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Occurrence: N. America, Spain since 1996 Age affected:
Weaners | ||
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Photo: Ananmnŏse |
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Effects: Wasting, poor growth, breathing difficulty, diarrhoea, jaundice, death.
Pig health & diseases main page
Post-weaning multisystemic wasting syndrome (PMWS) is a multifactorial disease. Porcine circovirus type II (PCV2) plays a major role in PMWS, but management factors and other disease agents seem to be important also. 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 trace, macrophages (white blood cells which kill bacteria, and T and B lymphoctes (which control immunity). In some cases, the virus has been accompanied by porcine parvovirus and porcine circovirus type I, which appears to be innocuous alone. Recent studies have confirmed that type II PCV can cause PMWS on its own, but clinical signs do not occur in every case and other agents may be needed to cause clinical disease consistently. Infection with PCV type II appears to have an incubation period of 10-12 days and 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 of the clinical signs. The virus may be involved in Congenital tremor AII and in the Porcine dermatitis and nephropathy syndrome.
Both epidemic and endemic forms 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% morality. 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. 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 tonsil and ileal Peyer's patches. The bronchiloar lesions and inclusion bodies are also present. Confirmation is by demonstration of PCV type 2 in cells by immunoperoxidase or in situ hybridsation or PCR of tissues. Antibody may be demonstrated using an indirect immunofluorescence test.
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. There is
currently no vaccine. 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.
Isolation and hygiene appear to have maintained some herd free from the disease
which is introduced with carrier pigs.
Several international animal health companies have introduced
vaccines against PCV2 infections.