Objectives The aim of the study was to describe the ultrasonographic and endoscopic appearance and characteristics of the caecum in asymptomatic cats, and to correlate these findings with histology. Methods Ex vivo ultrasonographic and histologic evaluations of a fresh caecum were initially performed. Then, 20 asymptomatic cats, privately owned or originating from a reproductive colony, were recruited. All cats had an ultrasonographic examination of the ileocaecocolic junction, where the thickness of the caecal wall, ileocolic lymph nodes and the echogenicity of the local fat were assessed. They all underwent a colonoscopy with a macroscopic assessment of the mucosa and biopsies for histology. Results An ultrasonographic hypoechoic nodular inner layer, which corresponded to the coalescence of multiple lymphoid follicles originating from the submucosa and protruding in the mucosa on histology, was visible in all parts of the caecum. The combined mucosa and submucosa was measured ultrasonographically and defined as the follicular layer. Although all cats were asymptomatic, 3/19 cats showed mild caecal inflammation on histology. The most discriminatory ultrasonographic parameter in assessing this subclinical inflammation was the thickness of the follicular layer at the entrance of the caecum, with a cut-off value of 2.0 mm. All cats (20/20) showed some degree of macroscopic 'dimpling' of the caecal mucosa on endoscopy. Conclusions and relevance Lymphoid follicles in the caecal mucosa and submucosa constitute a unique follicular layer on ultrasound. In asymptomatic cats, a subtle, non-clinically relevant inflammation may exist and this is correlated with an increased thickness of the follicular layer on ultrasound. On endoscopy, a 'dimpled aspect' to the caecal mucosa is a normal finding in the asymptomatic cat.
Some strains of West Nile virus (WNV) are neuroinvasive and may induce fatal encephalitis/meningitis in a variety of animal species including humans. Whether, however, there is a strain-specific signature in the brain is as yet unknown. Here we investigated the neuropathogenesis induced by two phylogenetically distant WNV strains of lineage 1, WNVIS98 and WNVKUN35 911. While four-week old C57Bl/6J mice were susceptible to both strains and succumbed rapidly after intraperitoneal inoculation, differences were observed in virulence and clinical disease. WNVKUN35 911, the less virulent strain as judged by determination of LD50, induced typical signs of encephalitis. Such signs were not observed in WNVIS98-infected mice, although they died more rapidly. Histological examination of brain sections also revealed differences, as the level of apoptosis and inflammation was higher in WNVKUN35 911- than WNVIS98-infected mice. Moreover, staining for cleaved caspase 3 showed that the two WNV strains induced apoptotic death through different molecular mechanisms in one particular brain area. Finally, the two strains showed similar tropism in cortex, striatum, brainstem, and cerebellum but a different one in hippocampus. In summary, our data show that, upon peripheral administration, WNVIS98 and WNVKUN35 911 strains induce partially distinct lesions and tissue tropism in the brain. They suggest that the virulence of a WNV strain is not necessarily correlated with the severity of apoptotic and inflammatory lesions in the brain.
Schmallenberg virus infection is emerging in European domestic and wild ruminants. We investigated the serologic status of 9 red deer populations to describe virus spread from September 2010 through March 2012 among wildlife in France. Deer in 7 populations exhibited seropositivity, with an average seroprevalence of 20%.
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