An H1N2 influenza A virus was isolated from a pig in the United States for the first time in 1999 (A. I. Karasin, G. A. Anderson, and C. W. Olsen, J. Clin. Microbiol. 38:2453-2456, 2000). H1N2 viruses have been isolated subsequently from pigs in many states. Phylogenetic analyses of eight such viruses isolated from pigs in Indiana, Illinois, Minnesota, Ohio, Iowa, and North Carolina during 2000 to 2001 showed that these viruses are all of the same reassortant genotype as that of the initial H1N2 isolate from 1999

Propagated (free-field) ultrasonic energy at a frequency of 26 kHz was used to expose aqueous suspensions of bacteria (Escherichia coli, Staphylococcus aureus, BaciUus subtilis, and Pseudomonas aeruginosa), fungus (Trichophyton mentagrophytes), and viruses (feline herpesvirus type 1 and feline calicivirus) to evaluate the germicidal efficacy of ultrasound. There was a significant effect of time for all four bacteria, with percent killed increasing with increased duration of exposure, and a significant effect of intensity for all bacteria except E. coli, with percent killed increasing with increased intensity level. There was a significant reduction in fungal growth compared with that in the controls, with decreased growth with increased ultrasound intensity. There was a significant reduction for feline herpesvirus with intensity, but there was no apparent effect of ultrasound on feline calicivirus. These results suggest that ultrasound in the low-kilohertz frequency range is capable to some degree of inactivating certain disease agents that may reside in water. The physical mechanism of inactivation appears to be transient cavitation.

Pseudorabies is caused by Suid herpesvirus 1, a member of the Alphaherpesvirinae subfamily. Although pigs are the natural host of Pseudorabies virus (PRV), the virus has a broad host range and may cause fatal encephalitis in many species. The United States obtained PRV-free status in 2004 after the virus was eradicated from domestic swineherds, but the virus is still present in feral swine populations. The current report describes PRV infection in 3 dogs that were used to hunt feral swine. The dogs developed clinical signs including facial pruritus with facial abrasions, dyspnea, vomiting, diarrhea, ataxia, muscle stiffness, and death. Two were euthanized, and 1 died within approximately 48 hr after onset of clinical signs. The salient histologic changes consisted of neutrophilic trigeminal ganglioneuritis with neuronophagia and equivocal intranuclear inclusion bodies. Pseudorabies virus was isolated from fresh tissues from 2 of the dogs, and immunohistochemistry detected the virus in the third dog. Virus sequencing and phylogeny, based upon available GenBank sequences, revealed that the virus was likely a field strain that was closely related to a cluster of PRV strains previously identified in Illinois. Though eradicated from domestic swine in the United States, PRV is present in populations of feral swine, and should therefore continue to be considered a possible cause of disease in dogs and other domestic animals with compatible clinical history and signs. Continued surveillance is necessary to prevent reintroduction of PRV into domestic swine.