ABSTRACT
Twelve cases of neonates admitted to the neonatal unit of our hospital, between January 1, 2000, and December 31, 2005, because of otorrhea due to spontaneous perforation of the tympanic membrane within the first 10 days of life are presented. Data were collected retrospectively from medical records. Cultures of the middle ear exudate grew PSEUDOMONAS AERUGINOSA in 10, SERRATIA MARCENSCENS in 1, and STAPHYLOCOCCUS AUREUS in 1 neonate. Cultures of nasopharyngeal secretions grew P. AERUGINOSA in nine, S. MARCENSCENS in one, S. AUREUS in one, and STREPTOCOCCUS VIRIDANS in one neonate. Middle ear versus nasopharyngeal secretions cultures grew the same organism in 11 neonates. A 10-day course of parenteral antibiotics was administered (ampicillin-ceftazidime for all neonates except for the one neonate with the S. AUREUS otitis who received netilmicin-cloxacillin). All neonates had uneventful course and were discharged home in good clinical condition. Our findings suggest that neonates with eardrum perforation should receive antibiotics parenterally, as the most common pathogens is P. AERUGINOSA, for which there are no satisfactory antibiotics for oral use.
Subject(s)
Anti-Bacterial Agents , Otitis Media, Suppurative/complications , Pseudomonas aeruginosa , Serratia marcescens , Staphylococcus aureus , Tympanic Membrane Perforation/etiology , Tympanic Membrane Perforation/microbiology , Viridans Streptococci , Anti-Bacterial Agents/therapeutic use , Humans , Infant, Newborn , Microbial Sensitivity Tests , Otitis Media, Suppurative/drug therapy , Otitis Media, Suppurative/microbiology , Otitis Media, Suppurative/physiopathology , Pseudomonas Infections/complications , Pseudomonas Infections/drug therapy , Pseudomonas Infections/microbiology , Pseudomonas Infections/physiopathology , Pseudomonas aeruginosa/drug effects , Pseudomonas aeruginosa/isolation & purification , Pseudomonas aeruginosa/pathogenicity , Serratia Infections/complications , Serratia Infections/drug therapy , Serratia Infections/microbiology , Serratia Infections/physiopathology , Serratia marcescens/drug effects , Serratia marcescens/isolation & purification , Serratia marcescens/pathogenicity , Staphylococcal Infections/complications , Staphylococcal Infections/drug therapy , Staphylococcal Infections/microbiology , Staphylococcal Infections/physiopathology , Staphylococcus aureus/drug effects , Staphylococcus aureus/isolation & purification , Staphylococcus aureus/pathogenicity , Streptococcal Infections/complications , Streptococcal Infections/drug therapy , Streptococcal Infections/microbiology , Streptococcal Infections/physiopathology , Treatment Outcome , Tympanic Membrane Perforation/physiopathology , Tympanic Membrane Perforation/therapy , Viridans Streptococci/drug effects , Viridans Streptococci/isolation & purification , Viridans Streptococci/pathogenicityABSTRACT
Neisseria meningitidis serogroup A septicemia and the development of Kawasaki disease in a 10-month-old male infant are described. The patient also experienced a number of primary/septic manifestations as consequences of the direct infectious assault and secondary/hypersensitivity immune-mediated complications. The present observation indicates an etiological relationship between invasive meningococcal infection group A and Kawasaki disease, an association in favor of superantigen-induced theory for the latter occurrence.
Subject(s)
Meningococcal Infections/complications , Mucocutaneous Lymph Node Syndrome/etiology , Neisseria meningitidis, Serogroup A/isolation & purification , Sepsis/complications , DNA, Bacterial/analysis , Diagnosis, Differential , Humans , Infant , Male , Meningococcal Infections/diagnosis , Meningococcal Infections/microbiology , Mucocutaneous Lymph Node Syndrome/diagnosis , Neisseria meningitidis, Serogroup A/genetics , Sepsis/diagnosis , Sepsis/microbiologyABSTRACT
We describe 4 jaundiced neonates with acute pyelonephritis of whom family history was positive for or pointed to Gilbert's syndrome (GS). Uridine diphosphate glucuronosyltransferase 1A1 (UGT-1A1), (TA)7 polymorphism, associated with GS was found in these neonates. We suggest that extended (TA)7 promoter, acting as a predisposing factor, contributes substantially to hyperbilirubinaemia seen in a number of neonates with urinary tract infections (UTIs).
