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Item does not contain fulltext BACKGROUND: Sepsis is a leading cause of morbidity and mortality after surgery. Most studies regarding sepsis do not differentiate between patients who have had recent surgery and those without. Few data exist regarding the risk factors for poor outcomes in pediatric postsurgical sepsis. Our hypothesis is pediatric postsurgical, and medical patients with severe sepsis have unique risk factors for mortality. METHODS: Data were extracted from a secondary analysis of an international point prevalence study of pediatric severe sepsis. Sites included 128 pediatric intensive care units from 26 countries. Pediatric patients with severe sepsis were categorized into those who had recent surgery (postsurgical sepsis) versus those that did not (medical sepsis) before sepsis onset. Multivariable logistic regression models were used to determine risk factors for mortality. RESULTS: A total of 556 patients were included: 138 with postsurgical and 418 with medical sepsis. In postsurgical sepsis, older age, admission from the hospital ward, multiple organ dysfunction syndrome at sepsis recognition, and cardiovascular and respiratory comorbidities were independent risk factors for death. In medical sepsis, resource-limited region, hospital-acquired infection, multiple organ dysfunction syndrome at sepsis recognition, higher Pediatric Index of Mortality-3 score, and malignancy were independent risk factors for death. CONCLUSIONS: Pediatric patients with postsurgical sepsis had different risk factors for mortality compared with medical sepsis. This included a higher mortality risk in postsurgical patients presenting to the intensive care unit from the hospital ward. These data suggest an opportunity to develop and test early warning systems specific to pediatric sepsis in the postsurgical population.

Purpose: In mammography, the height of the image receptor is adjusted to the patient before compressing the breast. An inadequate height setting can result in an imbalance between the forces applied by the image receptor and the paddle, causing the clamped breast to be pushed up or down relative to the body during compression. This leads to unnecessary stretching of the skin and other tissues around the breast, which can make the imaging procedure more painful for the patient. The goal of this study was to implement a method to measure and minimize the force imbalance, and to assess its feasibility as an objective and reproducible method of setting the image receptor height. Methods: A trial was conducted consisting of 13 craniocaudal mammographic compressions on a silicone breast phantom, each with the image receptor positioned at a different height. The image receptor height was varied over a range of 12 cm. In each compression, the force exerted by the compression paddle was increased up to 140 N in steps of 10 N. In addition to the paddle force, the authors measured the force exerted by the image receptor and the reaction force exerted on the patient body by the ground. The trial was repeated 8 times, with the phantom remounted at a slightly different orientation and position between the trials. Results: For a given paddle force, the obtained results showed that there is always exactly one image receptor height that leads to a balance of the forces on the breast. For the breast phantom, deviating from this specific height increased the force imbalance by 9.4 ± 1.9 N/cm (6.7%) for 140 N paddle force, and by 7.1 ± 1.6 N/cm (17.8%) for 40 N paddle force. The results also show that in situations where the force exerted by the image receptor is not measured, the craniocaudal force imbalance can still be determined by positioning the patient on a weighing scale and observing the changes in displayed weight during the procedure. Conclusions: In mammographic breast compression, even small changes in the image receptor height can lead to a severe imbalance of the applied forces. This may make the procedure more painful than necessary and, in case the image receptor is set too low, may lead to image quality issues and increased radiation dose due to undercompression. In practice, these effects can be reduced by monitoring the force imbalance and actively adjusting the position of the image receptor throughout the compression.

In mammography, the height of the image receptor is adjusted to the patient before compressing the breast. An inadequate height setting can result in an imbalance between the forces applied by the image receptor and the paddle, causing the clamped breast to be pushed up or down relative to the body during compression. This leads to unnecessary stretching of the skin and other tissues around the breast, which can make the imaging procedure more painful for the patient. The goal of this study was to implement a method to measure and minimize the force imbalance, and to assess its feasibility as an objective and reproducible method of setting the image receptor height.A trial was conducted consisting of 13 craniocaudal mammographic compressions on a silicone breast phantom, each with the image receptor positioned at a different height. The image receptor height was varied over a range of 12 cm. In each compression, the force exerted by the compression paddle was increased up to 140 N in steps of 10 N. In addition to the paddle force, the authors measured the force exerted by the image receptor and the reaction force exerted on the patient body by the ground. The trial was repeated 8 times, with the phantom remounted at a slightly different orientation and position between the trials.For a given paddle force, the obtained results showed that there is always exactly one image receptor height that leads to a balance of the forces on the breast. For the breast phantom, deviating from this specific height increased the force imbalance by 9.4 ± 1.9 N/cm (6.7%) for 140 N paddle force, and by 7.1 ± 1.6 N/cm (17.8%) for 40 N paddle force. The results also show that in situations where the force exerted by the image receptor is not measured, the craniocaudal force imbalance can still be determined by positioning the patient on a weighing scale and observing the changes in displayed weight during the procedure.In mammographic breast compression, even small changes in the image receptor height can lead to a severe imbalance of the applied forces. This may make the procedure more painful than necessary and, in case the image receptor is set too low, may lead to image quality issues and increased radiation dose due to undercompression. In practice, these effects can be reduced by monitoring the force imbalance and actively adjusting the position of the image receptor throughout the compression.

Contains fulltext : 87344.pdf (Publisher’s version ) (Closed access) INTRODUCTION: Recruitment maneuvers (RMs) are advocated to prevent pulmonary collapse during low tidal volume ventilation and improve oxygenation. However, convincing clinical evidence for improved outcome is lacking. Recent experimental studies demonstrate that RMs translocate pulmonary inflammatory mediators into the circulation. To determine whether a single RM in ventilated children affects pulmonary and systemic cytokine levels, we performed a prospective intervention study. METHODS: Cardiorespiratory stable ventilated patients (0.5-45 months, n = 7) with acute lung injury were subjected to an RM determining opening and closing pressures (peak inspiratory pressure < or =45 cmH(2)O, positive end expiratory pressure (PEEP) < or =30 cmH(2)O). Before and after RM, cardiorespiratory parameters and ventilator settings were recorded, blood gas analysis performed, and bronchoalveolar lavage fluid and plasma TNF-alpha, IL-1beta, IL-6, IL-8, and IL-10 concentrations were determined. RESULTS: Fifteen minutes after the RM, an increase was observed in plasma tumor necrosis factor-alpha (400% +/- 390% of baseline, P = .04), IL-6 (120% +/- 35%, P = .08), and IL-1beta (520% +/- 535%, P = .04), which decreased at T = 60 minutes, hence indicative of translocation. Recruitment maneuver did not change the plasma levels of the anti-inflammatory IL-10 (105% +/- 12%, P = .5). Apart from a nonsignificant increase of IL-8 after 360 minutes (415% +/- 590%,P = .1), bronchoalveolar cytokine levels were not influenced by the RM. No increase in oxygenation or improvement of lung kinetics was observed. CONCLUSIONS: A single RM can translocate pro-inflammatory cytokines from the alveolar space into the systemic circulation in ventilated critically ill children. 01 maart 2010

Contains fulltext : 80528.pdf (Publisher’s version ) (Closed access) The long pentraxin 3 (PTX3) is an important element of the innate immune system and has potential as a diagnostic tool in inflammatory conditions. We studied PTX3 in patients admitted to an intensive care unit with severe meningococcal disease and compared it with the short pentraxin C-reactive protein (CRP). Twenty-six patients with meningococcal disease were studied, 17 patients presented with meningococcal septic shock (shock group), and 9 patients presented with meningococcal meningitis or bacteremia (no-shock group). Pentraxin 3 and CRP were measured by enzyme-linked immunosorbent assay. High plasma concentrations of PTX3 (median, 579 microg/L) were seen at admission in patients with meningococcal disease. Concentrations were significantly higher in patients with shock compared with patients without shock (medians, 801 and 256 microg/L, respectively; P = 0.006). In contrast, CRP at admission was lower in the shock group as compared with the no-shock group (medians, 58 and 165 mg/L, respectively; P = 0.008). High PTX3 and low CRP concentration at admission discriminated between presence and absence of shock (area under the receiver operating characteristic curve, 0.85; P = 0.007 for PTX3 and area under the receiver operating characteristic curve, 0.84; P = 0.01 for CRP). PTX3 did not correlate with disease severity (pediatric risk of mortality) and days spent in the intensive care unit. PTX3 at admission and PTX3 peak concentration both showed a negative correlation with plasma fibrinogen concentrations. C-reactive protein concentration at admission correlated negatively with disease severity. In conclusion, PTX3 was an early indicator of shock in patients with severe meningococcal disease that followed a pattern of induction distinct from CRP.

Item does not contain fulltext In total, 881 presumptive clinical isolates of Streptococcus pneumoniae collected from throughout The Netherlands were analysed to determine their mechanisms of macrolide resistance. Isolates were identified initially by participating laboratories using their own standard identification technique, followed by determination of MICs with Etests. Only 797 isolates were confirmed as pneumococci following bile-solubility tests, lytA PCR and 16S rRNA sequencing. Of these confirmed pneumococci, 59 (7.4%) isolates were macrolide-resistant. Analysis by PCR indicated that 34 (57.6%) isolates harboured only the erm(B) gene and 16 (27.1%) only the mef gene. Three (5.1%) isolates carried both erm(B) and mef, while six (10.2%) isolates were negative for both mechanisms. Of the six negative isolates, three had a mutation in the 23S rRNA gene, and three were negative for all mechanisms tested. No isolates with the erm(A) subclass erm(TR) gene were detected. Among the 19 mef-positive isolates, 14 (73.7%) carried the mef(A) gene, and only five (26.3%) carried the mef(E) gene. No linezolid cross-resistance or multiresistance (resistance to more than two classes of antibiotics) was observed.

Asplenie is een bekende risicofactor voor ernstige infecties met een mortaliteit van meer dan 50%. Wij beschrijven een gezin met twee kinderen met een geisoleerde, congenitale asplenie. De oudste presenteerde zich met ernstige sepsis, de jongste bleek bij screening Howell-Jolly-lichaampjes in het bloedbeeld te hebben en bij echografie een asplenie. Veelal is het afwezig zijn van een functionerende milt bekend door onderliggende hematologische aandoeningen, na extirpatie of in het kader van syndromale afwijkingen. Geisoleerde congenitale asplenie daarentegen wordt meestal pas ontdekt wanneer ernstige infecties optreden. In de helft van de gevallen is deze geisoleerde asplenie familiair. Daarom is bij het diagnosticeren van een patient met een geisoleerde asplenie familiaire screening middels bloedonderzoek naar Howell-Jolly-lichaampjes en echografie van de milt van belang. Gezien de hoge mortaliteit van ernstige infecties bij asplene patienten zijn preventieve maatregelen bestaand uit patientenvoorlichting, antibiotische profylaxe en vaccinaties essentieel.

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To study the role of surface-associated proteins in the virulence of Streptococcus pneumoniae , we used two serotype 3 strains, ATCC 6303 and WU2, and two PspA-negative mutants of WU2, an encapsulated one, JY1123 (Caps + /PspA − ), and an unencapsulated one, DW3.8 (Caps − /PspA − ). ATCC 6303 and WU2 were highly virulent in mice, while the virulence of JY1123 was slightly decreased (50% lethal doses [LD 50 s], 24, 6, and 147 CFU/mouse, respectively); DW3.8 was avirulent (LD 50 , 2 × 10 8 CFU). In vitro, ATCC 6303, WU2, and JY1123 (Caps + /PspA − ) strongly resisted complement activation and complement-dependent opsonophagocytosis, whereas DW3.8 (Caps − /PspA − ) was easily phagocytized in fresh serum. Trypsin treatment of ATCC 6303, WU2, and JY1123 (Caps + /PspA − ) resulted in enhanced complement activation and complement-dependent opsonophagocytosis. Trypsin had no deleterious effect on the polysaccharide capsule. In addition, trypsin pretreatment of ATCC 6303 strongly reduced virulence upon intraperitoneal challenge in mice. This indicated that surface proteins play a role in the resistance to complement activation and opsonophagocytosis and contribute to the virulence of type 3 pneumococci. In subsequent experiments, we could show that the modulation of complement activation was associated with surface components that bind complement regulator factor H; binding is trypsin sensitive and independent of prior complement activation. Immunoblotting of cell wall proteins of the virulent strain ATCC 6303 with anti-human factor H antibody revealed three factor H-binding proteins of 88, 150, and 196 kDa. Immunogold electron microscopy showed a close association of factor H-binding components with the outer surface of the cell wall. The role of these factor H-binding surface proteins in the virulence of pneumococci is interesting and warrants further investigation.

In 39 patients with acute meningococcal infections, the plasma concentrations of tumor necrosis factor-alpha (TNF) and its soluble receptors (sRs) TNFsR-p55 and TNFsR-p75 were measured from admission till recovery. At admission, patients with shock had significantly higher TNF, TNFsR-p55, and TNFsR-p75 values than patients without shock. In addition, during the first 24 hours, patients with shock had higher TNFsR-p75 to TNFsR-p55 ratios, indicating that in shock the increase of TNFsR-p75 exceeds that of TNFsR-p55. TNF measured more than 12 hours after admission failed to differentiate between shock and nonshock because TNF concentrations normalized within 12-24 hours. However, because concentrations of TNFsRs remained elevated for 5-6 days, at that time plasma TNFsRs still differentiated between shock and nonshock. Plasma exchange or whole blood exchange (PEBE), performed in 20 patients with shock, accelerated the decrease of plasma TNFsRs. However, because of a rebound after each PEBE session, the overall half-lives of both TNFsRs were not affected by PEBE.

Background: Current tools to predict the severity of respiratory syncytial virus (RSV) infection might be improved by including immunological parameters. We hypothesized that a combination of inflammatory markers would differentiate between severe and mild disease in RSV-infected children. Methods: Blood and nasopharyngeal samples from 52 RSV-infected children were collected during acute infection and after recovery. Retrospectively, patients were categorized into three groups based on disease severity: mild (no supportive treatment), moderate (supplemental oxygen and/or nasogastric feeding), and severe (mechanical ventilation). Clinical data, number of flow-defined leukocyte subsets, and cytokine concentrations were compared. Results: Children with severe RSV infection were characterized by young age; lymphocytopenia; increased interleukin (IL)-8, granulocyte colony-stimulating factor (G-CSF), and IL-6 concentrations; and decreased chemokine (C-C motif) ligand (CCL-5) concentrations in plasma. The combination of plasma levels of IL-8 and CCL-5, and CD4+ T-cell counts, with cutoff values of 67 pg/ml, 13 ng/ml, and 2.3 × 106/ml, respectively, discriminated severe from mild RSV infection with 82% sensitivity and 96% specificity. Conclusion: This study demonstrates that the combination of CD4+ T-cell counts and IL-8 and CCL-5 plasma concentrations correlates with disease severity in RSV-infected children. In addition to clinical features, these immunological markers may be used to assess severity of RSV infection and guide clinical management. Supplementary information The online version of this article (doi:10.1038/pr.2012.163) contains supplementary material, which is available to authorized users.

Amplified fragment length polymorphism versus pulsed-field gel electrophoresis was used for fingerprinting of 85 macrolide-resistant pneumococcal isolates identified by using primarily phenotypic methods. Confirmation of identification by 16S rRNA sequencing revealed that 27 isolates were actually nonpneumococci. Amplified fragment length polymorphism but not pulsed-field gel electrophoresis offered simultaneous and accurate discrimination between pneumococci and nonpneumococcal species.

A previously healthy 10-month-old boy was referred to our hospital because of coarse facial features that were suggestive of lysosomal storage disease. Apart from noisy respiration, there was no medical history. Elevated levels of urinary glycosaminoglycans and complete deficiency of leukocyte alpha-L-iduronidase indicated severe mucopolysaccharidosis type I. A chest radiograph revealed a markedly enlarged heart, and echocardiography revealed hypertrophic cardiomyopathy. While hematopoietic stem cell transplantation was being planned, progressive cardiac failure developed with a striking hypokinesia of the left-ventricle free wall. In combination with ischemic changes on the electrocardiogram, this was suggestive of coronary artery disease. Results of coronary echo Doppler interrogation were inconclusive, and intravascular ultrasound in this little infant was not feasible. Despite the patient's small size, a successful selective coronary angiography was performed and revealed diffuse narrowing of the left coronary artery with collateral flow from the right coronary artery. Enzyme-replacement therapy was started immediately in an attempt to improve myocardial performance. Evaluation after 3 months, however, revealed complete obliteration of the left coronary main stem with diffuse hypokinesia/akinesia of the left ventricle. At the age of 13 months the boy died of terminal cardiac failure. This case report illustrates the importance of considering early development of coronary artery disease in children with severe mucopolysaccharidosis type I and cardiomyopathy. Pediatrics 2011;127:e1343-e1346

A 13-year-old Moroccan boy in The Netherlands developed fever and a lesion resembling ecthyma gangrenosum on the abdomen during cytostatic drug treatment for a lymphoblastic B-cell lymphoma. Scytalidium dimidiatum was cultured from blood and the abdominal skin lesion. The patient was successfully treated with amphotericin B. The fungus Scytalidium dimidiatum is a fairly common plant pathogen in tropical and subtropical countries and is known to cause dermatomycoses in humans in these areas. This case demonstrates that it is necessary to be aware that immigrants from these areas can import their own fungal flora, some members of which may cause life-threatening disease in the case of patients with immune suppression.

Contains fulltext : 87317.pdf (Publisher’s version ) (Closed access) SUMMARY BACKGROUND: During invasive meningococcal disease, severe thrombocytopenia is strongly associated with a poor outcome. Objectives: In order to elucidate the pathophysiological mechanism behind the development of thrombocytopenia, we studied the role of von Willebrand factor (VWF) in meningococcal disease. PATIENTS/METHODS: Thirty-two children with severe meningococcal disease admitted to our university hospital were included in this study. VWF and related parameters were measured and results were correlated with the development of shock and thrombocytopenia. RESULTS: At admission, all patients had increased levels of (active) VWF and VWF propeptide. The highest VWF propeptide levels were observed in patients with shock, indicating acute endothelial activation. Although VWF propeptide levels in patients with shock, with or without thrombocytopenia, were similar, increased active VWF was significantly lower in patients with thrombocytopenia as compared with patients without thrombocytopenia. ADAMTS13 was moderately decreased. However, the VWF multimeric pattern was minimally increased. We assume that these findings are explained by VWF consumption and perhaps by granzyme B (GrB). In vitro experiments showed that GrB is able to cleave VWF multimers in plasma, whereas GrB was high in patients with shock, who developed thrombocytopenia. CONCLUSIONS: Our results demonstrate that consumption of VWF, derived from endothelial cells, could be a key feature of meningococcal disease and primary to the development of thrombocytopenia during shock. 01 mei 2010

Contains fulltext : 89555.pdf (Publisher’s version ) (Closed access) 01 oktober 2010

Contains fulltext : 80183.pdf (Publisher’s version ) (Closed access) OBJECTIVE: To analyze the role of the innate production capacity for tumor necrosis factor, interleukin-1beta, interleukin-12, and interleukin-10 in the clinical presentation and severity of meningococcal disease. DESIGN: Whole blood cultures from survivors of severe meningococcal disease obtained median 5.4 yrs after hospitalization were stimulated with meningococcal lipopolysaccharide and heat-killed Neisseria meningitidis bacteria. SETTING: Intensive care unit in academic hospital. PATIENTS: A total of 111 children were included. We classified these patients according to clinical manifestation in four groups: shock (n = 43); both shock and meningitis (n = 11); bacteremia (neither shock nor meningitis, n = 24); and distinct meningitis (n = 33). INTERVENTIONS:: None. MEASUREMENTS AND MAIN RESULTS: The classification into four groups stratifies these patients according to disease severity. No differences in whole blood cytokine production were found between the patients in these four groups. However, within the group of patients who had presented with shock, interleukin-1beta and the interleukin-1beta/interleukin-10 ratio were negatively correlated with disease severity (R = -.35, p = .03 and R = -.33, p = .04, respectively; Pediatric Risk of Mortality score). CONCLUSIONS: Clinical manifestation of meningococcal disease cannot be explained by the innate production capacity of whole blood cultures for the cytokines tumor necrosis factor, interleukin-1beta, interleukin-10, and interleukin-12. In patients who presented with shock, a low production capacity for interleukin-1beta and a low interleukin-1beta/interleukin-10 production ratio was associated with more severe disease.

Contains fulltext : 79869.pdf (Publisher’s version ) (Closed access) BACKGROUND: Systemic activation of complement during meningococcal disease is associated with severe disease and poor outcome. The exact mechanism of activation of complement is unknown but is important for future therapies aimed at modulating the complement system in this disease. METHODS: We studied complement activation in a group of 22 patients, including 18 with meningococcal septic shock and 4 with meningococcal disease without shock. Two of the patients with shock were MBL deficient: 1 patient was homozygous and 1 patient was compound heterozygous for exon 1 mutations in the gene for MBL. RESULTS: The MBL-deficient patients had relatively low disease severity and mild disseminated intravascular coagulation (DIC). At admission to the pediatric intensive care unit, the MBL-deficient patients had much lower circulating values of C3bc (indicating common pathway activation) and terminal complement complex (indicating terminal pathway activation) than did MBL-sufficient patients who presented with meningococcal septic shock. Levels of C4bc (indicating classical or lectin pathway activation) and C3bBbP (indicating alternative pathway activation) were also decreased in the MBL-deficient patients. Systemic activation of complement excellently correlated with disease severity and parameters of DIC. Testing of convalescent blood samples from 1 of the MBL-deficient patients in a model of meningococcal sepsis showed that a lack of lectin pathway activation leads to a reduced activation of complement. CONCLUSIONS: This indicates that MBL is critical for the systemic activation of complement seen during meningococcal septic shock.

Contains fulltext : 52923.pdf (Publisher’s version ) (Closed access) Macrophage migration inhibitory factor (MIF) is a mediator of innate immunity and important in the pathogenesis of septic shock. Lipopolysaccharide (LPS) and tumor necrosis factor (TNF) alpha are reported to be inducers of MIF. We studied MIF and cytokines in vivo in patients with meningococcal disease, in human experimental endotoxemia, and in whole blood cultures using a newly developed sensitive and specific enzyme-linked immunosorbent assay. Twenty patients with meningococcal disease were investigated. For the human endotoxemia model, 8 healthy volunteers were intravenously injected with 2 ng/kg Escherichia coli LPS. Whole blood from healthy volunteers was incubated with LPS or heat-killed meningococci. Macrophage migration inhibitory factor concentration in blood was increased during meningococcal disease and highest in the patients presenting with shock compared with patients without shock. Plasma concentration of MIF correlated with disease severity, the presence of shock and with the cytokines interleukin (IL) 1beta, IL-10, IL-12, and vascular endothelial growth factor, but not with TNF-alpha. MIF was not detected in blood in experimental endotoxemia, nor after stimulation of whole blood with LPS or meningococci, although high levels of TNF-alpha were seen in both models. In conclusion, MIF is increased in patients with meningococcal disease and highest in the presence of shock. Macrophage migration inhibitory factor cannot be detected in a human endotoxemia model and is not produced by whole blood cells incubated with LPS or meningococci.

Contains fulltext : 52993.pdf (Publisher’s version ) (Closed access) We describe the successful use of cardiac resynchronization therapy for treatment of mitral valve systolic anterior motion with left ventricle outflow tract obstruction after re-excision of a subaortic membrane and septal myectomy in a 12-year-old child. In the recovery phase, a total atrioventricular block persisted. Therefore a permanent atrioventricular pacing system was implanted.

Contains fulltext : 51083.pdf (Publisher’s version ) (Closed access) The complement system is an essential element in our innate defense against infections with Neisseria meningitidis. We describe 2 cases of meningococcal septic shock, 1 of them fatal, in 2 children of a Turkish family. In the surviving patient, alternative pathway activation was absent and factor D plasma concentrations were undetectable. Concentrations of mannose-binding lectin (MBL), C1q, C4 and C3, factor B, properdin, factor H, and factor I were normal. Mutation analysis of the factor D gene revealed a T638 > G (Val213 > Gly) and a T640 > C (Cys214 > Arg) mutation in the genomic DNA from the patient, both in homozygous form. The consanguineous parents and an unaffected sister had these mutations in heterozygous form. In vitro incubation of factor-D-deficient plasma of the boy with serogroup B N meningitidis showed normal MBL-mediated complement activation but no formation of the alternative pathway C3-convertase C3bBbP, and severely decreased C3bc formation and terminal complement activation. The defect was restored after supplementation with factor D. In conclusion, this is the second report of a factor D gene mutation leading to factor D deficiency in a family with meningococcal disease. This deficiency abolishes alternative-pathway dependent complement activation by N meningitidis, and leads to an increased susceptibility to invasive meningococcal disease.

We evaluated the applicability of ply PCR for confirmation of the identification of Streptococcus pneumoniae. lytA PCR, 16S rRNA sequencing, and amplified-fragment length polymorphism were used as reference methods. In contrast to the lytA gene, the ply gene proved to be not specific for S. pneumoniae . The presence of the ply gene in other streptococci, in particular Streptococcus mitis , suggests that pneumolysin plays a pathogenic role.

Background Apnea can be a presenting symptom in respiratory Synctial Virus (RSV) infection. The incidence of apnea in RSV infected infants varies between 16 and 25% with a particularly high risk associated with young age ( Objective The aim of the study is to assess autonomic dysfunction as indexed by Heart Rate Variability (HRV) in severe RSV infection. The secondary parameter is to analyze the effect of other viral pathogens on autonomic function in infants with LRTI requiring mechanical ventilation. Methods Prospective observational study in a tertiary PICU in infants with viral LRTI requiring mechanical ventilation. Controls were age matched infants without signs of infection. Autonomic function was assessed via HRV, monitoring low frequency (LF) and high frequency (HF) indices of short time recordings (5 min). Results In 7 patients and 13 controls 36 recording were analyzed. Total HRV, LF and LF/HF ratios were significant lower in RSV patients versus controls (p Conclusion RSV infection in infants is associated with autonomic dysfunction of central origin. This may be correlated with an increased risk for serious apnea or ALTE, for which prolonged cardio respiratory monitoring is indicated.

Background and aims Basal ganglia infarction is considered a complication of chronic refractory meningitis. In acute infection the basal ganglia are usually spared. Here we report an exceptional case of bilateral infarction of the basal ganglia in a child with acute S. pneumoniae meningoencephalitis. Methods A 4 year old girl with a short history of fever and left sided otalgia presented with drowsiness in a referral hospital. Cerebral spinal fluid (CSF) examination showed pleocytosis (900 leucocytes/mm 3 )and immediately corticosteroids, ceftriaxone and acyclovir were started. Because of a rapid decline inconsciousness she was transferred to our tertiairy PICU centre. Results Ad admission the girl had become unresponsive and was intubated. Her pupils were mid wide and non-reacting to light. Neurologic examination showed a bipyramidal syndrome with hypertonicity of the lower extremities, brisk deep tendon reflexes and bilateral positive Babinski’s. S.pneumoniae was cultured from CSF and blood. An MRI 4 days after admission showed bilateral sharply demarcated areas of high-signal intensity in the thalamus indicating infarction (Figure 1). In addition osteomyelitis of the tip of the petrous pyramid was observed. Her consciousness gradually improved with bilateral reactive pupils and spontaneous limb movements. Brainstem evoked response audiometry (BERA) of the left ear was negative. Gross motor deficits and impaired eye movements persisted. Conclusion Acute pneumococcal meningoencephalitis can cause bilateral basal ganglia infarction in a child.

Thomas Addison, working as a dermatologist in Guy’s Hospital, published in the London Medical Gazette of 1849 a case report of an anemic patient with apical pulmonary lesions and bilateral disease of the adrenals at autopsy. Although a similar case was described in 1823 by Addison’s colleague Richard Bright and in 1829 by the German pathologist Lobstein in 1829, the French clinician Armand Trousseau honored Addison by introducing the eponym Addison’s disease. Until 1900 it was generally believed that Addison’s disease was caused either by tuberculosis or cancer. Only at the end of the 19th century, did physicians start to recognize the clinical picture of acute adrenal insufficiency.

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The regulation of tumor necrosis factor-a (TNF) and interleukin-1b (IL-1b) production was studied in patients with meningococcal disease. Circulating TNF and IL-1b normalized within 1 day. TNF mRNA and IL-1b mRNA in white blood cells decreased over 3 ‐ 4 days. During the acute stage, TNF and IL-1b production in stimulated whole blood cultures was down-regulated. After 4 ‐ 5 days, this production was restored. The down-regulation was unlikely to be caused by circulating IL-6 and IL-10, as these cytokines normalized within 2 ‐ 3 days. TNF mRNA in stimulated cultures during the acute stage, with down-regulated production, did not differ from that at recovery, with restored production. In contrast, the down-regulated production of IL-1b was associated with significantly lower IL-1b mRNA levels. Thus, TNF and IL-1b production are differentially regulated. Whereas TNF production is regulated posttranscriptionally, IL-1b production is also regulated at the mRNA level. The cytokines tumor necrosis factor-a (TNF) and interleu- fore, we studied this regulation in patients with the prototypical kin-1b (IL-1b) are key mediators in the genesis of septic shock. disease of overwhelming endotoxin exposure and cytokine actiCurrently, only limited information is available on the regula- vation: acute meningococcal disease. This disease is charactertion of the production of these cytokines during sepsis. There- ized by a rather uniform pattern of circulating cytokines with high concentrations in the acute stage [1 ‐ 3]. Reportedly, the production of TNF and IL-1b in lipopolysaccharide (LPS)stimulated whole blood cultures is suppressed during the acute

To determine the value of the platelet count at admission for the assessment of the severity of disease in acute meningococcal infections.Retrospective and prospective, descriptive patient study.University Hospital Intensive Care Unit (ICU).All patients (n = 92) with acute meningococcal disease from 1985 to 1997, who arrived at the ICU within 12 h after hospital admission and had more than one platelet count during the first 12 h.After admission, platelets dropped in 95% of the patients. At admission, 2/41 (5%) of the non-hypotensive patients and 13/51 (25%) of the hypotensive patients had platelets fewer than 100 x 10(9)/l. During the following 12 h, these percentages increased to 15% and 71%, respectively. Fatalities had, at admission, a median platelet count of 111 x 10(9)/l (range, 19-302 x 10(9)/l), whereas the nadir, occurring at median 7.0 h (range, 1.3-12 h), was 31 x 10(9)/l (range, 12-67 x 10(9)/l). Plasma TNF, measured shortly after admission, correlated better with the platelet nadir (r = -0.65, p0.0001) than with the platelet count at admission. Similarly, serum lactate correlated better with the platelet nadir.As platelets drop after admission, the use of the platelet count at admission for the assessment of the prognosis in acute meningococcal disease may be misleading. Frequently repeated platelet counts are a better tool for evaluating the severity of disease.

Penicillin-resistant pneumococci are an increasing worldwide problem that until now has spared the Netherlands and a small number of other European countries. In countries with resistant pneumococci empirical therapy of otitis media and of meningitis is difficult. Special antibiotics such as clindamycin and ceftriaxone may be needed or combinations of vancomycin and high doses of cephalosporin. In spite of antibiotic resistance pneumococcal pneumonia can be treated successfully with high doses of benzylpenicillin or cephalosporin. In case of an infection outside the central nervous system, it is not clear what level of minimal inhibitory concentration indicates that therapy will fail, probably4 mg/l. Even in regions with much resistance such levels are rare. It is fortunate that antibiotic resistance only occurs in a limited number of pneumococcal strains, which in addition happen to be included in antipneumococcal vaccines.

Objective: Concomitant bacterial pneumonia (CBP)in children with respiratory syncytial virus (RSV)bronchiolitis is considered to be low and the use ofantibiotics is generally discouraged. Our experiencehowever suggested that this incidence is higher inchildren with RSV and acute lung injury (ALI). Ourobjective was to determine the incidence of CBP inchildren mechanically ventilated for RSV and ALI. Methods: We conducted a retrospective chartreview of all patients with RSV and ALI requiringmechanical ventilation and admitted to the PICU ofa tertiary care medical center from 2004 - 2009. Allpatients were identified in the PICU database andwere screened for ALI. Composite diagnosis of CBPwas made using 4 criteria: Results: A total of 95 patients were included. Fiftyfive(57.9%) were diagnosed as having CBP; 26(27.4%) met two criteria (possible CBP) and 29(30.5%) > 2 criteria (probable CPB). In infants withCBP a lower oxygenation index, a longer length ofstay and less ventilator free days were observed. All children with CBP and 97% of patients withoutCPB received antibiotics. Conclusion: A high incidence of CBP was observedin children with RSV and ALI requiring mechanicalventilation. The use of empiric antibiotics for pendingculture results may be justified in this specific patientgroup.

A pilot-study was carried out on support measures chosen by 40 families having a subsequent child after their experience with a cot-death infant. Cardio-respiratory monitors were used in one group and weighing scales in the other. General support measures given to both groups included the keeping of symptom charts and weekly visits by health-nurses. Parents who used a home-monitor relied upon the medical-technical approach of the problem, while parents using scales were mainly given confidence by the personal attention of the health-nurse. Monitor-parents more often called the paediatrician for advice than parents using weighing-scales. Especially parents who used weighing-scales commented on the great value of the symptom diary and the weekly home-visit of the health-nurse.

Background Candida species have been isolated with increasing frequency during intra-abdominal infection, yet their role as pathogens or co-pathogens and as determinants for outcome, especially in patients who are frequently reoperated on, is not well understood. Furthermore, the value of antimycotic therapy is the subject of discussion. Methods Candida cultures from the abdomen of surgical patients over the past 10 years (1989–1999) were documented. Medical records of the patients were reviewed for risk factors for morbidity and death. Results Some 72 patients (45 men, 27 women), of mean age 60 (range 18–88) years, had Candida cultured from the abdomen during operation. Indications for surgery included duodenal ulcer perforation in 15 patients (21 per cent), gastrointestinal malignancy in 15 (21 per cent), pancreatitis in nine (12 per cent) and various disorders in the remaining 33. A total of 361 relaparotomies was performed in 72 patients (mean 5, range 0–48). Cultures were positive at the first laparotomy in 19 patients, at the first relaparotomy in 20 patients and in 33 patients at the second or more relaparotomy. All but one patient were treated in the intensive care unit. Some 45 (62 per cent) of 72 patients died a mean of 44 (range 3–234) days after the first laparotomy. Risk factors for death, which appeared not to be significant, are shown in the Table. Died (n = 45) Survived (n = 27) * Values are mean (range) † values in parentheses are percentages. ‡ Daily ‘open’ abdomen wound lavage is counted as relaparotomy. § From identification of positive culture. AMT, antimycotic treatment No. of relaparotomies*‡ 5·3 (0–48) 4·5 (0–35) No. of co-morbid factors* 1·7 (0–4) 1·4 (0–4) Positive blood culture for Candida† 7 (16) 3 (11) Patients treated with AMT† 35 (78) 14 (52) Time to start of AMT (days)*§ 3·8 (0–18) 7·9 (0–21) Grade of infection* 2·2 (0·5–4) 1·7 (0·5–4) No. of bacterial types in abdominal cultures* 3·4 (0–8) 3·4 (0–8) Renal failure† 16 (36) 7 (26) Conclusion The number of relaparotomies among patients with Candida-positive cultures was high. No significant risk factors for death could be identified in surgical patients with intra-abdominal Candida infection in intensive care. © 2000 British Journal of Surgery Society Ltd

In positive pressure hand ventilation appropriate ventilatory pressures are essential for effectiveness and safety of treatment. Workers in a Neonatal Intensive Care Unit were asked to ventilate an imaginary patient. A diaphragm-manometer was used for measurements. This manometer was only visible to the investigator. Peak inspiratory pressure (PIP) and peak end expiratory pressure (PEEP) were recorded. Rather great differences in administered PIP were observed. Unintentionally, PEEP was given in many cases. It is concluded, that in positive pressure hand ventilation pressures should be monitored by measurement.

Many cephalosporins are presently available for clinical use. Although the cephalosporins are excellent antimicrobial agents for many infectious diseases in childhood, they have not replaced the older antibiotic regiments. In fact they offer the pediatrician a broader range of choices in treatment. This article gives a review on microbiological and pharmacokinetic properties of cephalosporins and an indication for the use of cephalosporins in pediatric therapy.