Embed Size (px)
Citation preview
Historical background ofPCV2 and PCVD
Historical background
• 1991 A veterinary practitioner, Dr. John Harding, and a pathologist, Dr. Edward Clark, observed a new syndrome in Saskatchewan, Canada
Edward Clark
John Harding
Historical background
This syndrome was characterized by:
↑ postweaning mortality
Wasting
Very specific microscopic lesions in the lymphoid tissue
Historical background
• 1996,1997 The disease was described and the name postweaning multisystemic wasting syndrome (PMWS) was proposed
(Harding, 1996; Clark, 1996)
• 1994 more similar clinical cases appeared again.
Historical background
• 1996: A variant of PCV was detected in abundance within the lesions observed in lymphoid tissues (Daft et al., 1996)
• 1998 - The virus was first isolated from PMWS affected pigs (Allan et al., 1998; Ellis et al., 1998)
• PCV1 and PCV2 are currently recognized as two different species by the International Committee on Taxonomy of Viruses (ICTV)
Porcine circovirus type 2 (PCV2)
Porcine circovirus type 1 (PCV1)
Genus Circovirus
PK-15 contaminant
PMWS
PCV2 and PCVD
• Ubiquitous in domestic swine
• Small (17 nm of diameter)
• Circular, single-stranded DNA (ssDNA)
• Icosahedric, non-enveloped(Mankertz et al., 2000) www.pcvd.eu
PCV2
PCV2
PCV2
• Resistent in the environment:– Extreme thermal and chemical resistance
(O’Dea et al., 2008)
– Resistant to lipid-dissolving disinfectants: based on alcohol, chlorhexidine, iodine and phenol
(Royer et al., 2001)
• PCV2 can be inactivated by:• alkaline disinfectants (sodium hydroxide)• oxidising agents (sodium hypochlorite)• quaternary ammonium compounds
(Martin et al., 2008)
• PCV2 and PCVD:
– PMWS– Subclinical infection– Reproductive disorders
– Porcine dermatitis and nephropathy syndrome (PDNS)– Enteritis– Proliferative and necrotising pneumonia (PNP)– Porcine respiratory disease complex (PRDC)
– Congenital tremor type AII not currently considered a PCVD
PCV2 and PCVD
1960 2009
First retrospectiveevidence of PCV2infection (1962)
First retrospectiveevidence of PMWS occurrence (1985)
First descriptionof PMWS in NA
(1991) – sporadic
First descriptionof PMWS in EU
(1995-97)
Major epizootic PMWS outbreaks in EU and
Asia (1998-2004)
Major epizootic PMWS outbreaks in North and South America (2004-07)
First PCV2vaccine available
(2004)
PCV2vaccines
Natural history of PCV2 and PMWS
PMWS distribution
•The clinico-pathological scope of PCV2 infection has expanded since 1991 (Chae, 2005; Segalés et al., 2005a; Opriessnig et al., 2007);
Countries in red mean that they have described at least one case of PMWS(based on available literature)
PCV2 Infection worldwide
PCV2 infectionand transmission
PC
V2
vira
l loa
ds (
qPC
R)
or
PC
V2
antib
ody
titre
s
Weeks of age
PCV2 antibodies
PMWS
1 3 7-9 2115
PCV2 viremia
PCV2 infection dynamics
• PCV2 has been detected in:– Nasal cavity– Oro-tonsillar secretions– Bronchial secretions– Salivary secretions– Ocular secretions– Faeces– Urine – Milk– Semen
Oro-nasal route: principal horizontal transmission
0,00
2,00
4,00
6,00
8,00
10,00
12,00
B F N T U S
Tested samples
Lo
g10 P
CV
2 g
en
om
e c
op
ies
A
B
C
Segalés et al., 2005
PMWS Affected
Wasted Non-PMWS Healthy
PMWS affected pigs harbour higher PCV2 amounts in those secretions/locations
PCV2 horizontal transmission
sow Boar
• PCV2 can be excreted by semen• Semen naturally infected with PCV2 (Opriessnig et al., 2007):
• Intraperitoneal inoculation of piglets : seroconversion and vireamia• Artificial Insemination in sows: no infection
Semen
• Naïve sows inseminated with PCV2 spiked semen (Madson et al., 2009):• Reproductive failure• Foetuses infection
PCV2 transmission by semen
Is the amount of PCV2 naturally shed in boar semen sufficient to infect sows or their fetuses?
Is it a frequent situation in the field?
Unfortunately it remains unknown
sow
• PCV2 intranasal infection of pregnant sows 3 wk PF (Park et al., 2005; Ha et al., 2008):• PCV2 present in aborted and live-born piglets
PCV2 vertical transmission
Can PCV2 be transmitted from sow to foetus?
√ Yes
• In utero infected foetuses (92-104 days of gestation) and allowed to live postnatally until 35 days PI (Sanchez et al., 2004):• PMWS-like histological lesions • but not PMWS
• Controversial paper and impact of PCV2 natural infection in reproductive failure:• Some rare event
(Ladekjaer-Mikkelsen et al., 2001; Maldonado et al., 2005)
• Others 13% of infected aborted fetuses and stillborns (Kim et al., 2004)
sow
PCV2 vertical transmission
Is the role of PCV2 in aborted foetuses and still born piglets clear nowadays?
Is it frequent in the field?
X Unfortunately it remains unknown
– Pigs held in adjacent pens (Kristensen et al., 2009).
– Direct contact more efficient than in separate pens (Andraud et al., 2008).
PCV2 and PMWShorizontal transmission
– Inter-mingling PMWS affected and healthy pigs (Dupont et al., 2009; Kristensen et al.,2009)
Can PCV2 be transmitted between piglets?
And PMWS?
√ Obviously Yes
√ Yes
PMWS
If PCV2 is ubiquitous,
¿WHY SOME FARMS
EXPERIENCE PMWS?
Pig genetics, sex, other
Co-infections
PCV2 genotype
Moment of infection
Sow status
Management: Madec’s 20 point plan
PMWS: a multifactorial disease
• Establishment of zootechnical measures in 10 french farms with PMWS (Guilmoto y Wessel-Robert, 2000):
• Facilities
• Management
• Hygiene
PMWS reduction through zootechnical measures
Measures directed to diminish the dissemination infectious agents and their infectious pressure
FarmRate of measures
complianceLoss rate before (%)
Loss reduction
1 81% 18.3 -13.7
2 86% 14.7 -12.7
3 59% 19.0 -9.3
4 84% 11.2 -5.8
5 79% 15.3 -6.4
6 70% 12.7 -4.7
7 82% 11.5 -4.4
8 55% 12.3 -3.5
9 54% 17.6 0.4
10 72% 11.3 0.7
Media 66% 13.1 -5.4
PMWS reduction through zootechnical measures
(Guilmoto y Wessel-Robert, 2000)
FarmRate of measures
complianceLoss rate before (%)
Loss reduction
1 81% 18.3 -13.7
2 86% 14.7 -12.7
3 59% 19.0 -9.3
4 84% 11.2 -5.8
5 79% 15.3 -6.4
6 70% 12.7 -4.7
7 82% 11.5 -4.4
8 55% 12.3 -3.5
9 54% 17.6 0.4
10 72% 11.3 0.7
Media 66% 13.1 -5.4
PMWS reduction through zootechnical measures
(Guilmoto y Wessel-Robert, 2000)
FarmRate of measures
complianceLoss rate before (%)
Loss reduction
1 81% 18.3 -13.7
2 86% 14.7 -12.7
3 59% 19.0 -9.3
4 84% 11.2 -5.8
5 79% 15.3 -6.4
6 70% 12.7 -4.7
7 82% 11.5 -4.4
8 55% 12.3 -3.5
9 54% 17.6 0.4
10 72% 11.3 0.7
Media 66% 13.1 -5.4
PMWS reduction through zootechnical measures
(Guilmoto y Wessel-Robert, 2000)
Where the same measures implemented in those “improved” farms and the “non-
improved” ones?
REMEMBER: PMWS is a multifactorial disease!
• Moment of infection
“Sow effect”
Calsamiglia et al., 2007
0
50
100
P
CV
2 p
reva
len
ce
Weeks of age
1-5
PMWS affected farms
Non-PMWS affected farms
6-10 11-15 16-20 21-25
Sibila et al., 2004
• Sow infection and immune status:
Factors related to PMWS development
The earlier the PCV2 infection, the higher the risk of developing PMWS
Higher mortality in piglets from:▪ Viraemic sows
▪ Sows with lower antibody titres
• PCV2 genotipe “b” vs “a” :
Experimental infections
50% PMWS with “b” (20 studies)
35% PMWS with “a” (75 studies)
PMWS with “b” 3,45 times > “a”(Tomás et al., 2008)
Factors related to PMWS development:The PCV2 genotype
PCV2 subclinicalinfection
PCV2 subclinical infection
160 piglets from two PMWS affected farms.
Weight and viral load analyses at 3, 9, 15 and 21 wks of age.
Area under the curve for weight and viral load was calculated.
The higher the AUCqPCR during the postweaning period, the lower AUCW (ρ=-0.203; p=0.010).
LaboratorialTechniques for
PCV2 and PMWS
PCR
Sibila et al., 2004
%
PCR (serum)
0
10
20
30
40
50
60
70
80
90
100
0-5 6-11 12-16 17-20 21-28
Weeks of age
Non-PMWS affected farms
Per
cent
age
PMWS affected farms
PCV2 is ubiquitous
Not useful for PMWS diagnosis
Laboratorial Analyses: PCR
Useful to monitor:
Infection dynamicSubclinical infection
-
2,00
4,00
6,00
8,00
10,00
12,00
14,00
0 1 2 3 4
Lo
g 1
0 co
pie
s/m
l ser
um
Slight Moderate Severe
PMWS lesions
a b c
Olvera et al., 2004
PMWS
SubclinicalPCV2
infection
Can PMWS be diagnosed in live animals???
Laboratorial Analyses: qPCR
Quantitative PCR
Not proved to be specific and/or sensitive enough to replace current diagnostic criteria (Fort et al., 2007; Grau-Roma et al., 2009)
Inter-laboratory and inter-assay variation (Harding et al., 2009; Hjulsager et al., 2009)
qPCR suggested applications for PMWS herd diagnosis.
Can qPCR be used as a diagnostictool for PMWS?
0
10
20
30
40
50
60
70
80
90
100
0-5 6-11 12-16 17-20 21-28
Non-PMWS affected farms
Weeks of age
PMWS affected farms
Serology (IPMA, ELISA)
Sibila et al., 2004
Per
cent
age
PCV2 is ubiquitous
All piglets seroconvert
Not useful for PMWS diagnosis
Laboratorial Analyses: Serology
Useful to monitor:
Maternal immunity transferInfection dynamicSeroconversion to
vaccination
2. Moderate to severe (lymphoid depletion and granulomatous inflammationin
lymphoid tissue)
3. Detection of moderate to high PCV2 amount within microscopic lesions in
lymphoid tissues
1. Compatible clinical signs:
growth retardation
H/E
PCV2 ISH
(Sorden, 2000; Segalés, 2002)
PMWS diagnosis
• Histopathology:– Optimally 5 live diseased pigs– Tissue samples:
• Lymphoid tissues: (Lymph nodes, tonsil, ileum [Peyer’s patch], timus)
• Lung• Liver• Kidney• Other…
Non essential for PMWS diagnosis
Laboratorial Analyses:Sample collection for histopathology
Preventionand
control
Prevention and controlPrevention and control
Initial efforts directed to counteract the known triggering factors
Since 2004 onwards PCV2 vaccination
• According to available data, probably yes…– Mortality reduction– Increase of ADG– Batch homogeneity– Reduction of antibiotics use – Reduction of infection pressure
• Of course, to be coupled with:– Good management practices– Control of concurrent diseases– Rational use of antibiotics
Prevention and controlIs PCV2 vaccination the solutionfor PMWS and PCV2 subclinical
infection?
PCV2 CReSA Team
