Upward trend in the frequency of community-acquired methicillin-resistant Staphylococcus aureus as a cause of pediatric skin and soft tissue infections over five years: a cross-sectional study.

BACKGROUND: The increasing prevalence of methicillin-resistant Staphylococcus aureus (MRSA) and its resistance to multiple antibiotics has become a serious challenge since the early 2000s. Especially, community-acquired MRSA (CA-MRSA) infections that appear mainly as skin and soft tissue infections (SSTIs) tend to increase worldwide. The objective of this cross-sectional study was to evaluate the trends in the frequency of SSTIs due to community-acquired S. aureus among children. METHODS: All children with SSTIs caused by culture positive community-acquired S. aureus during the period from 2013 to 2018 were included in this study. Data of the outpatients were collected from medical records. Annual alteration in frequencies of CA-MRSA and community-acquired methicillin-sensitive S. aureus (CAMSSA) were evaluated. RESULTS: A total of 112 cases was evaluated. Of these, 35 (31.25%) were CA-MRSA. The rates of CA-MRSA had emerged from an increasing annual frequency of 9.5 cases per 10,000 SSTIs as of 2014 to 96.8 cases per 10,000 SSTIs in 2018. The ratio of cases with CA-MRSA to cases with CA-MSSA was 0 - 0.09 in two years of the study period and increased to a maximum ratio of 0.6 - 0.72 in the last two years. Consequently, the frequency of S. aureus in cases with SSTIs was significantly higher in 2016 - 2018 compared to the initial study period within the years of 2013-2015 [p < 0.001, relative risk increase: 7 (2.6-28.7) for CA-MRSA and p=0.002, relative risk increase: 2.1 (1.2-3.5)]. Cases with CA-MRSA increased approximately eight-fold during the six-year-study period. CONCLUSIONS: The rates of CA-MRSA in SSTIs among children increased significantly compared to CA-MSSA. The clinical impact of this increase should be evaluated, especially in patients with SSTI who are unresponsive to empirical treatment.

Effect of Visible Light on Vasospasticity of Post-Subarachnoid Hemorrhage Cerebrospinal Fluid.

Background and Objective Cerebral vasospasm (CV) is a serious complication of subarachnoid hemorrhage (SAH) with high morbidity and mortality rates. The mechanism of CV has not been determined. There are many theories related to this unsolved issue, one of which supports CV as a two-stage phenomenon from a pathophysiologic perspective. The first stage consists of inhibition of neuronal nitric oxide synthase by oxyhemoglobin, which results in a decrease of nitric oxide (NO) production. The second stage consists of an increase in the levels of asymmetric dimethylarginine through bilirubin oxidation products (BOXes), which are oxidized by-products of hemoglobin metabolism. These in turn inhibit endothelial nitric oxide synthase (eNOS), which results in the blockage of the second NO production mechanism. BOXes are sensitive to visible light, as is their precursor bilirubin. The hypothesis of CV prevention using the photosensitivity of BOXes was tested in this study. Material and Methods Cerebrospinal fluid (CSF) obtained from two patients with SAH was divided in half and either exposed to a standard dose of visible light or not exposed to any light. The CSF was spectrophotometrically investigated and the concentration of BOXes was measured. A comparison between CSF samples exposed to light and not exposed to light was made. Using two groups of 16 rats each, the vasospastic effect of the CSF exposed and not exposed to light on arteries of the cortical surface was measured. The cortex was exposed using the cranial window. Results Spectrophotometric analysis revealed that the concentration of BOXes in the CSF decreased significantly after being exposed to visible light (p < 0.001). There was a significant difference of the vasospastic effect of CSF on exposed cortical arteries (p < 0.001). Conclusion The concentration of BOXes and the vasospastic effect of CSF taken from patients with SAH were significantly reduced after being exposed to visible light if compared with CSF not exposed to light.

Finding brands and losing your religion?

Religion is a powerful force in many people's lives, impacting decisions about life, death, and everything in between. It may be difficult, then, to imagine that something as seemingly innocuous as the usage of brand name products might influence individuals' commitment to religion. However, we demonstrate across 6 studies that when brands are a highly salient tool for self-expression, individuals are less likely to report and demonstrate strong religious commitment. We suggest that a desire to maintain consistency among self-identities is one important driver of this relationship and find that the effect is mitigated when the perceived distance between brands and religious values is minimized.

Differences between pediatric extra-pulmonary and pulmonary tuberculosis: a warning sign for the future.

BACKGROUND: Tuberculosis (TB) remains a major global health problem. The childhood tuberculosis has some unique features different which makes the diagnosis more complicated. Here we described the epidemiologic, clinical and microbiologic features of children with extra pulmonary and pulmonary TB. METHODS: The data of the patients <14 years with active TB were collected and compared in pulmonary (PTB) and extrapulmonary TB (EXPTB) patients. RESULTS: A total of 128 cases was included. Forty-two cases occurred in children were < 5 years of age; 41 cases between 6-10 years and 45 cases > 10 years. PTB was present in 75,0% of the cases, and EXPTB was present in 25% of cases. There was no significant difference between the EXPTB and PTB by means of distribution of age groups (p=0,201). The rate of patients free of constitutional symptoms were significantly higher in EXPTB compared to PTB(p=0,000). There was no significant difference between EXPTB and PTB by means of sources detection(p=0,069). CONCLUSION: TB is still a major public health problem. EXPTB has an insidious and silent onset without any constitutional symptoms, and both microbiological confirmation and the source by an adult are not frequently found. Moreover, detection of the adult source is mandatory for controlling the TB disease in children.

A single center's experience with Candida parapsilosis related long-term central venous access device infections: the port removal decision and its outcomes.

Pediatric cancer patients have an increased risk of potentially life-threatening fungal infections such as Candida parapsilosis, associated with long-term CVADs. The Infectious Diseases Society of America (IDSA) guidelines on Candida catheter-related bloodstream infections recommend systemic antifungal therapy and catheter removal. In this study, we focused on our experience with antifungal failure due to totally implanted catheter-associated C. parapsilosis bloodstream infections. We investigated cases leading to port removal in pediatric malignancy patients and the associated patient outcomes. In the first phase of the study, a retrospective chart review was performed to collect patient information, including primary disease; time from hospitalization to port-related candidemia; antifungal drug choice; and the time at which port removal occurred. During the second phase, antifungal susceptibility tests for C. parapsilosis were performed in our microbiology laboratory. All patients had fevers and were neutropenic at the time of candidemia diagnosis. The mean duration between the first isolation of Candida parapsilosis from the port samples to the port removal was 9.75 ± 5.29 days for 11 patients. Patient fevers lasted for a mean time of 16.22 ± 6.51 days. The median recovery duration from fever after CVC removal was four days (range 2-12 days). The median duration for achieving negative blood cultures, following antifungal treatment was 18 days (range 10-27 days). Our data favored the removal of catheters in the presence of ongoing fever, as suggested by the guidelines, independent of the chosen antifungal treatment. Future studies with large samples are needed to evaluate the effects of catheter removal on mortality rates and patient outcomes.

Effect of magnesium, MK-801 and combination of magnesium and MK-801 on blood-brain barrier permeability and brain edema after experimental traumatic diffuse brain injury.

OBJECTIVE: Glutamate antagonists are very attractive drugs in laboratory works to protect neural tissue against ischemia. In this work, the effects of magnesium, MK-801 and combination of magnesium and MK-801 on blood-brain barrier (BBB) and brain edema after experimentally induced traumatic brain injury are evaluated. METHODS: A standard closed head injury was induced on the rats by a controlled impact device using a 450-g free falling mass from a height of 2 m onto a metallic disc fixed to the intact skull. One of the following was injected to animals intraperitoneally 30 minutes after injury: saline, magnesium, MK-801 and magnesium plus MK-801. To quantify the brain edema, the specific gravity of the brain tissue was determined. To demonstrate the alteration of the BBB permeability, Evans blue dye was used as a tracer. RESULTS: In all treatment groups, the specific gravity of brain tissue values was significantly higher compared with the control group. Evans blue dye content in the brain tissue was significantly reduced in all three treatment groups with respect to the control group. There was no significant difference of effect between the groups of magnesium alone and MK-801 alone when compared with each other and when compared with their combination. CONCLUSION: The present data demonstrate that treatment with magnesium, MK-801 and combination of magnesium and MK-801 can reduce formation of brain edema and can help restore BBB permeability after experimental diffuse brain injury.

[Neurogenic pulmonary edema: a prospective study based on observation]. / Nörojenik pulmoner ödem: Gözleme dayali prospektif bir çalisma.

BACKGROUND: In this study, we evaluated the cause and the clinical course of neurogenic pulmonary edema which has developed abruptly in some of the patients in the neurosurgical intensive care unit. METHODS: We evaluated 223 patients in the neurosurgical ICU (116 males; 107 females; mean age 44.4+/-19.5). Five of these had worsening in neurological evaluation and oxygenation and were diagnosed as having a neurogenic pulmonary edema. Patients with pneumonia were excluded from the study. RESULTS: We identified acute hydrocephaly in three patients and re-bleeding of an aneurysm in one as the cause of neurogenic pulmonary edema. No cause could be identified in the remaining patient. Although four patients could be discharged from the ICU, one died due to multiorgan failure. CONCLUSION: Physicians should be careful about neurogenic pulmonary edema, a life-threatening clinical condition, that develops within hours of a neurologic event and usually resolves with neurologic recovery.

Effect of magnesium sulfate administration on blood-brain barrier in a rat model of intraperitoneal sepsis: a randomized controlled experimental study.

INTRODUCTION: Permeability changes in the blood-brain barrier (BBB) and their possible contribution to brain edema formation have a crucial role in the pathophysiology of septic encephalopathy. Magnesium sulfate has been shown to have a protective effect on BBB integrity in multiple experimental models. In this study we determine whether magnesium sulfate administration could have any protective effects on BBB derangement in a rat model of sepsis. METHODS: This randomized controlled experimental study was performed on adult male Sprague-Dawley rats. Intraperitoneal sepsis was induced by using the infected fibrin-thrombin clot model. To examine the effect of magnesium in septic and sham-operated rats, a dose of 750 micromol/kg magnesium sulfate was given intramuscularly immediately after surgery. Control groups for both infected and sham-operated rats were injected with equal volume of saline. Those rats surviving for 24 hours were anesthetized and decapitated for the investigation of brain tissue specific gravity and BBB integrity by the spectrophotometric assay of Evans blue dye extravasations. Another set of experiments was performed for hemodynamic measurements and plasma magnesium level analysis. Rats were allocated into four parallel groups undergoing identical procedures. RESULTS: Sepsis significantly increased BBB permeability to Evans blue. The dye content of each hemisphere was significantly lower in the magnesium-treated septic rats (left hemisphere, 0.00218 +/- 0.0005; right hemisphere, 0.00199 +/- 0.0007 [all results are means +/- standard deviation]) than in control septic animals (left hemisphere, 0.00466 +/- 0.0002; right hemisphere, 0.00641 +/- 0.0003). In septic animals treated with magnesium sulfate, specific gravity was higher (left hemisphere, 1.0438 +/- 0.0007; right hemisphere, 1.0439 +/- 0.0004) than in the untreated septic animals (left hemisphere, 1.0429 +/- 0.0009; right hemisphere, 1.0424 +/- 0.0012), indicating less edema formation with the administration of magnesium. A significant decrease in plasma magnesium levels was observed 24 hours after the induction of sepsis. The dose of magnesium that we used maintained the baseline plasma magnesium levels in magnesium-treated septic rats. CONCLUSIONS: Magnesium administration attenuated the increased BBB permeability defect and caused a reduction in brain edema formation in our rat model of intraperitoneal sepsis.

Effects of magnesium administration on brain edema and blood-brain barrier breakdown after experimental traumatic brain injury in rats.

In this study, we examined the effects of magnesium sulfate administration on brain edema and blood-brain barrier breakdown after experimental traumatic brain injury in rats. Seventy-one adult male Sprague-Dawley rats were anesthetized, and experimental closed head trauma was induced by allowing a 450-g weight to fall from a 2-m height onto a metallic disk fixed to the intact skull. Sixty-eight surviving rats were randomly assigned to receive an intraperitoneal bolus of either 750 micromol/kg magnesium sulfate (group 4; n = 30) or 1 mL of saline (group 2; n = 30) 30 minutes after induction of traumatic brain injury; 39 nontraumatized animals received saline (group 1; n = 21) or magnesium sulfate (group 3; n = 18) with an identical protocol of administration. Brain water content and brain tissue specific gravity, as indicators of brain edema, were measured 24 hours after traumatic brain injury. Blood-brain barrier integrity was evaluated quantitatively 24 hours after injury by spectrophotometric assay of Evans blue dye extravasations. In the magnesium-treated injured group, brain water content was significantly reduced (left hemisphere: group 2, 83.2 +/- 0.8; group 4, 78.4 +/- 0.7 [P <.05]; right hemisphere: group 2, 83.1 +/- 0.7; group 4, 78.4 +/- 0.5. [P <.05]) and brain tissue specific gravity was significantly increased (left hemisphere: group 2, 1.0391 +/- 0.0008; group 4, 1.0437 +/- 0.001 [P <.05]; right hemisphere, group 2, 1.0384 +/- 0.001; group 4, 1.0442 +/- 0.005 [P <.05]) compared with the saline-treated injured group. Evans blue dye content in the brain tissue was significantly decreased in the magnesium-treated injured group (left hemisphere: group 2, 0.0204 +/- 0.03; group 4, 0.0013 +/- 0.0002 [P <.05]; right hemisphere: group 2, 0.0064 +/- 0.0009; group 4, 0.0013 +/- 0.0003 [P <.05]) compared with the saline-treated injured group. The findings of the present study support that beneficial effects of magnesium sulfate exist after severe traumatic brain injury in rats. These results also indicate that a blood-brain barrier permeability defect occurs after this model of diffuse traumatic brain injury, and magnesium seems to attenuate this defect.