Occurrence: Most countries.
Age affected: Weaners.
Causes: Porcine circovirus 2; poor housing; stress.
Effects: Wasting, poor growth, breathing difficulty, diarrhoea, jaundice, abortion, skin discolouration, death.
Occurrence: Most countries.
Porcine Circovirus infection is almost ubiquitous. PCV is a small, resistant, circular, single-stranded DNA virus which can grow in a wide range of porcine cell lines. The virus multiplies in cells of the porcine intestine, respiratory tract, macrophages (white blood cells which kill bacteria), and T and B lymphoctes (which control immunity).
PCV type 1 (PCV1) is non-pathogenic, but PCV2a and, more recently, PCV2b infections cause or contribute to several conditions, most importantly PMWS, PDNS and reproductive conditions such as mummified pigs and abortions. In some cases, the virus has been accompanied by other viruses such as porcine parvovirus.
Infection is generally oronasal, transplacental or venereal, and disease is produced when infection of the cells of the lymphoid system allows high levels of virus to accumulate in the blood. In foetuses, this can result in foetal death, mummification and abortion, in weaned pigs it can cause PMWS, the commonest form of disease, resulting in wasting and mortality once maternal antibody levels have declined, and in older pigs with high viral loads and low antibody levels, in PDNS.
Clinical signs do not occur in every case. Infection with PCV2 appears to have an incubation period of 10-14 days and, in PMWS, produces jaundice, swelling of the liver and kidneys and granulomatous lesions in a wide range of tissues. Most consistent lesions develop in the lymph nodes which are infiltrated with macrophages, contain syncytia (fused cells) and inclusions in the cytoplasm and nucleus of some cells. Affected pigs develop antibody within 2-4 weeks of the clinical signs. PDNS may develop in older pigs where the antibody response has been weak and high levels of virus are present and is associated with haemorrhages in many organs and has a high mortality rate.
Pig to pig contact is the commonest mode of transmission. The virus is shed in urine, faeces and saliva within 1 day of infection and in semen from 5 days post infection. Virus can cross the placenta to infect embryos and foetuses. The virus is relatively resistant to heat and can persist in the environment but is sensitive to disinfectants and can infect mice and rats, but rodents play little part in transmission. Transmission to naïve farms is usually in carrier pigs, but can result from contact with contaminated clothing, implements and transport. Virus may be present in semen and can be introduced to a herd by AI. Although wild boar can be infected, they are only important where contact with domestic pigs occurs.
PMWS: Both epidemic and endemic forms of PMWS have been reported. In non-immune herds, an increase in pre-weaning mortality (13%) may occur to give low numbers weaned (6.3), but the effects are seen mainly in weaned pigs, where disease is most obvious between weeks 6-8 and mortality peaks at week 9. Mortality rates of 64.3% have been recorded in affected recently-weaned pigs, 92.3% in those weaned for 4 weeks and 64.3% in growers, but it does not affect finishers.
Few clinical signs may be seen in some cases. In immune herds first clinical signs appear at 42 +/- 13.5 days, in the flat deck or early grower stage and may give rise to 6.5 +/- 5.1% mortality. Affected pigs are unthrifty, have dyspnoea (difficulty in breathing) with a marked expiratory effort, pallor, rough hair coat, enlarged inguinal lymph nodes, jaundice and diarrhoea and may die after 2-8 days. In some cases, affected pigs are profoundly anaemic and there are rare cases of neurological signs, such as incoordination.
The clinical syndrome (stunting, pallor, dyspnoea, jaundice, diarrhoea and mortality) suggests PMWS, but confirmation is based on the pathological findings and demonstration of the virus in tissues. Antibody testing by ELISA.
PDNS: Affected pigs are usually aged between 11 and 14 weeks, may have had PMWS previously, become depressed, fevered and inappetant. They develop red or purple patches over the hindquarters and back and discoloured swellings occur on the lower limbs. The skin lesions can extend to the rest of the body and affected pigs recover or die within a few days. The skin lesions may fade or leave scars. The clinical syndrome (skin haemorrhages, haemorrhages and a high mortality rate in affected pigs and their age) suggests PDNS, but the changes seen in life and at post-mortem examination resemble those of the swine fevers, and should be treated as suspicious if there is doubt.
Reproductive effects: These are less well defined, but PCV2 may be involved in stillbirths, abortions and the birth of mummified piglets.
PMWS: Five to ten pigs may be required, as the lesions are not consistent. Wasting is present, the skin is pale and there may be jaundice. The lungs do not collapse, may be mottled and a tan colour. All body lymph nodes are enlarged, firm homogeneous in texture and whitish on the cut surfaces. The liver may be atrophic or pale, with white foci, there may be white foci in the kidneys or they may be enlarged, pale and oedematous. The spleen is often enlarged. Changes in the stomach include ulcers in the pars oesophagea. There may be oedema around the pancreas, the small intestine is thin-walled, the contents watery and the caecum distended and there is reddening of the caecal wall. Histiocytes and giant cells are visible by microscopy in lymphoid tissues, especially in the tonsil and in the ileal Peyer’s patches. Bronchiolar lesions and inclusion bodies are also present. Confirmation is by demonstration of PCV type 2 in cells by immunoperoxidase, in situ hybridsation or PCR of tissues. Determination of viral load by quantitative PCR is helpful if the laboratory is able to carry it out.
PDNS: The gross lesions on the skin are usually obvious, but may require washing to reveal them clearly. They are very obvious on slaughtered pigs after scalding. There is usually gross enlargement of the kidneys which are pale with a granular surface and appear to be petechiated, and haemorrhages can be found on the serous surfaces and in the swollen lymph nodes. The basic lesions found by microscopical examination are of a necrotising vasculitis, and, in the kidney an immune glomerulonephritis. The gross lesions must be differentiated from thos of the swine fevers.
Stillbirths and mummies:
Stillborn piglets have congestion of the liver and enlargement of the heart.
There is no treatment. Secondary infections with bacteria should be controlled and individual animals can be removed from the herd and nursed as they may grow normally if they recover. This is not possible on any large scale and high mortality often persists under farm conditions. When an outbreak occurs, strict hygiene should be practised and accompanied by all in, all out management. Prevention of spread within a farm may be possible as the virus is spread in faeces and spreads slowly within a building, but not easily from building to building. The use of an oxidising disinfectant on boots, implements and as a dip may be sufficient to reduce the chance of spread.
Prevention of the consequences of infection is based on reduction of the viral load by means of vaccination, but does not prevent infection. Current vaccines are all killed and are whole, inactivated PCV2 or contain the Open Reading Frame 2 (ORF2) viral protein which is protective against both PCV 2a and PCV 2b. All are adjuvanted. Passive protection of piglets can be provided for up to 5 weeks by sow vaccination prior to farrowing, and active protection can be provided within 2 weeks by piglet vaccination from 3 weeks onwards. Protection lasts for 14 weeks. Hygiene and improved management practices should be continued.
Vaccination of the sow population will reduce the reproductive effects of the infection and PDNS is much less likely in vaccinated herds.
Isolation and hygiene appear to have maintained some herds free from the disease which is introduced with carrier pigs.
PDNS may resemble the Swine Fevers both clinically and at post-mortem examination. When there is any doubt about the identity of the disease or where there is a risk of the swine fevers, the state veterinary service should be consulted.