Procedures to eliminate H3N2 swine influenza virus from a pig herd.

A three-site pig herd infected with a H3N2 swine influenza virus (SIV) underwent a herd SIV elimination programme using herd closure and partial depopulation. The herd consisted of sow, nursery and finishing units, 1 to 2 km apart. Disease was noted in the sow unit and then the nursery unit. The herd temporarily stopped introduction of replacement animals, and replacement gilt introductions in the breeding herd was changed from monthly to quarterly. Gilts from a serologically negative source were also introduced and monitored. Virus elimination from growing pigs was attempted by totally depopulating the nursery and finishing sites once there was evidence that shedding in site 1 had stopped. Sentinel gilts remained serologically negative by haemagglutination inhibition (HI) test (0 of 69 animals negative) for at least 20 months after the initial disease. After restoring the pig flow in site 2, pigs did not experience flu-like clinical signs and HI serology results remained negative (0 of 30 animals tested) for the six months following repopulation of sites 2 and 3. In addition, nursery mortality was improved by 2.2 per cent, the growth rate was improved by 0.123 kg/day and feed efficiency was improved 0.26 points. Based on these results, SIV elimination was considered successful.

Molecular characterization of the hemagglutinin-neuraminidase gene of porcine rubulavirus isolates associated with neurological disorders in fattening and adult pigs.

"Blue eye disease" is a viral infection of swine endemic in Mexico, which produces fatal encephalitis accompanied by respiratory signs and corneal opacity in suckling piglets. An atypical blue eye disease outbreak presented high rates of neurological signs in fattening and adult pigs from 2000 to 2003. In order to identify the basis of increased neurovirulence, the hemagglutinin-neuraminidase (HN) gene of several porcine rubulavirus isolates were sequenced and compared with that of La Piedad Michoacan virus and other isolates that did not produce neurological disorders in weaned pigs. Nine amino acid mutations distinguished the high neurovirulent PAC6-PAC9 viruses, whereas five mutations characterized the low neurovirulent PAC2 and PAC3 viruses. HN protein three-dimensional models showed that the main conformation and functional domains were preserved, although substitutions A223T and A291D occurred in PAC2 and PAC3 viruses, as well as A511K and E514K presented in PAC6-PAC9 viruses considerably modified the properties of the HN protein surface. The increased positive charge of the HN protein of PAC6-PAC9 viruses seems to be associated with their increased neurovirulence.