Abstract
The reason for reporting this case is to remind that some microorganisms may cause
hemolysis leading to early and severe hyperbilirubinemia by secreting hemolysin in
cases; where bilirubin levels cannot be successfully decreased despite effective phototherapy,
intravenous immunoglobulin, and even exchange transfusion, or in cases of increased
rebound bilirubin (although urinary tract infection is associated with increased conjugated
bilirubin fraction and prolonged jaundice). The most common causes of hemolysis are
ABO/Rh incompatibility and enzyme deficiencies such as glucose-6-phosphate dehydrogenase
(G6PDH), pyruvate kinase (PK), and galactose-1-phosphate uridyltransferase (GALT).
Our patient was a male infant, weighing 3,160 g, at 38 + 4 gestational week; he was
referred to our unit with total bilirubin level of 14.7 mg/dL recorded at the postnatal
20th hour and was initiated treatment with intensive phototherapy and prepared for
exchange transfusion. The G6PD, PK, and GALT enzyme levels studied at the postnatal
96th hour and reducing substances in urine were detected to be normal/negative, whereas
complete urinalysis revealed pyuria (7 leukocytes per each high power field). α-hemolysis-producing
105 colony-forming unit/mL Enterobacter cloacae grew on blood agar in the urine culture. As reported in our case, hemolysin-secreting
α and β-hemolytic bacteria can lead to severe and early hemolysis and unconjugated
hyperbilirubinemia, as in blood type incompatibility and enzyme deficiencies.
Keywords
hemolysis - unconjugated hyperbilirubinemia - neonate
