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Incidence and causes of sepsis in glucose-6-phosphate dehydrogenase-deficient newborn infants
Y K Abu-Osba1, A A Mallouh, R W Hann
1Department of Pediatrics, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia.
Insights
Newborn infants with glucose-6-phosphate dehydrogenase (G6PD) deficiency are more susceptible to sepsis, particularly infections caused by catalase-positive organisms. This increased risk is linked to G6PD deficiency and late-onset sepsis in neonates.
Area of Science:
- Neonatal Medicine
- Genetics
- Infectious Diseases
Background:
- Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a common genetic disorder.
- Neonatal sepsis remains a significant cause of morbidity and mortality worldwide.
- The relationship between G6PD deficiency and susceptibility to neonatal sepsis requires further elucidation.
Purpose of the Study:
- To investigate the association between G6PD deficiency and the incidence of sepsis in newborn infants.
- To identify specific types of organisms more frequently implicated in sepsis among G6PD-deficient neonates.
- To explore the timing of sepsis in relation to G6PD status.
Main Methods:
- A large-scale screening of 33,943 Saudi Arabian infants was conducted.
- G6PD deficiency was identified, and infants were monitored for sepsis.
- Sepsis diagnosis was confirmed by clinical signs and positive blood cultures.
Main Results:
- G6PD deficiency was identified in 18% of the screened infants.
- The incidence of sepsis was significantly higher in G6PD-deficient infants (3.4/1000) compared to those with normal G6PD activity (1.9/1000).
- G6PD-deficient infants showed a higher incidence of sepsis caused by catalase-positive organisms (2.9/1000 vs. 1/1000).
- G6PD deficiency was more prevalent in infants with late-onset sepsis (46%) compared to early-onset sepsis (21%).
Conclusions:
- Neonates with G6PD deficiency exhibit increased susceptibility to sepsis, particularly infections by catalase-positive organisms.
- G6PD deficiency is significantly associated with late-onset sepsis in newborns.
- Potential mechanisms include impaired leukocyte bactericidal activity and increased susceptibility due to hyperferremia from erythrocyte lysis.
Abstract:
To determine the susceptibility to sepsis in newborn infants deficient in glucose-6-phosphate dehydrogenase (G6PD), we screened 33,943 Saudi Arab infants. Deficiency of G6PD was found in 18%. Sepsis was determined by the presence of clinical signs of sepsis and confirmed by positive blood cultures. Sepsis was documented in 75 infants (2.2/1000). The incidence of sepsis was significantly higher in 6138 G6PD-deficient infants (3.4/1000) than in the 27,805 with normal G6PD activity (1.9/1000; p less than 0.02). The incidence of catalase-positive organism sepsis was higher in G6PD-deficient infants (2.9/1000) compared with those with normal G6PD activity (1/1000; p less than 0.0002), whereas the incidence of catalase-negative organism sepsis did not differ (p less than 0.2). Deficiency of G6PD was more common in infants with late sepsis (46%) than in those with early sepsis (21%) and in all infants screened (18%) (p less than 0.03 and p less than 0.001, respectively). We conclude that neonates with G6PD deficiency are more susceptible to late sepsis and to infection with catalase-positive organisms. The exact mechanism for the increased susceptibility is not clear, but a partial explanation could be lack of leukocyte bactericidal activity associated with G6PD deficiency, and an increased susceptibility to infection caused by hyperferremia resulting from lysis of G6PD-deficient erythrocytes.