I was particularly struck by a paper given by Danish workers, (Hjulsager and others), who showed the dynamics of PCV2 infections in piglets from naturally immune but PMWS affected herds in comparison with pigs, which did not show PMWS. PCV2 was found in the nose by quantitative PCR from as early as one week of age (see Graph 1). It was not proven, if this came directly from the sows, as they were not swabbed, although this early transmission is suggestive that it was the case. It could indicate that 'nasal shedding may play an important role in the route of infection', more than previously considered. In contrast, a significant viraemia (virus particles in the blood), which is the major determinant of potential disease expression, did not occur until 9 weeks of age and continued to increase to 12 weeks, when the trial was terminated. The late viraemia and subsequent faecal shedding was presumably due to circulating passive antibodies in the blood, passed on from the sow's colostrum. It had no effect on nasal colonisation and excretion in the piglets. In contrast, non-PMWS affected pigs showed a similar early nasal infection and viraemia at 9 weeks of age but this had started to fall by 12 weeks of age, presumably, as the pig's own immune system started to cope with the virus challenge. Faecal swabs followed a similar pattern to blood with an increasing virus shedding in the PMWS-affected pigs and a fall in the negative pigs (see Graph 2).
Graph 1. PCV2 copies/ml from serum and nasal and rectal swabs from piglets from PMWS-affected pigs
Log figures mean numbers are multiples of 10: - 1 = 10; 2 = 100; 3 = 1000 etc
(Source: Hjulsager and others, 2007)
Graph 2. PCV2 copies/ml from serum and nasal and rectal swabs from piglets from PMWS-free pigs
(Source: Hjulsager and others, 2007)
These findings emphasize Madec's earlier concerns of the potential spread of infection by nose to nose contact, across open pens, especially at a litter level or mixed-source group level. It also highlights that deficiencies in the immune response to the virus will allow it to continue to develop into PMWS. The causes of those deficiencies are only now becoming apparent e.g. stress, concurrent infections, breed etc. Immuno-enhancement, particularly by vaccination, was reported on by several authors under European conditions, confirming previous N. American field trial results.
Interestingly the only emerging or new disease was described in Australia by Kirkland and others. They described the porcine mycocarditis syndrome, where there was an increase in stillborn piglets, mummifications and increased preweaning losses upto 50%. Pathological changes were described as multifocal, non-suppurative myocarditis (inflamed heart muscle) consistent with a viral infection. A virus could not be initially cultured, although materials from affected piglets could affect foetuses when injected into the uterus. Specialised techniques using RNA fragments from the viral material showed the virus to be related to the pestivirus group, although unlike any existing pestivirus such as classical swine fever virus or bovine viral diarrhoea in cattle.
Porcine reproductive and respiratory virus (PRRSV) was also widely discussed. The major concern appears to be the large numbers of different strains that are proliferating around the world and the concern over the availability of suitable vaccines to control them. In a series of laboratory studies with live virus vaccines however, against a range of US isolates, lung lesions were reduced on average by 70%. In the US, there is a strong movement to try to eradicate the virus from the field but this is fraught with difficulties unless vaccines and diagnostics can be improved.
The main concern about swine influenza appears to be the potential link to human and avian influenza and the production of new pathogenic strains. Pigs have historically been considered to be susceptible to infection with both avian and human influenza viruses. Although persistent circulation of human lineage influenza viruses in swine populations would facilitate development of a pandemic virus in pigs through genetic reassortment, this phenomenon, fortunately is relatively rare. Regarding the avian influenza virus H5N1, this can infect pigs, if in close proximity to an avian source but there has been only a transient infection with limited virus replication and no transmission. There was a call for further surveillance and monitoring of influenza virus infection in pigs to address the potential establishment of novel avian influenza viruses as well as H5N1.
This excellent event was organised by the president, Prof Zygmunt Pejsak and his team from the National Veterinary Research Institute in Pulawy and was supported by the Jagiellonian University in Krakow, who provided the extensive conference facilities.
Pig Diseases & Medication: Pig Technical Reviews
