Abstract

Stunting syndrome (SS) is a viral enteric disease of turkey poults. The etiologic agent (stunting syndrome agent [SSA]) of this disease has been reported recently. The objective of this study was to develop a method for in vitro propagation of SSA. Primary cells, various continuous cell lines, and embryonated eggs were evaluated. Turkey embryos that were inoculated via the amniotic cavity at 24-25 days of incubation were susceptible to SSA infection. The jejunal maltase activity of SSA-inoculated turkey embryos was significantly (P < or = 0.001) lower than that of control embryos. D-xylose absorption was also altered in SSA-infected turkey embryos. The extent of reduction of D-xylose absorption and maltase activity in the infected embryos was nearly identical to that observed when day-old poults were infected with SSA. The intestines from the infected turkey embryos were pale, thin walled, and distended with fluid. Electron microscopic examination of the intestinal fluid and epithelial cell lysate of infected embryos revealed pleomorphic membraned SSA viral particles. SSA that had been serially passaged in turkey embryos retained its ability to induce SS in day-old poults. All the primary and continuous cells that were evaluated did not support the replication of SSA on the basis of cytopathic effects, electron microscopy, and turkey embryo inoculation. Inoculation of chicken embryos by various routes failed to support SSA. All routes of inoculation, other than the amniotic route at 24-25 days, failed to support SSA in turkey embryos. The results of the this study indicate that the SSA was successfully propagated in turkey embryos that exhibited alterations in embryo intestinal absorption and digestive enzyme activity similar to poults with SS. Successful propagation of SSA in turkey embryos should prove beneficial for future studies including characterization of SSA, prevention and control strategies, and enteric disease modeling.

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