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First Asian PigElite® 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
Demographics
100 Million Pigs
5.5 Million Sows
U.S. Pork Industry Structure Study, 2003
University of Missouri, Iowa State University, Pork magazine, Pig Improvement Company, National Pork Board, Monsanto Choice Genetics, and Land O’ Lakes.
Firm size
(thousand head mktd. annually)
Number of operations Market share
Less than 1 59,950 1%
1 - 3 6,630 8%3 - 5 950 4%
5 - 10 1,526 9%
10 - 50 915 19% 50 - 500 134 19%
500+ 25 40%Total 70,130 100%
Estimated Total Number of Operations & Share of U.S. Slaughter in 2003
by Size Category
Biggest barriers of swine production
PRRSPCVADMycoplasma
hyopneumoniae
What is the AASV doing The American Association of Swine Veterinarian
organization is taking several steps to confront two deadly diseases: PRRS and PCVAD affecting hog farms.
Formed PRRS committee Formed the PRRS Eradication Task Force Formed a Committee on PCVAD to develop a plan
of action and educate members Plans to offer the PRRS risk-assessment tool from
Boehringer Ingelheim for free to members to implement on their clients’ farms
AASV activities The AASV will continue to support the
country's core PRRS research initiative, the PRRS Coordinated Agricultural Project through the Department of Agriculture and the National Pork Board. The USDA National Research Initiative has committed about $4.4 million to the project, and the National Pork Board has committed about $2 million in Pork Check-off funding
the AASV is positioning itself for a leadership role in eradicating the disease by adoption of the following statement:
Porcine reproductive and respiratory syndrome (PRRS) is a significant production-limiting disease of swine that is estimated to cost the US industry approximately 560 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 eradication of the disease 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 eradication 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.
PRRSV and PCV2
‘A Terrible Gang of Two’
PRRSv: A very complex problem A quick review of PRRS virus
Where it multiplies Properties of the virus Sow herd infection Grow finish animal infection Symptoms Transmission and circulation of virus
Control methods Co-infections and what does this mean
enveloped RNA-Virus of the family Arteriviridae very sensitive virus outside of host (low tenacity)
The PRRS Virus
50-60 nm
Nukleocapsid
GlycoproteinsRNA
Membrane
Primary target cells are porcine alveolar macrophages (PAM`s) Infection itself does not cause generalized immuno-suppression
but
defence mechanism of the lung
is impaired
=> secondary pulmonary pathogens have easy access to the lung
The PRRSv infection
PRRS infected (dead) PAMPRRS infected (dead) PAM
Properties of PRRS virusProperties 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 duration of immunity due to viral mutations Short duration of immunity due to viral mutations (Lager et al., 1997)
Short colostral protection of piglets Short colostral protection of piglets
Abortions between day 105-Abortions between day 105-
110 of pregnancy are 110 of pregnancy are
commoncommon
Prolongation of pregnancy Prolongation of pregnancy
up to day 120 often due to up to day 120 often due to
dead fetiidead fetii
Delivery of stillborn, weak-Delivery of stillborn, weak-
born or mummified pigletsborn or mummified piglets
Increase of return to Increase of return to
breedersbreeders
PRRSv:PRRSv: symptoms in symptoms in sowssows
PRRSv Infection:PRRSv Infection:Time lag between infection and clinical Time lag between infection and clinical symptomssymptoms
Infection time ofsusceptible sows
(return tobreeders)
Lactation Pregnancy
Mating
Lactation
Farrowing
Late term abortions or litters with
weakborn, stillbornor mumified pigs
NO clinical symptoms
NO clinical symptoms
3-6 weeks
up to 6.5 weeks
-33 -19 -5 0 14 28 42 56 70 84 98 115
Time (days)
Reproductive disorders :Reproductive disorders :PRRSv differential diagnosisPRRSv differential diagnosisSymptom/Pathogen abortions re-breeders mummies small litters poor milkingAujeszky Virus + + + + +Ergotism + + + + +PEV + + + + -Parvovirus (+) + + + -Hog Cholera + + + + -Brucellosis + + + - -PRRSV + (late) + + (large) - -Strep./Staph. + + - - +E.coli + + - - +Erysipelas + + - - -Eperythrozoon + + - - -Mycotoxins + + - + -Leptospirosis + - + - +Past. multocida + - + - -Listeriosis + - - - -Salmonellosis + - - - -Influenza V. (+) (+) - - +PCV2PCV2 + + + + +Mycoplasma (+) (+) - - (+)Management + + + + -
PRRSv symptoms in boars without obvious without obvious
symptoms symptoms Influenza like Influenza like
symptomssymptoms exhaustionexhaustion in some cases transient in some cases transient
reduction in quantity reduction in quantity and and motility of sperms motility of sperms
PRRSv: PRRSv: reproductive losses reproductive losses
Decrease of fertility by -10% to -25%Decrease of fertility by -10% to -25%
Decrease of piglets per sow (-1.5 to -3.8 pigs/ sow per year)Decrease of piglets per sow (-1.5 to -3.8 pigs/ sow per year)
Decrease of feed convertion ratio (+0.02 to +0.5)Decrease of feed convertion ratio (+0.02 to +0.5)
Reduction of general health status and increased Reduction of general health status and increased susceptibility to other pathogens susceptibility to other pathogens
increased medication costs increased medication costs
Total financial losses due to PRRS infection of sows are Total financial losses due to PRRS infection of sows are (depending on field virus pathogenicity) is 255 $/sow/ year (depending on field virus pathogenicity) is 255 $/sow/ year (National Pork Board, 2003 PRRS Compendium)(National Pork Board, 2003 PRRS Compendium)
PRRSv:PRRSv: symptoms in pigs symptoms in pigs Conjunctivitis, eyelid edemaConjunctivitis, eyelid edema
Discoloration of ears, snout ...Discoloration of ears, snout ...
Increase losses in growth and Increase losses in growth and
mortalitymortality
Non-responding respiratory Non-responding respiratory
symptoms and symptoms and
secondary secondary
infectionsinfections
growth within pensgrowth within pens
and groups of finishingand groups of finishing
animals are not evenanimals are not even
Respiratory Disorders
Pathogen Resp.distress
Dis-coloration
ears
CoughConjuncti-vitis
SIV +- + ++
APP + - +++
Aujeszky virus - + ++-
Erisipelas + +++-
Past. multocida +- +- -
Ergotism + -- --
H. parasuis - + +- -
Salmonella sp. + -- --
M.hyopneumiae - + +- -
Hog Cholera ++ ++ -
Eperythrozoon + -- +-
E. coli ++ + +-
PRRS ++ - (+) -
PCV 2 +- + ++
Difficult breathing
PRRSv: PRRSv: losses in losses in pigs pigs Increase of losses (+1% to +8%)Increase of losses (+1% to +8%) Increase of feed conversion ratio (+0.01 to +0.5)Increase of feed conversion ratio (+0.01 to +0.5) Decrease of daily weight gain (-15g to -150g/ Decrease of daily weight gain (-15g to -150g/
animal /day)animal /day) Increase of uneven growth within groups and pensIncrease of uneven growth within groups and pens Decrease of general health status and by this Decrease of general health status and by this
increased susceptibility for secondary pathogens increased susceptibility for secondary pathogens (Thacker, 2000)(Thacker, 2000)
Increased rates of culls and light pigs (Keffaber, 1989)Increased rates of culls and light pigs (Keffaber, 1989) Increse of medication costs due to worsening health Increse of medication costs due to worsening health Reduction of carcass qualityReduction of carcass quality Average cost of PRRS in the growing pig: Average cost of PRRS in the growing pig: 6.25 – 6.25 –
15.25$ per pig15.25$ per pig
Transmission of PRRSV
Animals- direct contact and aerosolsAnimals- direct contact and aerosols Airborn transmission supporting factors: - low Airborn transmission supporting factors: - low
temperatures, low UV radiation and weather changes temperatures, low UV radiation and weather changes (wind and clouds) (wind and clouds)
Transmission up to 2 - 3 km possible but still needs Transmission up to 2 - 3 km possible but still needs supporting evidencesupporting evidence
Scott Dee‘s current research – 5 replicates so farScott Dee‘s current research – 5 replicates so far
Spread by flies in two reps Spread by flies in two reps
Aerosol spread in two repsAerosol spread in two reps
Personal communications – August, 2006Personal communications – August, 2006
Infected semen - Boars usually are shedding virus via Infected semen - Boars usually are shedding virus via semen between day 3 to 21 post infection but can be semen between day 3 to 21 post infection but can be sporadic shedding for long timesporadic shedding for long time
Vehicles – are very common problem in US, especially Vehicles – are very common problem in US, especially in winterin winter
People and fomites – boxes, tools, insects, etc.People and fomites – boxes, tools, insects, etc.
PRRS-virusPRRS-virus circulationcirculation
-- ++++ ----
--
+++++/-+/-+/-+/- +/-+/-++++
sowssowsgiltsgilts
finishersfinishers
pigletspiglets
3-43-4 5-65-6 7-97-9
(+)(+) +/-+/-+/-+/- +/-+/--- ---- ++++++++ --
++++immune animal
++partly immune animal
-- non- immune animal
+/-+/-infected animal (virus shedding)
(+)(+)maternal immune animal
pig flow virus circulation
age of pigs (weeks)age of pigs (weeks)
PRRS-virus circulationPRRS-virus circulation
++++ ++++++++ ++++++++
--
++++++++++++ ++++++++
sowssowsgiltsgilts
finishersfinishers
pigletspiglets
3-43-4 5-65-6 7-97-9
(+)(+) +/-+/-(+)(+) ++++(+)(+) +/-+/-+/-+/- ++++++ ++++
++++immune animal
++partly immune animal
-- non- immune animal
+/-+/-infected animal (virus shedding)
(+)(+)maternal immune animal
pig flow virus circulation
age of pigs (weeks)age of pigs (weeks)
++ ---- ++++
--
------ --++
sowssowsgiltsgilts
finishersfinishers
pigletspiglets
3-43-4 5-65-6 7-97-9
(+)(+) ++(+)(+) ++++(+)(+) ++++ ++++++ ++++
++++immune animal
++partly immune animal
-- non- immune animal
+/-+/-infected animal (virus shedding)
(+)(+)maternal immune animal
pig flow virus circulation
age of pigs (weeks)age of pigs (weeks)
Interruption of infection chain due tovaccination of piglets
Sows become highly susceptible about 3-4 month after start of vaccination
PRRS-virus circulationPRRS-virus circulation
Proper diagnosis prior to vaccination!!
Whole herd vaccination of sows (and boars): Depends on producing SEW piglets (3 times per year) or nursery on site
(4 times per year)
Piglet vaccination: 10-21 days of age or initial mass vaccination
then 10-21 days of age
Gilt vaccination on arrival:
2 x (4 wks apart) in farms with high infection pressure
Serological success: titers should be low in sows at the time of
revaccination and in fatteners at the time of slaughter? Should be checked or monitored often – 2 x per year at least
General recommendations for General recommendations for PRRSv vaccinationPRRSv vaccination
Ingelvac® PRRS MLV vaccination in farrow to finish farmsaccination in farrow to finish farms
Start of vaccination:Start of vaccination: All All sowssows on one day on one day
irrespective of irrespective of gestation stagegestation stage All All nursing pigletsnursing piglets 3 3
weeks of age and weeks of age and olderolder
All All nursery pigsnursery pigs (when clinically (when clinically healthy)healthy)
All All finishing pigsfinishing pigs (when clinically (when clinically healthy)healthy)
Maintenance program for vaccinations:
Sows:Sows: first revaccination after 4 to 8 weeks, all first revaccination after 4 to 8 weeks, all following revaccinations with consideration of:following revaccinations with consideration of:44 الال month interval when piglets are continuously month interval when piglets are continuously
vaccinated at 3 weeks of age or nursery and vaccinated at 3 weeks of age or nursery and finishing animals are located at a different sitefinishing animals are located at a different site
33 الال month interval when piglets are not vaccinated month interval when piglets are not vaccinated and at the same siteand at the same site
Gilts:Gilts: two times ( two times (3 to 4 week interval3 to 4 week interval) upon ) upon arrivalarrival
Piglets: at 10 days of age to 3 weeks of age, If no infectious pressure, one dose at 5 weeks of age (need to explain further...)
PRRS vaccine is used in a mass vaccination program Depends on the site, if single site then will vaccinate all
animals on the site two times to start program Sows – does not matter what stage of gestation If two sites, then will vaccinate all of the animals on each site
It depends on your goal if two doses are needed in the nursery finisher flows
Important to remember that it takes about 4 weeks to develop protective immunity
Place vaccine 4 weeks prior to exposure When active field virus, two doses of vaccine are given 4
weeks apart
Take home messages on vaccines:Typical PRRS vaccination program in a US (continuous farrow-finish) herd
PRRSv Control Interventions Control principles Subpopulation effects Persistence Major considerations Population immune
management tools reviewed
Case presentations Summarize what I have
learned
PRRSv Control Principles Employ protocols that minimize viral replication and
transmission within a population of animals Fundamental to this is Population Immune
Management Population based implementation of immune management
tools Implement in an effort to create a homogenous population
giving field virus No Place to Go........ Create a non-infectious population
Often employed with a form of herd/population closure
PRRSv Control Principles Goal is to minimize and stop all viral replication and
transmission within a population Develop a homogenous population based on immune status Can be negative or positive which depends on what you are
trying to achieve Nursery – negative Sows – positive or negative
Create a non-infectious population Subpopulations exist in all population of animals
Subpopulations will maintain an environment for chronic field virus circulation
Subpopulation Principles Subpopulations exist
PRRS virus infection results when inconsistent exposure throughout the population occurs
Subpopulations are fundamental for maintenance of chronic field virus circulation
Subpopulations can co-exist for extended periods of time
Animals will “shift” from one subpopulation status to another subpopulation over time
Importance of these Principles Persistence PRRSv can persist in breeding age females
and persistently infected sows can shed virus to naïve contacts
Studies demonstrate PRRSv transmission at 49, 56, 86, & 99 days. Also demonstrate persistence beyond 100 days.
Major Considerations Establish the farm or site’s goal for PRRSv
Control viral activity so clinical improvement is observed Diagnostic support of present clinical signs to determine
recent status of PRRSv and classify as negative, stable, unstable or active Gilt Pool Breeding Gestation Lactation Growing Pigs Semen source
Control options for population immune management tools Initial stabilization Maintenance of stabilization Herd closure and immune management tools
Natural exposure, killed vaccine, live virus inoculation (LVI) and modified live vaccine
PRRS Control Program:Systematic Approach Goals of the Farm/System
Stabilize attain and maintain a stable PRRS positive population production of PRRSv negative offspring
Eliminate Depopulation Test and Remove Extended Herd Closure
Current data would suggest that at least 120 days is necessary to deal with persistently infected animals
Immune Management Tools Natural exposure
Takes considerable amount of time even in small groups of replacement females
Inconsistent in large populations of animals Little control over viremia
Killed vaccine Very little data that supports predictable efficacy
Live virus inoculation (LVI or serum therapy) High risk (virulent) and unreliable
Modified live vaccine The best immune management tool with proven success
Summary: importance of these principles Must eliminate subpopulations to attain and maintain
homogenous population
Population immune management is fundamental to attain and maintain this homogenous population and PRRS control/stability
Must decide which of the immune management tools has the best fit and probability of success for your unit or system
A: Goal – Determine the desired PRRS status B: Current PRRS Status – must know with
current diagnosticsC: PRRS Risk Assessment – AASV tool that
will soon become web basedD: Control Options
>> Initial Stabilization >> Immune management tool: MLV
>> Maintenance Stabilization>> Utilizing immune management tools and
herd closureE: Create Realistic ExpectationsF: Measure and Monitor Intervention
Summary: PRRS Control Methodology
Systematic Approach
Multiple Strains This is more common then one thinks It has been my experience that multiple strains in
a site or a population will alter the perceived program’s success Complete control and elimination is still possible but
often more difficult Could take longer to stabilize a population May need a more intense vaccine program May be the reason that abortions occur post mass
vaccination
Case report Single site unit – farrow to finish, 1000 sow Very well managed Sow herd responded well to vaccinations Continued to find field viruses in the nursery
flow with mild clinical signs Clinical signs will vary, so mortality rates vary Occasionally associated with PRDC in the
finisher animals Complicated with PCV 2 associated diseases
Narrative:
• Sequences beginning with AAA, AAC, AAD, AAF, AAK and CAA are available in the public domain database and are included to illustrate the diversity of PRRSV ORF 5 sequences
• VR-2332 is the prototype U.S. PRRSV strain
• Ingelvac and IngelvacATP are modified-live vaccine strains
0.1
AAF36254
AAC54599
VR-2332
AAD37086
CAA1108869325 Ingelvac
AAA67155
AAC41215
7179471065
6621362136
63628
AAC54591
66909
65554AAC57953
AAK25810
AAF36277 AAF36239
AAC5795772978
75088 InglvacATP
Group Dendogram
01/16/2004
05/19/200410/29/2003
09/23/2004
11/24/2004 12/22/2004
02/8/2005
04/20/2005
04/20/2004
06/18/2004
What I Have Learned Communication is vital
Expectations of the owner and staff “Sterilizing immunity” “Gold bullet”
Compliance issues with breaks Is all members of the unit on the “same page” Biosecurity example – employee lived on a separate
unit where different pigs were housed We still do not know how pathogens like PRRSv
“gets up to” or next to units
What I Have Learned Multiple strains exist on
farms An intense diagnostic program
is needed to find the different strains over time
Confusion will often occur early in any program
Develop a team approach to controlling the circulating virus
All members of the team need to “buy in” to the control measures
Current Knowledge This started a paradigm shift in our thinking in the late ’90’s
1998/19990 and my first client’s response One major change was the selling of breeding stock as naïve
not positive stable Management techniques that are successful
Herd closure, nursery depopulations, complete herd depopulations, etc.
Biosecurity issues – new knowledge Exposure of naïve replacements with MLV vaccine prior to
entry into a positive herd Natural exposure did not work well due to inconsistent exposure (not
like TGE)
Current Knowledge Elimination of virus from a population and
even a unit/ system is achievable Many units have been clean for years
Located in low dense areas High hog dense areas – can not keep clean as long
It is not if I can eliminate the virus from a unit, but can I keep the unit clean long enough to return a profit from the dollars spent on elimination
Summary: What I have learned Routine population immune management by
vaccination Long term stability can be attained and maintained for
resident PRRSv Prevent new entry of virus
Replacement animals Semen Biosecurity
Create realistic expectations for the unit Evaluate co-factors; i.e. other major pathogens,
environment, genetics and management issues
Summary: What I have learned Controlling PRRSv is challenging and involves
many factors Effective control requires a systemic approach that
effectively implements numerous PRRS management tools
First goal is to attain stability of the breeding herd Minimize circulating virus Eliminate subpopulations Influences PRRSv status of growing pigs
Gilt pool management is critical in maintaining sow herd stability
Summary: What I have learned I “attack” what I know first
I control what I can control first Mycoplasma, PRRSv and SIV
Aujesky virus, Classical Swine Fever, FMD Mhyo vaccine: 1-dose
Secondary bacterial infections I use antibiotic therapies
Management issues Environmental issues Mycotoxin control
Porcine Circovirus 2 Is PCV2 involved? AASV Task Force
committee work Porcine Circovirus
Associated Disease (PCVAD) The disease Diagnosis Economic costs Control measures Sequencing of virus European experience
PCV2 is involved 1) At least six different teams of researchers have reproduced
clinical signs, typical PMWS lesions and mortality with PCV2 alone. These lesions (lymphoid depletion, granulomatous inflammation and inclusion bodies) are considered as characteristic of PMWS, and have only been reproduced, at least so far, with PCV2. Please note that several of the studies have used small
sample size populations.
2) There are at least 18 (maybe 19 now) papers showing that there is a direct relationship between the quantity of PCV2 in blood and tissues, and the severity of clinical signs and lesions. If PCV2 was not important in that condition, why would that be? Viral loading can only be taken so far in understanding the
clinical signs.
Personal conversation with Dr. Robert Desroiers, April, 2006 My comments follow each category.
PCVAD Task Force Committee Members
Butch Baker (ISU); David Pyburn (USDA); Francois Cardinal (Qubec); Joaquin Bacerril (Mexico); John Harding (U. of Saskatchewan); Mark Engle (PIC); Pam Zaabel (NPB); Pat Halbur (ISU); Rodger Main (Murphy Brown West); Russ Nugent (Tyson); Tim Loula (Minn); William Starke (Land O’Lakes); Kelly Lager (USDA)
Others on list to step in if someone decides to leave the committee
PCVAD Task Force Committee for AASV was formed
First order of business was to decide on what to call this problem Porcine Circovirus
Associated Disease Covers all clinical
expressions, although the primary economic concern is PMWS
PCVAD Porcine Circovirus Associated Disease Why did we select this name?
At the time there were several veterinarians describing what the clinical expressions were being observed
Input from veterinarians and researchers from Canada and Europe
Dealing with a very complex problem
Early challenge Develop a database to
track occurrence of the disease
Eastern Canada Minnesota – Dr. Peter
Davies Purdue – Dr. Sandy
Amass
Main challenges associated with conducting an epidemiological survey on this syndrome:
the variation in clinical presentation observed
how do you define “high” mortality
the difficulty in determining a case definition that appropriately describes the syndrome. It was decided that the committee should review existing case definitions in light of the newly described syndrome being reported (i.e. high mortality with little to no wasting) to determine if an appropriate case definition could be derived. This was considered important if accurate and meaningful case reporting was to occur
producer’s potential sensitivity
associated with reporting this information into any type of database to which there would be public access
on what do you base epidemiological reports (i.e. diagnostic sample results, clinical presentation, etc).
Early challenge USDA’s Center for
Emerging Issues (CEI) and the National Surveillance Unit (NSU) to determine what role they should play in tracking this disease and, in a broader sense, analyzing the syndrome in general
The committee also discussed the need to explore the role of allied groups such as:
USDA’s Agricultural Research Service (ARS) for a research focus
National Pork Board to facilitate funding and outreach.
Early challenge Educational material
Discussed the linking of web sites www.pcvd.org (Gordon Allen) www.thepigsite.com (very popular site) www.pmwsinpigs.com www.pighealth.com Developed a page within the AASV website as an
educational page (menu AASV >committee >PCVAD) The page has a focused on recognition, diagnosis and
current therapies which includes vaccine response
Literature articles Current research projects that are being conducted
Early challenge Vaccine response
Need to report to industry at some point
Literature and research updates National Pork Board
will help facilitate this information
Information from some articles will be included
The disease As early as 1991 the problem was mentioned
Retrospective testing of stored sera may go as far back as 1969 (Staebler, S. et al, 2005)
Sporadic cases of PCVAD in Spain and England may be as early as 1986 (Rodriguez-Arrioja, G. et al, 2003)
Global explosion since the mid-1990’s Drs. Harding and Clark coined PMWS in 1996
PCV 2 not a “new” pathogen and PCVAD is not a “new” disease Epidemiological studies in UK and Denmark
strongly suggest since 1999 that the spread of PCVAD has been consistent with the introduction of a “new” infectious agent
MONTANA
WYOMING
IDAHO
WASHINGTON
OREGON
NEVADA
UTAH
CALIFORNIA
ARIZONANEW MEXICO
TEXAS
OKLAHOMA ARKANSAS
LOUISIANA
NEBRASKA
COLORADOKANSAS
MISSOURI
NORTH DAKOTA
SOUTH DAKOTA
IOWA
MINNESOTA
TENNESSEE
MISS ALABAMAGEORGIA
FLORIDA
SOUTHCAROLINA
NORTH CAROLINA
WISCONSIN
ILLINOISINDIANA
KENTUCKYVIRGINIA
WV
OHIO
MICHIGAN
MARYLAND
NEW YORK
PENN
DELAWARE
NEWJERSEY
CONN RI
MASS
MAINE
VT
NH
ALASKA
HAWAII
PCVAD – High or rapidly increasing, low, not yet reported
PCVAD – High or rapidly increasing, low, not yet reported
Self reporting incidence in US
Supplied by Dr. John Kolb, Boehringer Ingelheim Vetmedica
The individual pig: A starting point!
Growth retardation, dyspnea, enlargement of lymph nodes, diarrhea, and/ or jaundice (Allan, G. et al, 2000. Segales, J. et al, 2002)
Clinical signs will vary Enlarged lymph nodes and non-
collapsing lungs are most common Need to necropsy and submit tissue
from at least 5 animals
Tissue submissions: PCVAD is a broad categorization of
multisystemic diseases with the following histopathological findings in affected pigs: Depletion of lymphoid cells Detection of PCV2 within the lesions Disseminated granulomatous inflammation in
multiple tissues (e.g. spleen, thymus, ileum, lymph nodes (sternal, bronchial, inguinal and mesenteric), lung, kidney, liver, tonsil, etc.).
Reproductive diagnosis requires the presence of PCV2 antigen in lesions associated with fetal myocarditis
The herd: “Muddy waters” This is a “work in
progress” Primary reason is that
many herds can have an occasional animal with fulfills an individual case definition but does not have a herd problem
AASV committee reviewed CDC’s approach to describing a new clinical problem
Also looked at our European colleagues approach 1a) historical level of
mortality +1.6 X SD2 1b) if no records,
increase that exceeds regional level by 50%
Work in progress: herd definition PCVAD can be subclinical or include one or more of
the following clinical manifestations concurrently: Multisystemic disease with weight loss (formerly
known as PMWS) High mortality: Doubling of historical mortality
rate without introduction of a new known pathogen.
Respiratory signs including pneumonia Porcine Dermatitis and Nephropathy Syndrome
(PDNS) Enteric signs including diarrhea and weight loss Reproductive disorders including abortions,
stillbirths and fetal mummification (diagnosis requires the presence of fetal myocarditis associated with PCV2 antigen in lesions)
PCVAD: Diagnosis PMWS/ High mortality is the most common
and most economically damaging clinical expression Is considered the major clinical manifestation of
PCVAD Co-factors are probably the most important
aspect to consider Infectious co-factors
Viruses - PRRSv, Parvovirus, SIV Bacteria - Mycoplasma, Salmonella
PCV2 coinfections in 484 U.S. field cases: ISU-VDLPCV2 coinfections in 484 U.S. field cases: ISU-VDL
99
164164
1010
7777
1313 33
92926868
37371111
002020404060608080
100100120120140140160160180180
PCV2 Alon
e
PCV2 Alon
e
PCV2+PRRSV
PCV2+PRRSV
PCV2+PRRSV+SIV
PCV2+PRRSV+SIV
PCV2+PRRSV +
M.h
yo.
PCV2+PRRSV +
M.h
yo.
PCV2+SIV
PCV2+SIV
PCV2+SIV
+M
.hyo
.
PCV2+SIV
+M
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.
PCV2+M
. hyo
.
PCV2+M
. hyo
.
PCV2+Bac
teria
l sep
ticem
ia
PCV2+Bac
teria
l sep
ticem
ia
PCV2+Bac
teria
l pne
umon
ia
PCV2+Bac
teria
l pne
umon
ia
PCV2+ O
ther
s
PCV2+ O
ther
s
Num
ber
of C
ases
Num
ber
of C
ases
Rarely see PCV2 singular infection
PCV 2Strains Co-factors
InfectionsNon-infectious
Immune stimulation
Low viremia
Seroconversion
Host susceptibility
Subclinical disease
High viremia leukopenia
+/- seroconversion
Systemic spread
Clinical disease- 70/80% mortality
PCV 2 VirusInfection in lymphoid tissues +/- other tissues
Lymphoid depletion + histiocytic replacement, antigen
PCV 2 particle
1 to 20 % of the animals
Porcine Circovirus Associated Disease
Information courtesy of Dr. Pat Halbur
Economics of PCVAD PMWS is perplexing,
interesting but very costly when clinical signs contribute to mortality and attrition.
Attrition is best defined as pigs that do not make full market weight on time Culls, lights, under
market weights, etc
Other expressions of PCVAD Enteric disease in
grow finish stage Infectious and
nutritional causes
PCV2 Induced Granulomatous Enteritis in Growing Pigs
Kolb, J. Genzow, M. and Roof, M. IPVS, 2006 pg. 272.
Pathogen # cases % cases
Lawsonia 12 32%
Salmonella 7 19%
PCV2 14 38%
Brachyspira 1 2%
total 37* 100%
*includes mixed infections; sum does not total to 100%
Other expressions of PCVAD
Reproductive expression is rare Abortions, stillborns, mummified fetuses The presence of fetal heart lesions
Necrotizing myocarditis The presence of PCV2 antigen in the
myocardial lesions and in other fetal tissues if possible
Other expressions of PCVAD
PCV2 is considered a contributor to Porcine Respiratory Disease Complex (PRDC) Pneumonia is one of the more common
expressions associated with PCV2 PDNS
The incidence is often increased when other expressions of PCVAD occur
Has not been supported by research
Control – Develop an action plan
Get an accurate diagnosis!! Identify concurrent infections and implement an
action plan to control and or eliminate PRRSv/ SIV/ HPS/ Salmonella/ Mycoplasma
Evaluate timing of when you are vaccinating Mycoplasma vaccines especially Enteric vaccines do not seem to be as “sensitive”
Treat bacterial infections Therapeutic “CTC” levels and therapies to control
bacterial co-infections Use vitamin E and Selenium Nutritional enhanced diets
Control – Develop an action plan
Try removing effected animals very early in the clinical expression – does not always work
Practice strict All In All Out Stop mixing and resorting animals post weaning Make sure you provide 0.28 square meter (3
square feet) in the nursery and 0.74 square meter (8 square feet) in the finisher
Use detergents and disinfectants Virkon S, Roccal D and Synergize Anthium Dioxide + Acidic Detergent (foam with air)
Weaning age may become a factor?
Madec 20-point rules Control without PCV2 vaccination
sometimes works, sometimes does not work!
Control programs have focused on co-factors and other risk factors
Madec rules will significantly decrease mortality because the measures are designed to reduce “infection pressure” of PCV2 and other infectious pathogens, improve hygiene and reduce stress
Summary– Develop an action plan Transmission studies
No research studies that I can find An “on farm” study placed 140 day old from
source with no clinical signs and tested with animal > 140 days old that had recovered from PCVAD PCR positive serum in >140 day olds Did not “transfer” PCV2 to sentinels or clinical signs
Canadian/ Midwest/ N.C. strains are very similar to European strain Virus will change over time??
Maternal antibody studies Kelly Lager – found in 3 week old pigs
May not be held back by maternal antibodies?
Summary
Environmentally stable virus We do not know this for sure Do not know how long it will survive in
manure One common comment is how well
the sow herds are performing for a severe problem in the finishers
Vaccines – piglets have been vaccinated two times (efficacy varies)
Summary-Genetic influences Landrace and
Large White Pat Halbur – one
study implicated Landrace as more suspectable
Duroc and Pietrain More information
is needed!
Period of timeDuroc A
mortality
Duroc B mortality
Jan-June 2005 (before PMWS)
2.5% (245,945)*
3.5% (316,29
7)
Jan-Dec 2005 2.6% (278,704)
4.3% (898,28
0)
Jan-April 2006 (with PMWS) 3.0% (29,504)
7.5% (490,31
9)
Mortality in finishing units in the progeny of two different Duroc boar lines
*number of animals per group
Matt Turner, personal communication, July 2006
Information supplied by Dr. Tim Loula, Swine Vet Center
a) Sequencing and building dendograms are useful but limited in providing information on severity of virus isolated
b) There may be distinct and conserved PCV2 genotypes, which may equate to distinct PCV2 strains and this may be important in the understanding of PCVAD
Summary thoughts Management issues are important and may start in the sow
herd Get an accurate diagnosis Cross fostering techniques stopped in the sow herd Stop resorting in nursery Remove the affected animals from the general population Be aggressive on treatments if improvement is observed Needle management? Sanitation program updated Replacement animal “stabilized” Genetic changes Others?
Summary thoughts Vaccine will be a tool to consider
Sow vaccination vs. piglet vaccines
Control other pathogen activity – important! Especially PRRS if present Easier said then done!
Transmission and viremia Lots to learn yet! Started at 6 weeks and still viremic by PCR tests
on serum at 135 days in one case of mine
You may also concern:Mycoplasma vaccination
Piglet vaccination will work if given at the right time Single dose vaccines are common and given at 5 to 6
weeks of age In some flows the exposure to mycoplasma is so high
that a two dose program is needed I have been vaccinating sow herds for three years
Reduces the amount of organism in the piglets at weaning
Have stopped vaccinating the piglets in two flows Are using naïve sentinels in both flows to see if we have
completely eliminated the organism or reduced to very low levels
Most boar studs that I service are mycoplasma naïve Again we used vaccine at first to stabilize the stud After a couple of years, purchased mycoplasma naïve
boars and used them as sentinels initially
Questions?Questions?
THANK YOU! THANK YOU! Special thank you to Dr. Marika Genzow Special thank you to Dr. Marika Genzow
and Dr. Mike Murtaughand Dr. Mike Murtaugh