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Background. Staphylococcal scarlet fever (SSF), a rare disease, was first described in 1900. The clinical features and outcomes in children with SSF caused by Panton-Valentine leukocidin (PVL)-positive and PVL-negative Staphylococcus aureus strains have not been compared prospectively. Methods. The demographic data, selected clinical features, laboratory values, and outcomes for 49 consecutive children with community-acquired S. aureus SSF prospectively identified during an 11-year period were collected for analysis. Results. The male-to-female ratio was 1.88, and the median age of the patients was 37 months. Cutaneous abscesses predominated among children with SSF. Methicillin-susceptible S. aureus (MSSA) andmethicillin-resistant S. aureus (MRSA) caused SSF in 26 and 23 children, respectively. Twenty-four isolates had results that were positive for PVL (5 MSSA and 19 MRSA isolates), and 25 had results that were negative for PVL (21 MSSA and 4 MRSA isolates). Polymerase chain reaction revealed that most (92%) contained only staphylococcal enterotoxin B (23 MSSA and 22 MRSA isolates). By multivariate analysis, children with PVL-positive isolates had significantly larger abscess sizes, higher white blood cell counts, higher C-reactive protein levels, and longer durations of fever, generalized scarlatiniform rashes, and hospital stays. Most (17 isolates; 89%) of the 19 PVL-positive MRSA isolates carried the staphylococcal cassette chromosome mec VT and all were multilocus sequence type 59. Conclusion. SSF caused by PVL-positive S. aureus strains were associated with more-exacerbated skin manifestations and a greater systemic inflammatory response, compared with those cases caused by PVL-negative S. aureus. Clinical improvement after incision and drainage was achieved for most children with SSF caused by PVLpositive MRSA strains, despite treatment with an ineffective antibiotic. [ABSTRACT FROM AUTHOR]

Background. A 1400-bed tertiary medical center in northern Taiwan was used to conduct an epidemiological study of children hospitalized with community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) infection during a 5-year period. Methods. Nineteen previously healthy children with predominantly skin and soft-tissue CA-MRSA infections were enrolled into the study. Seventeen CA-MRSA isolates were examined for antimicrobial susceptibility and molecular typing. Results. A comparison of our results with the reported resistance rates among CA-MRSA isolates from other countries showed uniformly high macrolide resistance (100%). Of the 17 MRSA isolates in our study, all had the macrolide-lincosamide-streptogramin-constitutive phenotype and the ermB gene. Moreover, on the basis of molecular typing results, 11(65%) of 17 CA-MRSA isolates were genetically related (as determined by pulsed-field gel electrophoresis), and multilocus sequence typing revealed a sequence type of 59 in all isolates. Staphylococcal toxin genes lukS -P V and lukF -P V were detected in all isolates. However, staphylococcal cassette chromosome mec type IV was only detected in 3 (17.6%) of 17 isolates; the remaining 14 isolates were untypeable. Conclusions. Analysis of our data suggests the predominance of a single endemic CA-MRSA strain with high macrolide resistance in our community. Clinical improvement with incision and drainage was noted for most patients, despite treatment with an ineffective antibiotic, so the need for a change in treatment guidelines should be addressed. [ABSTRACT FROM AUTHOR]

This study retrospectively reviewed all pediatric cases of staphylococcal scarlet fever (SSF) that occurred during a 10-year period in a 1400-bed tertiary medical center in northern Taiwan. All 20 cases of SSF occurred in previously healthy individuals. Skin and soft-tissue infections predominated among children from whom Staphylococcus aureus was isolated. Polymerase chain reaction testing was used to detect known staphylococcal toxin genes, and of the isolates studied, most (18 [90%I of 20) contained only the staphylococcal enterotoxin B. One of the other strains was positive for staphylococcal enterotoxin A only, and the last strain was positive for both staphylococcal enterotoxin G and staphylococcal enterotoxin I. Pulsed-field gel electrophoresis identified a small cluster of isolates (6 [30%] of 20) that were genetically related, but these strains came from epidemiologically unrelated patients during a 3-year period. [ABSTRACT FROM AUTHOR]

Both erythropoietin (EPO) and haem oxygenase-1 (HO-1), an anti-oxidative stress protein, have proven protective roles in experimental autoimmune encephalomyelitis (EAE), a reliable animal model of multiple sclerosis. In this study, EPO delivered intraperitoneally could reduce disease severity in myelin oligodendrocyte glycoprotein (MOG)-EAE mice. To assess the effect of EPO on endogenous HO-1 in EAE, we investigated expression of HO-1 mRNA by real-time polymerase chain reaction (RT-PCR), protein expression centrally and peripherally by Western blot and immunohistochemistry and mean fluorescence intensity of splenic HO-1 by flow cytometry. A significantly higher expression of HO-1 in both the central nervous system (CNS) and spleen was shown in EPO-treated MOG-EAE mice than in controls. We further examined the immunomodulatory effect of EPO in EAE, and via RT-PCR demonstrated significantly lower expression of interferon-γ, interleukin (IL)-23, IL-6 and IL-17 mRNA, and significantly higher expression of IL-4 and IL-10 mRNA in CNS of EPO-treated MOG-EAE mice than in controls. Using flow cytometry, we also observed a significantly decreased ratio of both T helper type 1 (Th1) and Th17 lymphocyte subsets isolated from CNS and a significantly increased ratio of splenic regulatory CD4 T cells in EPO-treated MOG-EAE mice. In addition, we demonstrated that MOG-specific T cell proliferation was lower in the EPO-treated group than in controls and showed amelioration of EAE by adoptive transfer of splenocytes from EPO-treated MOG-EAE mice. Together, our data show that in EAE, EPO induction of endogenous HO-1 and modulation of adaptive immunity both centrally and peripherally may involve the repression of inflammatory responses. [ABSTRACT FROM AUTHOR]