OBJECTIVE:This study assessed clinical differences between invasive pneumococcal disease (IPD) caused by penicillin-resistant and penicillin-sensitive Streptococcus pneumoniae.MATERIAL AND METHOD:Patients with IPD confirmed during January 1996-December 2007 at three hospitals were included. Clinical characteristics and outcomes were compared between patients infected with penicillin-resistant Streptococcus pneumoniae (PRSP) and penicillin-sensitive Streptococcus pneumoniae (PSSP).RESULTS:Sixty-nine patients with IPD were identified during the study period, 20 (29%) of whom were infected with PRSP and 49 (71%) with PSSP. Sex, mean age, underlying diseases and seasonal variation did not differ statistically between the two groups. No significant differences were identified in clinical course as measured by time until defervescence, duration of hospitalization and clinical outcome. Minimum inhibitory concentrations (MIC) for other antibiotics were determined; 20% and 10% of PRSP isolates were nonsusceptible to cephalosporins and meropenem, respectively, but all isolates were sensitive to vancomycin.CONCLUSION:There were no significant differences identified in the clinical epidemiology of lPD cases caused by PRSP and PSSP.

Background: Crigler-Najjar syndrome (CN) clinically manifests as intense unconjugated hyperbilirubinemia without evidence of hemolysis. At present, over 90 genetic variations such as mutations, insertions, or deletions have been described in the five exons of the UDP-glucuronosyltransferase (UGT1A1) gene responsible for defect of bilirubin conjugation. Objective: To report a case of a female CN type I child who presented with unconjugated hyperbilirubinemia, normal liver function tests, and normal ultrasonographic images of the liver. Results: Peak total bilirubin in this patient was 27.6 mg/dL. She developed kernicterus despite prolonged daily home phototherapy. Exons 1-5 of the UGT1A1 gene were amplified by polymerase chain reaction (PCR) and the UGT1A1 gene was screened for mutations by direct DNA sequencing. Molecular genetic analysis showed that this patient was homozygous for a nonsense mutation at nucleotide number 715 (715C→T) in exon 1 resulting in the replacement of glutamine (CAG, amino acid 239) by a stop codon (TAG). Conclusion: Detection of this genetic defect is essential for gene therapy and can be used as a prenatal screening test to identify the affected offspring.

Background: Overwhelming strongyloidiasis defined by multi-organ dissemination causes severe morbidity and high mortality.Objective: To report a case of disseminated strongyloidiasis presenting with unusual gastrointestinal manifestations in an immunocompromised host.Methods: A Thai girl with myasthenia gravis treated by chronic administration of corticosteroids presented with disseminated strongyloidiasis. Pulmonary and gastrointestinal symptoms were the clinical manifestations of hyperinfection or disseminated strongyloidiasis.Results: Strongyloid larvae were found in her sputum, stool, and peritoneal fluid. They were present in all layers of the intestinal wall. She did not respond to oral antihelminthic drugs (albendazole). Subcutaneous ivermectin was administered. She succumbed to unresponsive cardiac arrest that was unresponsive to standard resuscitation protocols due to severe septicemia. Pulmonary and gastrointestinal symptoms were the clinical manifestations of hyperinfection or disseminated strongyloidiasis.Conclusion: Serial stool examination should be performed prior to the onset and during immunosuppressive treatment.