Prospective observational study in two Dutch hospitals to assess the performance of inflammatory plasma markers to determine disease severity of viral respiratory tract infections in children.

Introduction: Respiratory viruses causing lower respiratory tract infections (LRTIs) are a major cause of hospital admissions in children. Since the course of these infections is unpredictable with potential fast deterioration into respiratory failure, infants are easily admitted to the hospital for observation. The aim of this study was to examine whether systemic inflammatory markers can be used to predict severity of disease in children with respiratory viral infections.

Force balancing in mammographic compression.

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.

CD4+ T-cell counts and interleukin-8 and CCL-5 plasma concentrations discriminate disease severity in children with RSV infection.

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.

Fatal coronary artery disease in an infant with severe mucopolysaccharidosis type I.

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 α-l-iduronidase indicated severe mucopolysaccharidosis type I.

von Willebrand factor activation, granzyme-B and thrombocytopenia in meningococcal disease.

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.

Mannose-binding lectin is a critical factor in systemic complement activation during meningococcal septic shock.

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.

Influence of innate cytokine production capacity on clinical manifestation and severity of pediatric meningococcal disease.

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.

A single recruitment maneuver in ventilated critically ill children can translocate pulmonary cytokines into the circulation.

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.

Anomalous coronary artery from the wrong sinus in a 15-year-old boy.

Congenital coronary artery anomalies are a well-recognized risk factor for sudden cardiac death in children as well as young adults, mostly during or immediately after intense exertion on the athletic field. Because these malformations are amenable to surgical treatment, timely identification is crucial. Unfortunately, antemortem diagnosis is notoriously difficult, partly due to the absence of abnormal test results in routine investigations.

Pentraxin 3 and C-reactive protein in severe meningococcal disease.

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).

Cardiac resynchronization therapy for mitral systolic anterior motion in a child.

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.

Macrophage migration inhibitory factor (MIF) in meningococcal septic shock and experimental human endotoxemia.

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.

Deficient alternative complement pathway activation due to factor D deficiency by 2 novel mutations in the complement factor D gene in a family with meningococcal infections.

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.

The absent and vanishing spleen: congenital asplenia and hyposplenism--two case reports.

Unlabelled: Two unrelated patients are reported: one with isolated familial asplenia diagnosed postmortem, the other with isolated hyposplenism diagnosed after recurring invasive bacterial infections. Because both children died of fulminant septic shock, the importance of early diagnosis of splenic dysfunction is evident. Clues for an early diagnosis of congenital asplenia are recurrent invasive bacterial infections, Howell-Jolly bodies in the blood smear or a relative with congenital isolated asplenia.

In-vitro susceptibility and molecular characterisation of macrolide resistance mechanisms among Streptococcus pneumonia isolates in The Netherlands: the DUEL 2 study.

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.

Pneumolysin is a key factor in misidentification of macrolide-resistant Streptococcus pneumoniae and is a putative virulence factor of S. mitis and other streptococci.

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.

Amplified fragment length polymorphism fingerprinting is an effective technique to distinguish streptococcus pneumoniae from other Streptococci and an efficient alternative to pulsed-field gel electrophoresis for molecular typing of pneumococci.

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.

Resistance to both complement activation and phagocytosis in type 3 pneumococci is mediated by the binding of complement regulatory protein factor H.

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.

Plasma patterns of tumor necrosis factor-alpha (TNF) and TNF soluble receptors during acute meningococcal infections and the effect of plasma exchange.

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.

Posttranscriptional down-regulation of tumor necrosis factor-alpha and interleukin-1beta production in acute meningococcal infections.

The regulation of tumor necrosis factor-alpha (TNF) and interleukin-1beta (IL-1beta) production was studied in patients with meningococcal disease. Circulating TNF and IL-1beta normalized within 1 day. TNF mRNA and IL-1beta mRNA in white blood cells decreased over 3-4 days.