Porcine Reproductive and Respiratory Syndrome

PRRSv biosecurity – key points to stop entry to your farm

PRRSv biosecurity – reducing the spread around your farm

 

Other issues

 

Other names

PRRS,  Blue Ear Disease, Mystery Swine Disease, Swine Infertility and Respiratory Syndrome (SIRS), Porcine Endemic Abortion and Respiratory Syndrome (PEARS)

Causal agent

Virus.  Porcine Reproductive and Respiratory Syndrome Virus – RNA enveloped

Differences in virulence are being detected through variation in the structural genes.  The highly pathogenic form in China is associated with two deletions in NPS2 region.

Age group

Adult: Clinical signs generally reproductive, mild fever and anorexia

Piglets through to finishing: clinical signs generally associated with secondary infections

Clinical signs

Naive herds

Reproductive losses and a decreased farrowing rate

Early farrowings, at 105 to 112 days

Increase in stillborn, mummified and weak liveborn pigs

Increased pre-weaning mortality often associated with increase in bacterial infections for example diarrhoea and greasy pig disease

Increased numbers of unthrifty pigs post weaning

Increased nursery mortality often associated with an increase in bacterial infections for example post-weaning diarrhoea and meningitis

On established herds

Neonatal Pigs

Respiratory Distress Unthrifty and failure to thrive Increased secondary bacterial infections- diarrhoea and pneumonia

Growing pigs

Increased mortality Decreased appetite Fever Rough hair coat, unthrifty pigs

Increased respiratory problems, pneumonia and atrophic rhinitis

Increased secondary bacterial infections for example meningitis, Greasy pig disease

High Fever Problem in China associated with a novel deletion of ORF 5 (NPS2) region

Adults

North America strains can cause major reproductive problems with massive abortions

Late mummifications and abortions occur later in pregnancy may be due to the fact that the early embryo and foetus have no receptors to PRRSv and are therefore unaffected by the virus.  But as they mature, they can become infected.

PRRS mummified

prrsConjunctivitis%2001sw

PRRSv blue ear sow

prrs Abortus 01SW

Later mummified piglets with early farrowing

Sick pig with complicated PRRSv

“Blue ears” in a sow

Abortions

Infectivity

The virus particles have an envelope and rapidly becomes inactivated in the environment and in the presence of disinfectants

Pig to pig contact is the major means of spread, through infected faeces, urine and milk to piglets without colostral antibodies

Transmission through needles and insects is possible, especially when blood transfer occurs

Air transmission possible, but mainly when major outbreaks are present

While virus particles are seen in boar semen for 90+ days and experimentally gilts can contract the disease through insemination.  Thousands of inseminations from serologically positive boars to naive herds has not resulted in the spread of disease, therefore the risk through AI is small

When the disease first enters a country or new area, the level of disease locally can be very high and aerosol spread possible.  Once the disease has stabilised in an area the risk of disease spread by semen or air is reduced.

 

Post-mortem lesions

There are very few visible post-mortem changes associated with PRRSv, majority of the signs relate to secondary infections.  Histologically the major finding is a interstitial pneumonia and lack of air spaces.  The disease selectively kills the lung macrophage, essential for the defense of the lung.  The macrophages are killed or damaged for 26 days.  After 7 weeks of age the alveolar macrophage becomes more resistant to PRRSv infection

PRRS Macrophage healthy

PRRS Macrophage dead

Anat normal lung histo

PRRS intersitial pneumonia histo

Healthy macrophage

Dead macrophage

Normal lung

Interstitial pneumonia

Diagnosis

PRRSv is suspected on the basis of the clinical signs

The presence of PRRSv on a unit is confirmed by the use of antibody tests.  However, it can take 2-3 weeks for the antibody level to rise before the test becomes positive.  Unfortunately the antibodies may also disappear 6 months after exposure.  

Examination of the lung tissue by histology -immunohistochemistry can reveal the organism in the lung

PCR examination of tissues, in particular used for semen and serum examination

Gene sequencing can be useful to monitor epidemiology of PRRSv between farms

Treatment and control

Infected Herds

There is no specific anti viral treatment for PRRSv infection

The treatment regimes aim to minimise the effect of secondary infections.  Aim to keep the pigs warm and in the draught free environment and possibly increase feed density to compensate for the anorexia.  Review the control measures for the secondary infections.  Elimination of PRRSv from units

Control

SEW programmes can help to control the spread of the disease around the farm and minimise the effect of the disease on the farm's economy

All-in/ all-out and hygiene are essential precursors to controlling the disease

Current live vaccines result in excretion from vaccinated pigs and therefore cannot be used on PRRSv negative herds.  The use of live vaccines in incoming breeding animals in PRRS +ve herds helps to maintain farm stability.  The vaccinated stock must be kept separate from the farm until shedding has stopped

Home (Autogenous) vaccines from serum or tonsilar scrape therapy may be utilised to help gilt and boar introduction programmes.  These should be restricted to the single farm

Gilts and boars must be stabilised before service.  Discuss introduction programmes with your veterinarian

Vaccines

Dead vaccines generally confer little or no protection in naive animals, but it will reduce excretion of virus and assist reducing farm clinical signs in infected herds.

Modified live vaccines (MLV) – these can be very variable in response depending on the modification carried out.   Several MLV can cause severe clinical signs without field virus.  In addition, there can be little protection provided for heterologous virus strains.   Allowing sufficient time between vaccination and field infection essential part of control.   MLV general reduce excretion of virus particles.

Review fly and mosquito control programmes

PRRS-ve herds

Before purchasing breeding or other incoming stock ensure you match serostatus.  Unfortunately the testing procedures are not 100% accurate.  Practice on-farm AI collection, do not rely on a commercial AI stud

Common differentials

The clinical signs associated with Swine Influenza can mimic many of the signs of PRRSv

Zoonotic implications

There are no zoonotic implications

 

 

Other issues relating to Porcine Reproductive and Respiratory Syndrome Virus

 

PRRSv biosecurity – key points to stop entry to your farm

PRRSv biosecurity – reducing the spread around your farm

 

Treatment and control following a PRRSv break in a naïve herd

 

Eradication of PRRSv in a positive herd without depopulation

 

Depopulation and repopulation

 

Biosecurity for PRRSv and Biosecurity in detail

 

PRRSv biosecurity manual AASV

 


 

 

PRRSv the genome and genetic identity

 

Porcine Reproductive and Respiratory Syndrome Virus

None enveloped, Positive sense single stranded RNA virus of the family Arteriviridae.

The Arteriviridae and Coronaviridae families are combined into the Nidovirales order

PRRS viral particle

 

 

The appearance down the electron microscope.

Dr KJ Yoon

 

PRRSv genome

The general layout of the 15 kb of the PRRSv genome, illustrating the two long Open Reading Frame (ORF)1 and ORF2 and the smaller other frames.  Note there are some overlapping with the ORF

 

There are 7 regions of the positive sense RNA genome of the PRRSv genome.

ORF 1

RNA replicase ORF1a and ORF1b

None structural proteins

ORF 2

Minor membrane glycoprotein GP2a

GP2b

 

Structural proteins

ORF 2-7

Nucleocapsid protein N, nucleolar localization

ORF 3

Membrane glycoprotein GP3

ORF 4

Membrane glycoprotein GP4

ORF 5

Major membrane glycoprotein GP5

ORF 6

Membrane associated protein - M

ORF 7

Nucleocapsid protein - N

 

The GP5 protein is the most variable structural protein, with only 51-55% aminoacid identity between North American and European isolates, whereas the M protein is the most conserved protein with 78-80% aminoacid identity.`                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    
Identification of the PRRSv genome is through two systems:

Restriction pattern using MLU1; SacII and HincII enzymes

For example the predicted RFLP Pattern of the PRRSv isolated illustrated below is a

   1-? - 4 Atypical Hinc II Pattern.  This method does not produce satisfactory results.

 

Sequence bases within ORF5

The ORF5 area is selected because this area demonstrates a high degree of variability and evolutionary change.

 

This results in a table of results – for example – chronograph

A=Adenine; T= Thymine – Uracil in original RNA; G=Guanine; C=Cytosine as the base pairs.   Each 3 base pairs (a codon) codes for a different aminoacid, which when combined together produce the protein.  Note the RNA is converted into a cDNA for sequencing as the RNA degenerates too quickly.  However, the pattern of bases represents the actual Codons for their respective aminoacids.

 

10

   20

      30

40

Bases

atg

ttg

ggg

aaa

tgc

ttg

acc

gcg

ggc

tgc

tgc

tcg

caa

ttg

ctt

ttt

48

ttg

tgg

tgt

atc

gtg

ccg

ttc

tgt

ttt

gtt

gcg

ctc

gtc

aac

gcc

gac

96

AAC

aac

agc

agc

tcc

cat

tta

cag

ttg

att

tat

aac

ctg

aca

ata

tgt

144

gag

ctg

aat

ggc

aca

gat

tgg

cta

act

aca

aat

ttt

gat

tgg

gca

gtg

192

gag

acc

ttt

gtc

atc

ttt

cct

gta

ttg

act

cac

atc

gtc

tcc

tat

ggt

240

Gcc

ctc

acc

acc

agc

cat

ttc

ctt

gac

aca

gtc

ggt

ttg

gtc

act

gtg

288

tcc

gcc

gcc

gga

tac

tgc

cac

ggg

cgg

tat

gtc

cta

agt

agc

att

gtg

336

gct

gtc

tgc

gcc

ctg

gcc

gcg

ctg

att

tgc

ttc

gcc

atc

agg

ctg

acg

384

aaa

aac

tgc

atg

tcc

tgg

cgc

tac

tca

tgt

act

aga

tat

act

aac

ttt

432

ctt

cta

gac

acc

aag

ggg

aaa

ctc

tat

cgt

tgg

cgg

tct

ccc

gtc

atc

480

ata

gag

aaa

ggg

gga

aaa

atc

gag

gtt

aac

ggt

cac

ttg

atc

gac

ctc

528

aag

aga

gtt

gtc

ctt

gat

ggt

tcc

gcg

gca

act

cct

gta

acc

aaa

gtt

576

tcaa

gcg

gaa

caa

tgg

tgt

cgt

cct

tag

603

 

This can then be compared with other published sequences, from vaccine strains for example, or from other sequenced isolated from the farm or possible source.  When there is less than 99% difference (<6 nucleotides), the isolates can be considered similar or at least related. 

 

For example, the above isolate was classified as similar to the following sequences:

Ingelvac ATP

PrimePac

RespPRRS

Suvaxyn

PRRomiSe

Lelystad

86.1%

86.2%

86.7%

86.7%

86.9%

53.4%

 

Therefore, this isolate was unrelated to any vaccine strain and the European strain (Lelystad) of PRRSv.

 

These patterns do not infer anything about virulence.  Also note that the technique examines only 4% of the total genome of the virus. 

 

Also remember that it takes 3 base pairs to code for an aminoacid and several types of codons code for the same aminoacid – so a change in a single base may not necessarily result in a change in aminoacid selected.

 

More on PRRSv genome