PRRS

Porcine Reproductive and Respiratory Syndrome Virus (PRRSV)

Porcine reproductive and respiratory syndrome virus (PRRSV) is endemic in most swine-producing regions worldwide. Infections (PRRS) are first characterized by:

outbreaks of severe reproductive losses,
respiratory disorders,
reduced growth rate,
and increased mortality.

Two types of PRRSV (1 and 2) exist. PRRSV1 and PRRSV2 are considered two distinct species within the Arteriviridae family. The two prototype genomes (PRRSV‑1 Lelystad strain and PRRSV‑2 VR‑2332 strain) were discovered around 1991, respectively in Europe and North America.
Despite this, they differ by approximately 44% in their nucleotide sequence.

Today, both species are distributed worldwide:

PRRSV‑1 predominates in Europe,
PRRSV‑2 predominates in the Americas and Asia.

These two small RNA viruses are extremely diverse.

Intra-type variation can reach up to 30% for PRRSV‑1
and more than 21% for PRRSV‑2.

Infected animals shed the virus through:

oral and nasal secretions,
urine,
blood,
semen,
mammary secretions,
and sometimes feces.

PRRS is transmitted through direct contact, fomites, and aerosols.

These RNA viruses have limited environmental survival, except in moist organic material at neutral pH and temperatures ≤4 °C.
At temperatures ≤ −18 °C, their survival is virtually indefinite.
They are highly sensitive to common detergents and disinfectants, but in cold conditions, product selection and contact time must be carefully assessed.

Clinical presentation

Clinical presentation varies greatly:

between strains,
between herds,
and within the same herd over time.

It can range from subclinical to devastating.

Outbreaks occur in populations naïve to the newly introduced strain, even if the herd is endemic for other strains.

All age groups are affected.

In endemic PRRS, the disease primarily affects susceptible subpopulations:

nursery piglets,
early finishing pigs,
replacement gilts,
naïve sows,
and their congenitally infected offspring.

In an endemic farm, more than 4 strains can circulate simultaneously.
Recombination between wild-type strains and modified live vaccine viruses is common.

Recent research shows that PRRSV does not circulate as a homogeneous virus, but as a cloud of variants undergoing constant evolution.
The more variants present in the herd, the more severe the disease.

Acute phase (phase 1)

Occurs approximately 2 weeks after introduction:

anorexia,
fever,
lethargy,
respiratory signs,
increased mortality (virulent strains).

Duration: ≥ 2 weeks, affecting all age groups.
It begins in one or a few areas and then spreads rapidly throughout the site.

Reproductive phase (phase 2)

Occurs simultaneously with or shortly after the acute phase.
Duration: 1 to 4 (up to 6) months.

Manifestations:

infertility,
abortions,
increased pre-weaning mortality,
poor viability of liveborn piglets.

When reproductive performance returns close to pre‑outbreak levels, most herds remain endemic.

During the acute phase:

sow mortality: 1–4%,
litter losses: 1–3% (mainly 21–109 days of gestation),
irregular returns to estrus,
non-pregnant sows,
anorexia,
agalactia,
ataxia,
major exacerbation of endemic diseases.

During the reproductive phase:

5–80% of sows: late abortions / premature farrowings
Piglets born:
- normal
- weak
- of varying sizes
- stillborn
- autolytic (brown)
- partially or completely mummified

Liveborn piglets may show:

neonatal diarrhea,
increased susceptibility to infections,
pre-weaning mortality: 25–50%.

Surviving sows show:

delayed return to estrus
low conception rates

Boars:

loss of libido
reduced semen quality (2–10 weeks after infection)

In highly virulent strains:

80–100% abortions,
piglet mortality > 20%,
sow mortality > 20%,
neurological signs (ataxia, circling, paresis).

Acute PRRS in nursery / finishing pigs

Typical signs:

anorexia,
lethargy,
cutaneous hyperemia,
dyspnea / abdominal breathing,
variable cough,
rough hair coat,
reduced ADG,
mortality 12–20% (may exceed 50% with highly virulent strains).

Frequent co-infections

During acute PRRS, endemic diseases increase:

streptococcal meningitis,
Glässer’s disease,
exudative dermatitis,
sarcoptic mange,
bacterial bronchopneumonia.

Epidemiology and persistence

After introduction, PRRSV almost always becomes endemic.
Persistence is due to:

chronic infections of lymphoid tissues,
carrier animals,
continuous introduction of susceptible animals.

Viremia occurs 6–48 h after exposure, lasts 2–4 (up to 8) weeks, and is longer in young animals.
In lymphoid tissues, the virus can persist up to 250 days post‑exposure.The virus is maintained through:

in utero transmission,
post‑partum transmission,
mixing of susceptible and infected animals.

Modes of infection

Increasing susceptibility:

oral
vaginal
intra‑uterine
intranasal
parenteral (very sensitive: ≤20 viral particles)

Indirect transmission:

aerosols over ≥10 km,
equipment, clothing, vehicles, feed, water,
arthropod vectors (possible).

Contaminated semen and infected pigs play a major role in transmission between herds.

Control and vaccination

Vaccination is a key component of PRRSV control, along with:

strict internal and external biosecurity,
rigorous hygiene.

However, control remains difficult and economic losses are significant.
The cost of PRRS is estimated between $6.25 and $15.25 USD per pig sold.The complementary use of inactivated vaccines with PRRS MLV vaccines, combined with strict batch production, has shown a highly reliable strategy.
It provides robust protection, both colostral and direct, enabling full control of the virus in breeders and their piglets up to the end of the nursery phase.