IJNHCR Journal

Introduction

Preterm (<37 weeks’ gestation) and low birth weight (LBW) (<2.5 kg) infants have limited nutrient reserves at birth, which makes them subject to many physiologic and metabolic stresses that increase their nutrient needs [1]. Formula milks (i.e. artificial/powdered infant formulas) can typically be manipulated to contain higher amounts of nutrients (e.g. protein) than the mother’s own milk [2,3]. However, formula milks lack the immunomodulators and nutrients present in human milk that stimulate the immune system, protect the immature gut, and promote neurodevelopment [2,4].

Breast milk, aside from being the optimal source of nutrition, has immunologic properties that prevent infection in neonates [5]; for instance, lysozyme which acts directly against bacteria and indirectly potentiates the bactericidal activity of antibodies [6,7].

Despite the benefits of breast milk on infants, for the reason that admitted NICU patients typically cannot be fed directly, a high reliance on EBM is inevitable [8]. Mostly due to improper protocol follow-through (e.g. incorrect thawing after freezing or storage temperatures) and lack of hygiene when extracting, the prevalence of contamination within NICUs has been highly estimated to reach almost all admitted patients. Moreover, these occurrences have also been found in both manual expressions and breast pumps [9]; which, consequently, hold a concerning high risk of infections and sepsis for the patients.

Sepsis among very low birth weight (VLBW) infants is a major worldwide health care concern in NICUs that has been associated with increased morbidity and mortality [10-12]. Neonatal sepsis is most commonly categorized into early-onset sepsis (EOS), occurring within the first 72 hours of life, and late-onset sepsis (LOS), occurring 72 hours or later after birth [10,13]. Although EOS is related to maternal and perinatal factors, LOS is more closely related to neonatal and nosocomial factors [10,13-16].

This case report presents the clinical intervention of a set of preterm neonate twins, one presenting with sepsis and the second one with urinary tract infection (UTI)-pyelonephritis.

Case 1

At 34-week gestational age, Twin A was born vaginally to a gravida 1, para 2 Caucasian woman. Artificial Rupture of Membranes (AROM) was recorded at delivery. Maternal serologies and group B streptococcus (GBS) presented all negatives. At birth, the baby developed respiratory distress due to transient tachypnea of the newborn and no antibiotics were given at the time. The indication of preterm delivery resulted from maternal pregnancy induced hypertension (PIH) with severe features. On day of life (DOL) number nine, the baby developed mild abdominal distension and hypotonia. Blood, urine, and cerebro-spinal fluid (CSF) cultures were obtained; in which blood culture grew enterococcus faecalis, and urine culture, collected through urinary catheterization, grew enterococcus faecalis and klebsiella aerogenes. Following that, the patient received ten days of antibiotics. Repeated blood and urine cultures after the completion of antibiotic therapy showed no organisms.

Case 2

At 34-week gestational age, Twin B was born vaginally to a gravida 1, para 2 Caucasian woman. Artificial Rupture of Membranes (AROM) was seen at delivery. Maternal serologies and group B streptococcus (GBS) presented all negatives. At birth, the baby developed respiratory distress due to transient tachypnea of the newborn and no antibiotics were given for the time being. The indication of preterm delivery was ordered due to maternal pregnancy induced hypertension (PIH) with severe features. On day of life (DOL) number ten, the baby developed decreased breast milk oral intake and mild hypotonia. Blood, urine, and cerebro-spinal fluid (CSF) cultures were obtained; where only the urine culture, collected through urinary catheterization, grew Klebsiella aerogenes. Subsequently, the patient received seven days of antibiotics. Repeated blood and urine cultures after completion of antibiotic therapy showed no presence of organisms.

Results

With the speculation of infection in both twins, the stored expressed breast milk samples that were used for feeding these patients were sent to the microbiology laboratory for aerobic and anaerobic cultures. Confirming the belief; Klebsiella aerogenes, enterococcus faecalis, and staphylococcus epidermidis colonies grew on both samples.

Discussion

Considering the details of this case report, the occurrence of grave infections in preterm twin neonates was traced to the frozen expressed breast milk (EBM) that was used for feeding these patients, which was administered through orogastric tubes. With the twins being born at 34 weeks’ gestation, they both initially presented with respiratory distress that was not treated with antibiotics at first. Ultimately, Twin A presented signs of sepsis, mild abdominal distension, and hypotonia on day nine of life, Twin B exhibited decreased oral intake and hypotonia on day ten of life. Additionally, Twin A’s urine and blood cultures confirmed the presence of Enterococcus Faecalis and Klebsiella Aerogenes, whereas the urine cultures of Twin B just presented Klebsiella Aerogenes. To treat these infections, both patients received antibiotic therapy.

Conclusion

This case highlights several important points. Preterm infants are especially vulnerable due to their underdeveloped immune systems, making them highly susceptible to infections from non-sterile EBM. Proper hygiene during the expression storage, and handling of EBM is essential, including maintaining sterile conditions, appropriate storage temperatures, and correct thawing procedures. Additionally, raising awareness about the risks of contaminated EBM in NICUs is crucial. Evidence-based protocols and educational interventions for both mothers and staff can help reduce these risks [17].

In conclusion, the infections in these preterm twins underscore the importance of strict protocols for EBM storage and administration. The presence of pathogenic bacteria in the EBM serves as a reminder of the need for enhanced safety measures to protect vulnerable infants in the NICUs.

Acknowledgements

N/A

Funding

The author(s) received no financial support for the research, authorship, and/or publication of this article.

Ethical Guidelines

Ethics approval and consent to participate: N/A

Consent for publication

Consent was obtained from the guardian at the time of admission.

Conflict of Interest

The authors declare that they have no competing interests.

References

1. World Health Organization (2006) Optimal Feeding of the Low Birth Weight infant. Technical review. ISB 9241595094. Geneva: WHO.
2. Agostoni C, Buonocore G, Carnielli VP, Darmaun D, Decsi T, et al. (2010) ESPGHAN Committee on Nutrition. Enteral nutrient supply for preterm infants: commentary from the European Society of Paediatric Gastroenterology, Hepatology and Nutrition Committee on Nutrition. J Pediatr Gastroenterol Nutr 50: 85-91.
3. Emblenton ND, Berrington JE, Dorling J, Ewer AK, Juszczak E, et al. (2017) Mechanism affecting the gut of preterm infants in enteral feeding trials. Front Nutr 4:14.
4. Walsh V, McGuire W (2019) Immunonutrition for preterm infants. Neonatology. 115: 398-405.
5. American Academy of Pediatrics (1997) Policy statement: breast-feeding and the use of human milk. Pediatrics. 100:1035-1039.
6. Hill IR, Porter P (1974) Studies of bactericidal activity to Escherichia coli of porcine serum and colostral immunoglobulins and the role of lysozyme with secretory IgA. Immunology. 26:1239-1250.
7. Kliegman RM, Pittard WB, Fanaroff AA (1979) Necrotizing enterocolitis in neonates fed human milk. J Pediatr 95: 450-453.
8. Gad S, Sheta MM, Al-Khalafawi AI, Abu El-Fadl HA, Anany M, et al. (2021) Expressed Breast Milk Contamination in Neonatal Intensive Care Unit. Pediatric Health Med Ther 12:307-313.
9. Boo NY, Nordiah AJ, Alfizah H, Nor-Rohaini AH, Lim VK (2001) Contamination of breast milk obtained by manual expression and breast pumps in mothers of very low birthweight infants. J Hosp Infect. 49: 274-281.
10. Shane AL, Sánchez PJ, Stoll BJ (2017) Neonatal sepsis. Lancet. 390:1770-1780.
11. Dong Y, Speer CP (2014) Late-onset neonatal sepsis: recent developments. Arch Dis Child Fetal Neonatal Ed. 100: F257-F263.
12. Qazi SA, Stoll BJ (2009) Neonatal sepsis: a major global public health challenge. Pediatr Infect Dis J 28: S1-S2.
13. Dong Y, Glaser K, Speer CP (2019) Late-onset sepsis caused by Gram-negative bacteria in very low birth weight infants: a systematic review. Expert Rev Anti Infect Ther 17:177-188.
14. Wójkowska-Mach J, Chmielarczyk A, Strus M, Lauterbach R, Heczko P (2019) Neonate Bloodstream Infections in Organization for Economic Cooperation and Development Countries: An Update on Epidemiology and Prevention. J Clin Med 8: 1750.
15. Hornik CP, Fort P, Clark RH, Watt K, Benjamin DK Jr, et al. (2012) Early and late onset sepsis in very-low-birth-weight infants from a large group of neonatal intensive care units. Early Hum Dev. Suppl 2: S69-S74.
16. Flannery DD, Mukhopadhyay S, Morales KH, Dhudasia MB, Passarella M, et al. (2022) Delivery Characteristics and the Risk of Early-Onset Neonatal Sepsis. Pediatrics. 149: e2021052900.
17. Karimi M, Eslami Z, Shamsi F, Moradi J, Ahmadi AY, et al. (2012) The effect of educational intervention on decreasing mothers' expressed breast milk bacterial contamination whose infants are admitted to neonatal intensive care unit. J Res Health Sci 13: 43-47.