathogenic variant of type 2
PRRSV with 90 nucleotides deletion, namely 30-amino-acid
(30-aa in 481 and 533–561) deletion in its Nsp2- coding.
There have also been descriptions of East European strains
of type 1 PRRSV with a high degree of polymorphism.
virus is only moderately resistant to environmental
degradation. The virus is easily inactivated by phenol,
formaldehyde, and most common disinfectants. Strains of
PRRSV vary markedly in virulence.
The pig (Sus
whether domestic or feral, is the only species known to be
naturally susceptible to this disease. Other species of wild
pig and members of family
may be susceptible.
probably the most important swine disease of the last
half-century. Although reported initially in only a few
countries in the late 1980s, PRRS now occurs worldwide in
most major swine-raising countries, except for a few
countries including Sweden, Switzerland, New Zealand, and
Australia which claim to be free of this disease.
testing has revealed there are many infected herds in which
signs are not apparent. Where signs are apparent, they vary
and are influenced by several factors such as virulence of
the virus, the age of animals, herd size and management
practices, whether it is an initial infection or ongoing
(endemic with herd immunity, presence of other disease
causing agents in the population, etc.
reproductive and respiratory syndrome virus (PRRSV) occurs
in all age groups. Reproductive impairment or failure, more
obvious in sows or gilts, also affects some boars. The
respiratory syndrome is seen more often in young growing
pigs but also occurs in naïve finishing pigs and breeding
age gilts, sows, and boars:
Clinical signs may include a period of anorexia, fever,
lethargy, depression, and perhaps respiratory distress or
vomiting. Mild cyanosis of the ears, abdomen and vulva has
been reported in some outbreaks. Reproductive problems,
often the most obvious signs, include a decrease in the
number of dams that conceive or farrow. There is usually an
increase in premature farrowings, 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.
There is evidence that subpopulations within large breeding
herds escape initial infection but are infected when exposed
later and serve as sources of continued virus shedding.
Also, herds may be infected with multiple, heterologous
strains of PRRS virus that are not completely
cross-protective. In boars, clinical signs are similar to
sows and are accompanied by a decrease in semen quality.
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. Older pigs, especially naïve, high-health swine,
have similar respiratory signs. Heterologous infections may
lead to prolonged or repeated outbreaks of respiratory
there are no pathognomonic symptoms, 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).
Serology provides indirect evidence of infection but does
not determine if there is actual disease caused by PRRS
Antibody can be detected by ELISA and by the indirect
staining of pre-prepared monolayers of infected cells (Immunoperoxidase
monolayer assay (IPMA)
Commercially available ELISA kits are also commonly being
used for PRRSV antibody detection. All serological tests can
give rise to false positives and false negatives on
individual animals, but on a group basis, they are reliable
in indicating whether the herd has been infected or not.
test and removal programs, RTPCR has been used to detect
viremic animals or carriers, primarily using serum, tonsil
biopsy, or oropharyngeal scrapings. This assay has also been
used to detect PRRSV RNA in semen samples, with an advantage
over the virus isolation technique because of the toxicity
of semen on the cells used for virus isolation. Although
seldom used for diagnostic purposes, in-situ
hybridisation is capable of detecting and differentiating
type 1 and 2 PRRSV genotypes in formalin-fixed tissues. The
sensitivity and specificity of the methods for detection of
PRRSV genome or antibody are compromised by the very high
genetic diversity of PRRSV.
Collection of specimens for laboratory diagnosis
following specimens should be collected and sent to the
virus isolation and RT-PCR: whole blood (in EDTA)
and serum, lung, lymph nodes, respiratory tract, spleen and
tonsils of affected animals. Samples from mummified or
aborted litters are unlikely to yield virus, but can still
be useful for RT-PCR.
antibody testing (serology):
Serum from up to 20 exposed animals in the herd. Specimens
should be chilled and forwarded unfrozen on water ice or
with frozen gel packs.
Lung, tonsil, heart, brain, and nasal turbinate fixed in 10%
neutral buffered formalin should be submitted for histologic
should be chilled and forwarded to the laboratory unfrozen
on water ice or with frozen gel packs.
There is no
single successful strategy for control of PRRS, largely
because of genetic and antigenic variability between
viruses, large swine populations, and unresolved issues of
transmission. Intervention strategies to prevent PRRSV
spread are the keys to success. 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.
disease is confirmed, a strategy should be decided either to
eliminate the disease or to control (or “live with”) PRRS.
Current control measures include the management of incoming
replacement gilts, the use of vaccines and implementation of
biosecurity protocols validated to reduce the risk of PRRSV
spread within and between herds. Methods of eliminating
virus from endemically infected herds include whole herd
depopulation/repopulation, test and removal and herd
There is no
specific treatment for PRRS. Broad-spectrum antibiotics may
be useful in controlling secondary infections.
Anti-inflammatory products are commonly administered during
acute disease. Other helpful techniques include early
weaning and isolation of piglets, regular serologic
monitoring, testing (ELISA, PCR and IFA) and removal of
persistent carriers in herds with <10% infection, and
PRRS virus, the control strategies, and the specific farm
situations are so variable, it is important that field
veterinarians, diagnosticians and research workers continue
to objectively expand their knowledge for better control and
eventual elimination of this financially devastating