Submitted to: Avian Pathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/8/2013
Publication Date: 1/27/2014
Publication URL: http://handle.nal.usda.gov/10113/60107
Citation: Franca, M., Howerth, E.W., Carter, D., Byas, A., Poulson, R., Afonso, C.L., Stallknecht, E. 2014. Co-infection of mallards with low virulence Newcastle disease virus and low pathogenic avian influenza virus. Avian Pathology. 43(1):96-104. Interpretive Summary: Newcastle disease and Avian Influenza viruses circulate worldwide in chickens and in wild birds. The virulent forms of both viruses cause significant disease in poultry and the attenuated form of those viruses are very commonly isolated in wild birds. Attenuated forms are a cause of concern for poultry producers because they can become virulent. The introduction of attenuated Newcastle Disease or Avian Influenza viruses into poultry occurs frequently, however the role of Mallards in the ecology and transmission of the viruses, or the effect of the interaction among these viruses in Mallards is poorly understood. Here under highly controlled conditions we have studied the replication and interaction of those viruses in Mallards and demonstrated that infection with Avian Influenza may affect the capacity of Newcastle disease virus to replicate in the intestinal tract.
Technical Abstract: Waterfowl are considered the natural reservoirs of low pathogenic avian influenza viruses (LPAIV) and low virulence Newcastle disease viruses (loNDV). The objective of this study was to investigate the effect of co-infections with loNDV and LPAIV on the infectivity and excretion of these viruses in Mallards. One-month old Mallards were intranasally inoculated with 106 median embryo infectious doses (EID50) of a wild bird-origin loNDV and A/Mallard/MN/199106/99 (H3N8) LPAIV on the same day or received the LPAIV 2 or 5 days after loNDV inoculation. Co-inoculation with LPAIV and loNDV did not affect the ability of Mallards to be infected with either virus. However, co-infection caused more productive LPAIV cloacal (CL) shedding in some groups and markedly reduced or ceased loNDV CL shedding. Less productive oropharyngeal (OP) LPAIV and loNDV shedding was detected in Mallards co-infected with both viruses on the same day. Co-infection did not affect LPAIV replication in epithelial cells of the lower intestine and bursa of Fabricius. The results of this study suggest that LPAIV may reduce or inhibit loNDV replication in the intestinal tract of co-infected Mallards. Competition for replication sites may have affected loNDV CL shedding in all co-infection groups as well as OP shedding of LPAIV and loNDV when both viruses were inoculated on the same day.