porcine parvovirus infection
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PicturesTop of page
IdentityTop of page
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
OverviewTop of page
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 AffectedTop of page
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:
- a vesicular skin disease (Kresse et al., 1985)
- piglet diarrhoea (Yasuhara et al., 1995)
- piglet myocarditis (Bolt et al., 1997)
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 TableTop of page
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/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|China||Present||Lu et al., 1995; You et al., 1995|
|-Guangdong||Present||Lu et al., 1995|
|-Ningxia||Present||Wang et al., 1994|
|-Sichuan||Present||Wu et al., 1986|
|Israel||Present||Brenner et al., 1996|
|Korea, Republic of||Present||Hwang et al., 1998|
|Malaysia||Present||Sharifah et al., 1996|
|Taiwan||Present||Tsai and Chen, 1979|
|Thailand||Present||Wattanavijarn et al., 1983|
|Vietnam||Present||Pham and Ho, 1998|
|Mozambique||Present||Rivera et al., 1995|
|South Africa||Present||Pini, 1975|
|Canada||Present||Present based on regional distribution.|
|-Ontario||Present||Gagnon and Dulac, 1979|
|Mexico||Present||Ramírez et al., 1998|
|USA||Present||Stein et al., 1982|
|-Kansas||Present||Gipson et al., 1999|
|-Oklahoma||Present||Saliki et al., 1998|
Central America and Caribbean
|Uruguay||Present||Sienra et al., 1988|
|Venezuela||Present||Arriojas et al., 1998|
|Bulgaria||Present||Peev et al., 1990|
|Croatia||Present||Roic et al., 1996|
|Finland||Present||Schulman et al., 1982|
|France||Present||Tillon et al., 1981|
|Greece||Present||Xilouri et al., 1987|
|Hungary||Present||Kudron et al., 1982|
|Ireland||Present||O'Conner et al., 1984|
|Italy||Present||Bonaduce and Iovane, 1991|
|Poland||Present||Pejsak and Markowska-Daniel, 1996|
|Portugal||Present||Vieira and Perestrelo, 1981|
|Spain||Present||Perea et al., 1988|
|Switzerland||Present||Zanoni et al., 1984|
|Yugoslavia (Serbia and Montenegro)||Present||Pancic et al., 1987|
|Australia||Present||Parke and Burgess, 1993|
|New Zealand||Present||Fairley, 1997|
PathologyTop of page
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).
DiagnosisTop 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/SignsTop of page
|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 CourseTop of page
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.
EpidemiologyTop of page
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: EconomicTop of page
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 TreatmentTop of page
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 ControlTop 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.
ReferencesTop of page
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Harding MJ; Molitor TW, 1988. Porcine parvovirus: replication in and inhibition of selected cellular functions of swine alveolar macrophages and peripheral blood lymphocytes. Archives of Virology, 101(1-2):105-117; 35 ref.
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O'Conner M; Lenihan P; Dillon P, 1984. Irish Veterinary Journal, 9, 162.
Peev Ya; Motovski A; Jordanov S; Petrov N, 1990. Investigation of reproductive disorders caused by parvovirus on a pig farm. Veterinarna Sbirka, 88(3):26-29; 5 ref.
Perea A; Maldonado A; Hermoso de Mendoza M; Miranda A; Carranza J; Arenas A; Poveda JB, 1988. Epidemiological study of porcine parvovirus in the province of Malaga. Medicina Veterinaria, 5(7/8):341.346; 13 ref.
Pini A, 1975. Journal of the South African Veterinary Association 3, 241.
Ramírez Mendoza H; Trigo Tavera F; Correa Girón P; Castillo Juárez H; Mercado García MC, 1998. Determination of porcine parvovirus antigens and antibodies in fetuses collected in abattoirs. Veterinaria México, 29(4):337-343; 21 ref.
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.
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.
Soares RM; Durigon EL; Bersano JG; Richtzenhain LJ, 1999. Detection of porcine parvovirus DNA by the polymerase chain reaction assay using primers to the highly conserved nonstructural protein gene, NS-1. Journal of Virological Methods, 78(1/2):191-198; 27 ref.
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Tarry DW; Lucas M, 1977. Persistance of some livestock viruses in the cockroach Blatta orientalis. Entomologia Experimentalis et Applicata, 22:200-202.
Taylor DJ, 1999. Pig Diseases, 7th Edition, ISBN 09506932 6X, 18-23.
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.
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Wang Dong; Xie Qin; He CunLi; Chen ZhuSan; Yu GuiFa, 1994. Investigation of the epidemics of porcine parvovirus in Ningxia. Ningxia Journal of Agricultural and Forestry Science and Technology, No. 5:30-31; 9 ref.
White MEC, 1987. Experiences with parvovirus [immunization]. Pig Veterinary Society Proceedings, 17:116-121.
Wrathall AE, 1988. Porcine parvovirus vaccination. Veterinary Record, 123(5):138-139.
Wrathall AE; Cartwright SF; Wells DE; Jones PC, 1987. Maternally-derived antibodies to porcine parvovirus and their effect on active antibody production after vaccination with an inactivated oil-emulsion vaccine. Veterinary Record, 120(20):475-478; 16 ref.
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Yasuhara H; Yamanaka M; Izumida A; Hirahara T; Nakai M; Inaba Y, 1995. Experimental infection of pigs with a parvovirus isolated from the diarrheic feces of a pig. Journal of Veterinary Medical Science, 57(4):629-634; 16 ref.
You YongJin; Xu QuanXing; Zhou Zhiai, 1995. Recent status of studies on porcine parvovirus. Acta Agriculturae Shanghai, 11(3):90-96; 36 ref.
Zanoni RG; Henn V; Rutishauser UP; Wyler R, 1984. Prevalence of porcine parvovirus in Switzerland and a new method of detection by immune electron microscopy. Zentralblatt für Veterinärmedizin, B, 31(10):729-742; 42 ref.
Distribution MapsTop of page
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