In February 2000, a low pathogenic H6N2 virus was detected for the first time in commercial egg layers in southern California, an area with a population of approximately 15 million chickens. At that time fewer than 10 farms were found to be infected with this low-pathogenic virus in an area with about 60 large farms ranging in size from about 30,000 to 1.2 million birds. The infection was asymptomatic—egg production and mortality were not affected—thus little was done to eradicate the virus. The state performed some vaccination of layer farms, but because it was not accompanied by depopulation or stamping-out, the measure proved futile.
Over the next 2 years, the virus persisted on some farms where it found a continual stream of naïve hosts. Sporadic infections occurred in additional farms in the area, bringing the total number of affected (H6N2 antibody positive) farms to 15. Three different genotypes of H6N2 virus were found to be circulating; in January 2002, one form emerged to cause clinical disease in San Diego County, where an infected flock suffered a 50 percent decrease in egg production and a 10-fold increase in mortality. The farmer had his birds tested, but during a 2-week period before the diagnosis was made, chicken manure was removed from the farm, young hens were brought in, and eggs continued to be taken to be processed. The virus immediately spread to approximately 10 farms and the outbreak continued to expand over the next 2 months.
A major expansion of the outbreak subsequently occurred in Turlock, a town in northern California where layer hens from several states were slaughtered and processed. Infected layer hens from southern California were sent to the Turlock plant, into the heart of a densely populated poultry region. Shortly thereafter, three egg-laying flocks in the Turlock region were found to be positive for avian influenza detected through passive surveillance; a drop in egg production prompted the producers to have the birds tested.
One week later a broiler flock was found to be positive for avian influenza at slaughter. Once the virus got into broilers, it spread very rapidly among turkeys and layers as well. This acceleration resulted from the unfortunate coincidence
reduce human exposure as well (ProMED-mail, 2004r; Sibartie, 2004). However, as several conference participants stressed, vaccination must be accompanied by strong surveillance to prevent the spread of asymptomatic infection among vaccinated birds. This can be accomplished either through the use of unvaccinated sentinel birds or of recombinant vaccines that elicit a distinct “marker” antibody (ProMED-mail, 2004s). Should a “silent epidemic” of influenza manage to erupt under these conditions, it could serve as an incubator for the evolution of a more deadly viral strain. This apparently occurred in Mexico after chickens were vaccinated against highly pathogenic H5N2 influenza in 1995; today, antigenically distinct variants of the vaccine strain are spreading among the country’s poultry flocks (Lee et al., 2004).