Evaluation of immunity to feline infectious peritonitis in cats with cutaneous viral-induced delayed hypersensitivity()

Delayed-type hypersensitivity (DTH)-like reactions to feline infectious peritonitis (FIP) virus (FIPV) were induced in the skin of nine cats that were asymptomatic after a previous challenge-exposure with FIPV. Four of the nine previously challenge-exposed cats were negative for virus-neutralizing antibodies against FIPV at the time of intradermal (ID) testing for DTH. Two other cats tested for DTH when acutely ill with clinical FIP did not have cutaneous DTH responses to FIPV. Gross skin reactions to FIPV injected ID were observed in six of nine asymptomatic cats (67%) at postintradermal inoculation hours (PIH) 24, 48, and/or 72. The reactions consisted of focal, 1–5-mm to 2.5-cm diameter indurated or semi-firm, nonerythematous, slightly raised nodules. Microscopically, DTH-like reactions were observed in biopsies taken from the FIPV-inoculated skin of asymptomatic cats at PIH 24 to 72. The lesions consisted of perivascular and diffuse dermal infiltrations by macrophages, lymphocytes, and polymorphonuclear leukocytes (PMN). The dermal infiltrates, which were maximal at PIH 48 or 72, were predominantly mixed inflammatory cells (five of nine cats) or PMN (four of nine cats) at PIH 24, but later were predominantly mononuclear cells (six of nine cats) or mixed inflammatory cells (two of nine cats) at PIH 72. Five of nine cats (56%) with positive DTH skin responses had increased survival times after lethal ID challenge-exposure with FIPV compared to mean survival times in FIPV-naive, non-immune control cats that were DTH-negative when ID challenge-exposed. Four of nine DTH-positive cats (44%) resisted an ID challenge-exposure dose of FIPV that was fatal in both control cats, and two of the four remaining DTH-positive cats survived a third challenge-exposure with highly lethal doses of FIPV given intraperitoneally. Four of the six DTH-positive cats (67%) that died after re-challenge and were necropsied had lesions of noneffusive FIP, suggesting that cellular immunity may also be involved in the pathogenesis of noneffusive disease, whereas both control cats and both DTH-negative cats with clinical disease succumbed to effusive FIP. Seemingly, DTH responses to FIPV can be associated with an increased level of resistance to disease; however, this state of immunity is variable and apparently can be lost with time in some cats.