[Toxic shock syndrome toxin level in wound samples of hospitalized children with burn: a case control study]

Background: Toxic shock syndrome [TSS], a dangerous consequence of Toxic shock syndrome toxin-1 [TSST-1] caused by Staphylococcus aureus. The early detection for infections of Staphylococcus aureus in burned children is very important, also the prevention for consequences of TSST-1. Fever is one of the most noticeable sign in burned children. On the other hand, fever is one of the important consequences of TSST-1 production

Methods: This study aimed to assess the toxic shock syndrome toxin-1 level in the wound's specimens of two groups febrile and afebrile in the hospitalized burned children in Motahari hospital Tehran, Iran in the year 2013. In this case-control study, 90 children who admitted to the burn unit, divided in two groups of 45 patients: febrile [cases group] and afebrile [control group]

All of burned children under went wound biopsy, and then all of wound's specimens were tested by PCR for specific primer of toxin producing genome. Finally all of data collected and statistically analyzed. This data include group febrile and afebrile, demographic characteristics, percentage of burned surface severity and result of PCR

Results: The positive result for PCR test, production of TSST-1 in febrile burned children [cases group] was 37.7% and in afebrile burned children [control group] was 11.1% that this different was statistically significant [P=0.003]

The mean and standard deviation for percentage of burned surface [severity] in samples with positive result for PCR test was 30.9+/- 16.93 and in samples with negative result for PCR test was 20.09+/-11.02 that this different was statistically significant [P<0.01]. There was no difference between positive PCR result and negative PCR result of age and sex

Conclusion: Direct association was approved between the production of TSST-1 and the occurrence of fever in burned children. Increased surface severity

[Streptococcus super antigen in polyp tissue of patients with nasal polyposis and chronic rhinosinusitis in comparison to normal population]

Nasal polyp [NP] is a benign mucosal mass located in both sinuses and nares which is mostly seen in association with cystic fibrosis, asthma or oversensitivity to aspirin. The prominent histological feature of NP is inflammatory cell infiltration with eosinophil predominance. Superantigens role in causing NP complications is already proven. Superantigens, which are mostly originated from Streptococci and Staphylococci, activate T cells strongly and increase the process of production and release of cytokines, and secretion of IgE from B cells, which in turn directly affects proinflammatory cells such as eosinophils, both in their tissues infiltration and functions. The samples are collected from patients referring to ENT clinic in Rasoul Akram training Hospital in Tehran after thorough clinical and paraclinical examinations. For control group the samples collected from patients undergoing rhinoplasty. All the samples kept frozen and sent to immunology lab. The DNA of the excised tissues extracted and amplified by using the superantigens specific primers and PCR product detected by gel electrophoresis. The date analyzed by using mean and SD and CHI[2] analytical tools. Fifteen healthy individuals, 25 patients with rhinosinusitis and 24 with polyposis entered this trial. Group A Streptococcus toxin detection was significantly more frequent in those with nasal polyp and rhinosinusitis compared to healthy individuals [P=0.001 and 0.005, respectively], but the results were almost the same for those with nasal polyp and rhinosinusitis [P=0.4]. Streptococci may play an important role in induction or clinical exacerbation of polyposis and group A Streptococcus pyogenes exotoxin [SPEs] with superantigenic effects may have a crucial role in etiology and pathogenesis of polyps with or without rhinosinusitis. It is postulated that, T cells polyclonal activation by SPEs may cause recruitment of inflammatory cells in nasal mucosa. These inflammatory cells include IgE producing B cells leading to allergic and inflammatory reactions in NP.

[Determination of STREM-1 level in synovial fluid for diagnosis of septic arthritis in children]

Triggering receptors expressed on myeloid cells i.e soluble triggering expressed on myeloid cells-1 [STREM-1] is inducible on monocyte/macrophages and neutrophils and accelerates tissue destruction by propagating inflammatory responses in disease related to bacterial infections. The aim of this study was to investigate the role of STREM-1 in the synovial fluid to identify septic arthritis from aseptic ones. A cross sectional study [2007-2009] was conducted in the Pediatric and Orthopedic wards of Hazrat-e-Rasool Akram hospital, Tehran . Synovial fluid was aspirated in 53 cases with arthitis and searched for diagnosis of bacterial arthritis by conventional diagnostic tests. About 0.5-3cc of synovial fluid was stored at -70°C, and quantification of STREM-1 was done in 53 synovial fluid samples [Quantikine, R and D systems, USA] by EIA; results were compared between septic and aseptic arthritis. Septic arthritis was detected in 49% [26/53] and aseptic arthritis in 51%[27/53]. Positive synovial fluid culture was detected in 20.3%, and positive latex particle agglutination for bacteria was found in 8.5%. Positve direct smear was obtained in 10.5% of the cases. Cut off level 825 pg/ml for SF-STREM-1 yielded 50% sensitivity, 70% specificity, 64% Positive Predictive Value [PPV], and 64%, Negative Predictive Value [NPV]. Poor agreement was seen between SF -STREM-1 levels and positive culture [p value: 0.037; Kappa=0.28]. The area under the ROC curve for discriminating between septic and aseptic arthitis was 0.603 [95% CI; 0.757-0.448, p = 0.1]. SF-STREM-1 level with cutoff 825pg/ml had 50% sensitivity, and 70% specifity in discriminating between proved cases with septic arthitis from aseptic ones. Searching for bacterial antigens in synovial fluid [Latex Particle Aagglutination test] and synovial fluid -STREM-1 level could potentially assist clinicians in better diagnosis of septic arthitis if added to the conventional tests including smear and routine analysis of synovial fluid. It might prevent unnecessary empiric antibiotic theray in children with arthritis. In clinical decision making; randomized studies on the potential synovial fluid - STREM-1 -level guided antimicrobial therapy in bacterial arthritis would be useful.

[ comparison of TH1 and TH2 cytokines gene expression in allergic and non-allergic patients with nasal polyps by PCR]

Too many studies are in the process of determining the probable role of immune system in the etiopathogenesis of nasal polyposis. This study was designed to identify the probable participation of Th1, Th2 lymphocytes in the induction and progression of nasal polyposis. Seventy-five patients, 42 male and 33 female, with nasal polyposis were examined for total serum IgE, specific serum IgE and reaction to skin test for differentiating allergic from non-allergic participants in Rasoul Akram Hospital during 2010. To determine the possible correlation of allergic reactions in the upper respiratory tract and nasal polyposis, cytokine gene expression was evaluated on the extracted RNA by RT-PCR. The data were analyzed by using c2, independent t-test, correlation and Receiver operating characteristic [ROC] curve. The mean age of participants was 38 years [18-81 years]. IFN-gamma and IL-4 gene expressions were more prevalent in allergic than non-allergic individuals [IFN-gamma: 39.5% vs. 14.2%, P=0.3 and IL-4: 44.7% vs. 18.9%, P=0.02, respectively]. IL-10 and IL-12 [P35 and P40 fractions] genes were not significantly different between the two groups. IL-10 and IL-12 [P35, P40] genes did not differ significantly either. This research suggests that overproduction of cytokines and an imbalance of Th1 and Th2 cell production may play an important role in the pathophysiology of allergic or non-allergic nasal polyp formation. Thus, although nasal polyposis is a multifactorial disease with several different etiological factors, chronic persistent inflammation is undoubtedly a major factor irrespective of the etiology