Influenza A viruses occur worldwide in wild birds and are occasionally associated with outbreaks in commercial chickens and turkeys. However, avian influenza viruses have not been isolated from wild birds or poultry in South America. A recent outbreak in chickens of H7N3 low pathogenic avian influenza (LPAI) occurred in Chile. One month later, after a sudden increase in deaths, H7N3 highly pathogenic avian influenza (HPAI) virus was isolated. Sequence analysis of all eight genes of the LPAI virus and the HPAI viruses showed minor differences between the viruses except at the hemagglutinin (HA) cleavage site. The LPAI virus had a cleavage site similar to other low pathogenic H7 viruses, but the HPAI isolates had a 30 nucleotide insert. The insertion likely occurred by recombination between the HA and nucleoprotein genes of the LPAI virus, resulting in a virulence shift. Sequence comparison of all eight gene segments showed the Chilean viruses were also distinct from all other avian influenza viruses and represent a distinct South American clade.

Pandemic (H1N1) 2009 virus was detected in breeding turkeys on 2 farms in Valparaiso, Chile. Infection was associated with measurable declines in egg production and shell quality. Although the source of infection is not yet known, the outbreak was controlled, and the virus was eliminated from the birds.

Porcine reproductive and respiratory syndrome (PRRS) is endemic in most pork producing countries. In Chile, eradication of PRRS virus (PRRSV) was successfully achieved in 2009 as a result of the combined efforts of producers and the animal health authorities. In October 2013, after several years without detecting PRRSV under surveillance activities, suspected cases were confirmed on a commercial swine farm. Here, we describe the PRRS epidemic in Chile between October 2013 and April 2015, and we studied the origins and spread of PRRSV throughout the country using official surveillance data and Bayesian phylogenetic analysis. Our results indicate that the outbreaks were caused by a PRRSV closely related to viruses present in swine farms in North America, and different from the strain that circulated in the country before 2009. Using divergence time estimation analysis, we found that the 2013–2015 PRRSV may have been circulating in Chile for at least one month before the first detection. A single strain of PRRSV spread into a limited number of commercial and backyard swine farms. New infections in commercial systems have not been reported since October 2014, and eradication is underway by clearing the disease from the few commercial and backyard farms that remain positive. This is one of the few documented experiences of PRRSV introduction into a disease-free country.

No abstract

The objective of this study was to determine clinical features, shedding and transmission of a Chilean Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) strain upon experimental inoculation of 4-week-old pigs. Six groups of five animals each were used. The G1 (donor) group was inoculated with PRRSV, maintained in an isolation unit for 35 days, and sampled daily to determine shedding in mucosal secretions and faeces, viraemia and seroconversion. An uninfected control group (G6) was equally maintained and sampled under strict isolation. Four other groups (G2 to G5) were exposed to PRRSV via direct contact with G1 for 5-day periods in a staggered manner, throughout the 35-day period, and were later placed in an independent isolation unit to monitor infection status for 7 days. All the animals in G1 and G6 were killed at 35 days post-inoculation (dpi) and the contact groups at 12 days post-contact (dpc). Samples were obtained from diverse organs for histopathological, immunohistochemical (IHC) and virological analysis. No clinical symptoms were evident in any group, except for a transient fever observed in G1. Histopathologically, all the animals of G1 had interstitial pneumonia, although scarce PRRSV-positive cells were detected in the lung using IHC. PRRSV-positive cells (IHC) were detected in the lymphoid tissue of all animals in infected groups, but especially in G3 and G4. Viraemia was detected in G1 (3-35 dpi) and in the all contact groups (5-12 dpc). Likewise, ranging from 3 to 19 dpi, PRRSV was detected in at least one animal from the tonsils and lungs in all infected groups, in nasal and ocular secretions, saliva or faeces. These results indicate that the donor group excreted infectious PRRSV and was able to transmit the infection to susceptible pigs. The critical shedding period was 7-19 dpi, during which, most likely, transmission took place.