Does mixing acute medical admissions with burn patients increase infective complications from paediatric thermal injuries?

In the winter of 2005–2006, the management at our children's hospital elected to admit ‘overspill’ acute medical admissions to the ward used for plastic surgery and burns for logistical reasons. This study was conducted to assess the effects of that change on the incidence of infective complications in thermally-injured patients. Seventy-three patients were studied, 23 in the sample winter and 50 in the two preceding control winters. The data gathered included days on IV fluids and antibiotics, transfer to the Paediatric Intensive Care Unit (PICU), microbiology and a ‘septic signs score’ – based on pyrexia, irritability, diarrhoea/vomiting, wound colonization, bacteraemia. The outcomes studied were: the maximum ‘septic signs score’; patients with a score ≥3; wound colonization; PICU admission; days on antibiotics and IV fluids. A statistically significant increase in patients with septic episodes was demonstrated by an increase in the mean septic signs score (0.66–1.48, P = 0.044) and the number of patients with a score ≥3 (4–22%, P = 0.017). Other analysed variables did not reach statistical significance although the raw data suggested a trend. It was concluded that there is an association between mixing acute medical admissions with thermally-injured patients and an increase in the incidence of infective complications in the latter group

Persistence survey of Toxic Shock Syndrome toxin-1 producing Staphylococcus aureus and serum antibodies to this superantigen in five groups of menstruating women

Background: Menstrual Toxic Shock Syndrome (mTSS) is thought to be associated with the vaginal colonization with specific strains of Staphylococcus aureus TSST-1 in women who lack sufficient antibody titers to this toxin. There are no published studies that examine the seroconversion in women with various colonization patterns of this organism. Thus, the aim of this study was to evaluate the persistence of Staphylococcus aureus colonization at three body sites (vagina, nares, and anus) and serum antibody to toxic shock syndrome toxin-producing Staphylococcus aureus among a small group of healthy, menstruating women evaluated previously in a larger study. Methods: One year after the completion of that study, 311 subjects were recalled into 5 groups. Four samples were obtained from each participant at several visits over an additional 6-11 month period: 1) an anterior nares swab; 2) an anal swab; 3) a vagina swab; and 4) a blood sample. Gram stain, a catalase test, and a rapid S. aureus-specific latex agglutination test were performed to phenotypically identify S. aureus from sample swabs. A competitive ELISA was used to quantify TSST-1 production. Human TSST-1 IgG antibodies were determined from the blood samples using a sandwich ELISA method. Results: We found only 41% of toxigenic S. aureus and 35.5% of non-toxigenic nasal carriage could be classified as persistent. None of the toxigenic S. aureus vaginal or anal carriage could be classified as persistent. Despite the low persistence of S. aureus colonization, subjects colonized with a toxigenic strain were found to display distributions of antibody titers skewed toward higher titers than other subjects. Seven percent (5/75) of subjects became seropositive during recall, but none experienced toxic shock syndrome-like symptoms. Conclusions: Nasal carriage of S. aureus appears to be persistent and the best predicator of subsequent colonization, whereas vaginal and anal carriage appear to be more transient. From these findings, it appears that antibody titers in women found to be colonized with toxigenic S. aureus remained skewed toward higher titers whether or not the colonies were found to be persistent or transient in nature. This suggests that colonization at some point in time is sufficient to elevate antibody titer levels and those levels appear to be persistent. Results also indicate that women can become seropositive without experiencing signs or symptoms of toxic shock syndrome

Upregulation of IgE synthesis by staphylococcal toxic shock syndrome toxin-1 in peripheral blood mononuclear cells from patients with atopic dermatitis

BACKGROUND: Atopic dermatitis (AD) is a chronic skin disease associated with increased IgE synthesis and colonization with Staphylococcus aureus secreting exotoxins, such as Toxic Shock Syndrome Toxin-1 (TSST-1). OBJECTIVES: In this study, we were interested in determining the in vitro effects of TSST-1 on IgE synthesis in peripheral blood mononuclear cells from patients with AD. METHODS: We stimulated peripheral blood mononuclear cells (PBMC) from AD patients with a wide range of TSST-1 concentrations and measured IgE synthesis by enzyme-linked immunosorbent assay (ELISA) after 14 days. RESULTS: We show herein that TSST-1 produced antagonistic effects on IgE synthesis by PBMC from AD patients, depending on the concentration used: IgE synthesis was inhibited at 1000 pg/mL (P < 0.05) and enhanced at 0.01 pg/mL (P < 0.01) of toxin. TSST-1 was found to induce the production of much higher amounts of interferon-gamma (IFN gamma) at 1000 pg/mL than at 0.01 pg/mL of toxin (P = 0.0001). More importantly, immunoglobulin E (IgE) synthesis was enhanced by TSST-1 at 1 pg/mL in the presence of antibodies blocking IFN gamma activity. The other immunoglobulin (Ig) isotypes were also increased after TSST-1 stimulation suggesting that the enhanced IgE synthesis was secondary to a polyclonal B cell activation rather than an isotype switch. TSST-1-stimulated IgE synthesis was T cell-dependent because purified tonsil B cells were only able to synthesize increased amounts of IgE when small numbers of T cells were added to the cultures. Anti-HLA-DR and anti-LFA-1 monoclonal antibodies (MoAb) inhibited TSST-1-enhanced IgE synthesis, suggesting that the bridging of the T cell receptor (TCR) and major histocompatibility complex (MHC) class II on B cells was necessary for activation of B cell differentiation. CONCLUSION: These data indicate that staphylococcal superantigens are able, at concentrations inducing low amounts of IFN gamma, to stimulate IgE synthesis by PBMC from AD patients, and suggest that staphylococcal toxins may contribute to elevated IgE synthesis in AD