Objective—To assess the use of measuring anti-coronavirus IgG in CSF for the diagnosis of feline infectious peritonitis (FIP) involving the CNS in cats.
Sample Population—CSF and serum samples from 67 cats.
Procedures—CSF and serum samples were allocated into 4 groups: cats with FIP involving the CNS (n = 10), cats with FIP not involving the CNS (13), cats with CNS disorders caused by diseases other than FIP (29), and cats with diseases other than FIP and not involving the CNS (15). Cerebrospinal fluid was evaluated for concentrations of erythrocytes, leukocytes, and total protein. Anti-coronavirus IgG was measured in CSF and serum by indirect immunofluorescence assay.
Results—CSF IgG (range of titers, 1:32 to 1:4,096) was detected in 12 cats, including 6 cats with neurologic manifestation of FIP, 4 cats with FIP not involving the CNS, and 2 cats with brain tumors. Cerebrospinal fluid IgG was detected only in cats with correspondingly high serum IgG titers (range, 1:4,096 to 1:16,384) and was positively correlated with serum IgG titers (r = 0.652; P < 0.01), but not with any other CSF parameter. Blood contamination of CSF resulted in ≤ 333 erythrocytes/μL in cats with CSF IgG.
Conclusions and Clinical Relevance—The correlation between serum and CSF IgG and the fact that CSF IgG was detected only in strongly seropositive cats suggested that CSF anti-coronavirus IgG was derived from blood. Measurement of anti-coronavirus IgG in CSF was of equivocal clinical use.
Objective—To evaluate the effects of recombinant human interferon α-2b (rHuIFN-α2b) and recombinant feline interferon ω (rFeIFN-ω) on in vitro replication of feline herpesvirus (FHV)-1.
Sample Population—Cultures of Crandell-Rees feline kidney (CRFK) cells.
Procedures—CRFK cells were treated with rFeIFN-ω or rHuIFN-α2b at concentrations ranging from 100 to 500,000 U/mL. Cultures were then inoculated with FHV-1. Constant concentrations of interferon products were maintained throughout the study. Reductions in the number and size of plaques were used as indicators of antiviral activity. Six plaque reduction assays were performed in duplicate. A 3-(4, 5-dimethylthiazolyl-2)-2, 5-diphenyltetrazolium bromide assay was used to detect cytotoxic effects of interferon. A 1-way ANOVA and Dunnett test were used to determine significant differences.
Results—Treatment with rFeIFN-ω at various concentrations resulted in significant reductions in the number of plaques (100,000 U/mL, 54.7%; and 500,000 U/mL, 59.8%) and in plaque size (100,000 U/mL, 47.5%; 250,000 U/mL, 81.0%; and 500,000 U/mL; 70.5%). Treatment with various concentrations of rHuIFN-α2b resulted in a significant reduction in plaque size (100,000 U/mL, 56.0%; 250,000 U/mL, 75.7%; and 500,000 U/mL, 69.0%). None of the tested concentrations of interferon caused significant cellular toxicosis.
Conclusions and Clinical Relevance—At some of the higher concentrations, the antiviral effect of rFeIFN-ω was greater than the antiviral effect of rHuIFN-α2b. Reduction in plaque size appeared to be a good indicator of the antiviral activity of interferon against FHV-1.