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First Asian ® Tour Pig. Elite Thomas Gillespie, DVM, Diplomate ABVP Rensselaer Swine Services, Rensselaer, IN tom. [email protected] com www. rssvet. com
Demographics o 100 o 5. 5 Million Pigs Million Sows
U. S. Pork Industry Structure Study, 2003 Estimated Total Number of Operations & Share of U. S. Slaughter in 2003 by Size Category Firm size (thousand head mktd. annually) Number of operations Market share Less than 1 1 -3 3 -5 5 - 10 10 - 50 50 - 500+ Total 59, 950 6, 630 950 1, 526 915 134 25 70, 130 1% 8% 4% 9% 19% 40% 100% University of Missouri, Iowa State University, Pork magazine, Pig Improvement Company, National Pork Board, Monsanto Choice Genetics, and Land O’ Lakes.
Biggest barriers of swine production o. PRRS o. PCVAD o. Mycoplasma hyopneumoniae
What is the AASV doing o o o 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 o 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: o 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 PCV 2 ‘A Terrible Gang of Two’
PRRSv: A very complex problem o A quick review of PRRS virus n n n o o 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
The PRRS Virus Glycoproteins RNA Membrane Nukleocapsid 50 -60 nm enveloped RNA-Virus of the family Arteriviridae o very sensitive virus outside of host (low tenacity) o
The PRRSv infection o Primary target cells are porcine alveolar macrophages (PAM`s) o 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 PRRS infected (dead) PAM
Properties of PRRS virus ð Replication in porcine alveolar macrophages (PAMs) ð Long term viremia (more than in some cases 3 weeks) ð Persistent infections (157 days; Wills et al. , 1997) ð Subclinical infections (Morrison et al. , 1992) ð Differences in virulence (Mengeling et al. , 1996/1998) ð High infectivity (<10 infectious particles) but slow transmission (Yoon et al, 1998; Wills et al. , 1997) ð Short duration of immunity due to viral mutations (Lager et al. , 1997) ð Short colostral protection of piglets
PRRSv: symptoms in sows í Abortions between day 105 -110 of pregnancy are common í Prolongation of pregnancy up to day 120 often due to dead fetii í Delivery of stillborn, weak-born or mummified piglets í Increase of return to breeders
PRRSv Infection: Time lag between infection and clinical symptoms Farrowing Mating Lactation -33 Infection time of susceptible sows -19 -5 0 Lactation Pregnancy 14 28 42 56 70 84 98 115 Time (days) (return to breeders) 3 -6 weeks NO clinical symptoms Late term abortions or litters with weakborn, stillborn or mumified pigs up to 6. 5 weeks
Reproductive disorders : PRRSv differential diagnosis Symptom/ Pathogen Aujeszky Virus Ergotism PEV Parvovirus Hog Cholera Brucellosis PRRSV Strep. /Staph. E. coli Erysipelas Eperythrozoon Mycotoxins Leptospirosis Past. multocida Listeriosis Salmonellosis Influenza V. PCV 2 Mycoplasma Management abortions re-breeders mummies small litters poor milking + + + (+) + + + (late) + + + + + (+) + + + (large) + + + + + (+) -
PRRSv symptoms in boars o o without obvious symptoms Influenza like symptoms exhaustion in some cases transient reduction in quantity and motility of sperms
PRRSv: reproductive losses í Decrease of fertility by -10% to -25% í Decrease of piglets per sow (-1. 5 to -3. 8 pigs/ sow per year) í Decrease of feed convertion ratio (+0. 02 to +0. 5) í Reduction of general health status and increased susceptibility to other pathogens í increased medication costs í Total financial losses due to PRRS infection of sows are (depending on field virus pathogenicity) is 255 $/sow/ year (National Pork Board, 2003 PRRS Compendium)
PRRSv: symptoms in pigs í Conjunctivitis, eyelid edema í Discoloration of ears, snout. . . í Increase losses in growth and mortality í Non-responding respiratory symptoms and secondary infections í growth within pens and groups of finishing animals are not even
Respiratory Disorders Pathogen PRRS Hog Cholera E. coli APP Erisipelas Eperythrozoon Ergotism Salmonella sp. PCV 2 SIV Aujeszky virus M. hyopneumiae H. parasuis Past. multocida Discoloration ears + + + + - Conjunctivitis + + + - Cough (+) + + + + + Resp. Difficult distress breathing + + + +
PRRSv: losses in pigs í Increase of losses (+1% to +8%) í Increase of feed conversion ratio (+0. 01 to +0. 5) í Decrease of daily weight gain (-15 g to -150 g/ animal /day) í Increase of uneven growth within groups and pens í Decrease of general health status and by this increased susceptibility for secondary pathogens (Thacker, 2000) í Increased rates of culls and light pigs (Keffaber, 1989) í Increse of medication costs due to worsening health í Reduction of carcass quality í Average cost of PRRS in the growing pig: 6. 25 – 15. 25$ per pig
Transmission of PRRSV Ê Animals- direct contact and aerosols Ë Airborn transmission supporting factors: - low temperatures, low UV radiation and weather changes (wind and clouds) Transmission up to 2 - 3 km possible but still needs supporting evidence Scott Dee‘s current research – 5 replicates so far Spread by flies in two reps Aerosol spread in two reps Personal communications – August, 2006 Ì Infected semen - Boars usually are shedding virus via semen between day 3 to 21 post infection but can be sporadic shedding for long time Í Vehicles – are very common problem in US, especially in winter Í People and fomites – boxes, tools, insects, etc.
PRRS-virus circulation pig flow ++ immune animal + partly immune animal - non- immune animal virus circulation +/(+) sows gilts infected animal (virus shedding) maternal immune animal +/- + - - +/- ++ +/- - piglets +/- (+) 3 -4 5 -6 - ++ ++ 7 -9 age of pigs (weeks) +/- finishers
PRRS-virus circulation ++ immune animal + partly immune animal - non- immune animal +/(+) pig flow sows gilts infected animal (virus shedding) maternal immune animal ++ virus circulation - ++ ++ ++ piglets (+) (+) +/- +/3 -4 5 -6 + ++ ++ ++ 7 -9 age of pigs (weeks) finishers
PRRS-virus circulation ++ immune animal + partly immune animal - non- immune animal +/(+) pig flow virus circulation sows gilts infected animal (virus shedding) maternal immune animal - Sows become highly susceptible about 3 -4 month after start of vaccination - - + + - - - + Interruption of infection chain due to vaccination of piglets (+) (+) 3 -4 + + 5 -6 + + ++ ++ ++ 7 -9 age of pigs (weeks) finishers
General recommendations for PRRSv vaccination prior to vaccination!! í Proper diagnosis í Whole herd vaccination of sows (and boars): í Depends on producing SEW piglets (3 times per year) or nursery on site (4 times per year) í Piglet vaccination: 10 -21 days of age or initial mass vaccination then 10 -21 days of age í Gilt vaccination on arrival: í 2 x (4 wks apart) in farms with high infection pressure í Serological success: titers should be low in sows at the time of revaccination and in fatteners at the time of slaughter? í Should be checked or monitored often – 2 x per year at least
Ingelvac® PRRS MLV vaccination in farrow to finish farms Start of vaccination: o All sows on one day irrespective of gestation stage n n n All nursing piglets 3 weeks of age and older All nursery pigs (when clinically healthy) All finishing pigs (when clinically healthy) Maintenance program for vaccinations: Sows: first revaccination after 4 to 8 weeks, all following revaccinations with consideration of: 4 month interval when piglets are continuously vaccinated at 3 weeks of age or nursery and finishing animals are located at a different site 3 ﻼ month interval when piglets are not vaccinated and at the same site ﻼ Gilts: two times (3 to 4 week interval) upon arrival 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. . . )
Take home messages on vaccines: Typical PRRS vaccination program in a US (continuous farrow-finish) herd o PRRS vaccine is used in a mass vaccination program n 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 o If two sites, then will vaccinate all of the animals on each site o n n 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 o When active field virus, two doses of vaccine are given 4 weeks apart o
PRRSv Control Interventions v v v v Control principles Subpopulation effects Persistence Major considerations Population immune management tools reviewed Case presentations Summarize what I have learned
PRRSv Control Principles o o Employ protocols that minimize viral replication and transmission within a population of animals Fundamental to this is Population Immune Management n n n 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 noninfectious population Often employed with a form of herd/population closure
PRRSv Control Principles o Goal is to minimize and stop all viral replication and transmission within a population n n Develop a homogenous population based on immune status Can be negative or positive which depends on what you are trying to achieve o o o Nursery – negative Sows – positive or negative Create a non-infectious population n Subpopulations exist in all population of animals o Subpopulations will maintain an environment for chronic field virus circulation
Subpopulation Principles o Subpopulations exist n n 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 o o o 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 o Establish the farm or site’s goal for PRRSv n o Diagnostic support of present clinical signs to determine recent status of PRRSv and classify as negative, stable, unstable or active n n o Control viral activity so clinical improvement is observed Gilt Pool Breeding Gestation Lactation Growing Pigs Semen source Control options for population immune management tools n n n Initial stabilization Maintenance of stabilization Herd closure and immune management tools o Natural exposure, killed vaccine, live virus inoculation (LVI) and modified live vaccine
PRRS Control Program: Systematic Approach o Goals of the Farm/System n Stabilize o o n attain and maintain a stable PRRS positive population production of PRRSv negative offspring Eliminate o o o Depopulation Test and Remove Extended Herd Closure n Current data would suggest that at least 120 days is necessary to deal with persistently infected animals
Immune Management Tools o Natural exposure n n n o Killed vaccine n o Very little data that supports predictable efficacy Live virus inoculation (LVI or serum therapy) n o Takes considerable amount of time even in small groups of replacement females Inconsistent in large populations of animals Little control over viremia High risk (virulent) and unreliable Modified live vaccine n The best immune management tool with proven success
Summary: importance of these principles o Must eliminate subpopulations to attain and maintain homogenous population o Population immune management is fundamental to attain and maintain this homogenous population and PRRS control/stability o Must decide which of the immune management tools has the best fit and probability of success for your unit or system
Summary: PRRS Control Methodology Systematic Approach Goal – Determine the desired PRRS status B: Current PRRS Status – must know with current diagnostics C: PRRS Risk Assessment – AASV tool that will soon become web based D: Control Options A: >> Initial Stabilization >> Immune management tool: MLV >> Maintenance Stabilization >> Utilizing immune management tools and herd closure E: Create Realistic Expectations F: Measure and Monitor Intervention
Multiple Strains o o 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 n Complete control and elimination is still possible but often more difficult o o o 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 o o 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 n n Clinical signs will vary, so mortality rates vary Occasionally associated with PRDC in the finisher animals o Complicated with PCV 2 associated diseases
AAF 36277 AAF 36239 Group Dendogram AAK 25810 04/20/2004 65554 AAC 57953 AAC 57957 06/18/2004 04/20/2005 66909 02/8/2005 Narrative: 72978 75088 Inglvac. ATP AAF 36254 AAC 54599 AAC 54591 VR-2332 09/23/2004 AAD 37086 CAA 11088 69325 Ingelvac • 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 Ingelvac. ATP are modified-live vaccine strains 01/16/2004 63628 10/29/2003 62136 0. 1 05/19/2004 66213 AAA 67155 11/24/2004 12/22/2004 71065 71794 AAC 41215
What I Have Learned o Communication is vital n Expectations of the owner and staff o o o “Sterilizing immunity” “Gold bullet” Compliance issues with breaks n n n 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 o Multiple strains exist on farms n o o o 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 o This started a paradigm shift in our thinking in the late ’ 90’s n o o One major change was the selling of breeding stock as naïve not positive stable Management techniques that are successful n o o 1998/19990 and my first client’s response 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 n Natural exposure did not work well due to inconsistent exposure (not like TGE)
Current Knowledge o o Elimination of virus from a population and even a unit/ system is achievable Many units have been clean for years n n o 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 o Routine population immune management by vaccination n n Long term stability can be attained and maintained for resident PRRSv Prevent new entry of virus o o o n n 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 o o o 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 n n n o 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 o I “attack” what I know first n n I control what I can control first Mycoplasma, PRRSv and SIV o o n Secondary bacterial infections o n n n Aujesky virus, Classical Swine Fever, FMD Mhyo vaccine: 1 -dose I use antibiotic therapies Management issues Environmental issues Mycotoxin control
Porcine Circovirus 2 o o o Is PCV 2 involved? AASV Task Force committee work Porcine Circovirus Associated Disease (PCVAD) n The disease n Diagnosis n Economic costs n Control measures n Sequencing of virus n European experience
PCV 2 is involved o 1) At least six different teams of researchers have reproduced clinical signs, typical PMWS lesions and mortality with PCV 2 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 PCV 2. n o 2) There at least 18 (maybe 19 now) papers showing that there is a direct relationship between the quantity of PCV 2 in blood and tissues, and the severity of clinical signs and lesions. If PCV 2 was not important in that condition, why would that be? n o Please note that several of the studies have used small sample size populations. Viral loading can only be taken so far in understanding the clinical signs. Personal conversation with Dr. Robert Desroiers, April, 2006 n My comments follow each category.
PCVAD Task Force Committee o Members n o 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 o First order of business was to decide on what to call this problem n n Porcine Circovirus Associated Disease Covers all clinical expressions, although the primary economic concern is PMWS
PCVAD o o Porcine Circovirus Associated Disease Why did we select this name? n n n 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 o Develop a database to track occurrence of the disease o o ü ü ü 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 ü ü 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 o 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 o The committee also discussed the need to explore the role of allied groups such as: n n USDA’s Agricultural Research Service (ARS) for a research focus National Pork Board to facilitate funding and outreach.
Early challenge o Educational material n Discussed the linking of web sites o o o n n 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 o o Vaccine response n Need to report to industry at some point Literature and research updates n National Pork Board will help facilitate this information n Information from some articles will be included
The disease o o o As early as 1991 the problem was mentioned n Retrospective testing of stored sera may go as far back as 1969 (Staebler, S. et al, 2005) n 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 n Drs. Harding and Clark coined PMWS in 1996 PCV 2 not a “new” pathogen and PCVAD is not a “new” disease n 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
Self reporting incidence in US ALASKA PCVAD – High or rapidly increasing, low, not yet reported MAINE WASHINGTON VT MONTANA NORTH DAKOTA NH MINNESOTA MASS OREGON NEW YORK WISCONSIN SOUTH DAKOTA IDAHO WYOMING MICHIGAN PENN NEBRASKA INDIANA WV NEVADA COLORADO KANSAS NEW JERSEY DELAWARE MARYLAND OHIO IOWA ILLINOIS UTAH VIRGINIA KENTUCKY MISSOURI NORTH CAROLINA TENNESSEE CALIFORNIA ARIZONA CONN RI OKLAHOMA SOUTH CAROLINA ARKANSAS NEW MEXICO MISS ALABAMA GEORGIA TEXAS LOUISIANA FLORIDA HAWAII Supplied by Dr. John Kolb, Boehringer Ingelheim Vetmedica
The individual pig: A starting point! o o 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 n o Enlarged lymph nodes and non-collapsing lungs are most common Need to necropsy and submit tissue from at least 5 animals
Tissue submissions: o PCVAD is a broad categorization of multisystemic diseases with the following histopathological findings in affected pigs: n n Depletion of lymphoid cells Detection of PCV 2 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 PCV 2 antigen in lesions associated with fetal myocarditis
The herd: “Muddy waters” o o 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 o o AASV committee reviewed CDC’s approach to describing a new clinical problem Also looked at our European colleagues approach n 1 a) historical level of mortality +1. 6 X SD 2 n 1 b) if no records, increase that exceeds regional level by 50%
Work in progress: herd definition o PCVAD can be subclinical or include one or more of the following clinical manifestations concurrently: n Multisystemic disease with weight loss (formerly known as PMWS) n High mortality: Doubling of historical mortality rate without introduction of a new known pathogen. n Respiratory signs including pneumonia n Porcine Dermatitis and Nephropathy Syndrome (PDNS) n Enteric signs including diarrhea and weight loss n Reproductive disorders including abortions, stillbirths and fetal mummification (diagnosis requires the presence of fetal myocarditis associated with PCV 2 antigen in lesions)
PCVAD: Diagnosis o PMWS/ High mortality is the most common and most economically damaging clinical expression n o o Is considered the major clinical manifestation of PCVAD Co-factors are probably the most important aspect to consider Infectious co-factors o o Viruses - PRRSv, Parvovirus, SIV Bacteria - Mycoplasma, Salmonella
Number of Cases PCV 2 coinfections in 484 U. S. field cases: ISU-VDL 180 160 140 120 100 80 60 40 20 0 164 92 77 9 10 13 3 68 37 11 ia a s o. o. o. V ni IV y y em er S o. h. h R th +S m tic M R u O 2 +M P V 2 SV V + ep +M + ne V R 2 2+ IV ls C V 2 PC S R l p CV a V S P i R ia +P PC R P 2+ er PC er 2 t t P V V ac ac 2+ C PC V P +B +B C P V 2 PC PC Rarely see PCV 2 singular infection ne o Al
Porcine Circovirus Associated Disease PCV 2 Strains Co-factors ·Infections ·Non-infectious PCV 2 particle PCV 2 Virus Infection in lymphoid tissues +/- other tissues Immune stimulation Host susceptibility Lymphoid depletion + histiocytic replacement, antigen 1 to 20 % of the animals Low viremia Seroconversion High viremia leukopenia +/- seroconversion Systemic spread Subclinical disease Clinical disease - 70/80% mortality Information courtesy of Dr. Pat Halbur
Economics of PCVAD o o 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 n Culls, lights, under market weights, etc
Other expressions of PCVAD o Enteric disease in grow finish stage n n n Infectious and nutritional causes PCV 2 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% PCV 2 14 38% Brachyspira 1 2% total 37* 100% *includes mixed infections; sum does not total to 100%
Other expressions of PCVAD o Reproductive expression is rare n n Abortions, stillborns, mummified fetuses The presence of fetal heart lesions o n Necrotizing myocarditis The presence of PCV 2 antigen in the myocardial lesions and in other fetal tissues if possible
Other expressions of PCVAD o PCV 2 is considered a contributor to Porcine Respiratory Disease Complex (PRDC) n o Pneumonia is one of the more common expressions associated with PCV 2 PDNS n n The incidence is often increased when other expressions of PCVAD occur Has not been supported by research
Control – Develop an action plan o o Get an accurate diagnosis!! Identify concurrent infections and implement an action plan to control and or eliminate n o Evaluate timing of when you are vaccinating n n o o Mycoplasma vaccines especially Enteric vaccines do not seem to be as “sensitive” Treat bacterial infections n o PRRSv/ SIV/ HPS/ Salmonella/ Mycoplasma Therapeutic “CTC” levels and therapies to control bacterial co-infections Use vitamin E and Selenium Nutritional enhanced diets
Control – Develop an action plan o o o 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 n n o Virkon S, Roccal D and Synergize Anthium Dioxide + Acidic Detergent (foam with air) Weaning age may become a factor?
Madec 20 -point rules o o o Control without PCV 2 vaccination sometimes works, sometimes does not work! Control programs have focused on cofactors and other risk factors Madec rules will significantly decrease mortality because the measures are designed to reduce “infection pressure” of PCV 2 and other infectious pathogens, improve hygiene and reduce stress
Summary– Develop an action plan o Transmission studies n No research studies that I can find o 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 n n o o PCR positive serum in >140 day olds Did not “transfer” PCV 2 to sentinels or clinical signs Canadian/ Midwest/ N. C. strains are very similar to European strain n Virus will change over time? ? Maternal antibody studies n Kelly Lager – found in 3 week old pigs o May not be held back by maternal antibodies?
Summary o Environmentally stable virus n n o o 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 o Landrace and Large White o o Pat Halbur – one study implicated Landrace as more suspectable Duroc and Pietrain o More information is needed! Mortality in finishing units in the progeny of two different Duroc boar lines *number of animals per group Period of time Jan-June 2005 (before PMWS) Jan-Dec 2005 Jan-April 2006 (with PMWS) Duroc A mortality Duroc B mortali ty 2. 5% (245, 945) * 3. 5% (316, 29 7) 2. 6% (278, 704) 4. 3% (898, 28 0) 3. 0% (29, 504) 7. 5% (490, 31 9) 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 PCV 2 genotypes, which may equate to distinct PCV 2 strains and this may be important in the understanding of PCVAD
Summary thoughts o Management issues are important and may start in the sow herd n Get an accurate diagnosis n Cross fostering techniques stopped in the sow herd n Stop resorting in nursery n Remove the affected animals from the general population n Be aggressive on treatments if improvement is observed n Needle management? n Sanitation program updated n Replacement animal “stabilized” n Genetic changes n Others?
Summary thoughts o Vaccine will be a tool to consider n o Control other pathogen activity – important! n n o Sow vaccination vs. piglet vaccines Especially PRRS if present Easier said then done! Transmission and viremia n n 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 o o Piglet vaccination will work if given at the right time n Single dose vaccines are common and given at 5 to 6 weeks of age n 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 n Reduces the amount of organism in the piglets at weaning o o o 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 n Again we used vaccine at first to stabilize the stud n After a couple of years, purchased mycoplasma naïve boars and used them as sentinels initially
Questions? THANK YOU! Special thank you to Dr. Marika Genzow and Dr. Mike Murtaugh