Second Asian Pig Elite® Tour
Thomas Gillespie, DVM, Thomas Gillespie, DVM, Diplomate ABVPDiplomate ABVP
Rensselaer Swine Services, Rensselaer Swine Services, Rensselaer, INRensselaer, IN
[email protected]@rssvet.com
www.rssvet.com
Primary target cells are porcine alveolar macrophages
(PAM`s) (T. Molitor et al., 1996, AASP proceedings)
Infection itself does not cause generalized immuno-suppression butdefense mechanism of the lung is impaired
Secondary pulmonary pathogens have easy access to the lung
(Zimmerman et al., Diseases of Swine,
2006)
The PRRSV infection
PRRS PRRS infected (dead) PAMinfected (dead) PAM
Aspects that we know of PRRS virusAspects that we know of PRRS virus
Replication in porcine alveolar macrophages (PAMs)Replication in porcine alveolar macrophages (PAMs)
Long term viremia Long term viremia (more than in some cases 3 weeks)
Persistent infections Persistent infections (157 days; Wills et al., 1997)
Subclinical infections Subclinical infections (Morrison et al., 1992)
Differences in virulence Differences in virulence (Mengeling et al., 1996/1998)
High infectivity High infectivity (<10 infectious particles) but slow transmission but slow transmission
(Yoon et al,1998; Wills et al., 1997)
Short colostral protection of piglets Short colostral protection of piglets
Inconsistent results across all farmsInconsistent 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)
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)
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
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)
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)
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
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.
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
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
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
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
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
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
PCVAD: When immunology goes wrong, life on the farm becomes
very expensive!Thomas Gillespie, DVM, Thomas Gillespie, DVM,
Diplomate ABVPDiplomate ABVPRensselaer Swine Services, Rensselaer Swine Services,
Rensselaer, INRensselaer, [email protected]@rssvet.com
www.rssvet.com
PMWS“Post weaning Multisystemic
Wasting Syndrome”
Outline
1. What is it?• Case definition
2. What causes it?• Experimental & diagnostic info
3. Where did it come from?• Clinical trends
4. How is it spread?• Transmission information and questions
PCVAD – case definition
“…we would expect to see a herd syndrome of wasting in post-weaning
pigsthat is generally unresponsive to intervention, with characteristic histopathology and abundant PCV2 in lesions.”
Gardner Murray, Australian Chief Veterinary Officer/Special AdviserDate: Thu, 10 Nov 2005 16:28:06 -0500 (EST)
From: ProMED-mail <[email protected]>Subject: PRO/AH> Post weaning multisystemic wasting synd., porcine - Australia(02)
Mortality curve example from PCVAD herd
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19
Week in finish barn
2%
1%
0%
Percent risk of death by week
Expected mortality rate
Ileum Lung
PCVAD: Microscopic changes
“…and abundant PCV2 in lesions.”
Sorden: Case Definition
An individual or group case:
1. FIELD - Clinical signs of growth retardation,“ill thrift” or wasting (and others)
2. LAB - Characteristic histopathological lesions3. LAB - Detection of PCV2 within lesions
Sorden, 2000
Outline
1. What is it?• Case definition
2. What causes it?• Experimental & diagnostic info
3. Where did it come from?• Clinical trends
4. How is it spread?• Transmission information and questions
Etiology
Three Main Camps:
1. New PCV2 “strains”
2. Cofactors such as concomitant disease or management factors.
3. Novel pathogen:“Agent X”
Circovirus
Photo: Stewart McNulty
• Circoviruses Family of small viruses “Circular” DNA PCVAD-like diseases
• Porcine Circoviruses PCV1 – no disease PCV2 – associated with disease
PCV2 “a” and “b”
Etiology
Henle-Koch Postulates:
1. Organism present in every case of disease2. Organism NOT present when non-diseased3. Organism isolated as pure culture from tissue4. Organism induces disease experimentally
PCVAD – clinical severityClinical severity a function of:
1. Co-infection• Parvovirus (Ellis et al 1999)• Mycoplasma hyopneumoniae (Opriessnig et al 2004)• PRRS virus (Harms et al 2001)
2. Co-factors• M. hyopneumoniae vaccine (Allan et al 2000)
• A. pleuropneumoniae vaccine (Allan et al 2000)
• Vaccine adjuvant (Krakowka et al 2001)
• Influenza
PCVAD – clinical diseaseClinical severity a function of:
3. Virus genotype (Fenaux et al 2004)
• Two amino acid difference = changed virulence• PCV2 A & B (Rowland 2006)
4. Host genotype? • Found no effect experimentally (Rose et al 2003)
• Found effects experimentally (Bergstrom 2006)
• Danes eliminating Hampshires
Outline
1. What is it?• Case definition
2. What causes it?• Experimental & diagnostic info
3. Where did it come from?• Clinical trends
4. How is it spread?• Transmission information and questions
Albers Equal Area Conic Projection
‘91‘94
‘96
Albers Equal Area Conic Projection
‘97
‘97
‘98
‘98
‘98
‘98
‘98
‘99
‘99
‘00
‘00
‘00
‘00
‘00
‘01‘01
‘01
‘02
‘03
‘03
‘03
‘04
‘04
Segales, 2006
Overal trend of PCV2-associated disease cases submitted to the ISU-VDL
0
200
400
600
800
1000
1200
1993 1994 1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 2005
year
num
ber
of c
ases
Halbur, 2006
Over 1200 cases in 2006
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
Clinical trends: Practitioners
• Higher rate of “background” wasting• Dramatic cases since Fall of ‘05:
Very high rates of wasting, mortalityHigher health pigs less affectedVaccines appear to be effective
Outline
1. What is it?• Case definition
2. What causes it?• Experimental & diagnostic info
3. Where did it come from?• Clinical trends
4. How is it spread?• Transmission information and questions
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.
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.
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
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
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%
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
Management of PCVAD
• Management practices to help control PCVAD– Health Co-
infections
– Biosecurity
– Environment issues
– Production/ management issues
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
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
Management of PCVAD
• Management practices to help control PCVAD– Health Co-
infections
– Biosecurity
– Environment issues
– Production/ management issues
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
Management of PCVAD
• Management practices to help control PCVAD– Health Co-
infections
– Biosecurity
– Environment issues
– Production/ management issues
Environmental Stressors
• Mixing/sorting of pigs• High stocking density• Suboptimal
temperatures or ventilation
• Out-of-feed events– Gastric ulcers
Management of PCVAD
• Management practices to help control PCVAD– Health Co-
infections
– Biosecurity
– Environment issues
– Production/ management issues
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