Transcript First Asian PigElite® Tour

First Asian
PigElite® Tour
Thomas Gillespie, DVM,
Diplomate ABVP
Rensselaer Swine Services,
Rensselaer, IN
[email protected]
www.rssvet.com
Demographics
 100
 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
500+
Total
59,950
6,630
950
1,526
915
134
25
70,130
1%
8%
4%
9%
19%
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
PRRS
PCVAD
Mycoplasma
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
The PRRS Virus
Glycoproteins
RNA
Membrane
Nukleocapsid
50-60 nm

enveloped RNA-Virus of the family Arteriviridae
 very sensitive virus outside of host (low tenacity)
The PRRSv infection

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
PRRS infected (dead) PAM
Properties 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 duration of immunity due to viral mutations (Lager et al., 1997)

Short colostral protection of piglets
PRRSv: symptoms in sows
Abortions between day 105-110 of pregnancy
are common
Prolongation of pregnancy
up to day 120 often due to dead fetii
Delivery of stillborn, weak-born or mummified
piglets
Increase of return to
breeders
PRRSv Infection:
Time lag between infection and clinical symptoms
Farrowing
Mating
Lactation
-33 -19
Infection time of
susceptible sows
-5 0
Lactation
Pregnancy
14 28
42 56 70
84 98
115
Time (days)
(return to
breeders) 3-6 weeks
NO
clinical symptoms
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.
PCV2
Mycoplasma
Management
abortions
re-breeders
mummies
small litters
poor milking
+
+
+
(+)
+
+
+ (late)
+
+
+
+
+
+
+
+
+
(+)
+
(+)
+
+
+
+
+
+
+
+
+
+
+
+
+
(+)
+
(+)
+
+
+
+
+
+
+
+ (large)
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
(+)
-
PRRSv symptoms in boars




without obvious
symptoms
Influenza like
symptoms
exhaustion
in some cases transient
reduction in quantity
and
motility of sperms
PRRSv: reproductive losses
 Decrease of fertility by -10% to -25%
 Decrease of piglets per sow (-1.5 to -3.8 pigs/ sow per year)
 Decrease of feed convertion ratio (+0.02 to +0.5)
 Reduction of general health status and increased susceptibility to other pathogens
 increased medication costs
 Total financial losses due to PRRS infection of sows are (depending on field virus pathogenicity) is
255 $/sow/ year (National Pork Board, 2003 PRRS Compendium)
PRRSv: symptoms in pigs
 Conjunctivitis, eyelid edema
 Discoloration of ears, snout ...
 Increase losses in growth and mortality
 Non-responding respiratory symptoms and
secondary
infections
 growth within pens
and groups of finishing
animals are not even
Respiratory Disorders
Pathogen
PRRS
Hog Cholera
E. coli
APP
Erisipelas
Eperythrozoon
Ergotism
Salmonella sp.
PCV 2
SIV
Aujeszky virus
M.hyopneumiae
H. parasuis
Past. multocida
Discoloration
ears
+
+
+
+
+
+
+
+
-
Conjunctivitis
+
+
+
+
+
-
Cough
(+)
+
+
+
+
+
+
+
+
+
+
Resp.
distress
+
+
+
+
+
+
Difficult
breathing
+
+
+
+
+
+
+
+
+
+
-
PRRSv: losses in pigs
 Increase of losses (+1% to +8%)
 Increase of feed conversion ratio (+0.01 to +0.5)
 Decrease of daily weight gain (-15g to -150g/ animal /day)
 Increase of uneven growth within groups and pens
 Decrease of general health status and by this increased susceptibility for secondary
pathogens (Thacker, 2000)
 Increased rates of culls and light pigs (Keffaber, 1989)
 Increse of medication costs due to worsening health
 Reduction of carcass quality
 Average cost of PRRS in the growing pig: 6.25 – 15.25$ per pig
Transmission of PRRSV
 Animals- direct contact and aerosols
 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
 Infected semen - Boars usually are shedding virus via semen between day 3 to 21 post
infection but can be sporadic shedding for long time
 Vehicles – are very common problem in US, especially in winter
 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
gilts
infected animal
(virus shedding)
maternal immune animal
-
+/(+)
pig flow
virus circulation
sows
++
++
++
++
++
++
++
++
++
++
(+)
(+)
(+)
+/-
+/-
+/-
+
++
++
++
piglets
3-4
5-6
7-9
age of pigs (weeks)
finishers
PRRS-virus circulation
++
immune animal
+
partly immune animal
-
non- immune animal
gilts
infected animal
(virus shedding)
maternal immune animal
-
+/(+)
pig flow
virus circulation
sows
Sows become highly susceptible about 3-4 month after start of
vaccination
-
-
+
-
+
+
-
-
-
+
Interruption of
infection chain due to
vaccination of piglets
piglets
(+)
(+)
3-4
(+)
+
+
+
+
++
5-6
++
7-9
age of pigs (weeks)
++
finishers
General recommendations for PRRSv vaccination
 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
Ingelvac® PRRS MLV
vaccination in farrow to finish farms
Start of vaccination:

All sows on one day
irrespective of
gestation stage



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
‫ ﻼ‬3 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
 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

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 noninfectious 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


Diagnostic support of present clinical signs to determine
recent status of PRRSv and classify as negative, stable,
unstable or active





Control viral activity so clinical improvement is observed
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




Killed vaccine


Very little data that supports predictable efficacy
Live virus inoculation (LVI or serum therapy)


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

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
Summary: PRRS Control Methodology
Systematic Approach
A: 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
>> 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


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
AAF36277
AAF36239
Group Dendogram
AAK25810
04/20/2004
65554
AAC57953
AAC57957
06/18/2004
04/20/2005
66909
02/8/2005
Narrative:
72978
75088 InglvacATP
AAF36254
AAC54599
AAC54591
VR-2332
AAD37086
09/23/2004
• 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
CAA11088
69325 Ingelvac
01/16/2004
63628
0.1
05/19/2004
10/29/2003
62136
66213
AAA67155
11/24/2004 12/22/2004
71065
71794
AAC41215
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



One major change was the selling of breeding stock as naïve
not positive stable
Management techniques that are successful



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

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



Secondary bacterial infections




Aujesky virus, Classical Swine Fever, FMD
Mhyo vaccine: 1-dose
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.


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?


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

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

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).
 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
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
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
MICHIGAN
WYOMING
PENN
NEBRASKA
INDIANA
WV
NEVADA
VIRGINIA
COLORADO
KENTUCKY
KANSAS
MISSOURI
NORTH
CAROLINA
TENNESSEE
CALIFORNIA
OKLAHOMA
ARIZONA
SOUTH
CAROLINA
ARKANSAS
NEW MEXICO
MISS
ALABAMA
GEORGIA
TEXAS
LOUISIANA
NEW
JERSEY
DELAWARE
MARYLAND
OHIO
IOWA
ILLINOIS
UTAH
CONN RI
FLORIDA
HAWAII
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 noncollapsing 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
Number of Cases
PCV2 coinfections in 484 U.S. field cases: ISU-VDL
180
160
140
120
100
80
60
40
20
0
164
92
77
9
10
Rarely see PCV2 singular infection
13
68
37
3
11
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
 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 cofactors 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
Mortality in finishing units in the progeny
of two different Duroc boar lines
 Landrace and
Large White
*number of animals per group
 Pat Halbur – one
study implicated
Landrace as more
suspectable
 Duroc and Pietrain
 More information
is needed!
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 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?
THANK YOU!
Special thank you to Dr. Marika Genzow
and Dr. Mike Murtaugh