Limitations of using feline coronavirus spike protein gene mutations to diagnose feline infectious peritonitis

Barker, Emily N.; Stranieri, Angelica; Helps, Chris R.; Porter, Emily L.; Davidson, Andrew D.; Day, Michael J.; Knowles, Toby; Kipar, Anja; Tasker, Séverine

Detection of FCoV by RT-qPCR in colonic tissue of 3 cats without FIP was not surprising as enteric infection has been described in otherwise clinically healthy cats [7, 8, 32] . These 3 cats were euthanized as a result of clinical signs relating to pyothorax, brain tumour and nasal adenocarcinoma, had unremarkable histopathological examination and negative IHC of colonic tissue. In the 2 of the 3 cats where faeces were available for testing there was no detectable viral shedding. In 1 cat the FCoV was non-mutated, another cat had mutated FCoV, and in the remaining cat mixed non-mutated and mutated FCoV was detected. Of note, the cat with pyothorax also had non-mutated virus detected at a low level in its brain, and mutated virus detected at low level in its liver, suggesting that it was viraemic at the time of death and that the virus persisted not only in the colon but also in extraintestinal tissue macrophages [7] . If colonic tissue samples are excluded, all but one tissue sample from the non-FIP cats that were FCoV RT-qPCR-positive for which sequence data were available (n = 13) had mutated FCoV, confirming our previous findings that S gene mutations are a marker of systemic spread [20] .