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Cats with feline infectious peritonitis (FIP) are usually lymphopenic and have lymphoid depletion evident in spleen and lymph nodes. In particular, the number of CD4+ lymphocytes in tissues decreases during the evolution of FIP lesions. This decrease is most likely due to increased lymphocyte apoptotic rate. In contrast, cats infected with the Feline Coronavirus (FCoV) develop a follicular hyperplasia in the peripheral lymph nodes. The current study was devised to evaluate the possible pathogenic role of shifts in circulating lymphocyte subsets in FIP. Peripheral blood from cats with FIP was evaluated and compared with peripheral blood from clinically healthy cats living in both FCoV-free and FCoV-endemic catteries. Blood from cats with diseases other than FIP was also examined in order to define the diagnostic relevance of the changes. Lymphocyte subsets were analysed by flow cytometry, using a whole blood indirect immunofluorescence technique and mAbs specific for feline CD5, CD4, CD8, CD21. The results of the current study suggest that cats recently infected with FCoV that do not develop the disease have a transient increase in T cells; cats from groups with high prevalence of FIP have a moderate but persistent decrease in T cell subsets; cats with FIP have a very severe decrease in all the subsets of lymphocytes. Moreover, during FIP many lymphocytes do not express any membrane antigen, most likely due to early apoptosis. Cats with diseases other than FIP also had decreased number of lymphocytes: as a consequence, the diagnostic relevance of these findings is very low. Nevertheless, the lack of flow cytometric changes had a high negative predictive value (NPV), thus allowing to exclude FIP from the list of possible diagnoses in cats with normal cytograms.

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Mice, rats, guineapigs and rabbits that were apparently healthy and did not present skin lesions were examined for the presence of dermatophytes. A small proportion of them were found to be carriers of Trichophyton mentagrophytes, Trichophyton rubrum, Microsporum canis (8/140 = 5·7% of mice; 2/185 = 1·1% of rats; 1/70 = 1·4% of guineapigs; 1/215 = 0·5% of rabbits).

"Transmissible Spongiform Encephalopathies" (TSE) are a group of degenerative progressive fatal disorders of the CNS, affecting both humans and animals. The main pathogenic event is the conversion of cellular prion protein from the normal, enzyme-sensitive (PrPsen), to the insoluble proteinase K-resistant isoform (PrPres). Since the new juvenile variant of Creutzfeldt-Jakob disease (vCJD) is probably due to the transmission of Bovine Spongiform Encephalopathy (BSE) prion protein to man, therapeutic and preventive compounds for animals and humans are urgently needed. Congo Red (benzidine-diazo-bis-1-naphthylamine-4-sulfonic acid sodium salt, CAS 573-58-0, CR), an azoic dye that inhibits amyloid deposition, and some newly synthesized derivatives, more lipophilic and less toxic, were tested for their anti-prionic activity, in different experimental models. Cell-free experiments using the synthetic peptide PrP 106-126, homologous to amino acid residues 106-126 of the human PrP, were run to determine the anti-amyloidogenic properties of some of the molecules. Peptide solutions containing each compound were incubated at 37 degrees C, for increasing times, to analyse the kinetics of aggregation of PrP 106-126 peptide. After incubation, the amount of non-aggregated peptide was measured by RP-HPLC. While CR enhanced the amyloidogenicity of PrP 106-126, derivatives "1a" and "1b" both showed the opposite behaviour, reducing aggregation by 15-20%. In other experiments using electron microscopy PrP 106-126 was assayed with the same molecules to assess the number and size of fibrils formed. CR showed its typical interaction, producing amyloid aggregates, "1a" did not interfere with fibril formation, while "1b" seemed to partially affect the structure of PrP 106-126 fibrils. Using a different cell-free model, it was investigated whether CR derivatives could reverse the protease-resistant PrPres, extracted from Syrian hamster infected brain, into the normal protease sensitive PrPsen. Samples containing fixed amounts of PrPres were incubated at 37 degrees C for 1 h with all the newly synthesized molecules, at concentrations ranging from 50 micrograms/mL to 750 micrograms/mL. After treatment with proteinase K, half of each sample was incubated with 3 mol/L guanidine thiocyanate in order to exclude over-stabilisation of the PrPres aggregates already observed with CR. The remaining amount of PrPres was assessed by Enhanced Chemoluminescence (ECL) Western blotting analysis. None of the compounds induced the reversion of PrPres to PrPsen; nevertheless, 6 of the 8 molecules interacted with PrPres molecules, over-stabilising the PrPres aggregates, from this aspect being similar to CR in activity. Finally, the inhibition of the generation of PrPres in the S12 clone of a mouse neuroblastoma cell line (N2a S12), persistently infected by the mouse adapted Chandler strain of scrapple, was evaluated. Increasing amounts of CR, "1a" and "1b" were added to the culture medium at each cell passage. After various days of treatment, the cells were c...