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.