1. Second Asian Pig Elite® Tour
Thomas Gillespie, DVM,
Diplomate ABVP
Rensselaer Swine Services,
Rensselaer, IN

2. The PRRSV infection
Primary target cells are porcine alveolar macrophages
(PAM`s) (T. Molitor et al., 1996, AASP proceedings)
Infection itself does not cause generalized immuno-suppression but defense mechanism of the lung is impaired
Secondary pulmonary pathogens have easy access to the lung
(Zimmerman et al., Diseases of Swine,
2006)
Detrimental effect of PRRS virus infection
Source: Boehringer Ingelheim Vetmedica GmbH
Date: October 1999
Comment:
Primary target cells of the PRRS virus are the porcine alveolar macrophages (PAM`s), a cell type of the immune system which is responsible to inactivate and eliminate inhaled pathogens in the lung.
By replicating within PAM`s, these macrophages are no longer able to carry out their "Police-function" in the lung properly. Inhaled pathogens may replicate without restraint until PAM`s have recovered from PRRS infection. PRRS infection is therefore considered to be a primary infection which - especially in farms with insufficient management and hygiene - supports secondary pathogens.
PRRS infection does impair local defence mechanism in the lung for some weeks but it does not cause general immuno deficiency.
PRRS infected (dead) PAM

3. Aspects that we know of PRRS virus
Replication in porcine alveolar macrophages (PAMs)
Long term viremia (more than in some cases 3 weeks)
Persistent infections (157 days; Wills et al., 1997)
Subclinical infections (Morrison et al., 1992)
Differences in virulence (Mengeling et al., 1996/1998)
High infectivity (<10 infectious particles) but slow transmission (Yoon et al,1998; Wills et al., 1997)
Short colostral protection of piglets
Properties of PRRS virus
Source: Boehringer Ingelheim Vetmedica GmbH
Date: October 1999
Comment:
Beside the replication and by this destruction of a cell population of the immune system in the lung, the PRRS virus has several other properties which influence the infection control possibilities:
Compared to other virus infections, PRRSV induces viremia for a long period of time (usually 3 weeks but in some animals viremia has been described for more than 150 days) which means infected animals do infect others for a long time, even if they already are seropositive. In addition transmission is very slow compared to other virus infections so that it may take some month until all animals are infected (first infected animals may be already susceptible again when last infected animal still sheds virus).
Subclinical infections are frequent so that viremic animals (infecting others) may not be obviously seen.
Due to differences in virulece of the PRRS virus also clinical symptoms are different. Some isolates cause just mild symptoms, others are extremely „agressive“; some isolates induce mainly respiratory problems, others mainly reproductive problems. Therefore the diagnosis MUST ALWAYS be confirmed by laboratory diagnostics.
Another factor which supports virus circulation within a herd is the short duration of colostral immunity. Even if piglets get maximum amount of maternal antibodies, protection is no longer than 3-4 weeks so that already in the farrowing room fist piglets may get infected.

4. Inconsistent results across all farms
Techniques that have been proposed to eliminate subpopulations and reduce the risk of PRRSV shedding such as:
Herd closure
(Dee et al., 1995; Torremorell et al., PRRS Compendium, 2003)
Gilt acclimatization
(Dee et al., 1997; Batista et al., 2002; Fano et al., 2005)
Mass exposure
(Desrosiers et al., 2002; Batista et al., 2004; Wagner et al., 2005 and FitzSimmons et al., 2005)

5. Another alternative to maximize population immunity to PRRSV is vaccination
The induction of both humoral and cell-mediated immune (CMI) responses has been described following the application of PRRS modified-live virus (MLV) vaccines in pigs.
(Chareratanakul et al., 2006; Foss et al., 2002 and Meier et al., 2003)
Multiple experiments have shown significant reduction in lesions and clinical signs of vaccinated pigs following both homologous and heterologous PRRSV challenge
(Chareratanakul et al., 2006; Foss et al., 2002; Mengeling et al., 2003 and Opriessnig et al., 2005)

6. PRRS Efficacy: Take Home Message
Independent confirmation of vaccine efficacy at Iowa State University.
Improved ADG
Reduction of Lung Lesions
Reduction of Clinical Disease
Reduction of Post-challenge Viremia
Trial conducted by Dr. Pat Halbur et al.
Trial used Ingelvac ATP modified live vaccine
Used 3 recent heterologous challenge isolates
No correlation between sequence homology and protection….. Heterologous Protection Exists

7. Killed Vaccine
Although it has been reported that vaccination with MLV provides incomplete heterologous protection against PRRSV infection
(Labarque et al., 2003)
Research on PRRS killed virus (KV) vaccines has generated contrasting results regarding the stimulation of the production of neutralizing antibody and cell-mediated immune response in pigs
(Nilubol et al., 2004)
or the absence of these responses following the application of KV vaccines
(Meier et al., 2003 and Plana-Duran et al., 1997)

8. Commercial Conditions
In commercial conditions, the strategic combination of mass vaccination using PRRS MLV products with herd closure and unidirectional pig flow has been found to be a successful approach to control and in some cases to eliminate PRRSV from swine herds.
(Dee et al., 1998; Gillespie et al., 2003, Ridremount et al., 2006 and Rodriquez et al., 2006)

9. Commercial Application
The challenge is to develop a farm specific program to control PRRSV activity:
Using the proven “tools” that are available
Each farm will present with unique situations
The challenge is to control the different PRRS field isolates
In some cases there are multiple isolates in the herd
Monitoring program is vital to understand if the program is working

10. PRRSV is expensive!
Porcine reproductive and respiratory syndrome (PRRS) has been estimated to cost the US swine industry 560 million dollars in losses a year.
(Neumann et al., 2005)
The same study estimates that 88% of the total cost of PRRS in the US is due to increased mortality and decreased growth performance in post-weaning pigs, while the impact of the disease on breeding herds represents only 12% of the total cost.

11. General information of case farm
Originally SPF herd – has remained closed except for semen entry
Does not have finisher space for entire production
Has sold weaners in the past, but started selling feeder pigs last summer/fall when the weaner buyer quit
Pigs that are sold off-site do OK
Site is continuous flow
Farrowing rooms are one large room with 84 crates per room
Nursery, grower and finishers are one large barn with a center aisle
Separate pits for each barn – nursery, grower, finisher, etc.
No restrictions on people (or dog) flow within barns
3/30/07

12. General information of this farm
Owner has a young son that is getting involved in the operation
May not be wanting to keep sows long-term
Son would like to go to contract wean-to-finish production
Have used both MLV and ATP vaccine for sow herd mass vaccinations and pig vaccinations
Have closed herd and bred gilts off-site along with nursery and finisher depopulation and mass vaccination in 2005
No clinical signs in sow herd, but can have an occasional disastrous nursery production
Last nursery group closed out with 44% mortality due to PRRS and PCVAD and it looks like will lose another 15-20% from chronic poor doing pigs
Following group will close out Monday 4/2/07 at 4% to 5% mortality and pigs look good
Pigs have been vaccinated with HP-1 at 7 days, Ingelvac PRRS MLV and CircoFLEX at weaning and Ingelvac M. hyo at 4 weeks of age
3/30/07

13. Major issues
Use Ingelvac PRRS MLV to develop humoral and cell mediated immunity in the sow herd
Need to understand by phase of production, i.e. sows, farrowing, nursery, grower and finisher phases
As the sow herd “stabilizes”, shedding to their offspring will eventually stop
Negative offspring will be weaned
Develop an action plan so negative pigs will stay negative through out the nursery and finisher stages
Develop an action plan to deal with the home raised replacement animals

14. Action Plan
Separate the unit into two “halves” so people do not move freely
Stop all dog movement
Mass vaccinate sow herd two times 30 days apart
May need to mass vaccinate a third time
Practice needle management
Unidirectional animal flow
Strict sanitation program

15. Action Plan Monitoring program
In this case profiling the replacement gilts and sows to determine incidence of viremia in each population
Start testing nursing piglets four weeks after the second mass vaccination
Consider the use of sentinels at the proper time
Use both ELISA and PCR tests

16. Summary
It is important to understand about PRRSV and know the virus’s limitations
It is important to know what tools are available to you to control PRRS virus activity within a unit
Time is on your side – do not hurry through the program

17. Rensselaer Swine Services,
PCVAD: When immunology goes wrong, life on the farm becomes very expensive!
Thomas Gillespie, DVM,
Diplomate ABVP
Rensselaer Swine Services,
Rensselaer, IN

18. “Post weaning Multisystemic
PMWS
“Post weaning Multisystemic
Wasting Syndrome”

19. Outline What is it? What causes it? Where did it come from?
Case definition
What causes it?
Experimental & diagnostic info
Where did it come from?
Clinical trends
How is it spread?
Transmission information and questions

20. PCVAD – case definition
“…we would expect to see a
herd syndrome of wasting in post-weaning pigs
that is generally unresponsive to intervention,
with characteristic histopathology and
abundant PCV2 in lesions.”
Gardner Murray, Australian Chief Veterinary Officer/Special Adviser
Date: Thu, 10 Nov :28: (EST)
From: ProMED-mail
Subject: PRO/AH> Post weaning multisystemic wasting synd., porcine - Australia(02)

21. Mortality curve example from PCVAD herd2% 1% 0%
Percent risk of death by week
Expected mortality rate
Week in finish barn

22. PCVAD: Microscopic changes
“…and abundant PCV2 in lesions.”
Ileum
Lung

23. Sorden: Case Definition
An individual or group case:
FIELD - Clinical signs of growth retardation,
“ill thrift” or wasting (and others)
LAB - Characteristic histopathological lesions
LAB - Detection of PCV2 within lesions
Sorden, 2000

24. Outline What is it? What causes it? Where did it come from?
Case definition
What causes it?
Experimental & diagnostic info
Where did it come from?
Clinical trends
How is it spread?
Transmission information and questions

25. Etiology Three Main Camps: 1. New PCV2 “strains”
2. Cofactors such as concomitant disease or management factors.
3. Novel pathogen:
“Agent X”

26. Circovirus Circoviruses Porcine Circoviruses Family of small viruses
“Circular” DNA
PCVAD-like diseases
Porcine Circoviruses
PCV1 – no disease
PCV2 – associated with disease
PCV2 “a” and “b”
Photo: Stewart McNulty

27. New Problem
Old Virus
PCV2
PCV2

28. Etiology Henle-Koch Postulates:
Organism present in every case of disease
Organism NOT present when non-diseased
Organism isolated as pure culture from tissue
Organism induces disease experimentally

29. PCVAD – clinical severity
Clinical severity a function of:
Co-infection
Parvovirus (Ellis et al 1999)
Mycoplasma hyopneumoniae (Opriessnig et al 2004)
PRRS virus (Harms et al 2001)
Co-factors
M. hyopneumoniae vaccine (Allan et al 2000)
A. pleuropneumoniae vaccine (Allan et al 2000)
Vaccine adjuvant (Krakowka et al 2001)
Influenza

30. PCVAD – clinical disease
Clinical severity a function of:
Virus genotype (Fenaux et al 2004)
Two amino acid difference = changed virulence
PCV2 A & B (Rowland 2006)
Host genotype?
Found no effect experimentally (Rose et al 2003)
Found effects experimentally (Bergstrom 2006)
Danes eliminating Hampshires

31. Outline What is it? What causes it? Where did it come from?
Case definition
What causes it?
Experimental & diagnostic info
Where did it come from?
Clinical trends
How is it spread?
Transmission information and questions

32. ‘91
‘94
‘96
Albers Equal Area Conic Projection

33. ‘04
‘03
‘00
‘98
‘01
‘99
‘97
‘02
Segales, 2006
Albers Equal Area Conic Projection

34. Over 1200 cases in 2006
Halbur, 2006

35. Clinical Trends: Labs PCV2 detection “constant”
Elevation in percentage of pigs PCV2 +
New PCV2 genetic patterns identified
Increase in PCVAD-like lesions
More Minnesota pigs with typical lesions
More pigs with PCVAD herd histories

36. Clinical trends: Practitioners
Higher rate of “background” wasting
Dramatic cases since Fall of ‘05:
Very high rates of wasting, mortality
Higher health pigs less affected
Vaccines appear to be effective

37. Outline What is it? What causes it? Where did it come from?
Case definition
What causes it?
Experimental & diagnostic info
Where did it come from?
Clinical trends
How is it spread?
Transmission information and questions

38. PCV2 Shedding Routes
PCV2 is shed in respiratory, nasal, fecal, urine and other secretions, and at a higher level in PMWS affected pigs
(Magar et al, 2000, Segales et al 2005).
Milk can also be contaminated
(Shibata et al., 2006).
PCV2 is shed in semen.

39. PCVAD Transmission
Pig to pig transmission of PCV2 and PCVAD documented in field and experimentally.
Incubation appears to be two to four weeks experimentally and observationally.
PCVAD transmission by direct and indirect contact despite PCV2 status of farm of origin.
PCVAD transmitted to PCV2 seropositive pigs, with clinical disease developing when maternal antibodies are low or gone.
Maternal antibodies are protective at high levels and/or are associated with disease.
Sows shedding virus have pigs more likely to develop disease.

40. Timing of vaccine
When vaccine became available, this site was just starting to be refilled
Oldest pigs were approximately 9 weeks of age
Vaccine was given to all animals within one week of time so the youngest were about 4 weeks of age
Oldest vaccinated animals did not perform as well as the animals that were vaccinated younger

41. Circovirus Vaccine In United States
Minnesota
Mortality has decreased to below 5% in previously infected herds
Illinois
Prior group had 18% mortality
Current group at 150 days of age
No vaccine = 4.4% mortality
With vaccine= 1.76% mortality
North Carolina
No vaccine=10-14% mortality
With vaccine=5% mortality

42. Circovirus Vaccine in Canada
Ontario
Mortality in previous groups= 12-17%
Next groups
No vaccine= 5-6%
With vaccine=1-2%
Quebec
Mortality Pre-Madec= 9-10%
Mortality with Madec= 5-6%
Mortality with Madec and Vaccine=2.85%

43. Summary PCVAD is a very costly disease when it is active
Mortality, ADG and FC are the primary areas measured and often compared
Light market animals and cull animals become a major cost
Vaccine for PCVII is a good tool when PCVAD is active

44. Management of PCVAD Management practices to help control PCVAD
Health Co-infections
Biosecurity
Environment issues
Production/ management issues

45. Co-infections diagnosed with PCVAD
Porcine Reproductive and Respiratory Syndrome (PRRS)
Swine Influenza
Mycoplasma hyopneumoniae
Haemophilus suis
Pasteurella multocida
Salmonella species especially typhimurium
Maybe chronic Streptococcus suis

46. Health issues Sow herd stability to major pathogens
Examine internal biosecurity issues
Animal flow
People flow
Needle management especially in the nursery and early finisher
Farrowing management practices to minimize transmission of infections between litters

47. Management of PCVAD Management practices to help control PCVAD
Health Co-infections
Biosecurity
Environment issues
Production/ management issues

48. Biosecurity issues Use a detergent in the soak/prewash period
Ensure that ceilings, walls, flooring and equipment are cleaned and disinfected between groups of pigs
Allow the facilities to dry before animals are placed

49. Management of PCVAD Management practices to help control PCVAD
Health Co-infections
Biosecurity
Environment issues
Production/ management issues

50. Environmental Stressors
Mixing/sorting of pigs
High stocking density
Suboptimal temperatures or ventilation
Out-of-feed events
Gastric ulcers

51. Management of PCVAD Management practices to help control PCVAD
Health Co-infections
Biosecurity
Environment issues
Production/ management issues

52. Production/ management issues
Wash sows and treat for parasites before farrowing
Ensure adequate colostrum intake by piglets at birth
Stop cross fostering after 48 hours
Milk replacer system or “Rescue” decks
Examine hygiene of needle teeth clippers and other instruments
Consider increasing weaning age
Do not move pigs between rooms and try to maintain pen integrity within a room
Hospital pen management
Nutritional issues