Molecular typing of Salmonella typhi strains from Dhaka (Bangladesh) and development of DNA probes identifying plasmid-encoded multidrug-resistant isolates

Seventy-eight Salmonella typhi strains isolated in 1994 and 1995 from patients living in Dhaka, Bangladesh, were subjected to phage typing, ribotyping, IS200 fingerprinting, and PCR fingerprinting. The collection displayed a high degree of genetic homogeneity, because restricted numbers of phage types and DNA fingerprints were observed. A significant number of the S. typhi strains (67%) were demonstrated to be multiple drug resistant (MDR). The vast majority of the MDR strains were resistant to chloramphenicol, ampicillin, trimethoprim, streptomycin, sulfamethoxazole, and tetracycline (R type CATmSSuT), a resistance phenotype that has also frequently been observed in India. Only two strains displayed a distinct MDR phenotype, R type AT-mSSuT. Pulsed-field gel electrophoresis demonstrated the presence of large plasmids exclusively in the MDR strains of both R types. The plasmids present in the S. typhi strains of R type CATmSSuT could be conjugated to Escherichia coli and resulted in the complete transfer of the MDR phenotype. PCR fingerprinting allowed discrimination of MDR and susceptible strains. The DNA fragments enabling discrimination of MDR and susceptible S. typhi strains by PCR were useful genetic markers for identifying MDR encoded by large plasmids of the H1 incompatibility group

Bone mineral density assessed by phalangeal radiographic absorptiometry before and during long-term growth hormone treatment in girls with Turner's syndrome participating in a randomized dose-response study

To assess bone mineral density (BMD) in girls with Turner's syndrome before and during long-term treatment with GH, longitudinal measurements using phalangeal radiographic absorptiometry were performed in 68 girls with Turner's syndrome. These previously untreated girls, age 2-11 y, participating in a randomized, dose-response trial, were randomly assigned to one of three GH dosage groups: group A, 4 IU/m(2)/d ( approximately 0.045 mg/kg/d); group B, first year 4 IU/m(2)/d, thereafter 6 IU/m(2)/d ( approximately 0.0675 mg/kg/d); or group C, first year 4 IU/m(2)/d, second year 6 IU/m(2)/d, thereafter 8 IU/m(2)/d ( approximately 0.090 mg/kg/d). In the first 4 y of GH treatment, no estrogens for pubertal induction were prescribed to the girls. Thereafter, girls started with 17beta-estradiol (5 microg/kg body weight/d, orally) when they had reached the age of 12 y. BMD results were adjusted for bone age and sex, and expressed as SD scores using reference values of healthy Dutch girls. At baseline, almost every individual BMD value of bone consisting predominantly of cortical bone, as well as that of bone consisting predominantly of trabecular bone, was within the normal range of healthy girls and the SD scores were not significantly different from zero [mean (SE) 0.38 (0.22) and -0.04 (0.13)]. During 7 y of GH treatment, BMD SD scores showed a significant increase to values significantly higher than zero [mean (SE) 0.87 (0.15) and 0.95 (0.14)]. The increment in BMD SD score of bone consisting predominantly of cortical bone was significantly higher in group C compared with that of the other two GH dosage groups. The pretreatment bone age was significantly negatively related to the increment in BMD SD score. We found no significant influence of spontaneous puberty or the use of low-dose estrogens in the last 3 y of the study period on the increment in BMD SD score during 7 y of GH treatment. In conclusion, most untreated young girls with Turner's syndrome have a normal volumetric BMD. During 7 y of GH treatment with 4, 6, or 8 IU/m(2)/d, the BMD SD score increased significantly