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Porcine parvovirus infection

Porcine parvovirus infection

G R THOMSON AND M-L PENRITH

GENERAL INTRODUCTION: PARVOVIRIDAE

Introduction

Porcine parvovirus (PPV) causes reproductive failure in pigs, principally due to foetal death and mummification.

The association between infection with PPV and porcine infertility was first demonstrated in 1967,13 although the virus had previously been identified in stocks of classical swine fever (hog cholera) virus grown in cell culture.43 Subsequent investigation showed that PPV is widespread in all pig populations but that it is non-pathogenic in pigs infected after birth. In pregnant animals, however, the virus is able to cross the placental barrier and infect embryos and foetuses. In foetuses younger than approximately 60 to 70 days of gestation, infection is usually fatal. The ability of older foetuses to withstand infection appears to be associated with the onset of immunological competence.

Porcine parvovirus has been identified as one of the most important causes of the porcine SMEDI (S = stillbirth, M = mummification, ED = embryonic death, I = infertility) syndrome, which may be reflected as variation in litter size.21, 27, 61, 62 The prevalence of reproductive losses due to PPV has greatly declined during the last decade, probably owing to routine vaccination of herds.

This is reflected in the number of papers on PPV presented at the biennial International Pig Veterinary Society congresses between 1976 and 2000 (Figures 73.1),23 the proceedings of which are a strong indication of the most important diseases constraining pig production at a given time. Porcine reproductive and respiratory syndrome (PRRS) (see Porcine reproductive and respiratory syndrome) which emerged almost simultaneously in Europe, the USA, and Asia in the 1980s, has superseded PPV as the most important cause of breeding losses in the major pig-producing countries of the world. Nevertheless, when PPV enters a fully susceptible breeding herd it can have a devastating effect.9, 22, 70 It has periodically caused reproductive failuren in pigs in southern Africa.83, 88, 93.

Porcine parvovirus infection

Figure 73.1 Number of papers on porcine parvovirus infection presented at the biennial International Pig Veterinary Society congresses between 1976 and 2000.23 (The data for 1998 and 2000 have been added by the authors)

Aetiology

The genus Parvovirus is one of three genera classified in the subfamily Parvovirinae of the family Parvoviridae.

Virions of PPV are 18 to 26 nm in diameter, unenveloped and cubic in shape, and have icosahedral symmetry. Mature virions have two or three capsid proteins, 32 capsomeres, and a weight of 5,3 × 106 kDa.56 Infectious virions have a buoyant density of 1,39 to 1,42 g/ml in CsCl,2 while ‘empty’ (DNA-deficient) particles have a lower density (1,30 g/ml).66

The genome of PPV, as in other members of this virus family, comprises a single linear strand of DNA made up of approximately 5 000 bases68 with Mr about 1,5 to 1,8 × 106 .82 During viral replication, the single-stranded DNA is converted to a double-stranded replicative form that serves both as a template for viral-messenger RNA synthesis and as an intermediate for the generation of progeny genomic DNA. It has been inferred that single DNA strands with negative (minus) polarity are encapsulated.67 Genomic DNA has terminal hairpin structures at both ends as a result of palindromic (inverted repeat) sequences67, 87, 98 and two open reading frames, the left encoding the structural polypeptides and the right the non-structural polypeptide NS1.87 Complete nucleotide sequences of infectious clones of PPV are available.5, 87, 91, 98

Three structural polypeptides (VP1, VP2 and VP3, with Mr values of 83 000, 64 000 and 60 000 respectively), and at least one non-structural polypeptide (NS1 of Mr 8 400) are encoded by the genome, VP3 being the most abundant structural protein.66, 68 The three structural polypeptides have similar amino acid sequences and therefore, as is the case with other members of the Parvoviridae, the lower molecular weight polypeptides are thought to be subsets of the largest polypeptide, probably derived from a common precursor.67, 82

Porcine parvovirus has a predilection for rapidly proliferating cells both in vivo and in vitro and there is a requirement that one or more cellular functions be associated with the late S or early G phase of the cell cycle.82 During replication, viral proteins accumulate and are packaged in the nucleus with the formation of intranuclear inclusion bodies, margination of the chromatin and slight swelling of the nucleoli.2 Staining with haematoxylin and eosin is usually employed to make these changes evident microscopically. In cell cultures the cytopathic effects (CPE) of viral replication develop slowly and are rarely pronounced. They eventually become evident as granulation, rounding and finally lysis of the cells. For this reason, CPE in unstained preparations are difficult to detect or to differentiate from non-specific cell degeneration.

Primary and secondary cultures of pig tissues and organs are susceptible to infection, the most commonly employed being kidney or thyroid cell cultures. Most cell lines of porcine origin have low sensitivity to PPV infection, as is the case of cells derived from animals other than pigs.43, 84 At least three porcine cell lines, two derived from lung tissue and one from kidney, have been shown to be suitable for the propagation of vaccine virus.25, 86 A comparative study in swine testicle cells (permissive for porcine parvovirus) and Madin-Darby canine kidney cells (non-permissive) indicated that the virus entered both cell types with equal ease but that replication was markedly reduced in non-permissive cells.74

No significant antigenic heterogeneity between PPV isolates has been detected.14, 37, 38, 69, 90 However, strain variation in ability to infect different host cells, apparently dependent upon the NS and capsid coding regions, has been described,99 as well as differences in tissue tropism between strains.75 Four distinct groups of PPV have been differentiated on the basis of cellular tropism and pathogenicity.95

Intact virions of PPV agglutinate erythrocytes from a variety of species including guinea pigs, rats, humans (type O), monkeys, mice, fowls and cats but not those of cattle, sheep or pigs.43 Haemagglutination is most efficient at 4 °C34, 54 and, because of the close association between haemagglutinating and virus neutralizing antibody, it is possible that a common antigen(s) is responsible for the induction of both antibody types.43 On the other hand, animals inoculated with experimental vaccines that induce protection against foetal infection on challenge may fail to induce the development of significant haemagglutination inhibiting antibody.25. Haemagglutinating activity is not destroyed by heating, ultraviolet irradiation or treatments with inactivants such as 0,5 per cent formalin or 0,2 per cent propiolactone which destroy infectivity.14, 43

A striking overall DNA homology (approximately 63 per cent) between minute virus of mice, canine parvovirus and PPV has been reported, and in the left open reading frame encoding NS1 this is even more marked (70 per cent).87 Homologies with human parvovirus B19 and bovine parvovirus are much lower (approximately 20 per cent). Despite this generic relationship, there are only minor antigenic similarities between porcine parvovirus and canine and feline parvoviruses.58

Porcine parvovirus is extraordinarily resistant to environmental conditions and can, for example, survive heating to 56 °C for 48 hours or 70 °C for two hours, but not to 80 °C for five minutes.14 It survives pH values between 3 and 9 for 18 hours.69 Sodium hypochlorite (1:16 or 1:32) is an effective and safe disinfectant and destroys 105,5 TCID50 within five minutes.10 Five per cent sodium hydroxide is equally effective but is less desirable because of its caustic and toxic properties.10 Other agents such as formaldehyde solution or gas, gluteraldehyde and ultraviolet irradiation have also been evaluated but are less practical disinfectants than is sodium hypochlorite.10

Epidemiology

Infection with PPV is ubiquitous in pig populations throughout the world, including those of southern Africa.2, 9, 13, 37, 55, 62, 73, 83, 88, 90, 97 The result is that only a small proportion of herds (probably less than 5 per cent) contain exclusively serologically negative individuals, usually as a consequence of a closed-herd policy.40 Most herds consist of adults with high antibody prevalence rates71 and animals less than 12 months of age with lower rates of active immunity.40 In South Africa and Zimbabwe, herd infection rates of 90 and 50 per cent respectively were reported, based on a serological survey of herds with a history of reproductive failure.83

The antibody level in the colostrum of a sow may exceed that in her serum by a 5- to 100-fold factor.40 Most piglets born to multiparous sows acquire antibodies, and consequently immunity, to PPV within the first few hours of life, when they ingest colostrum. Thereafter, levels of circulating antibody in piglets decline progressively, the half-life being approximately 20 days.81 In practice, maternally acquired antibody levels have usually declined below protective levels by the time pigs are between 12 and 26 weeks of age,39, 53, 81, 96 although protection may persist for up to 36 weeks in a small proportion of pigs.40 Thus pigs become susceptible to infection at approximately the time when gilts are first bred (24 to 30 weeks of age).86

After becoming infected, pigs excrete the virus in faeces and oral secretions for about two weeks,40, 63, 80 but the quantities of virus excreted have not so far been determined. Periodic shedding of virus by persistently infected animals has been suggested, but this has not been demonstrated.40 A persistent carrier state has been suggested as a possibility in those pigs that survive intra-uterine infection prior to the onset of immunological competence, i.e. in immunologically tolerant animals.15, 37, 38, 39, 40, 56Shedding of virus by such animals has, however, not been demonstrated.40

Infection is presumed to occur via the oronasal route, most frequently when susceptible animals encounter individuals actively excreting the virus. However, because PPV is very resistant to environmental conditions, premises that have housed infected pigs may continue to be a source of infection for four months or more.40, 63 Gilt pens, as might be expected, are more heavily contaminated than other housing on pig farms.40 Contaminated fomites are also likely to be infectious for protracted periods, and personnel are probably able to transfer the infection unless effectively decontaminated.43 It has been suggested that rats may act as vectors of PPV,43 but subsequent investigation has shown that this is unlikely to be important in practice.17

Transmission of PPV from infected boars to susceptible sows and gilts may occur during mating, since it has been shown by DNA hybridization that PPV binds ‘tightly’ to the spermatozoa of experimentally infected boars, with 0,01 to 0,32 genome copies of PPV per spermatozoon being detectable.32 Although isolation of PPV from the semen of infected boars has usually been unsuccessful,92 it has been reported.13, 14Reproductive failure as a result of infection of females via semen has not been proven. In one experiment, even when large quantities of PPV were mixed with semen and introduced artificially into the uteri of five seronegative gilts, only mild lesions were evident, and four of the gilts conceived normally and contained uninfected embryos when killed 10 to 20 days later.106 This supports the finding that PPV is incapable of penetrating the zona pellucida, 6, 105 but, on the other hand, as PPV may adhere to the surface of the zona pellucida, embryo transfer to susceptible sows may result in transmission of the virus.3, 31, 106 The possibility also exists that the virus could penetrate the zona via the open tracks left by spermatozoa, or traumatic damage caused to it by manipulation of the embryo.3 The importance of sexual transmission of PPV is rather that females so infected may act as foci for dissemination of the virus to susceptible pregnant animals. Likewise, susceptible boars may acquire the infection by serving sows with PPV present in the vaginal mucus.50 Regardless of their immune status, boars may be responsible for mechanical transmission of the virus to susceptible gilts.56.

Porcine parvovirus is not confined to commercially produced pigs, nor is it confined to Sus scrofa. A survey in Australia demonstrated antibody to PPV in 58,4 per cent of feral pigs.12 Antibody to PPV, detected by haemagglutination inhibition tests, has been reported in 1 to 18 per cent of sera of warthogs (Phacochoerus aethiopicus) tested in South Africa, Zimbabwe and Namibia.94 The pathogenic potential of PPV for warthogs, however, remains to be determined.

The role of PPV in post-weaning multisystemic wasting syndrome, caused by porcine circovirus 2 (see Post weaning multi systemic wasting syndrome in swine), has been investigated. While co-infection with PPV is not necessary for development of the syndrome, lesions may be more severe when both viruses are involved.1, 26, 45, 101

Pathogenesis

In a large number of experiments and field observations designed to assess the effect of PPV on embryos (up to 30 days after conception) and foetuses (more than 30 days after conception) of different ages, the consensus is that if infection occurs at less than approximately 60 to 70 days, the conceptus is usually severely affected and is likely to die.6, 18, 19, 33, 39, 41, 48, 59, 64, 65, 72, 85, 106 Older foetuses, although they frequently still develop lesions and occasionally succumb, are less severely affected and respond immunologically to infection.33, 41, 60, 72, 85, 97

The precise mechanism whereby transplacental infection occurs remains to be determined. Examination of tissues at the maternal–foetal junction at various stages of infection failed to reveal virus in the uterine tissues, but large amounts were present in the endothelial and mesenchymal cells of the chorion.56 However, the possibility of infection via the uterine epithelium or trophectoderm could not be definitively excluded,56 and possible transfer via macrophages that phagocytose the virus has also been investigated.79 The source of the virus is presumably the lowgrade viraemia that persists for one to six days.2, 43, 72 Intrauterine spread of virus from infected to uninfected foetuses is a significant cause of infection, especially during early gestation.72 This, as well as persistent viraemia, explains why foetuses frequently die at different stages of development.56, 57

The virus may also affect the uterus directly and contribute to foetal loss due to placental insufficiency.48, 65, 85 Hormonal effects, such as the failure of oestrone sulphate values to increase in sows infected experimentally during early pregnancy, may lower endometrial activity, with similar consequences.65 Nevertheless, there is general consensus that the direct cytolytic effects of PPV on embryos and foetuses is far more important than uterine insufficiency in the causation of reproductive failure. Damage to any vital organ of a foetus prior to the development of an adequate immune response could result in death, but the most striking effects of the virus appear to be upon the foetal circulatory system due to extensive involvement of the endothelium.56 

Experimentally induced infection of one-day-old and six-week-old piglets produced no discernible ill effects,11, 18 although PPV was present in all the tissues tested, particularly in lymphoid tissues.18 Porcine parvovirus is able to replicate in peripheral blood lymphocytes (T, B and null cells), but only if they are stimulated to proliferate by mitogens.79 Monocytes and peritoneal macrophages are able to phagocytose the virus, but no replication in them occurs.79 The numbers of T and B cells are unaffected by infection, as are their responses to mitogens.11

In six- to seven-week-old pigs infected experimentally, PPV has been recovered from, or antigen detected in, a wide variety of tissues and organs (lymph nodes, salivary glands, tonsils, thymus, lungs, spleen, nasal turbinates, and blood). This indicates that in acutely infected pigs the virus is widely distributed in the body of the animal, but the quantities of virus present have not, as yet, been accurately determined. 78, 80

The decreased pathogenicity of PPV for older foetuses and piglets has been ascribed to the ability of foetuses to mount humoral responses after approximately 55 days of conception.8 However, the hypothesis that there is a direct relationship between the onset of immunological competence and increasing resistance to the effects of infection with PPV has not been definitively proven.72

The association of PPV with other syndromes in piglets, such as diarrhoea and cutaneous vesicle-like lesions, is not supported by evidence that the virus replicates to any extent in gastric or cutaneous epithelium.20, 56 Replication of a virus morphologically compatible with a parvovirus has been reported in intestinal crypt epithelium of diarrhoeic piglets,24 but its identity with PPV was not established. Experimental infection to investigate the association of PPV with cutaneous lesions suggested that it would likely be isolated from cutaneous lesions during a natural infection, but failed to indicate that it is a primary cause of such lesions.47

Clinical signs

Infection with PPV is probably only important in the causation of embryonic and foetal death and the signs associated therewith. Abortion, although it has been ascribed to PPV infection,13, 28, 85, 88 is not usually a feature of foetal death caused by PPV.16, 30, 35, 56 Because PPV is more or less ubiquitous in pig populations, caution should be exercised in diagnosing PPV as the cause of abortion, particularly abortion storms, even if PPV is detected. Other adverse reproductive effects such as infertility, stillbirth, and neonatal death or reduced vitality are also considered to be unusual. 56 The virus has been reported as being associated with a variety of post-natal conditions, such as respiratory disease,14, 54 diarrhoea,20, 24, 108 and a cutaneous vesicular disease-like condition of pigs in mid-western states of the USA.46 Diarrhoea has been induced with a parvovirus isolated from the faeces of piglets with diarrhoea, but it was demonstrated that the virus was different from PPV which causes reproductive failure.109

The stage of gestation at which infection of gilts or sows occurs determines the particular signs of reproductive failure that become apparent. Frequently, the first sign of PPV infection in a herd is an increase in the number of gilts or sows returning to oestrus three to eight weeks after service or artificial insemination, i.e. ‘repeat breeders’. This is caused by infection of embryos and young foetuses, which die and are rapidly resorbed. Such sows may show a slight vaginal discharge.97 Experimentally, it has been shown that it takes 23 to 32 days for PPV to cross the placenta following oral infection; intramuscular inoculation of the virus reduces this period to 15 days.41

Older foetuses in which ossification has occurred are not easily resorbed and tend to be retained and become mummified. If all the foetuses are so affected, sows or gilts that were apparently pregnant lose abdominal girth and do not farrow. They are infertile and do not return to oestrus. The cause of the infertility generally only becomes apparent when they are examined after slaughter. More frequently, only a proportion of the foetuses becomes infected and, at farrowing, smaller than normal litters are produced in which there are often one or more mummified foetuses, a characteristic feature of PPV infection.17 In addition, there may be piglets that are smaller than normal, stillborn piglets, or even weak individuals that do not survive, but that is uncommon.

Pathology

Lesions in foetuses before they become immunologically competent include various degrees of stunting, widespread haemorrhages with the accumulation of serosanguinous fluid in body cavities, and eventually foetal death with resorption or mummification. Microscopic changes are characterized by widespread necrosis, sometimes accompanied by mineralization, and the presence of intranuclear inclusions in various organs including the liver, lungs, kidneys, brain and mesenteric and mediastinal lymph nodes.42, 48, 59, 60, 89

Macroscopic changes usually do not occur in foetuses infected after approximately 70 days of gestation, but in one experiment piglets that survived into the neonatal period following infection with PPV showed multifocal hepatic necrosis, accumulation of fluid in the body cavities and myocarditis.97 Microscopic changes have been reported in foetuses exposed to PPV during the second half of gestation. 19, 59 These varied in extent and included perivascular infiltration of mononuclear cells (lymphocytes, lymphoblasts and plasma cells) in various tissues including the meninges, brain and kidneys, accompanied by endothelial hypertrophy and hyperplasia of small blood vessels.19, 33, 59,85A round cell infiltration in the heart, in the absence of noteworthy damage to myocytes, and perivascular cuffing in the cerebral cortex, brain stem and cerebellum have been described.97 Direct proof that these lesions were caused by PPV was not obtained, but a subsequent study using polymerase chain reaction (PCR) demonstrated a strong association of PPV DNA with round cell infiltrates in the myocardium of suckling piglets.7

Uterine lesions in seropositive dams infected by transplacental inoculation of virus during either the first or second half of gestation comprised focal accumulation of mononuclear cells in the mucosa and perivascular cuffing of endo- and myometrial vessels.33, 85 Seronegative gilts infected at 70 days of gestation had, in addition to the lesions described in the uteri of seropositive dams, perivascular cuffs of plasma cells and lymphocytes in the brain, spinal cord and choroid of the eyes.33, 48

Diagnosis

A sudden increase in the number of repeat breeders followed some months later by a decrease in average litter size and litters with increased numbers of mummified foetuses is characteristic of PPVinfection. Delayed returns to oestrus are, however, uncommon.16 The initial sign of repeat breeding is sometimes missed by the farmer, with the result that the first indication of a problem is a sudden increase in the number of mummified foetuses and apparently infertile sows or gilts. Because a number of viruses that commonly cause foetal death of pigs do not occur in southern Africa, reproductive problems of this nature in pigs justify a provisional diagnosis of PPV infection. Confirmation requires laboratory support.

Foetuses that have died and become mummified before the onset of immunological competence (less than approximately 160 mm crown–rump length) are usually rich in PPV antigens, although live virus is often no longer recoverable.43 The antigens can be demonstrated in foetal tissue suspensions (lungs, liver and kidneys) by their ability to agglutinate guinea pig erythrocytes (the specificity of the reaction can be proved by inhibition with PPV antiserum) or by direct immunofluorescence on the same foetal organs.19,41, 42 An enzyme-linked immunosorbent assay (ELISA) for antigen detection has also been described as a rapid, sensitive and specific diagnostic test.36 In older (larger) foetuses, virus and viral antigens may be masked by the presence of antibody. However, if antibody to PPV can be demonstrated in the blood of foetuses (the chambers of the heart are the best source of blood) that are not too autolysed, in tissue suspensions prepared from decomposing foetuses, or in neonatal piglets that have not ingested colostrum, it is a good indication that infection occurred in utero. Methods not affected by the presence of antibody that have been used in diagnosis include electron microscopy,27 in situ hybridization,100 and PCR.4, 31 Porcine parvovirus can also be detected immunohistochemically in formalin-fixed, paraffinembedded tissues.102

Isolation of PPV from infected foetuses and piglets is not an efficient method for diagnosing the infection because it may take up to 21 days to recover the virus.43 In addition, not only is virus recovery from foetuses that are autolysed ineffi- cient,43 but primary cell cultures vary in their sensitivity.25, 86

Serological diagnosis of infection in gilts or sows with unequivocal association with disease is usually difficult to achieve because the infection is ubiquitous. For this reason, examination of paired serum samples (acute and convalescent phase) are essential, but acute-phase sera are almost impossible to obtain because the acute phase of the infection is usually past by the time infection is suspected. On the other hand, finding sows or gilts that are serologically negative to PPV after suffering reproductive failure would preclude the possibility of PPV being the cause of such failure.

The conventional serological test for PPV is haemagglutination inhibition, which is unusually sensitive, and titres of over 1:100 000 are common. However, in this system relatively high titres (e.g. over 1:256) are necessary to be sure of the specificity of the reaction.43 High haemagglutination inhibition titres develop and persist for four years or longer after the initial infection.43 A competition ELISA that is equally sensitive but amenable to automation has been developed.102 ELISAs that detect antibodies to the non-structural protein (NS1) may assist in distinguishing between vaccinated and naturally infected pigs.51

Differential diagnosis

Infection with classical swine fever (hog cholera), Aujeszky’s disease (pseudorabies), and porcine picornaviruses may all cause reproductive failure, although other signs usually occurin the former two diseases. The role of porcine picornaviruses in the SMEDI syndrome in Africa is unknown, as it has never been reliably determined.

A number of other infections cause reproductive failure in pigs, but these are usually associated with abortion or the birth of weak piglets, e.g. porcine reproductive and respiratory syndrome (PRRS) (see Porcine reproductive and respiratory syndrome) infection with porcine circovirus 2 that is associated with post-weaning multisystemic wasting syndrome and dermatitis-nephropathy, Japanese encephalitis virus (a flavivirus that occurs in Asia), Menangle virus (a paramyxovirus) recently described in Australia,49 Brucella suis and Leptospira serovars. Abortion can also be caused by an array of factors such as endotoxaemia or hormonal dysfunction, which may result in maternal failure to maintain the pregnancy.104 Because PPV infection rarely causes abortion, it should not be difficult to differentiate it from these conditions. Porcine circovirus 2 has, in addition, been described as a cause of myocarditis in piglets after intra-uterine infection,101 and co-infection with the two viruses is not uncommon.1, 26, 45, 101

Control

There are basically two approaches to the control of disease caused by PPV. The first involves ensuring that the virus is actively maintained in breeding herds so that gilts are infected, and become immune, before first mating. Alternatively, gilts can be immunized prior to breeding and the immunity maintained by booster inoculations.

Since the virus is present in most large breeding herds, infection of gilts prior to first service can be promoted by enabling contact between gilts and as many other age groups as possible on the farm, particularly those aged between three and eight months. The rationale is that pigs in the latter age category are likely to have the highest infection rate. Promoting transmission on the farm can also be achieved by spreading small amounts of dung between pens, which is simpler than moving the pigs themselves. The disadvantage of this approach is that it also promotes the transmission of other infections that may not be desirable, and it is not compatible with modern approaches to intensive pig management that demand strict separation of different age groups. Furthermore, one cannot ensure that all gilts become infected in the period between the waning of maternal immunity (12 to 26 weeks) and the time of mating (six to seven months of age). To increase the likelihood of infection prior to mating it is sometimes recommended that gilts not be bred until they are at least eight months old. This would have important economic consequences on large breeding units and is of doubtful value, since in the UK it has been found that approximately 20 per cent of multiparous sows are susceptible to infection.71 

Immunization is a more effective way of ensuring immunity in sows and gilts, although protection derived from vaccination is of shorter duration than that acquired by natural infection.35 Both live attenuated and inactivated vaccines have been produced, but presumably because they are safer, inactivated products are used. Inactivated vaccines are available in South Africa.

A PPV, designated NADL-2, which has undergone 54 passages in cell culture has been shown to be immunogenic when as little as 100 median cell-culture infective doses are administered intramuscularly to seronegative pigs. The virus is apparently incapable of crossing the placenta to infect embryos and foetuses, but if inoculated directly into the fluids surrounding the foetuses, replication of the virus and foetal death occur.77, 78 The virus is excreted in the faeces of vaccinated pigs and is able to infect susceptible animals. Oral administration of this virus is inefficient in stimulating immunity when compared to that obtained following intramuscular inoculation.78.

Vaccines containing inactivated PPV derived from suspensions prepared from infected foetuses,25, 107 primary porcine cell cultures,44, 57 or continuous porcine line cells25, 86 have been shown to be effective and safe. The latter have considerable advantages with respect to characterization for microbial purity and achievement of reproducible yields.86 A variety of inactivants encompassing aziridine compounds, formalin and β-propiolactone are effective, as are both aluminium hydroxide and water-in-oil adjuvants.25, 86

A recombinant vaccine produced by cloning the VP2 protein in a baculovirus system and expressing it in insect cells was demonstrated experimentally to elicit an immune response identical to that of commercial vaccines.52

Efficient application of a vaccination programme should greatly reduce the rate of circulation of PPV on large farms, and for that reason immunization of both gilts and sows according to the vaccine manufacturers’ instructions is vital when a vaccination programme is instituted. Although some animals may develop a longer-lasting immunity, studies elsewhere have shown that serological testing to limit vaccination to serologically negative pigs is generally not cost-effective.29, 35, 76 Parvoviral vaccines are usually combined with vaccines against erysipelas, and are administered to gilts, sows and boars twice a year.

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