RESULTS: Differences in disease outcome provided an opportunity to investigate the role of T cell immunity to FIP determined by T cell subset proliferation after stimulation with different viral antigens. Reduced total white blood cell (WBC), lymphocyte and T cell counts in blood were observed during primary acute infection for all experimental groups including cats that survived without clinical FIP. Antiviral T cell responses during early primary infection were also similar between cats that developed FIP and cats remaining healthy. Recovery of antiviral T cell responses during the later phase of acute infection was observed in a subset of cats that survived longer or resisted disease compared to cats showing rapid disease progression. More robust T cell responses at terminal time points were observed in lymph nodes compared to blood in cats that developed FIP. Cats that survived primary infection were challenged a second time to pathogenic FIPV and tested for antiviral T cell responses over a four week period. Nine of ten rechallenged cats did not develop FIP or T cell depletion and all cats demonstrated antiviral T cell responses at multiple time points after rechallenge.
CONCLUSIONS: In summary, definitive adaptive T cell responses predictive of disease outcome were not detected during the early phase of primary FIPV infection. However emergence of antiviral T cell responses after a second exposure to FIPV, implicated cellular immunity in the control of FIPV infection and disease progression. Virus host interactions during very early stages of FIPV infection warrant further investigation to elucidate host resistance to FIP.
METHODS: A case-control study was carried out among patients with CSOM (cases) and controls were those with no ear pathology. The presence of CSOM was made through a medical history and otoscopic examination. Allergen testing was done by the skin prick test.
RESULTS: In all 124 subjects were recruited in this study with equal number of the cases and controls. The commonest positive reaction in the skin prick test in both groups was to house dust mites. Among CSOM cases, half (50%) of them had an allergy to Blomia tropicalis and 48.4% to Dermatophagoides while in the control group, 27.4% to Dermatophagoides and 25.8% to B. tropicalis. There were significant associations between CSOM and allergy to B. tropicalis (p=0.005), Dermatophagoides (p=0.016) and Felis domesticus (p=0.040). The prevalence of allergy at 95% confidence interval (95%CI) in CSOM and control groups were demonstrated as 59.7% (95%CI: 47.5, 71.9) and 30.6 % (95%CI: 19.1, 42.1) respectively. There was a significant association between allergy and CSOM (p=0.001).
CONCLUSION: Indoor allergens are the most prevalent in our environment and therefore good control may difficult to achieve. The hypersensitivity states of the subject are likely to have a role in the pathogenesis of CSOM especially in the tropical countries where allergy occurs perennially.
RESULTS: The prevalence rates of H. pylori infection in animals were 22.2% and 16% in antibody and stool antigen tests, respectively. The detection rates were 28%, 24%, 12%, 10%, and 4.7% in cats, dogs, buffaloes, sheep, and cattle, respectively. On the other hand, the prevalence rate of H. pylori infection in human stool samples was 74.8%, and a statistically significant association was observed between prevalence and several factors, such as sex, age, and locality. PCR was performed to detect the glmM gene of H. pylori, and this gene was found in 21 of 27 human antigen-positive samples and 5 of 13 animal milk samples.
CONCLUSIONS: H. pylori was detected in both human and animal samples. Furthermore, glmM was found in milk and human samples. Our findings suggest that pet and farm animals could transmit H. pylori infection to humans.