Development of icterus gravis in a preterm infant with G71R UGT1A1 polymorphism

BACKGROUND: Uridine diphosphate-glucuronosyltransferase (UGT) gene family is involved in the detoxification of biomaterials and drugs in the liver. Among the UGT gene family members, only UGT1A1 is involved in bilirubin conjugation. As a result, deficient UGT1A1 activity causes jaundice. One disease that is characterized by reduced UGT1A1 activity is Gilbert’s syndrome. Two prevalent UGT1A1 polymorphisms responsible for Gilbert’s syndrome have been identified: G71R in exon 1 and A(TA)7TAA in the TATA box of the promoter region. Recently, the G71R polymorphism has been associated with breastfeeding jaundice and neonatal hyperbilirubinemia in term infants. However, its association with jaundice in very low birth weight infants (VLBWIs) has never been reported. CASE PRESENTATION: The patient was a female born at 28 weeks, 4 days gestation with a birth weight of 1172 g. On day 21, intense yellowing of the skin and eyes was noted, and the patient’s total bilirubin level was 23.7 mg/dL (her direct bilirubin level was 2.1 mg/dL). Therefore, an exchange transfusion was conducted. She had neither blood type incompatibility nor a family history of constitutional jaundice. Metabolic screens for amino and organic acids were negative. No elevation of any of the examined antibody titers was noted, and no evidence of an inflammatory reaction was observed. In addition, no hematological abnormalities were detected. The direct/indirect Coombs test, irregular antibody test and red blood cell antibody dissociation test were all negative, and her thyroid function was normal. We performed sequence analysis of the UGT1A1 gene after the patient’s parents provided written informed consent. Exon 1 of the UGT1 gene on chromosome 2 was analyzed by direct sequencing. A heterozygous substitution from G to A (211G→A: G71R) in base 211 was noted. CONCLUSION: We speculated that this preterm infant with carrying the G71R polymorphism reduced UGT1A1 activity and developed severe jaundice that was likely triggered by factors such as breast feeding and medications. The polymorphism appears at some frequency among VLBWIs, which would necessitate adequate care of severe jaundice even after the acute phase

Controlling highly prevalent Staphylococcus aureus mastitis from the dairy farm

In 57 Holstein cows where the dairy farm uses a milking parlor system, the somatic cell count (SCC) increased persistently in the bulk milk (monthly mean 52.3 × 10^4 cells/ml; range 21 to 94 × 10^4 cells/ml). We detected S. aureus in 24 (41.2%) of the 54 lactating cows and in 29 (12.8%) of 227 quarters of the 57 milking cows in the herd. A control program was implemented in an effort to eradicate S. aureus mastitis from this dairy farm. The control plan established improved handling of the lactating cows, improved milking procedures, dry-cow therapy, and culling of infected cows. The program was monitored for 3.5 years by frequent checkups on the rate of S. aureus infection, the SCC, and the changes in milk composition. Eighteen months after the control program was started, the rate of S. aureus infection in the quarter milk decreased dramatically, and no S. aureus isolates were found in the milk of the remaining cows. The SCC in the bulk milk of the herd dropped to a monthly mean of <20 × 10^4cells/ml. In conclusion, the control program was effective for controlling persistent S. aureus mastitis in this dairy herd