PRRSv Guide Porcine Reproductive and Respiratory Syndrome

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PRRSv GUIDE PORCINE REPRODUCTIVE AND RESPIRATORY SYNDROME VIRUS Alejandro Ramírez

PRRSv Guide Porcine Reproductive and Respiratory Syndrome

PRRSv GUIDE PORCINE REPRODUCTIVE AND RESPIRATORY SYNDROME VIRUS Alejandro Ramírez

Author: Alejandro “Alex” Ramírez.

Format: 11 x 20 cm.

Number of pages: 112.

Number of images: 30.

Binding: hardcover, wire-o.

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35 €

The objective of this guide is to provide a practical summary regarding current knowledge and understanding of porcine reproductive and respiratory syndrome (PRRS). The information presented is focused on clinically relevant and practical information to help field veterinarians and farm team personnel interested in animal health.

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PRRSv Guide. Porcine Reproductive and Respiratory Syndrome

Presentation of the book Porcine reproductive and respiratory syndrome (PRRS) is, without any doubt, one of the diseases with greatest economic significance around the world. It has led to noticeable changes in pig production worldwide, especially regarding biosecurity protocols. Its causative agent, first identified in 1991, is a virus that evolves very rapidly; the diversity of the virus is therefore high both in Europe and North America, with highly pathogenic variants in Asia, Europe and the United States.

This book shows the data from the most recent studies on this disease from a practical point of view. To do so, this guide starts with a brief introduction and the economic importance of PRRS followed by its pathogenesis, epidemiology, and immunity. Diagnostic testing and herd monitoring techniques are described, followed by an extensive discussion on biosecurity for a better understanding of disease transmission, control and elimination.

The quality of the contents and their presentation make the book even more pleasant and easy to read and use for reference.

PRRSv Guide. Porcine Reproductive and Respiratory Syndrome

The author Alejandro “Alex” Ramírez Alex Ramírez is originally from Guadalajara, Mexico where he lived until he graduated from high school. He obtained a BS degree in Animal Science in 1989 and his DVM degree in 1993 from Iowa State University. He practiced in a rural private clinic primarily as a large animal veterinarian with an emphasis in swine for almost 11 years. He left private practice to pursue his interest in teaching and working with students. In 2004 he obtained his Master’s in Public Health from The University of Iowa. In 2005 he became board certified by the American College of Veterinary Preventive Medicine.

He has been working at Iowa State University since 2004. In 2008, he joined the Veterinary Diagnostic and Production Animal Medicine Department in swine production medicine where he currently holds the title of Associate Professor with duties in teaching, research, and professional practice. In 2011 he received his PhD in Veterinary Microbiology with emphasis in Preventive Medicine from Iowa State University.

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He has over 100 peer- and non-peer reviewed written works. He has authored several book chapters and is a coeditor for several books including the 4th edition of the American Associations of Swine Veterinarian’s Swine Disease Manual and the ultimate reference on swine diseases, the 10th edition of Diseases of Swine.

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PRRSv GUIDE PORCINE REPRODUCTIVE AND RESPIRATORY SYNDROME VIRUS Alejandro Ramírez

Table of contents 1. Introduction Brief history Agent Structure Small Enveloped Shape Single strand RNA Nine open read fragments (ORFs 1a, 1b, 2, 2b, 3, 4, 5, 6, and 7)

2. Economic impact Economic impact of PRRS

3. Clinical signs Clinical signs of PRRS General clinical signs Reproductive clinical signs Respiratory clinical signs

5. Epidemiology PRRSv epidemiologic characteristics Highly infectious Low transmission potential

Incubation time Routes of transmission Persistent infections Mutations and quasispecies Subpopulations

6. Immunity Introduction Innate immunity Definitions

Adaptive cell-mediated immunity Humoral immunity Maternal immunity Cross-protection

4. Pathogenesis Tissue tropism

7. Diagnostic tests

Lesions

Agent detection

Lung

Best samples

Lymph nodes

Histopathology

Other lesions

Virus isolation (VI)

Polymerase chain reaction (PCR) Direct fluorescent antibody test (FA) Immunohistochemistry (IHC) Genetic sequencing Restriction fragment length polymorphism (RFLP)

Antibody detection

10. Control and elimination Role of vaccines Killed vaccines Modified live virus (MLV) vaccines

Basics of control McRebel program

Enzyme-linked immunosorbent assay (ELISA)

Herd closure

Serum virus neutralization (SVN or SN)

Homogenize

Indirect fluorescent antibody assay (IFA) Immunoperoxidase monolayer assay (IPMA)

PrRsv elimination AASV position statement regarding PRRS Depopulation and repopulation (depop-repop)

8. Herd monitoring Monitoring program design Serum Oral fluids Herd classification Important notes regarding breeding herd classification

9. Biosecurity PRRSv resistance in the environment Environmental stability Water and manure Pork meat Vectors

Biosecurity practices PADRAP

Test and removal Herd rollover Regional elimination

Porcine reProductive and resPiratory syndrome

PRRSv guide

Agent

structure

1 introduction

Small

Porcine reproductive and respiratory syndrome virus (Prrsv): order: Nidovirales family: Arteriviridae genus: Arterivirus

~15,000 nucleotide base pairs; 50-70 nm in diameter.

SiZe ComPaRiSon WiTH oTHeR viRuSeS

Other viruses in same family: Equine arteritis virus (EAV).

Lactate dehydrogenase-elevating virus (LDV) of mice.

Simian hemorrhagic fever virus.

There are two recognized genotypes which share only approxi-

0.05-0.07 µm

mately 60 % nucleotide sequence. Within each genotype, there is

0.08-0.12 µm

Prrsv influenza (Arteriviridae) (Orthomyxoviridae)

great genetic variation which could be further classified into several phylogenetic clusters (Tables 1 and 2).

175-215 µm african swine fever virus (Asfaviridae)

enveloPed

Table 1. Prrs virus genotypes.

Genotype

Primary region affected

Prototype virus

type 1

Europe (Eu)

Lelystad

type 2

north America (nA)

Vr-2332

Enveloped viruses tend to be more susceptible to environmental degradation.

PRRS viRuS Structure:

Table 2. Vr-2332 strain nucleotide sequence match (% identity).

ORF

Lelystad

EAV

LDV

orF3

58 %

22 %

34 %

orF4

68 %

20 %

36 %

orF5

59 %

20 %

49 %

orF6

78 %

26 %

52 %

orF7

65 %

28 %

51 %

nucleocapsid rna GP5 (orF5) m protein (orF6) n protein (orF7)

orF: open reading frame.

Source: Murtaugh et al., 1995.

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ECONOMIC IMPACT OF PRRS

In the US, Neumann et al. estimated the overall cost of PRRS

2 Economic impact

to be around $560 million/year, making it the most economically

The economic impact of PRRS is significant worldwide. A major

significant disease in the US swine industry. This cost was sig-

factor when considering the economic costs of an outbreak is the

nificantly higher than that of classical swine fever ($360 million/

virulence of the specific PRRSv strain. Because of the great diver-

year) and Aujeszky’s disease ($36 million/year) combined, based

sity of field strains, the economic consequences can be quite vari-

on estimates prior to eradication and adjusted to the 2004 dollar

able from herd to herd. There is no question that, as a general rule,

exchange rate.

type 1 PRRSv (European) is considered to be significantly less virulent than the strains found in North America (type 2) (Fig. 1).

Figure 1 summarizes some of the better known peer-reviewed

However, many cases of severe outbreaks with type 1 PRRSv

studies published that have estimated the costs of PRRS. It is im-

have been reported, just as there have been some cases of herds

portant to recognize that the costs associated with PRRS involve

with type 2 PRRSv with no significant clinical signs.

all stages of production. It is also interesting to note that all countries do show a significant cost associated with PRRSv.

Figure 1. Studies on the economic cost of pRRS.

uS coStS

england (uK) coStS

2003 Holck and Polson

2011 Richardson

$255 per sow per outbreak

Based on a 500 sow farm

$6.25 - $15.25 per growing pig

REPROduCTIvE £80 per sow per outbreak (acute phase)

2005 Neumann et al. $560.32 million per year

11.9 %

88.1 %

$4.75 per weaned pig

$66.75 million in breeding herd $493.57 million in growing pigs

£107.18 per sow per year in chronic phase 40.8 %

$201.34 million in nursery

59.2 %

$292.23 million in grow-finishing

RESPIRATORy £104.36 per sow per year

netheRlandS coStS

$74 per litter

1994 Brouwer et al.

2013 Holtkamp et al. $663.91 million per year $1.8 million per day $52.19 per sow per year $2.36 per weaned pig $114.71 per sow in breeding inventory

45,5 %

54.5 %

£65 per sow

$302.06 million in breeding herd

2012 Nieuwenhuis et al. €126 per sow per outbreak (18 week period)

$361.85 million in growing pigs

Range of €59 to €379 per outbreak cost after outbreak ranged from €3 to €160 per sow

$4.67 per marketed pig 10

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3 Clinical signs

RePRoduCtive CliniCal SignS Females

Piglets

abortions, especially late-term abortions (>90 days gestation) (Figs. 2 and 3).

Early farrowing. irregular return to estrus. agalactia. incoordination.

Sow mortality (usually only in highly virulent strains). low conception rates. general reproductive failure.

increased stillbirth rate. increased number of mummified fetuses (Fig. 4). low birth weight (premature weak pigs). low live birth rate.

High preweaning mortality (20-60 %).

Slight doming of foreheads of newborns (infrequent) (Fig. 5).

Rough hair coat.

Figure 2. late-term abortion.

Figure 4. Mummified fetus.

Figure 3. late-term abortion.

Figure 5. Domed forehead (infrequent).

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INCUBATION TIME

table 1. Differences in the ID50 for the different routes of transmis-

5 Epidemiology

sion (source: Yoon et al., 1999; Benfield et al., 2000; Hermann et al., 2005).

The incubation period for PRRS can be quite variable depending on the virulence of the strain involved, and is therefore related to

Route

the clinical signs of the disease, which may range from being non-

ID50

Parenteral (subcutaneous)

~101

~20

reported to be as short as 12 hours; however, it most often ranges

Intranasal

104.0

10,000

between 1 and 7 days. Incubation periods of up to 37 days have

Artificial insemination

104.5

~31,600

also been reported. Under research conditions, incubation peri-

Oral

105.3

~200,000

ods are highly associated with the challenge dose, regardless of

Aerosol (strain dependent)

??

??

existent to high mortality rates. The incubation period has been

the route of infection.

ID50 = infectious dose 50, which corresponds to the amount of virus particles necessary to infect 50 % of the experimental animals. if there are ten animals in a group, the id50 would correspond to the amount of PRRSv necessary to infect five of these animals.

ROUTES OF TRANSMISSION The shedding routes of PRRSv are: Oral fluids (including saliva) for weeks.

Nasal secretions for up to 9 days.

Urine for up to 14 days.

Semen:

PERSISTENT INFECTIONS

Intermittent.

Start: 2-7 days.

The persistence of PRRSv in pigs is the single most important

Duration: up to 92 days with an average of 39 days.

epidemiological characteristic with an impact on the control and

Feces +/-.

possible elimination of the virus from a herd. Pigs can become

Mammary secretions both in colostrum and milk.

persistently infected regardless of their age at exposure (in utero to adult). How or why a pig can become persistently infected with

Table 1 summarizes the differences in the ID50 for the different

PRRSv is still unknown. Although PRRSv can be found in lung tis-

routes of transmission.

sue for a long period of time, the tonsils appear to play a major role in helping the virus evade its host’s active immune system. Persistently infected animals seem to have low rates of viral mutation.

Several research studies have documented persistent infections lasting 100-165 days. The virus tends to remain in the tonsil or lymphoid tissues for longer periods than those detected in blood.

The role of these persistent infections in PRRS recurring outbreaks is unknown.

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MUTATIONS AND QUASISPECIES

The term “quasispecies” refers to the recognition that within one

As is characteristic of RNA viruses, PRRSv is constantly mutating.

PRRSv. These differences are very small, but very important, since

This is because RNA viruses do not have the proofreading capac-

when a laboratory is performing the genetic sequencing of PRRSv

ity of DNA viruses. The latter have a proofreading mechanism that

from a single sample, it is actually reporting the consensus se-

works hard to ensure each new virus produced is an exact copy

quence for the sample. This consensus sequence is a summary

of the original. In the case of RNA viruses, spontaneous mutations

of the quasispecies or normal genetic diversity found in the ani-

are introduced into the genetic sequence of the offspring as the vi-

mal. This quasispecies does not appear to be driven or directed

rus replicates, without any corrections being made. If the mutation

by the immune system in any way. It appears to be more related to

introduced does not result in a fatal mutation (i.e. a mutation that is

the simple fact that the PRRSv has a high mutation rate.

5 Epidemiology

animal, there are several slightly different genetic sequences for

deadly to the virus itself), then the host cell becomes infected with

The diagram (Fig. 4) shows the great PRRSv genetic diversity

several, slightly different PRRSv.

within a host.

When calculating mutation rates, we usually calculate substitution rates. A substitution rate is defined as a mutation rate that a

is not fatal to the virus. PRRSv has been reported to have a

b

mutation rate many times higher than that of the human im-

c

munodeficiency virus (HIV); a virus that has challenged the hu-

d

man medical profession for many years due to its high muta-

e

tion rate. It has been calculated that PRRSv has a substitution

f

rate of 3.7 × 10-5 errors/site/replication. This is equivalent to

g

one substitution/genome/replication. It is important to remem-

h

ber that it takes three nucleotides to code for one amino acid

i

and that many times, one can change the last nucleotide in

j

a sequence of three and yet not change the amino acid the

k

sequence codes for (see Wobble hypothesis).

l m n

Wobble hypothesis: francis crick discovered that the rules for base pairing are relaxed at the third position, so that a nucleotide base can pair with more than one complementary base, but still result in the same amino acid formation.

o p q r

a h j k n q s u b e i m o t c f g r

t

d p

u

l

s

Figure 4. PRRSv genetic diversity within a host (source: Domingo et al., 2012).

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6 Immunity

INTRODUCTION PRRSv immunology is a very challenging subject. It has been ex-

Figure 1. The pulmonary alveolar macrophages are a primary target for PRRSv and thus play a primary role in the host’s immune response.

tensively studied but there is still a lot we do not know. This virus is very different from most reproductive or respiratory viruses we deal with in swine. There are still many gaps in the knowledge of PRRSv and most certainly our current understanding will continue

AlveolAR SPAce

to evolve with time. This section on immunity is not complete or

1

comprehensive, but rather focuses on our current understanding of the subject and some of the key concepts with the greatest clinical relevance.

3

As a basic premise, it is well accepted that exposure to live viruses produces good immunity, although its development is slow. Some have proposed that natural PRRSv exposure causes sterilizing (full 3

protection) and lifelong immunity to homologous (same) viruses.

This is supported by several research studies which have been performed under controlled conditions. Under field conditions, the results are not always clear. Sometimes, field experiences can be contradictory as there are usually many other co-infections

5

or confounders involved, including exposure to multiple PRRSv

2

strains at the same time.

4

As discussed in the pathogenesis section, the pulmonary alveolar macrophages are a primary target for PRRSv and thus play a pri-

6

mary role in the host’s immune response (Fig. 1). There appear to

7

8

5

be some differences in the immune response between individual pigs within a group and depending on the strain. These differ-

1. type i pneumocyte

ences seem to be directly related to the virulence of each strain.

2. type ii pneumocyte

Most research has been done involving PRRSv type 2 (North

3. alveolar macrophage

American strains), although it appears to be the same for type 1

4. interstitial macrophage

strains (European).

5. monocytes 6. sequestered monocyte 7. capillary endothelium 8. intravascular macrophage

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We do know that research studies as well as field experiences

Figure 2. Relative PRRS virus humoral immunity response curves.

have demonstrated that several modified live virus vaccines do

IgM IgG IgA Neutralizing (SN)

VI old VI young PCR

6 Immunity

provide some degree of protection against heterologous strains.

This cross-protection has been most commonly demonstrated through a significant reduction in clinical signs (abortions, ADG, mortality, coughing, etc.), reduced viremia or lower lung scores at necropsy. Protection against homologous strains is much stronger than that provided against heterologous strains. Studies have

PosÂ

also shown that cross-protection exists between PRRSv type-1

Neg 2

4

6

8

10

12

14

16

and type-2 strains.

18

A challenge for veterinarians has always been to know when a

Weeks postexposure vi old: virus isolation in old animals.

new strain has been identified on the farm (see Sections 5 and 7).

vi young: virus isolation in young animals.

Viral genetic sequencing is commonly performed for epidemiological investigations, but currently there are no peer-reviewed

MATERNAL IMMUNITY

publications demonstrating the value of this genetic sequence in identifying immunologically similar or different strains or ways to

It is essential to remember that piglets can be infected with PRRSv

anticipate cross-protection between different strains. There are

in utero and can thus be born viremic. The passive maternal im-

currently some proprietary technologies that are purported to be

munity (IgG) found in colostrum is protective against the develop-

valuable in helping sort the different PRRSv strains into immuno-

ment of clinical signs. This protection appears to wane off once

logical groups based on amino acid sequences. Although the

maternal antibodies disappear. Maternal antibody decay has

explanation of these technologies seems logical, plausible, and

been reported to occur between 16.2 days and 3 weeks when

has had some field anecdotal successes, the lack of independent

testing using ELISA and 8.1 days for SN. Maternal antibodies can

peer-reviewed literature makes it difficult to evaluate the validity of

be expected to be found in pigs of up to 10 weeks of age, with

such grouping system.

usual seroconversion occurring between 6 and 12 weeks of age.

One must remember that cross-protection can be defined in many different ways. Because of this, it is critical to be very objec-

CROSS-PROTECTION

tive when evaluating vaccine selection as well as its expectations.

The role of vaccination in controlling or eliminating PRRSv from a

It is a given fact that there is great genetic diversity between the

farm is discussed in detail under Section 10.

many different PRRSv strains found today. One of the greatest unknowns and challenges in PRRSv immunology is the lack of understanding of protective immunity. We currently do not know which epitopes are vital for protection. As such, there is no way to predict cross-protection between different strains. Also, there currently is no perfect vaccine available that provides full protection against all PRRSv strains.

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iMPoRtant noteS RegaRding BReeding HeRd ClaSSiFiCation

8 Herd monitoring

if the operation is farrow-to-finish or the herd contains growing pigs, these must also test negative.

PRRSv testing requirements:

Provisional negative herds (Category iii) must meet

Assays:

the following criteria: Herds have a negative PrrSv shedding status, but a

exposure (antibodies): eLiSA, iFA, or iPMA.

positive exposure status (older breeding herd animals

Shedding: PCr.

and some weaned pigs may have PrrSv antibodies).

number of animals:

Category iii starts 60 days after negative breeding

random sampling.

replacements are first introduced during a herd rollover

30 wean-age pigs (defined as pigs within seven days

with diagnostic evidence that they remain uninfected.

before to three days after weaning).

if the operation is farrow-to-finish or the herd contains

one pig per litter.

growing pigs, these must also test negative.

Frequency: Monthly or more frequent.

Positive stable herds (Category ii) must meet

need at least four sampling periods to start

the following criteria: Herds have an uncertain shedding status (either with

classification.

a prevalence below 10 % or negative) and a positive

negative herds (Category iV) must meet

exposure status.

the following criteria:

no PrrSv clinical signs in the breeding herd.

Herds have a negative PrrSv shedding status and a

no detectable viremia in weaned pigs when sampling

negative exposure status.

30 pigs every month, at least, over a 90-day period. the

Adult breeding animals must test negative for PrrSv

30-pig sampling protocol suggests that one is 95 %

antibodies:

certain that the herd prevalence is no more than 10 %

if a herd rollover* was done, test as soon as the last previously

assuming tests are 100 % sensitive and specific.

infected animals have been removed from the farm.

Positive unstable herds (Category i) must meet

if the herd is a startup or a depopulation-repopulation, test at least 30 days after population of premises with

the following criteria:

negative breeding replacements.

Herds have a positive exposure status and a positive shedding status.

if the herd was previously classified as Category iii, after

Herds going through a new PrrSv virus outbreak or herds with

one year of testing with no positive result (excluding

chronic PrrSv shedding will be classified as Category i.

false positives), the herd automatically becomes a

Herds with no PrrSv testing done will automatically

Category iV herd.

default to this category.

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* Herd rollover: any elimination procedure that relies upon cessation of viral shedding in the population and removal of previously infected animals, with subsequent introduction of negative breeding replacements (Holtkamp dJ, polson dd, torremorell M, et al. terminology for classifying swine herds by porcine reproductive and respiratory syndrome virus status. J Swine Health Prod. 2011;19(1):44-56).

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9 Biosecurity

Loading and unloading chutes: Chutes can be difficult to clean and disinfect, especially during winter months.

Create a line of separation.

Those inside the barn should not cross the line and come out of the barn.

Those outside the line (truck drivers) should not cross the line and go inside barn.

Chutes should not be shared between operations.

The exchange of animals could actually occur at the perimeter of the farm.

Two trailers can back up end-to-end to transfer animals.

This limits the access of external trailers to the farm site.

Equipment and supplies: Use of the double-bag technique: supplies are removed from an outside bag before entering the farm.

Figure 3. Poor biosecurity: rendering vehicle loading dead animals close to the buildings.

Use of disinfectant sprays: the outside surface of everything that is brought onto the farm is previously sprayed.

Use of a fumigation room: all supplies are fumigated and allowed to sit for at least 30 minutes before they can be remo-

– Prevent wildlife from being attracted to the piles.

ved from the room to enter the farm.

– Temperatures reached easily inactivate PRRSv. – Harder to manage, but still feasible, in areas with cold

Removal of dead pigs:

weather.

Proper animal disposal is critical in minimizing spread.

There is a whole science to proper composting.

Check local, state, or national laws or restrictions applicable

Incineration:

to each method.

Minimal biosecurity risk.

Rendering (Fig. 3): Major risk factor for the introduction of new diseases.

Concerns with environmental contamination by smoke.

Must provide pickup area away from the farm to avoid the

Equipment requires high maintenance.

Fuel costs to completely incinerate a carcass can be quite

rendering vehicle from entering the farm.

expensive, especially for an adult animal.

Ideally, there should be a different driveway for the rende-

Limited capacity for higher mortalities.

ring vehicle that does not cross paths with the on-farm vehicle traffic.

Burial:

Composting:

Not recommended due to environmental concerns/res-

Minimal biosecurity risk.

trictions.

Composting piles must be managed properly:

Only feasible for very small farms.

– Ensure proper breakdown of deads.

Burial sites must be away from any water sources.

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HeRd cloSuRe

In this section, when we talk about herd closure, we are specifi-

One of the most common methods for PRRS control involves

netic reference. Herd closure is a critical component of any dis-

herd closure. It is important to differentiate between a “closed

ease control plan. The ultimate goal is to eliminate all susceptible

herd” from a genetic standpoint and a “closed herd” from a PRRS

animals from the population long enough for the virus to have

disease standpoint.

nowhere to go. This is similar to stop adding wood to a fire, which

10 Control and elimination

cally referring to it in terms of PRRS and not to the traditional ge-

will ultimately result in the fire putting itself out as no new material (susceptible animals) is available for burning.

Herd closure (genetics): in this case, the herd is closed to replacement animals. The genetic pool of the herd is completely closed. No outside replacement gilts or replacement boars (including semen) have been purchased. A farm continues to produce its own replacement animals within the herd.

The goal of this closure is to minimize new disease introductions by eliminating animals raised off the farm from entering the farm.

Unfortunately, we do not have a perfect answer as to how long a herd should be closed to stabilize PRRSv within the herd. Based on field experiences, we can say that in herds that have been known to be PRRSv positive for many months with no acute clinical signs, a herd closure of 60 days may be enough. However, and more commonly, for herds that are undergoing an acute outbreak, 6-7 months is preferred. Anecdotal reports in the field suggest that as herd closures reach 200 days, the success for PRRSv elimination significantly increases.

Herd closure must occur as early as possible in order to maximize the ability to stabilize the herd. Herd closure should occur within

Herd closure (PRRS): in this case, the herd is closed to any “new” susceptible animals from being added to the herd. A susceptible animal is defined as an animal that can become newly infected with PRRSv. This not only includes no new replacement animals (regardless of whether home-raised or purchased) from being added to the herd, but also requires all pigs that are weaned, to be moved off-site. In this case, semen from a PRRS-negative boar stud is still allowed to enter the farm. The goal of this closure is to minimize possible disease spread by eliminating susceptible animals and allowing time for the entire herd to reach immunological stability (immunity and no viremia).

the first 2-4 weeks of an outbreak. The biggest challenge for herd closure is the limited space for the introduction of replacement animals. Replacement animals should be of different age groups so as to continue to maximize replacement rates through as much of the period of closure as possible.

Some farms will actually start an off-site breeding project while the herd is closed. In this case, gilts will be delivered to an offsite facility where these animals will be bred and kept off-site until they can be brought back to the main farm to farrow. This off-site breeding project should start just over 90 days after the start of herd closure (90 days + 115 day for gestation = 205 days) to ensure no animals need to be introduced into the herd (due to farrow dates) before the minimum 200 days needed for herd closure.

Any off-site facility poses a biosecurity risk for the main farm, as this adds one more location where new PRRSv exposure could occur. The advantage of an off-site breeding project is that it will

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PRSSv ELIMINATION

It is important to make an economic analysis for each farm, ahead

The ultimate goal for everyone should be to eliminate PRRSv from

information, together with the expected cost of the elimination

their herd. PRRSv elimination would allow the herd to achieve a

program and expected increase in productivity due to PRRSv

PRRSv-negative status (Category IV) as described in Section 8.

elimination, will help determine how long a farm must remain neg-

10 Control and elimination

of time, to calculate the current actual cost of the disease. This

ative in order to offset these costs. Herds do not have to remain PRRSv negative forever after the elimination of the virus to make

aaSV PoSiTion STaTeMenT RegaRding PRRS

the program economically feasible. A report by Yeske and Holtkamp (2012) suggested that a complete depopulation-repopulation would only require the farm to remain negative anywhere from

On October 11, 2011, the American Association of Swine Veterinarians (AASV) developed the following position statement regarding PRRS:

one to two years to offset the costs of the program.

dePoPulaTion and RePoPulaTion (dePoP-RePoP)

“Porcine reproductive and respiratory syndrome (PRRS) is a significant production-limiting disease of swine that is estimated to cost the North American swine industry in excess of 664 million dollars per year. Control of the disease via traditional methods has not been effective in all cases; therefore, it is the position of the AASV that elimination of the PRRS virus from the North American swine industry is the long-term goal. The AASV will take a leadership role by partnering with the swine industry to promote collaborative PRRS virus elimination efforts at the local, regional, and national levels; communicating the need and identifying sources of funding to support such initiatives; and assisting in the transfer of new PRRS-related information and technology across its membership, in order to achieve this goal”.

Depop-repop of the whole herd is the quickest and simplest way to obtain a PRRSv-negative herd (Category IV).

This is the most expensive approach to PRRSv elimination.

The entire farm site, not just a building, must be completely depopulated before negative replacement animals are allowed back on-site.

All buildings and equipment must be fully cleaned, disinfected, and allowed to fully dry for at least two weeks and preferably 30 days before animals are placed back in any building.

This is ideally done during summer months.

Winter months are the worst time for depop-repop due to the lack of ability to fully clean and disinfect all facilities.

Any equipment that is difficult to completely clean and disinfect should be removed from the site.

It is safer to buy new heat lamps, floor mats, boots, sorting panels, etc. than to try and ensure they are completely clean

When doing a PRRSv elimination program, it is a good time to

and disinfected.

evaluate what other pathogens could be eliminated at the same time. In the US, many farms starting a PRRSv elimination program

The cost of replacing all of these items is significantly lower

take advantage of the occasion to make slight modifications to

compared to the overall cost of the depop-repop project and

their elimination plans (such as the strategic use of antimicrobials)

can have a significant impact on preventing exposure to pre-

to also eliminate Mycoplasma hyopneumoniae.

vious virus.

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