SPI1 and infection: Although infection is usually sub-clinical, except in newly hatched chicks, the mechanisms of pathogenesis and host response to infection are broadly similar to those seen in mammalian models of gastroenteritis, with the induction of an inflammatory response largely mediated through the actions of the SPI1 T3SS and host recognition via TLR5 and TLR21 resulting in increased expression of CXC chemokines and an influx of polymorphonuclear cells into the intestine associated with architectural damage [13]–[17].