Age affected: All ages (effects only obvious in pregnancy).
Causes: Porcine parvovirus.
Effects: Delayed returns, not-in-pig, mummies, stillbirths.
Porcine parvovirus is a small DNA virus which appears to be stable over a wide range of pH and can resist heating, but is killed after exposure to 80°C for 5 minutes. The commonest antigenic type of the virus is PPV1 but other subtypes have been described. The virus replicates in cells about to divide and may be grown in primary pig kidney cell monolayers or continuous cell lines. Porcine parvovirus enters by the oronasal or venereal routes and enters the blood followed by passage into the reproductive tract taking 10-14 days from infection to cross the placenta.
In boars, it may be found on sperm from days 5-9 post-infection. Embryos and foetuses dying before 33-35 days are resorbed, while those dying later become mummified, stillborn or, occasionally, aborted. Foetuses develop neutralising antibody or become immunotolerant and remain infected for up to 8 months after birth. Recovered infected piglets may be stunted. Serum antibody appears at 7-10 after infection and rises rapidly.
The virus is shed in urine, faeces, tonsillar debris and nasal secretions from 2 weeks after infection and pigs remain infectious for approximately 2 weeks. Recovered pigs are solidly immune and passive immunity is passed in colostrum to piglets and can be detected for 4-6 months after birth.
Transmission is normally oronasal from virus shed in the faeces, urine and in mummified foetuses and foetal membranes. The virus can persist in the environment for up to 4 months and can also infect rats, although these are unlikely to infect pigs. Infection can also be venereal, as the virus can be found in semen. Maternal immunity can persist for16 weeks or longer, and transmission may be prevented until it has disappeared. Introduction to a farm is in carrier pigs, especially following the introduction of infected pregnant gilts, in semen and in contaminated clothing, vehicles and implements.
Returns to oestrus, failure to farrow, the production of small litters, mummified pigs, stillbirth and, rarely, abortion are the main clinical syndromes associated with parvovirus infections in pigs and are particularly prominent in newly introduced and first litter gilts in which a mean loss of 1.1 pigs per litter results from parvovirus infection.Farrowing rate to first service may be as low as 36% (first litter); small litters (especially those containing 5 or less) and the presence of mummified and stillborn pigs may all occur. Irregular returns to oestrus may also be seen. Clinical signs may occur in a whole susceptible herd if disease is introduced. Infection in boars is asymptomatic and appears to have no effect on semen quality or fertility. The virus has been recovered from a vesicular skin condition and from diarrhoeic faeces after weaning. Reports of the experimental production of pneumonia, leucopoenia, diarrhoea and encephalitis in piglets exist.
Returns to service, small litters, mummified and stillborn pigs in gilts, rather than sows with little or no abortion and no history of maternal illness, is suggestive of parvovirus infection. Gross lesions are restricted to the uterus of the sow. Embryos may be shrunken and may die, appearing as small areas of necrotic material on the uterine wall. Foetuses may be reduced in size, congested and oedematous prior to death. Dead foetuses become mummified. Mummified foetuses may increase in size along the uterus until stillborn animals are found. The diagnosis may be confirmed by the demonstration of virus in mummified foetuses of less than 70 days’ gestation age, by isolation or more commonly, by the demonstration of parvovirus antigen microscopically in frozen sections of lung and liver by specific immunofluorescence, immunoperoxidase or using radio-labelled, digoxin or biotin labelled DNA probes.
Extracts of foetuses may be tested for viral antigen by latex particle agglunination and by ELISA. A number of polymerase chain reaction primers have been used successfully. Neutralising antibody may be detected in the sera of infected sows, of newborn piglets and in foetal fluids, including exudates and transudates in stillborn piglets from infected litters.
Changes are restricted to the uterus and litter and have been described above. When examining products of conception for mummies, it is necessary to tease out the afterbirth and examine it carefully, as small, dehydrated mummies may resemble faecal pellets and be tightly bound in the membranes. The crown-rump length can be measured and used to estimate the age at which the foetus died.
There is no treatment. Prevention is by vaccination of susceptible stock. A typical vaccine is inactivated and oil-adjuvanted and is administered as two doses, 3-4 weeks apart with boosters every two years and produces long-term immunity and overcomes waning passive immunity if given intramuscularly (i/m) at 5 months of age.
Second or subsequent vaccinations, should be given at least 2 weeks before service. Boars should also be vaccinated at 6 months of age, 6 months later and then annually. Maternal antibody may not disappear until 6-7 months of age and the vaccine used much overcome this for gilt vaccination. In herds with solid immunity, it may not be cost-effective to vaccinate, but vaccination should be undertaken in the whole herd, a significant portion of the younger stock or introduced gilts are seronegative.
Where a seronegative unvaccinated herd exists, and vaccination is not to be carried out, incoming stock should be vaccinated and disinfection practised. Where seronegative and seropositive stock exist, hygiene may reduce the spread amongst pregnant sows. The virus can be destroyed within 5 minutes, using sodium hydroxide and sodium hypochlorite. Glutaraldehyde 2% and formaldehyde 8% are also effective but take longer. Steam cleaning may be used.