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Introduction:

These syndromes (the disease) first became known to most UK pig producers in late 1999. At that time, the problems seemed largely confined to outdoor herds and multi site operations. During 2000, it gradually became clear that the disease was spreading more widely, particularly in East Anglia.

Initially, many of those affected remained silent about the disease, and I still believe there is considerable under-reporting of infected herds. Because the problem seemed initially confined to East Anglia, and reports of the effects of the disease in other countries seemed to show that producers could live with it, there was a slow reaction from bodies commissioning new research.

Information within the UK on symptoms, causes and possible treatments was slow in coming forward, partly as a result of an attitude of ‘denial’ by producers, but also because of the swine fever crisis shifting veterinary and producer priorities. Sadly, the foot and mouth epidemic 2001 has further diverted and delayed proper attention to the disease. Yet the economic consequences for affected producers are very serious and the disease now appears to be spreading throughout the UK.

Unlike many diseases in pigs, which flare up and disappear within a relatively short time span, the effects of PMWS/PDNS seem to last a long time. Reports from other countries suggest that herds may be seriously affected for 6 to 24 months, and many producers in the UK are already in their second year of problems with no sign of reduction in mortality. The causes and trigger factors are inadequately understood, and the de-stocking and cleansing of units is no guarantee of freedom from further outbreaks. Unless there is some mitigation in the disease or a successful treatment is quickly found, the UK pig production sector, already under great financial pressure, will suffer a further significant decline.

This paper charts the course and effects of the disease on a single herd as well as highlighting the economic impact. Every herd appears to suffer different symptoms, but exchanging information offers some prospect of identifying causal linkages.

Progress of the Disease:

Expert advice to those producers who have not yet contracted PMWS/PDNS is to maintain a high level of herd bio-security. My own breeding/finishing herd was once a multiplication herd for a national breeding company, with an unusually good system for bio-security. It has been closed to all intake of stock (except for 2 or 3 boars each year – strictly quarantined off-site), for 5 years. Despite all of these precautions, the herd succumbed in February 2001. The most likely cause is bird transmission. The nearest infected pigs were 2 miles away, and the nearest pigs of any kind, more than 1 mile.

Throughout this paper I refer to PMWS and PDNS as one disease, although the scientists believe them to be quite different. On farm that distinction is not clear. If a pig dies in the finishing house, the reason tends to be recorded as PDNS. If it dies in the first or second stage post-weaning accommodation, then it is PMWS! On this farm the first symptoms showed in older pigs – between 10 and 16 weeks of age. Over time, the mortality record (Table 1), shows an increase in mortality of younger pigs, drawing down the average age of death to around 9 weeks.

Over the first 4 months mortality climbed steeply, flattening out during the mid summer period, then taking off with renewed vigour in September. The timing of this increase coincided with a general upsurge in the area, and caused suspicion to fall on nutritional factors associated with the wet harvest. To date any associations remain unproven, but the possibility of mycotoxin as one of, perhaps several, possible triggers to this disease needs proper scientific review. Averaged across 12 months, post weaning herd mortality has been 13.69%, compared to an average during the three previous years of 2.3%. There are indications that mortality has peaked and is now falling slowly, but other herds locally report another upsurge.

The economic effects are tabulated in Table 2. Overheads per pig sold increase substantially with such a large drop in output. Food efficiency suffers as a direct result of mortality and through slowing down growth rates generally. Veterinary and carcase disposal costs increase. Slower growth and reduced appetite

has a small compensatory effect in reducing backfat, thereby allowing pigs to grade better at higher slaughter weights. Staff morale suffers, because so little can apparently be done to bring the disease under control. Break-even cost increases by between10p/kg (£7.00/pig), and 15p/kg deadweight (£11.00/pig), depending on the parameters used in the calculation.

Treatment and Management changes:

During the first few months, many combinations of antibiotics were tried, to deal with the ‘secondary’ symptoms of disease. Prior to infection the herd was largely free of viral pneumonia and other lung complaints. The disease triggered a breakdown, and Stellamune vaccination of all young stock was started and continues. This alone has more than doubled our previous veterinary cost.

Initial post mortem inspections indicated a range of diseases, presumably as a result of the immune system being weakened by the causal agent of PDNS, thereby allowing any number of ‘secondaries’ to take hold. Some pigs in apparently good condition were simply found dead, while others exhibited the more typical ‘wasting’symptoms. No medicinal treatment was effective: removal from group competition was rarely successful for wasting pigs, and in most cases it was both cheaper and kinder to shoot such animals when first seen.

Some pigs showed symptoms of Mulberry heart disease indicating massive and sudden organ failure. Rations were supplemented with additional Vitamin E and with selenium. There was no discernible beneficial effect.

In recent months various mycotoxin inhibitors have been tried in feed to establish whether fungal toxins on grain might exacerbate the problem. Again, there have been no clear effects demonstrated to date, but trials continue.

Management changes are now held by many to hold the best chance of mitigating the disease. Weaning of smaller pigs is now delayed until they reach at least 6kg. Our system, unfortunately requires mixing of litters at weaning, and again at 8 weeks on entry to the second stage weaner housing. This is kept to a minimum, with gentle handling, and as much care and attention to hygiene of water and feed stations as possible. At 8 weeks the pigs transfer from dry feed to wet, and from temperature controlled slatted housing to strawed weaner pools. This is clearly a major stress point, and attempts have been made to reduce this stress by continuing to offer dry feed alongside the wet for a period, by constructing kennels, during the winter period, within the weaner pools, and by reducing group sizes. There has been little effect on mortality, which is now almost evenly spread before and after the move to 2nd stage accommodation. One observation, which cannot be statistically supported, is that mortality is somewhat less in smaller and less crowded groups.

On the theory that disease might be recycled through the breeding herd, records were kept of litter mortality related to the sows ear number and parity. No clear links were found (Table 3). As yet there is no indication of whether home reared gilts which have been challenged by the disease impart any immunity to their offspring. Following an observation that several early deaths were associated with poor tooth clipping and mouth abscesses, tooth clipping has now been effectively discontinued, with no adverse effects on the sows. It is too early to say whether this may ultimately reduce future mortality levels.

Records:

Too few records of on-farm experiences have been passed to VI Centres and researchers. Without adequate case histories the disease is proving difficult to understand, and without understanding, control measures will be largely futile. During 2000 we shared our sow parity records with Bury VI Centre and carried out an extended post mortem survey. The results are shown in Table 4. A few other farms have supplied similar or additional information. Most farms now have computer recording systems to assist herd management.

Much more could surely be learned by standardising and amalgamating these records?

The Future:

PMWS/PDNS is now appearing throughout the UK. Mortality rates of 30% plus are widely quoted. It is clear from the costings of my own herd that such levels are unsustainable if the disease remains active for more than a few months. Sadly, many are finding that it often lasts much longer. With little sign of a successful cure, the future of affected herds is bleak. Even if re-stocking is a viable option, (which has to be questioned, if the viral agent is as persistent as is widely reported), the ongoing export ban resulting from the foot & mouth outbreak make herd disposal very expensive.

The impact of the disease has been consistently under-rated. If it progresses throughout the UK herd as it already has done in East Anglia it threatens the entire viability of the sector. Comparative production costs, already above those in most competitor countries, will rise significantly.

Profitability will not return to fund urgent re-investment after a period of severe price pressure. Additional fieldwork and research into curing or mitigating the disease must be given urgent priority.