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porcine parvovirus infection

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porcine parvovirus infection

Summary

  • Last modified
  • 03 January 2018
  • Datasheet Type(s)
  • Animal Disease
  • Preferred Scientific Name
  • porcine parvovirus infection
  • Overview
  • Porcine parvovirus (PPV) has been recognised since 1969 as a major infectious cause of reproductive loss in pigs (Cartwright et al...

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Pictures

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PictureTitleCaptionCopyright
Variable aged mummified foetuses typical of a litter affected by PPV.
TitlePathology
CaptionVariable aged mummified foetuses typical of a litter affected by PPV.
CopyrightMark E.C. White
Variable aged mummified foetuses typical of a litter affected by PPV.
PathologyVariable aged mummified foetuses typical of a litter affected by PPV.Mark E.C. White
Porcine parvovirus has been implicated in the pathogenesis of post-weaning multisystemic wasting syndrome (PMWS) (along with porcine circovirus).
TitleSymptoms
CaptionPorcine parvovirus has been implicated in the pathogenesis of post-weaning multisystemic wasting syndrome (PMWS) (along with porcine circovirus).
CopyrightMark E.C. White
Porcine parvovirus has been implicated in the pathogenesis of post-weaning multisystemic wasting syndrome (PMWS) (along with porcine circovirus).
SymptomsPorcine parvovirus has been implicated in the pathogenesis of post-weaning multisystemic wasting syndrome (PMWS) (along with porcine circovirus).Mark E.C. White
Breeding results from a 300-sow herd experiencing an outbreak of porcine parvovirus.
TitleFertility records
CaptionBreeding results from a 300-sow herd experiencing an outbreak of porcine parvovirus.
CopyrightMark E.C. White
Breeding results from a 300-sow herd experiencing an outbreak of porcine parvovirus.
Fertility recordsBreeding results from a 300-sow herd experiencing an outbreak of porcine parvovirus.Mark E.C. White
Litter performance of herd affected by porcine parvovirus over 8-month period (November-July).
TitleLitter records
CaptionLitter performance of herd affected by porcine parvovirus over 8-month period (November-July).
CopyrightMark E.C. White
Litter performance of herd affected by porcine parvovirus over 8-month period (November-July).
Litter recordsLitter performance of herd affected by porcine parvovirus over 8-month period (November-July).Mark E.C. White

Identity

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Preferred Scientific Name

  • porcine parvovirus infection

International Common Names

  • English: parvovirus associated vesicular disease of pigs; parvovirus associated vesicular disease of pigs; parvovirus diarrhea in piglets; parvovirus diarrhea in piglets; porcine reproductive parvovirus; porcine reproductive parvovirus infection; SMEDI syndrome; stillbirth, mummification, embryonic, death and infertility syndrome

English acronym

  • SMEDI

Overview

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Porcine parvovirus (PPV) has been recognised since 1969 as a major infectious cause of reproductive loss in pigs (Cartwright et al., 1969). Prior to its identification, the SMEDI (stillbirth, mummification, embryonic death and infertility) syndrome had been described but it is now recognised that a Parvovirus is the most common cause of this syndrome, which may also be caused by enteroviruses V13 and F34 serotypes 3 and 8 (Taylor, 1999).

Prior to the development of effective vaccines in the late 1970s, PPV caused high levels of lost production in pig farms throughout the world. It remains a significant pathogen of pigs where active control measures are absent.

The infectious agent is known to be present in pig population throughout the world (Mengeling, 1999) and occurs in both domestic pigs and wild boar populations (Liebermann et al., 1986). In many populations the infection is enzootic, with disease incidence the result of the balance between individual or herd immunity and infectious challenge.

Hosts/Species Affected

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No one particular breed or type of pig has been shown to be more or less susceptible to PPV and the disease is recognised in both domesticated and wild populations (Liebermann et al., 1986; Mengeling, 1999).

The most important clinical and economic manifestation of PPV disease is reproductive loss; this occurs only in sows or gilts that are not solidly immune in the first half of gestation. Because of the ubiquitous nature and persistence of the virus, this is most likely to be in gilts served for the first time, although the cyclical pattern of immunity within a herd (as described by White, 1987, 1989) over a period of years has meant that some herds have suffered major disease breakdowns every few years (typically 3-4 years).

The young pig that has lost colostral immunity early in life (or never received any) is vulnerable to infection, and various diseases have been described in young pigs associated with PPV. Manifestations include:

In addition, it has been shown that PPV may be involved in the development of postweaning multisystemic wasting syndrome (PMWS) in association with porcine circovirus 2 (Allan et al., 1999). PPV is known to replicate in alveolar macrophages and lymphocytes, inhibiting phagocytosis and blastogenesis respectively (Harding and Molitor, 1988) and therefore may compromise the immune response to circoviruses.

Infection is not observed in other species. The pig is believed to be the only species affected with PPV and there is limited evidence that other species act as a significant reservoirs or vectors of infection, other than isolated reports of the cockroach (Blatta orientalis) (Tarry and Lucas, 1977) and rats (Cutler et al., 1982) carrying the virus for 1-3 weeks. The latter could act as a source of transmission of PPV between farms.

Distribution Table

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The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.

Continent/Country/RegionDistributionLast ReportedOriginFirst ReportedInvasiveReferenceNotes

Asia

ChinaPresentLu et al., 1995; You et al., 1995
-GuangdongPresentLu et al., 1995
-NingxiaPresentWang et al., 1994
-SichuanPresentWu et al., 1986
IsraelPresentBrenner et al., 1996
Korea, Republic ofPresentHwang et al., 1998
MalaysiaPresentSharifah et al., 1996
TaiwanPresentTsai and Chen, 1979
ThailandPresentWattanavijarn et al., 1983
VietnamPresentPham and Ho, 1998

Africa

MozambiquePresentRivera et al., 1995
South AfricaPresentPini, 1975

North America

CanadaPresentPresent based on regional distribution.
-OntarioPresentGagnon and Dulac, 1979
MexicoPresentRamírez et al., 1998
USAPresentStein et al., 1982
-KansasPresentGipson et al., 1999
-OklahomaPresentSaliki et al., 1998

Central America and Caribbean

PanamaPresentObaldia, 1991

South America

UruguayPresentSienra et al., 1988
VenezuelaPresentArriojas et al., 1998

Europe

BulgariaPresentPeev et al., 1990
CroatiaPresentRoic et al., 1996
DenmarkPresentThorup, 1995
FinlandPresentSchulman et al., 1982
FrancePresentTillon et al., 1981
GreecePresentXilouri et al., 1987
HungaryPresentKudron et al., 1982
IrelandPresentO'Conner et al., 1984
ItalyPresentBonaduce and Iovane, 1991
NetherlandsPresentHuysman, 1991
PolandPresentPejsak and Markowska-Daniel, 1996
PortugalPresentVieira and Perestrelo, 1981
SpainPresentPerea et al., 1988
SwitzerlandPresentZanoni et al., 1984
UKPresentNash, 1990
Yugoslavia (Serbia and Montenegro)PresentPancic et al., 1987

Oceania

AustraliaPresentParke and Burgess, 1993
New ZealandPresentFairley, 1997

Pathology

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PPV acts directly on the foetus to cause massive cellular death (Lenghaus et al., 1977) with no significant placentitis. In early gestation infection, it is suggested that some uterine changes are induced which affect the ability of the uterus to sustain developing embryos (Wrathall and Mengeling, 1979). The pathology of minor manifestations of PPV infection in young pigs has been described (Kresse et al., 1985, Yasuhara et al., 1995, Bolt et al., 1997).

Diagnosis

Top of page Introduction

Diagnosis in the field is based primarily on clinical signs of the disease over a period of time. Virus can be identified in mummified piglets, either by immunofluoresence (Mengeling, 1999) and more recently by PCR testing (Soares et al., 1999).

Serological testing is widely used to identify population trends, with the haemagglutination inhibition (HAI) test being most commonly used, although serum neutralisation (SN) test is said to be more sensitive (Mengeling, 1999). As with any serological test, a single sample does not indicate current disease; a 4-fold rising titre must be demonstrated to confirm active recent infection. However, experience in the field has suggested that in the wake of clinical outbreaks of disease, very high HAI titres (>1:20,000) will be common in the population, although titres will generally be lower where active disease has not been seen. The patterns of immunity, as measured by the HAI test, within a normal dynamic breeding herd, have been described by White (1987, 1989) and demonstrate the cyclical nature of infection and immunity within a population.

Differential Diagnosis

An increase in returns to service can occur as a result of a wide range of environmental, managemental, nutritional and disease factors (Britt et al., 1999).

Foetal mummification can result from foetal death following a number of viral diseases, the most important of which are:

  • Hog cholera (and other pestiviruses)
  • Aujeszky’s disease (pseudorabies)
  • Porcine reproductive and respiratory syndrome (PRRS)
  • Porcine parvovirus
  • Other SMEDI viruses (enteroviruses)
  • Japanese encephalitis
  • Blue eye disease
  • Porcine cytomegalovirus
  • Encephalomyocarditis virus

In addition, Leptospirosis (serovars pomona and bratislava) can produce weak piglets and mummification, although typically the mummification occurs in late gestation. Abortion is also a feature with this disease but is a rarity with PPV infection.

Foetal mummification will be seen sporadically in the normal litter (usually only affecting one or two foetuses) and is thought to be the result of placental insufficiency of individuals as a result of uterine crowding. On a herd basis, the overall incidence of mummification, in the absence of specific infectious disease, would be less than 2.5% of the total pigs born.

List of Symptoms/Signs

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SignLife StagesType
Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed Sign
Digestive Signs / Diarrhoea Pigs:Piglet Sign
Digestive Signs / Oral mucosal ulcers, vesicles, plaques, pustules, erosions, tears Sign
Digestive Signs / Tongue ulcers, vesicles, erosions, sores, blisters, cuts, tears Sign
General Signs / Dehydration Sign
General Signs / Forelimb lameness, stiffness, limping fore leg Sign
General Signs / Forelimb swelling, mass in fore leg joint and / or non-joint area Sign
General Signs / Generalized lameness or stiffness, limping Sign
General Signs / Hindlimb lameness, stiffness, limping hind leg Sign
General Signs / Hindlimb swelling, mass in hind leg joint and / or non-joint area Sign
Ophthalmology Signs / Chemosis, conjunctival, scleral edema, swelling Sign
Ophthalmology Signs / Conjunctival, scleral, redness Sign
Reproductive Signs / Abortion or weak newborns, stillbirth Pigs:Sow Diagnosis
Reproductive Signs / Anestrus, absence of reproductive cycle, no visible estrus Sign
Reproductive Signs / Female infertility, repeat breeder Pigs:Gilt,Pigs:Sow Diagnosis
Reproductive Signs / Mummy, mummified fetus Pigs:Sow Diagnosis
Reproductive Signs / Prolonged gestation Pigs:Gilt,Pigs:Sow Sign
Reproductive Signs / Small litter size Pigs:Gilt,Pigs:Sow Diagnosis
Respiratory Signs / Sneezing, sneeze Sign
Skin / Integumentary Signs / Nail, claw, hoof sloughing, separation Sign
Skin / Integumentary Signs / Skin crusts, scabs Pigs:Piglet Sign
Skin / Integumentary Signs / Skin necrosis, sloughing, gangrene Pigs:Piglet Sign
Skin / Integumentary Signs / Skin ulcer, erosion, excoriation Sign
Skin / Integumentary Signs / Skin vesicles, bullae, blisters Pigs:Piglet Sign

Disease Course

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The manifestation of disease depends on the stage of production of the animal infected. Non-pregnant adults will show no signs of disease and boars that become infected for the first time show no adverse clinical effects or deterioration in sperm quality (Bonte et al., 1984; Thacker et al., 1984). In young growing pigs, clinical signs of disease are rare, although vesicular skin disease (Kresse et al., 1985), piglet diarrhoea (Yasuhara et al., 1995) and myocardial disease (Bolt et al., 1997) have been described.

The most important and serious effects of primary infection are seen in the pregnant female. Initial exposure can occur at service from an infected boar and is likely to lead to a failure of pregnancy (Mengeling et al., 1980) with a return to service at 3 weeks. Infection slightly later will destroy embryos with two possible results:

  • Re-absorption of the whole litter and a return to oestrous at an abnormal interval (e.g. 30 days)
  • Re-absorption of some embryos, killed directly by the virus, but maintenance of pregnancy, such that a small litter is produced. A minimum of four embryos is required at implantation/attachment (14 days post service) for the sow to "recognise" that she is pregnant. Litters of less than four pigs will result in embryonic death after 14 days, before the foetal stage (30 days)

It is thought that transplacental infection does not occur until 10-14 days after initial challenge of the dam (Mengeling, 1999). Transplacental infection in the naive sow or gilt after 30 days gestation will kill the foetus directly (Lenghaus et al., 1977). However, very rarely will abortion occur. More commonly, the fluid is re-absorbed to leave a mummified foetus. Frequently, the virus infects initially a small number of foetuses, killing them, but then spreading to neighbouring foetuses, killing them later. Those that are infected after 70 days gestation may resist the challenge and survive, although they may be stunted. In this way, a typical "parvo" litter may include variable sized mummified pigs (indicating different stages of gestation at death) small or weak pigs, stillborn pigs and normal piglets.

The age of the pig at death can be calculated by measuring the crown rump length (L) in centimetres and applying the formula:

     Age (days) = (3 x L) + 20

Farrowing in the sow is triggered by cortisol release from the piglets. If the litter size is reduced substantially, for example to 1-3 piglets, the sow may well not farrow for several days after her expected due date. If the whole litter is mummified, farrowing will not take place, the sow remaining anoestrous unless the litter is removed with prostaglandin treatment. Often in such cases, very little material is voided 24 hours after treatment.

Typically, within a herd outbreak of PPV, returns to service will be seen first, followed by the appearance of mummified pigs and small litters.

Epidemiology

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Pigs may become infected by virus arising from:

  • Persistence within the environment, the virus being particularly resistant to disinfection and dehydration
  • Infection, multiplication and excretion from naive animals, be they young breeding stock or growing pigs

PPV is present in the faeces of many pigs following primary infection (Mengeling, 1999) and can thus be spread between and within farms by any physical carriers.

An infected animal is not generally a long-term source of infection, with excretion only lasting for 2 weeks post-infection (Mengeling and Paul, 1986). However, an infected boar can excrete virus in semen and thus can act as a source of infection either by artificial insemination (Thacker et al., 1984), or by direct physical contact and natural service.

Following infection, a strong immunity develops which is measurable by both haemagglutination inhibition tests (HAI) and sero-neutralization tests (SN). For practical purposes, this is likely to be life-long, although immunity may be topped-up by repeat exposures. A sow with a high level of circulating immunity will pass this onto her litter via colostrum and antibodies to PPV persist in the offspring for an unusually long period; up to 6 months or more (Mengeling, 1999). The significance of persistent maternally derived antibody titres (MDA) in the young pig is that it can block the development of natural immunity, either as a result of natural challenge or vaccination. Normal breeding policy within a commercial pig herd would be to serve gilts for the first time at an age of 6-7 months. Therefore gilts without active immunity may enter the herd prior to breeding, rendering them vulnerable to infection in early pregnancy, the most dangerous period.

The virus, once it has infected a naive animal, will replicate, produce a viraemia and cross the placenta of the pregnant female to infect the litter. If this occurs within the first half of pregnancy, disease is likely to result. Foetuses infected after they have become immune-competent (70 days), are capable of resisting infection and developing active immunity, detectable at birth by serological testing.

Infected immune-tolerant carrier piglet have been observed after infection has occurred in early pregnancy (before 55 days gestation) but failed to cause disease (Johnson and Collings, 1971). Such animals carry and may excrete the virus at least up to 8 months of age and hence can be a source of infection for the herd. Given that gilts are always likely to be more vulnerable to infection during pregnancy, (sows are more likely to be actively immune), prior to the advent of vaccination it was common veterinary advice not to retain offspring from gilts for breeding. The existence of active control programmes has rather negated this necessity.

There is very little strain variation between isolates of PPV, although a more virulent strain was reported by Kresse et al. (1985) to cause vesicular lesions in young piglets and this same strain has been shown to be capable of producing disease in late gestation foetuses (Oraveerakul et al., 1993).

Impact: Economic

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The impact of a typical (modelled) epizootic outbreak of parvovirus in a largely naive herd of 300 sows may follow a typical sequence of signs during an outbreak (MEC White, personal communication):

  • Initially an increase in returns to service, which are a mixture of regular 3 week returns and abnormal 4-5 week returns
  • As sows come through to farrow from groups served 1 month before the increase in returns to service, an increase in stillbirths and mummification occurs
  • 4% of sows had been earlier diagnosed pregnant but failed to farrow

The overall impact of the disease on this herd was to reduce the total output of pigs weaned over a 12-month period from 7050 to 6372, a shortfall of 678 weaned piglets or 2.26 pigs per sow per year.

Assuming that each piglet has a production cost of US $22, a total loss of $15,000 occurred ($50 per sow). If the capital costs and lost profit were added to the value of each piglet, the financial implications are:

  • Value of slaughter pig, $94
  • Cost of feed saved per pig, $50
  • Total loss per pig, $44

Allow 5% feeding herd mortality, therefore:

  • Total shortfall of pigs sold = 644
  • Loss to farm = $28,340 ($95 per sow)

Disease Treatment

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No treatment is available or effective for PPV infection and, in most cases, the disease is not suspected or diagnosed until the damage is done.

Prevention and Control

Top of page Immunization and Vaccines

Control lies in ensuring that breeding females are thoroughly immune to infection prior to breeding. Prior to the availability of commercial vaccines, control of parvovirus on a herd basis was achieved, with variable success, by operating a policy of deliberately exposing maiden gilts to virus-infected material at least 1 month prior to intended service. Material used includes:

  • Foetal material/placenta (under licence in some countries)
  • Sow and piglet faeces
  • Weaner faeces

Experience over many years showed that these proceedures could be effective but were unreliable; faeces from weaners of 8-12 weeks of age appeared to give the most reliable results.

Housing new gilts in a contaminated pen could be highly effective in producing PPV immunity, although there are considerable disadvantages with respect to other diseases (e.g. Leptospirosis or PRRS) if exposure is too close to service.

It must be remembered that this approach is a very crude form of on-farm vaccination without knowing:

  • If the relevant infectious agent is present in the material used
  • If other pathogens are present at sufficient levels to cause disease problems

This practice is to be recommended only when vaccine is not available.

Inactivated commercial vaccines have been available throughout the world since the late 1970s and many workers have reported the highly efficacious nature of such products (Mengeling, 1979; Wrathall et al., 1987; Heard, 1988; Wrathall, 1988; Hardy and Wilder, 1988; White, 1989), despite the fact that vaccines induce poor serological response as measured by HAI tests (Edwards et al., 1986).

Vaccine must be applied before breeding, but after decline of maternally derived antibody. The programmes available are variable and there is a strong argument for tailoring a herd programme to the specific requirements of that herd, as indicated by serological testing (Wrathall, 1988; White, 1989).

Vaccination of boars is also an area for dispute. Ulbrich and Schöne (1992) showed that a significant proportion of young boars were serologically negative when first working and recommended that vaccination of boars be undertaken. However, there is no evidence that vaccination prevents the temporary excretion of parvovirus from a challenged boar and, in many farms, boar vaccination is not undertaken for economic, logistic and safety reasons without apparent ill effect.

In some countries, commercial vaccines are available as monovalent PPV preparations. However, polyvalent vaccines are available with PPV combined variably with Erysipelas, Aujeszky’s disease and Leptospira antigens.

There are no state control programmes for PPV and no practical method of establishing a PPV-free herd on a commercial scale, although hysterectomy derivation from vaccinated dams may be feasible.

References

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Allan GM; Kennedy S; McNeilly F; Foster JC; Ellis JA; Krakowka SJ; Meehan BM; Adair BM, 1999. Experimental reproduction of severe wasting disease by co-infection of pigs with porcine circovirus and porcine parvovirus. Journal of Comparative Pathology, 121(1):1-11; 32 ref.

Arriojas NCde; Obando C; Hidalgo M; Montoya A; Cadenas V, 1998. Serological evaluation of porcine parvovirus in the towns of Aragua State, Venezuela. Veterinaria Tropical, 23(1):5-12; 11 ref.

Bolt DM; Häni H; Müller E; Waldvogel AS, 1997. Non-suppurative myocarditis in piglets associated with porcine parvovirus infection. Journal of Comparative Pathology, 117(2):107-118; 33 ref.

Bonaduce A; Iovane G, 1991. Porcine parvovirus infection. Occurrence of the disease in central and southern Italy. (Comparative serological studies). Acta Medica Veterinaria, 37(4):259-275; 76 ref.

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Roic B; Lojkic M; Jemersic L, 1996. Epidemiological situation and prevention of porcine parvovirus infections in Croatia between 1985 and 1995. Proceedings of the First Croatian Veterinary Congress, Cavtat, Croatia, 2-5 October, 1996., 229-233; 5 ref.

Saliki JT; Rodgers SJ; Eskew G, 1998. Serosurvey of selected viral and bacterial diseases in wild swine from Oklahoma. Journal of Wildlife Diseases, 34(4):834-838; 17 ref.

Schulman A; Neuvonen E; Ek-Kommonen C; Veijalainen P, 1982. Distribution of parvovirus infection in the Finnish swine population. Proceedings of the 14th Nordic Veterinary Congress, 6-9 July, 1982, Copenhagen, Denmark., 106-107; 5 ref.

Sharifah SH; Arunasalam V, 1993. Seroprevalence of porcine parvovirus in Perak. Jurnal Veterinar Malaysia, 5(1):53-54; 5 ref.

Sienra R; Vargas R; Guarino H, 1988. Prevalence of parvovirus infection of pigs in a breeding unit. Veterinaria, Uruguay, 24(101/102):9-25; 25 ref.

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Thacker B; Leman A; Joo H; Winkelman N, 1984. Porcine parvovirus infection in boars: absence of seminal shedding and changes in semen quality following experimental infection. Proceedings of the 8th International Pig Veterinary Society Congress., 9; 5 ref.

Thorup F, 1995. Porcine parvovirus. Occurrence in 12 Danish herds. Dansk Veterinærtidsskrift, 78(3):108-110; 7 ref.

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