Neonatal toxic shock syndrome‐like exanthematous disease (NTED) is a new entity of methicillin‐resistant Staphylococcus aureus (MRSA) infection. Most of NTED cases reported previously in the literature were sporadic ones. In the present report, we describe an outbreak of NTED that occurred in a neonatal intensive care unit (NICU) between April, 1999 and April, 2000 in Japan. All MRSA strains isolated from 14 patients (6 NTED, 2 infections and 6 colonizations) in this outbreak belonged to the group of coagulase II and produced toxic shock syndrome toxin 1 (TSST‐1). Of these, 14 strains produced staphylococcal enterotoxin C (SEC). No other superantigenic toxins were produced by these strains. The pulsed field gel electrophoresis (PFGE) patterns of genomic DNA digested with SmaI were indistinguishable each other due to no band shifting in all of the 13 strains except for strain O‐21 and M56. Strain M56 was different from the dominant type in the positions of only 2 bands, whereas the pattern of strain O‐21 had no similarity with the other pattern, suggesting that this outbreak was associated with the spread of a unique MRSA strain in the NICU. Two‐dimensional electrophoresis (2‐DE) analysis of exoproteins revealed that the patterns of these 14 strains were very indistinguishable to each other, and that these strains produced very large amounts of TSST‐1 and SEC3 subtype superantigens, as measured with computer‐assisted image analysis of the intensity of 2‐DE spots. The 2‐DE gel of O‐21 showed the different pattern from the others. These results as well as the profiles of toxin production also supported the conclusion drawn from PFGE analysis. Based on these results, the involvement of TSST‐1 and SEC3 in the pathogenesis of NTED is discussed.

Enzyme-linked immunosorbent assay using LPS derived from newly recognized serotype O165 verotoxin producing Escherichia coli (VTEC) could identify 4 cases of hemolytic uremic syndrome (HUS) associated with O165 VTEC. All 4 cases showed a typical clinical course seen in VTEC-associated HUS. We screened 33 cases of HUS whose pathogen was not identified by culture of serodiagnosis. The O165 serotype was not thought to be important not only as a VTEC but also as an enteropathogenic E. coli. However, the prevalence, 4 cases, was as high as of O111 serotype, which is the second major serotype of VTEC in Japan. We have to be careful for this serotype when we look for the pathogen of the patients with hemorrhagic colitis or with HUS.

We investigated the effect of three factors, namely dietary protein intake, age and sex, on the susceptibility of the renal glomerulus to the binding of antiglomerular basement membrane antibody (anti-GBM) in the early (heterologous) phase of anti-GBM nephritis, and the consequent reduction in glomerular filtration rate (GFR) as measured by inulin clearance (CIn). The effect of diet was examined in approximately equal to 8 week-old female Munich-Wistar rats fed a 40% high (HP) or a 6% low (LP) protein diet, and that of sex and age in male and female rats, 6 week or 10 month old. Following an intravenous dose (3 to 20 micrograms/g body wt) of radiolabeled nephritogenic anti-GBM, assessment of glomerular function was followed by quantitation of anti-GBM binding (values corrected for GBM surface area) in isolated glomeruli. At a given plasma level of antibody, the degree of binding of anti-GBM was slightly but significantly higher in HP than LP-fed rats; the decrease in GFR was significantly more pronounced in HP than LP-fed animals. The amount of anti-GBM binding was significantly greater in adult than young animals; however, the consequent decrease in GFR was more pronounced in the young than adult animals. Sex dependency was not discernible in anti-GBM binding or reduction in GFR. In all of the above experimental groups, the degree of anti-GBM binding was closely correlated with the plasma level of anti-GBM, but not with effective renal plasma flow rate, measured by PAH clearance. Separate groups of rats were subjected to experimental manipulation of single nephron GFR, glomerular capillary hydraulic pressure and glomerular plasma flow rate, by partial aortic constriction and saralasin administration. This set of experiments, using a tracer amount of non-nephritogenic anti-GBM, revealed that glomerular anti-GBM binding is independent of any of the above parameters. The studies indicate that dietary protein intake and age, but not sex, are among the factors determining the susceptibility of the glomerulus to acute immune injury. Since the binding of anti-GBM is determined by the affinity property of the glomerulus per se, and not by the prevailing hemodynamic pattern, the observed dependence of susceptibility to functional impairment on age and protein intake appears to also reflect a property of the glomerulus, which is influenced by age and the degree of dietary protein intake.