Isolation and characterization of a rare group A rotavirus G13P[18] strain from a diarrhoeic foal in Japan.

A rare genotype G13P[18] group A rotavirus (RVA/Horse-tc/JPN/MK9/2019/G13P[18]) was isolated from a diarrhoeic foal for the first time in 28 years. The genotype constellation of the virus was assigned to G13-P[18]-I6-R9-C9-M6-A6-N9-T12-E14-H11 and was the same as that of the first isolated strain, RVA/Horse-tc/GBR/L338/1991/G13P[18]. Phylogenetic analysis suggests that the virus is related to RVA/Horse-tc/GBR/L338/1991/G13P[18] and is distant from typical equine rotaviruses of the G3P[12] and G14P[12] genotypes.

Comparative endoscopic evaluation of normal and ulcerated gastric mucosae in Thoroughbred foals.

To contribute to early diagnosis and treatment of gastric ulcer of foals, we examined the gastric mucosa of healthy and affected foals using an endoscope. In healthy foals, the characteristic changes in the development of the squamous mucosa were seen mainly in the squamous mucosa, and maturation of the squamous mucosa in the greater curvature (GC-S) occurred more slowly than that of the squamous mucosa in the lesser curvature (LC-S). Epithelial desquamation in the LC-S and GC-S was observed between 6 and 90 days but was not observed in the LC-S at about 60 days, whereas it was observed in the GC-S until 90 days old. These findings suggest that there is a difference in the development of the gastric mucosa by region and that desquamation continues over a term longer than studies have reported in the past. In the affected foals, the minimum age at which gastric ulcer was observed was 4 days old. Gastric ulcers formed predominantly in the squamous mucosa (LC-S and GC-S) of foals with an immature mucosa before the weaning period, and the peak incidence occurred between 61 and 90 days old. The differences in the ulceration sites were considered to depend on the difference in the development (maturation) stage of the squamous mucosa. The grading score of the gastric ulcer increased with the growth of the affected foals. The gastric ulcer might be enhanced greatly by stress in the weaning period.

Antibody response in vaccinated pregnant mares to recent G3BP[12] and G14P[12] equine rotaviruses.

BACKGROUND: Both the G3P[12] and the G14P[12] type of equine group A rotavirus (RVA) have recently become predominant in many countries, including Japan. G3 types are classified further into G3A and G3B. The G3A viruses have been circulating in Europe, Australia, and Argentina, and the G3B viruses have been circulating in Japan. However, only an inactivated vaccine containing a single G3BP[12] strain is commercially available in Japan. To assess the efficacy of the current vaccine against recently circulating equine RVA strains, we examined antibody responses in pregnant mares to recent G3BP[12] and G14P[12] strains by virus neutralization test. FINDINGS: After vaccination in five pregnant mares, the geometric mean serum titers of virus-neutralizing antibody to recent G3BP[12] strains increased 5.3- to 7.0-fold and were similar to that against homologous vaccine strain. Moreover, antibody titers to recent G14P[12] strains were also increased 3.0- to 3.5-fold. CONCLUSIONS: These results suggest that inoculation of mares with the current vaccine should provide foals with virus-neutralizing antibodies against not only the G3BP[12] but also the G14P[12] RVA strain via the colostrum.

Molecular characterization and analysis of equine rotavirus circulating in Japan from 2003 to 2008.

Using a total of 2018 fecal samples collected between 2003 and 2008 from foals with diarrhea, the molecular epidemiology of group A equine rotaviruses circulating in Japan was investigated by the reverse transcription-polymerase chain reaction (RT-PCR) typing and sequence analysis of the VP4 (P type) and VP7 (G type) genes. A total of 1149 samples showed positive reactions with RT-PCR, of which 462 samples (40.2%) were positive for G3 type, 502 samples (43.7%) were positive for G14 type, and 185 samples (16.1%) were positive for both G3 and G14 types. To examine P types, 59 G3 and 56 G14 positive samples were used. The majority of the samples (96.5%) were characterized as P[12] type. In a phylogenetic analysis, the VP4 gene of the P[12] type in Japan was found to be conserved for a long time. The VP7 sequences of the G3 type were found to be clustered in the same group as the HO-5 strain, which is a G3 strain that was isolated in 1982 in Japan. In contrast, the VP7 sequences of the G14 type, which were in circulation between 2003 and 2008, were clustered differently from those of the G14 type strains isolated in Japan in the late 1990 s. These results suggest that the VP7 gene of the G3 type has been conserved over 25 years, while the VP7 gene of the G14 type circulating between 2003 and 2008 appears to have re-emerged in or invaded Japan around 2000.

Deficits in auditory P50 inhibition in obsessive-compulsive disorder.

Obsessive-compulsive disorder (OCD) is considered to involve abnormalities in inhibitory processes including gating systems. Auditory P50 inhibition, which is assessed by using a paired auditory stimulus paradigm to record P50 mid-latency evoked potential, is assumed to reflect sensory gating. In the present study, we investigated auditory P50 inhibition in subjects with OCD, and examined the relationship between P50 and clinical variables or neuropsychological performance. Twenty-six subjects with OCD and 26 age- and sex-matched healthy controls received P50 recording and neuropsychological tests. In the OCD subjects, we also evaluated clinical features including OC symptoms and subtypes of the disorder. P50 T/C ratios were significantly higher in OCD subjects than in control subjects (t=2.9, df=50, p=0.006). Compared to the controls, the OCD subjects performed significantly worse on the Symbol Digit Modalities Test (SDMT) and the Trail Making Test (TMT). There were no correlations between P50 T/C ratios and clinical variables or the results of neuropsychological tests. Our findings suggest that sensory gating deficits may be involved in the pathophysiology of OCD in a different way from clinical symptoms and executive attention dysfunction.