A case of fetal hyperthyroidism treated with maternal administration of methimazole.

Prenatal ultrasonography of a pregnant woman with a past history of total thyroidectomy for Graves' disease detected fetal tachycardia, fetal growth restriction and oligohydramnios at 30 weeks gestation. Because a high titer of thyroid-stimulating hormone receptor antibody was noted in maternal serum and the fetal goiter was detected on ultrasonography, fetal hyperthyroidism was strongly suspected and subsequently confirmed with cordocentesis at 31 weeks gestation. After treatment of fetal hyperthyroidism through oral maternal administration of methimazole (MMI) starting at 33 weeks gestation, fetal heart rate and amniotic fluid volume returned to normal ranges. Complete resolution of the fetal goiter was observed at 35 weeks gestation. A male infant was born at 35 weeks 6 days gestation via cesarean section in the absence of thyrotoxic findings; however, cord blood chemical analysis at birth indicated iatrogenic fetal hypothyroidism. In the present report, maternal therapy using MMI to resolve symptoms of fetal thyrotoxicosis, including fetal tachycardia and oligohydramnios, was successfully conducted.

FcγRIIB-nt645+25A/G gene polymorphism and periodontitis in Japanese women with preeclampsia.

FcγRIIB contains a unique immunoreceptor tyrosine-based inhibition motif (ITIM) and functions as a negative feedback regulator of leucocyte activation and antibody production. We have previously reported FcγRIIB-nt645+25A/G gene polymorphism to be associated with prevalence and severity of periodontitis, FcγRIIB expression level on peripheral B lymphocytes and the serum IgG level against periodontopathic bacteria. Previous studies have reported maternal periodontal disease to be associated with an increased risk for preeclampsia. Therefore, FcγRIIB-nt645+25A/G gene polymorphism may be associated with preeclampsia by affecting immune response to periodontopathic bacteria in pregnant women. To elucidate whether FcγRIIB-nt645+25A/G gene polymorphism has associations with preeclampsia and/or periodontitis in pregnant Japanese women, a case-control study was carried out on women with preeclampsia (n = 13) and without preeclampsia (n = 106). Maternal periodontal parameters and bacterial data of Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis and Prevotella intermedia in subgingival plaque were collected within 5 days of delivery. FcγR genotypes of each woman were determined using the genomic DNA isolated from peripheral blood. Serum IgG levels specific for each bacteria were determined. There was a significant association between FcγRIIB-nt645+25A/G polymorphism and preeclampsia (P = 0.013). The frequency of the FcγRIIB-nt645+25AA genotype was higher in the preeclampsia group compared with the nonpreeclampsia group (P = 0.007). The DNA level of A. actinomycetemcomitans from subgingival plaque was shown to be higher in the preeclampsia group (P = 0.017). In conclusion, maternal FcγRIIB-nt645+25A/G polymorphism and subgingival DNA level of A. actinomycetemcomitans were significantly associated with the prevalence of preeclampsia in a limited number of Japanese women independently with periodontal infection. Further investigations should be performed to confirm this association in a larger population and to determine the biological process of the association.

FcγRIIB polymorphisms, periodontitis and preterm birth in Japanese pregnant women.

BACKGROUND AND OBJECTIVE: Recently, numerous studies have investigated the association of preterm birth with periodontitis. FcγRIIb is a human low-affinity receptor for immunoglobulin G (IgG). We have previously demonstrated single nucleotide polymorphisms (SNPs) of FcγRIIb to be associated with periodontitis and the serum-specific IgG level against periodontopathic bacteria. In this study, we investigated whether FcγRIIB gene polymorphisms were associated with periodontitis and/or pregnancy outcome. MATERIAL AND METHODS: We assessed the periodontal conditions of 122 Japanese pregnant women within 5 d of delivery, and polymorphisms in FcγRIIB and in other Fcγ receptors were detected from the genomic DNA. Using clinical and genomic data, we analyzed the relationship between periodontitis, preterm birth and Fcγ receptor polymorphisms. RESULTS: A significant difference was observed in the distribution of FcγRIIB-nt645+25A/G (rs2125685) between preterm and term birth groups, with a higher prevalence of nt645+25AA in the preterm birth group (p = 0.032). Additionally, the FcγRIIB-nt645+25GG carrier showed significantly higher results for the prevalence of periodontitis (p = 0.048), mean pocket depth (p = 0.021), mean clinical attachment level (p = 0.010), percentage of sites with pocket depth ≥ 4 mm (p = 0.005) and percentage of sites with clinical attachment level ≥ 3 mm (p = 0.007) than the AA carrier. An association between preterm birth and periodontitis was not observed in this study. CONCLUSION: These findings suggest that FcγRIIB-nt645+25AA carriers are more likely to experience preterm birth than FcγRIIB-nt645+25AG and GG carriers. Also, women with FcγRIIB-nt645+25G exhibited a greater tendency to have periodontitis than those with nt645+25A.

Replication of hog cholera virus in porcine alveolar macrophage cultures.

Eight hog cholera viral strains were tested for virulence for pigs and ability to replicate in porcine alveolar macrophage cultures. Of them, five were virulent and replicated well in the macrophage culture. The other three were avirulent and grew less remarkably in this culture than them. It was suggested that the ability of the hog cholera viral strains to replicate in porcine macrophages might be correlated with their virulence.

Swine vesicular disease viruses isolated from healthy pigs in non-epizootic period. I. Isolation and identification.

A total of 524 fecal samples were collected from healthy swine of 36 hog farms scattered all over Japan from which had been detected neutralizing antibody against swine vesicular disease (SVD) virus. A virus was isolated from 21 of them. It was neutralized by antiserum against SVD virus. Of the 21 samples, 19 were derived from six farms, in areas which remained to be free from SVD in the past years and two from a farm where SVD broke out 18 months before. The cross-neutralization test was carried out with seven strains of SVD virus isolated from healthy pigs (SVDV-H) and five strains of SVD virus isolated from diseased pigs (SVDV-D). There was, however, no significant difference in antigenicity between the two groups. Some strains of SVDV-H were antigenically close to the Faulkner strain of Coxsackie B5 virus, and others to the freshly isolated strain of this virus. Neutralizing antibody of low titer against SVD virus was detected from pigs kept in areas free from SVD. It was presumed to have been produced in these pigs involved in silent infection with this virus.

Swine vesicular disease viruses isolated from healthy pigs in non-epizootic period. II. Vesicular formation and virus multiplication in experimentally inoculated pigs.

An infection experiment was carried out on pigs with swine vesicular disease virus isolated from healthy pigs (SVDV-H). Inoculation was done by two routes, intradermal in the coronary band of the foot and oral. Observation was made on the formation of vesicles and their spread, the virus contents of serum, swab of the oral cavity, and feces, the vicissitude of neutralizing antibody titers, and the distribution of virus in the body. From its results the pathogenicity of virus was judged. In the pigs inoculated intradermally there was a difference in the extension of the area involved in vesicular formation between any two strains of virus. That is, vesicular formation was restricted to the site of inoculation, involved the site of inoculation and the sole of the hoof, or spread over the oral and nasal regions. In every pig, however, vesicles developed only for 2 approximately 5 days after inoculation. After that, repair progressed rapidly. Some strains caused viremia, which was mild. The virus was detected from the site of vesicular formation, but not from any organ. Neutralizing antibody began to be detected 3 days after inoculation. Its titer reached a plateau about 10 days later. In the pigs inoculated perorally, no vesicles were formed. The virus was only detected from the tonsils and the intestinal contents. These findings made it clear that SVDV-H was less pathogenic than swine vesicular disease virus isolated from diseased pigs.

Outbreaks of swine vesicular disease in japan: virus isolation and epizootiological survey.

Outbreaks of a vesicular disease occurred among pigs in Kanagawa and Ibaraki Prefectures in Japan in November, 1973. Another outbreak was observed in Aichi Prefecture in December. The clinical signs of the disease observed included fever and vesicular lesions on the coronary bands, bulbs of the heel and in the interdigital spaces. In some pigs, vesicular lesions were observed on the snout, tongue and skin overlying the legs and abdomen. All the vesicular samples produced cytopathic changes on cultures of primary swine kidney cells of PK-15 cells. Three isolates of cytopathic agents tested were identified as swine vesicular disease virus from their physicochemical properties and antigenicity. The virus strains isolated from vesicular epithelial samples obtained from Ibaraki, Kanagawa and Aichi Prefectures were designated as Japan/Ibaraki/1/73, Japan/Kanagawa/1/73 and Japan/Aichi/1/73 strain, respectively. An outbreak of the disease among pigs due to swine vesicular disease virus was confirmed by the serum neutralization test with serum samples collected from pigs on affected farms. Approximately 80% of the pigs housed in affected shed showed high levels of neutralizing antibody titers. This is the first to report an occurrence of swine vesicular disease among pigs in Japan.