ABSTRACT
The epidemiology and microbiological characteristics of paediatric parapneumonic empyema (PPE) before the introduction of the new generation of conjugate pneumococcal vaccines (10-valent and 13-valent) are described. All patients <14 years old admitted to a tertiary paediatric hospital with a diagnosis of PPE were prospectively enrolled from January 2005 to December 2009. Pneumococcal serotyping of culture-negative pleural fluid samples was performed using a multiplex real-time PCR assay. Overall, 219 patients had PPE. Incidence rates for PPE remained stable during the study period with a not significant increase in 2009 compared with 2005 (p 0.13), and were temporally associated with higher circulation of pandemic influenza A H1N1 during the last quarter in our population (p 0.001). Pneumococci were detected in 72% of culture-positive and 79% of culture-negative samples. Serotypes were determined in 104 PPE cases. Serotype 1 was the most prevalent serotype identified (42%) followed by serotypes 7F (20%), 3 (16%), 19A (8%) and 5 (7%). Serotype distribution remained similar during all time periods. Pneumococcal serotype 1 remained the most common cause of PPE during the 5-year study. The new generation of pneumococcal conjugate vaccines offers potential serotype coverage of 73% (10-valent) and 99% (13-valent) in the population studied suffering from PPE. Continuous epidemiological and molecular studies are paramount to monitor the impact of pneumococcal vaccines on the epidemiology of PPE.
Subject(s)
Empyema/epidemiology , Empyema/microbiology , Pneumococcal Infections/epidemiology , Pneumococcal Infections/microbiology , Streptococcus pneumoniae/classification , Streptococcus pneumoniae/isolation & purification , Child , Child, Preschool , Female , Humans , Incidence , Male , Molecular Typing , Multiplex Polymerase Chain Reaction , Pneumococcal Vaccines/immunology , Prevalence , Prospective Studies , Real-Time Polymerase Chain Reaction , Serotyping , Spain/epidemiology , Streptococcus pneumoniae/geneticsABSTRACT
Necrotising pneumonia in young, previously healthy patients due to Panton-Valentine leucocidin (PVL) producing Staphylococcus aureus has been increasingly recognised. PVL pneumonia is often associated with influenza co-infection and high mortality. This case report describes the successful management of the first documented paediatric case of a previous healthy adolescent who developed necrotising pneumonia due to community-acquired methicillin-resistant (CA-MRSA) clone USA300 with pandemic influenza A (H1N1) co-infection, and highlights the importance of early recognition and initiation of appropriate therapy for this potentially fatal co-infection. PCR remains the gold standard to diagnose pandemic H1N1 since it may not be detected by rapid antigen tests. Bacterial necrotising pneumonia should be suspected in those presenting with worsening flu-like symptoms and clinical and/or radiological evidence of PVL infection (multifocal infiltrates, effusion and cavitation). These patients may benefit from the administration of toxin neutralising agents. In light of the current H1N1 pandemic, healthcare professionals will be increasingly confronted with this clinical scenario.
Subject(s)
Influenza A Virus, H1N1 Subtype , Influenza, Human/drug therapy , Methicillin-Resistant Staphylococcus aureus , Pneumonia, Bacterial/drug therapy , Pneumonia, Viral/drug therapy , Staphylococcal Infections/drug therapy , Child , Community-Acquired Infections/microbiology , Humans , Influenza, Human/complications , Influenza, Human/diagnostic imaging , Male , Pneumonia, Bacterial/complications , Pneumonia, Bacterial/diagnostic imaging , Pneumonia, Viral/complications , Pneumonia, Viral/diagnostic imaging , Radiography , Staphylococcal Infections/complications , Staphylococcal Infections/diagnostic imagingABSTRACT
Mannan-binding lectin (MBL) deficiency is determined by MBL gene polymorphisms and is associated with an increased infection risk. To clarify the role of MBL in Allo-SCT, 131 recipients-donors were analysed. MBL genotypes were determined by PCR and heteroduplex analyses, MBL serum levels by ELISA, and MBL oligomers by western blotting. MBL levels <400 ng/ml were associated with increased susceptibility to fungal pneumonia (7/12 vs 35/111; P=0.04, adjusted P=0.002), HSV/VZV (7/12 vs 26/111; P=0.03), CMV reactivation and acute GVHD. Donor genotypes had no influence. Pre-SCT MBL levels corresponded to recipients' genotypes (P<0.001), changed significantly post-SCT, but were not influenced by donors' genotypes. MBL oligomer profiles were similar pre-/post-SCT. Cultured CD34+ cells were found not to synthesise MBL. In conclusion, low MBL levels pre-transplant predisposed patients to sepsis, fungal and viral infection. Donors' MBL genotypes did not influence infection rates. Prospective studies should clarify the importance of MBL as a prelude for MBL replacement after SCT.
Subject(s)
Mannose-Binding Lectin/genetics , Stem Cell Transplantation/adverse effects , Adolescent , Adult , Aged , Disease Susceptibility , Female , Genotype , Graft vs Host Disease/etiology , Graft vs Host Disease/genetics , Humans , Male , Mannose-Binding Lectin/blood , Middle Aged , Mycoses/etiology , Phenotype , Prospective Studies , Retrospective Studies , Sepsis/etiology , Stem Cell Transplantation/mortality , Tissue Donors , Transplantation, HomologousABSTRACT
Chemotherapy-induced neutropenia increases the risk of infection. There appears to be a wide variability in the severity and length of infective episodes. Susceptibility to infections is determined by the underlying malignant disease and its treatment, environmental factors (e.g. nutritional state of the patient and hygiene) and genetically determined variations of the immune system. The majority of primary immunodeficiencies are rare (c. frequency one in 10 000), whereas some genetic polymorphisms in the innate immune system, such as profound mannose-binding lectin deficiency, are much more common (c. frequency one in 10). Here, we review the potential role of the innate immune system in determining susceptibility to infections in patients with neutropenia.
