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\n <\/a>\n <\/div><\/p>\nPig Diseases<\/h2><\/div>- All<\/a><\/li>
- B<\/a><\/li>
- C<\/a><\/li>
- D<\/a><\/li>
- E<\/a><\/li>
- G<\/a><\/li>
- L<\/a><\/li>
- M<\/a><\/li>
- P<\/a><\/li>
- R<\/a><\/li>
- S<\/a><\/li>
- T<\/a><\/li><\/ul><\/div><\/div>B<\/div>
- Blue Ear Disease<\/a><\/li><\/ul><\/div><\/div>C<\/div>
- Clostridia<\/a><\/li>
- Coccidiosis in Pigs<\/a><\/li>
- Colibacillosis in Pigs<\/a><\/li><\/ul><\/div><\/div>D<\/div>
- Diarrhea (Piglet)<\/a><\/li><\/ul><\/div><\/div>E<\/div>
- E. coli<\/a><\/li>
- Eimeria<\/a><\/li>
- Enteritis - Necrotic<\/a><\/li>
- Erysipelas<\/a><\/li>
- External Parasites<\/a><\/li>
- Edema Disease<\/a><\/li><\/ul><\/div><\/div>G<\/div>
- Greasy Pig Disease<\/a><\/li><\/ul><\/div><\/div>L<\/div>
- Lice<\/a><\/li><\/ul><\/div><\/div>M<\/div>
- Mange<\/a><\/li>
- Meningitis<\/a><\/li><\/ul><\/div><\/div>P<\/div>
- Parvovirus<\/a><\/li>
- PEARS<\/a><\/li>
- Piglet Diarrhea<\/a><\/li>
- Pneumonia<\/a><\/li>
- Porcine Epidemic Abortion and Respiratory Syndrome<\/a><\/li>
- Porcine Parvovirus<\/a><\/li>
- Porcine Reproductive and Respiratory Syndrome<\/a><\/li>
- Post-weaning Diarrhea<\/a><\/li>
- PRRS<\/a><\/li><\/ul><\/div><\/div>R<\/div>
- Respiratory Disease<\/a><\/li>
- Ringworm<\/a><\/li><\/ul><\/div><\/div>S<\/div>
- Scours<\/a><\/li>
- SIRS<\/a><\/li>
- Skin conditions<\/a><\/li>
- Streptococcal Infections<\/a><\/li>
- Swine Infertility and Respiratory Syndrome<\/a><\/li>
- Swine Pox<\/a><\/li><\/ul><\/div><\/div>T<\/div>
- Tetanus<\/a><\/li>
- Ticks<\/a><\/li><\/ul><\/div><\/div><\/div><\/div>\n
Porcine Parvovirus<\/h4>\n\nPorcine parvovirus (PPV) causes reproductive failure in pigs, characterized by embryonic and fetal death. Clinically, the disease in a herd manifests with decrease in litter size, return to service and increase in the number of mummified and\/or stillborn piglets (van Leengoed et al., 1983<\/a>; Mengeling, 1999<\/a>).<\/strong><\/p>\nContaminated sites and premises are the main reservoir for the virus, which survives major temperature changes and is resistant to disinfectants. While an infected pig only secretes the virus for a couple of weeks, the premises can remain infectious for up to four months (Mengeling and Paul 1986<\/a>).<\/strong><\/p>\nPigs do not exhibit any clinical signs if infection is prior to the reproductive phase. Clinical outcome in sows or pregnant gilts depends on the time of the infection during gestation. The virus is widely spread throughout the world and is endemic in most pig herds in the UK and the US (Mengeling, 1999<\/a>; Nash, 1990<\/a>; Robinson et al., 1985<\/a>).<\/p>\n<\/div>\n<\/strong><\/p>\n<\/div>\n
\nControl and Prevention<\/a>
\nNatural Infection<\/a>
\nVaccination against PPV<\/a>
\nTreatment Options<\/a>
\nGood Practice<\/a>\n<\/div>\n<\/div>\n\nControl and Prevention of Porcine Parvovirus<\/a><\/h4>\nDue to the ubiquitous nature of the disease, it is impossible to establish and\/or maintain PPV-free herds, therefore\u00a0gilts can be infected naturally or routinely vaccinated before breeding. However, the efficacy of the natural infection approach is not proven.<\/p>\n
Natural Infection with Porcine Parvovirus<\/h2>\n
To encourage natural infection, gilts can be\u00a0mixed with seropositive<\/a><\/span> sows before breeding or at entry to a herd. Attempts to stimulate immunity in gilts by exposing them to contamination on the site may work, but needs to be monitored by serological<\/a><\/span> testing, and this method rarely ensures 100% infection in gilts. Surveys carried out in indoor herds, where <\/a>natural infection control was practiced, have found that the infection prevalence in gilts varies significantly (Einarsson et al., 1987<\/a>; Pointon et al., 1983<\/a>; Robinson et al., 1985<\/a>; Too and Love, 1986<\/a>).<\/p>\nPoor infection levels in gilts as a result of managed exposure to PPV often appear to explain the clinical patterns of the disease when an outbreak occurs, i.e., gilts\/primiparous<\/a><\/span> sows exhibit greatest losses in terms of reproductive failure (Huysman et al., 1992;<\/a> Morrison and Joo, 1984<\/a>; Pointon et al., 1983<\/a>; Too and Love, 1986<\/a>).\n<\/div>\n\n<\/p>\n![\"outdoor](\"https:\/\/www.farmhealthonline.com\/wp-content\/uploads\/2015\/06\/outdoor-sow-and-piglets-300x292.jpg\")
<\/a>PPV is known as a common cause of reproductive failure in swine herds. PPV usually affects gilts although sows can still be susceptible.<\/strong><\/p><\/div>\n<\/span><\/div>\n
<\/div>\nVaccination Against Porcine Parvovirus<\/h2>\n
<\/p>\n![\"sow](\"https:\/\/www.farmhealthonline.com\/wp-content\/uploads\/2015\/09\/sow-injection-300x200.jpg\")
<\/a>In herds that are prone to porcine parvovirus, vaccination is advocated. Since gilts are most susceptible, it is recommended that gilts selected for breeding should be vaccinated prior to service (Leengoed et al., 1983<\/a>).<\/strong><\/p><\/div>\n<\/span>Vaccination is the only way to ensure active immunity in breeding gilts and sows (Edwards et al., 1986<\/a>). Both inactivated and live vaccines have been developed, but only inactivated vaccines are available in the UK. Gilts should be vaccinated after passive immunity<\/a><\/span> from colostrum has disappeared at about six months of age but before their first mating,\u00a0in accordance with the Specific Product Characteristics of the vaccine used.<\/p>\nThe use of routine vaccines in endemically<\/a><\/span> infected herds has been advocated by many, particularly on a cost-benefit basis (Gardner et al., 1996<\/a>; Nash, 1990<\/a>; Parke and Burgess, 1993<\/a>; Parsons et al., 1986<\/a>). Others have found that revaccination of breeding animals after first gestation<\/a><\/span> was not necessary (Einarsson et al., 1987<\/a>). In one vaccination trial that took place <\/a>between 1984 and 1986 and included 1243 gilts, from 12 herds in which approximately half of each herd was vaccinated, and half left un-vaccinated, there\u00a0was little difference in reproductive performance between\u00a0the groups. This is because incidence of PPV within different herds will vary. It is only when the same team looked closer at individual herds did the benefits of vaccination become apparent. From this it can be concluded that vaccination can be highly cost-effective for some farms, and not others (Wrathall, 1988<\/a>).<\/p>\n<\/div>\nTreating Porcine Parvovirus<\/h4>\n
There is no treatment for porcine parvovirus.<\/p>\n
<\/div>\nPorcine Parvovirus and Welfare<\/h4>\n
<\/a>As there is very little that can be done to alleviate the symptoms once the infection has entered the herd,\u00a0efforts should be concentrated on a robust\u00a0vaccination policy and careful screening of\u00a0all current and incoming stock,\u00a0especially gilts. It is important to adhere to good biosecurity measures<\/a>, including avoiding the use of stud boars that move from farm to farm, as this is a common way to spread parvovirus, as well as a range of other diseases from herd to herd.<\/p>\n<\/div>\nGood Practice Based on Current Knowledge<\/h4>\n\n- Monitor reproductive performance by good recording of service, farrowing and weaning<\/li>\n
- Investigate any indication of failure in reproduction<\/li>\n
- Investigate by laboratory examination any incidence of mummified foetuses<\/li>\n
- If failure to farrow (despite anestrus<\/a><\/span>) is a major symptom, have the uteri of the culled “sows\/gilts not in pig” examined<\/li>\n
- Choose the preferred method of maintaining immunity:\u00a0vaccination (vaccination of either all gilts and sows or only gilts) or natural infection\u00a0(although this method may lack efficacy).<\/li>\n
- Ensure adequate level of immunity in gilts entering the breeding herd either by purchasing vaccinated stock or by exposing gilts to infection before mating \u2013 see below on how to induce natural infection<\/li>\n<\/ul>\n
Guidelines on How to Induce Natural Infection<\/h4>\n
Natural infection may not cover the whole herd, however it is an alternative to routine vaccinations. Care should be taken as the efficacy of this approach is not proven and it can lead to ongoing fluctuations in reproductive performance. Your veterinarian can provide further guidance:<\/p>\n
\n- Buy in weaner gilts at an earlier age, at 30-35 kg liveweight<\/li>\n
- Allow a minimum of five weeks for the integration and immunity building period in maiden gilts of over 5 months of age and monitor the transfer of immunity by serological<\/a><\/span> testing<\/li>\n
- Start the acclimatization process at least seven weeks before mating<\/li>\n
- Expose gilts to pathogens from the breeding herd by placing piglet dung and scours<\/a><\/span> in the gilt paddock, repeating several times with fresh material<\/li>\n
- Introduce cull sows to the gilt paddock (preferably small ones)<\/li>\n
- Also, new boars should be subjected to a natural infection and acclimatization process for a minimum of four weeks before mating<\/li>\n<\/ul>\n
- All<\/a><\/li>
- B<\/a><\/li>
- C<\/a><\/li>
- D<\/a><\/li>
- E<\/a><\/li>
- G<\/a><\/li>
- L<\/a><\/li>
- M<\/a><\/li>
- P<\/a><\/li>
- R<\/a><\/li>
- S<\/a><\/li>
- T<\/a><\/li><\/ul>
<\/div><\/div>B<\/div>- Blue Ear Disease<\/a><\/li><\/ul><\/div><\/div>C<\/div>
- Clostridia<\/a><\/li>
- Coccidiosis in Pigs<\/a><\/li>
- Colibacillosis in Pigs<\/a><\/li><\/ul>
<\/div><\/div>D<\/div>- Diarrhea (Piglet)<\/a><\/li><\/ul><\/div><\/div>E<\/div>
- E. coli<\/a><\/li>
- Eimeria<\/a><\/li>
- Enteritis - Necrotic<\/a><\/li>
- Erysipelas<\/a><\/li>
- External Parasites<\/a><\/li>
- Edema Disease<\/a><\/li><\/ul>
<\/div><\/div>G<\/div>- Greasy Pig Disease<\/a><\/li><\/ul><\/div><\/div>L<\/div>
- Lice<\/a><\/li><\/ul><\/div><\/div>M<\/div>
- Mange<\/a><\/li>
- Meningitis<\/a><\/li><\/ul>
<\/div><\/div>P<\/div>- Parvovirus<\/a><\/li>
- PEARS<\/a><\/li>
- Piglet Diarrhea<\/a><\/li>
- Pneumonia<\/a><\/li>
- Porcine Epidemic Abortion and Respiratory Syndrome<\/a><\/li>
- Porcine Parvovirus<\/a><\/li>
- Porcine Reproductive and Respiratory Syndrome<\/a><\/li>
- Post-weaning Diarrhea<\/a><\/li>
- PRRS<\/a><\/li><\/ul>
<\/div><\/div>R<\/div>- Respiratory Disease<\/a><\/li>
- Ringworm<\/a><\/li><\/ul>
<\/div><\/div>S<\/div>- Scours<\/a><\/li>
- SIRS<\/a><\/li>
- Skin conditions<\/a><\/li>
- Streptococcal Infections<\/a><\/li>
- Swine Infertility and Respiratory Syndrome<\/a><\/li>
- Swine Pox<\/a><\/li><\/ul>
<\/div><\/div>T<\/div>- Tetanus<\/a><\/li>
- Ticks<\/a><\/li><\/ul>
<\/div><\/div><\/div><\/div>\nPorcine Parvovirus<\/h4>\n
\nPorcine parvovirus (PPV) causes reproductive failure in pigs, characterized by embryonic and fetal death. Clinically, the disease in a herd manifests with decrease in litter size, return to service and increase in the number of mummified and\/or stillborn piglets (van Leengoed et al., 1983<\/a>; Mengeling, 1999<\/a>).<\/strong><\/p>\n
Contaminated sites and premises are the main reservoir for the virus, which survives major temperature changes and is resistant to disinfectants. While an infected pig only secretes the virus for a couple of weeks, the premises can remain infectious for up to four months (Mengeling and Paul 1986<\/a>).<\/strong><\/p>\n
Pigs do not exhibit any clinical signs if infection is prior to the reproductive phase. Clinical outcome in sows or pregnant gilts depends on the time of the infection during gestation. The virus is widely spread throughout the world and is endemic in most pig herds in the UK and the US (Mengeling, 1999<\/a>; Nash, 1990<\/a>; Robinson et al., 1985<\/a>).<\/p>\n
<\/div>\n<\/strong><\/p>\n<\/div>\n
\nControl and Prevention<\/a>
\nNatural Infection<\/a>
\nVaccination against PPV<\/a>
\nTreatment Options<\/a>
\nGood Practice<\/a>\n<\/div>\n<\/div>\n\nControl and Prevention of Porcine Parvovirus<\/a><\/h4>\n
Due to the ubiquitous nature of the disease, it is impossible to establish and\/or maintain PPV-free herds, therefore\u00a0gilts can be infected naturally or routinely vaccinated before breeding. However, the efficacy of the natural infection approach is not proven.<\/p>\n
Natural Infection with Porcine Parvovirus<\/h2>\n
To encourage natural infection, gilts can be\u00a0mixed with seropositive<\/a><\/span> sows before breeding or at entry to a herd. Attempts to stimulate immunity in gilts by exposing them to contamination on the site may work, but needs to be monitored by serological<\/a><\/span> testing, and this method rarely ensures 100% infection in gilts. Surveys carried out in indoor herds, where <\/a>natural infection control was practiced, have found that the infection prevalence in gilts varies significantly (Einarsson et al., 1987<\/a>; Pointon et al., 1983<\/a>; Robinson et al., 1985<\/a>; Too and Love, 1986<\/a>).<\/p>\n
Poor infection levels in gilts as a result of managed exposure to PPV often appear to explain the clinical patterns of the disease when an outbreak occurs, i.e., gilts\/primiparous<\/a><\/span> sows exhibit greatest losses in terms of reproductive failure (Huysman et al., 1992;<\/a> Morrison and Joo, 1984<\/a>; Pointon et al., 1983<\/a>; Too and Love, 1986<\/a>).\n<\/div>\n
\n<\/p>\n<\/a>PPV is known as a common cause of reproductive failure in swine herds. PPV usually affects gilts although sows can still be susceptible.<\/strong><\/p><\/div>\n
<\/span><\/div>\n
<\/div>\nVaccination Against Porcine Parvovirus<\/h2>\n
<\/p>\n
<\/a>In herds that are prone to porcine parvovirus, vaccination is advocated. Since gilts are most susceptible, it is recommended that gilts selected for breeding should be vaccinated prior to service (Leengoed et al., 1983<\/a>).<\/strong><\/p><\/div>\n
<\/span>Vaccination is the only way to ensure active immunity in breeding gilts and sows (Edwards et al., 1986<\/a>). Both inactivated and live vaccines have been developed, but only inactivated vaccines are available in the UK. Gilts should be vaccinated after passive immunity<\/a><\/span> from colostrum has disappeared at about six months of age but before their first mating,\u00a0in accordance with the Specific Product Characteristics of the vaccine used.<\/p>\n
The use of routine vaccines in endemically<\/a><\/span> infected herds has been advocated by many, particularly on a cost-benefit basis (Gardner et al., 1996<\/a>; Nash, 1990<\/a>; Parke and Burgess, 1993<\/a>; Parsons et al., 1986<\/a>). Others have found that revaccination of breeding animals after first gestation<\/a><\/span> was not necessary (Einarsson et al., 1987<\/a>). In one vaccination trial that took place <\/a>between 1984 and 1986 and included 1243 gilts, from 12 herds in which approximately half of each herd was vaccinated, and half left un-vaccinated, there\u00a0was little difference in reproductive performance between\u00a0the groups. This is because incidence of PPV within different herds will vary. It is only when the same team looked closer at individual herds did the benefits of vaccination become apparent. From this it can be concluded that vaccination can be highly cost-effective for some farms, and not others (Wrathall, 1988<\/a>).<\/p>\n
<\/div>\nTreating Porcine Parvovirus<\/h4>\n
There is no treatment for porcine parvovirus.<\/p>\n
<\/div>\nPorcine Parvovirus and Welfare<\/h4>\n
<\/a>As there is very little that can be done to alleviate the symptoms once the infection has entered the herd,\u00a0efforts should be concentrated on a robust\u00a0vaccination policy and careful screening of\u00a0all current and incoming stock,\u00a0especially gilts. It is important to adhere to good biosecurity measures<\/a>, including avoiding the use of stud boars that move from farm to farm, as this is a common way to spread parvovirus, as well as a range of other diseases from herd to herd.<\/p>\n
<\/div>\nGood Practice Based on Current Knowledge<\/h4>\n
- \n
- Monitor reproductive performance by good recording of service, farrowing and weaning<\/li>\n
- Investigate any indication of failure in reproduction<\/li>\n
- Investigate by laboratory examination any incidence of mummified foetuses<\/li>\n
- If failure to farrow (despite anestrus<\/a><\/span>) is a major symptom, have the uteri of the culled “sows\/gilts not in pig” examined<\/li>\n
- Choose the preferred method of maintaining immunity:\u00a0vaccination (vaccination of either all gilts and sows or only gilts) or natural infection\u00a0(although this method may lack efficacy).<\/li>\n
- Ensure adequate level of immunity in gilts entering the breeding herd either by purchasing vaccinated stock or by exposing gilts to infection before mating \u2013 see below on how to induce natural infection<\/li>\n<\/ul>\n
Guidelines on How to Induce Natural Infection<\/h4>\n
Natural infection may not cover the whole herd, however it is an alternative to routine vaccinations. Care should be taken as the efficacy of this approach is not proven and it can lead to ongoing fluctuations in reproductive performance. Your veterinarian can provide further guidance:<\/p>\n
- \n
- Buy in weaner gilts at an earlier age, at 30-35 kg liveweight<\/li>\n
- Allow a minimum of five weeks for the integration and immunity building period in maiden gilts of over 5 months of age and monitor the transfer of immunity by serological<\/a><\/span> testing<\/li>\n
- Start the acclimatization process at least seven weeks before mating<\/li>\n
- Expose gilts to pathogens from the breeding herd by placing piglet dung and scours<\/a><\/span> in the gilt paddock, repeating several times with fresh material<\/li>\n
- Introduce cull sows to the gilt paddock (preferably small ones)<\/li>\n
- Also, new boars should be subjected to a natural infection and acclimatization process for a minimum of four weeks before mating<\/li>\n<\/ul>\n
- Ticks<\/a><\/li><\/ul>
- SIRS<\/a><\/li>
- Ringworm<\/a><\/li><\/ul>
- PEARS<\/a><\/li>
- Meningitis<\/a><\/li><\/ul>
- Mange<\/a><\/li>
- Lice<\/a><\/li><\/ul>
- Eimeria<\/a><\/li>
- E. coli<\/a><\/li>
- Coccidiosis in Pigs<\/a><\/li>
- Clostridia<\/a><\/li>
- B<\/a><\/li>