Infections & Immune Systems in preemies
The defence systems of a preemie baby are still immature and so they are at greater risk for developing an infection than full term babies.
Immature Systems
The skin and other membranes that line the respiratory and gastrointestinal systems help protect the body from foreign bodies. If the body is attacked by germs that can get through the physical barriers of the skin and membranes, the body uses another line of defence to help protect itself, this includes white blood cells, antibodies, and other substances in the blood that work to attack germs and foreign bodies. All of these defence systems are immature in premature babies, which means they are at greater risk of developing infections.
Incidence
Low gestational age is an important risk factor for infection due to immaturity of the immune system, which means they are inefficient at fighting off bacteria, viruses, and other organisms that can cause infection. Preterm infants are vulnerable to infection and as many as 65% of infants with birth weights less than 1,000 g have at least one infection during their initial hospitalisation. Approximately 35% of preemie babies delivered at less than 28 weeks’ gestation will develop a hospital-acquired infection during their stay. Micro preemies have an even greater risk for infection.
(Auriti et al., 2003; Lopez Sastre, Coto Cotallo, & Fernandez Colomer, 2002) (Bartels, Schwab, Geffers, Poets, & Gastmeier, 2007))
The most serious of infections commonly seen in preterm infants include;
- sepsis
- pneumonia
- meningitis, and
- urinary tract infections
Sepsis
Sepsis is a blood stream infection and is the most common infection in the neonatal intensive care units (NICU) setting. Premature infants can catch these infections at birth from their mothers or after birth through their immature skin, lungs, or gastrointestinal tract, which lack fully developed immunoprotective functions.
(Bartels, et al., 2007)
A general infection (sepsis: blood-borne infection) often develops in preemies because their immature immune systems mean it is difficult to stop infections from spreading. Septic infants are generally critically ill and infection can spread to other parts of the body, including the brain.
(Bartels, et al., 2007)
Hospital acquired infections
Hospital acquired infections, called nosocomial infections, affect up to 40% of infants in NICUs. Critically ill infants receiving care in NICUs are at an increased risk for infections due to the essential invasive procedures and treatments premature babies endure to save their lives. Injections, IV lines, catheters, and breathing and feeding tubes often mean the baby’s skin barrier is broken and bacteria can attack the body. The sicker a preterm infant is when they are admitted to the NICU the more at risk they are of contracting a hospital acquired infection.
(Auriti, et al., 2003; Moro et al., 1996) (Lopez Sastre, et al., 2002; Schelonka, Scruggs, Nichols, Dimmitt, & Carlo, 2006)
Technical Reference List
Auriti, C., Maccallini, A., Di Liso, G., Di Ciommo, V., Ronchetti, M. P., & Orzalesi, M. (2003). Risk factors for nosocomial infections in a neonatal intensive-care unit. J Hosp Infect, 53(1), 25-30.
Bartels, D. B., Schwab, F., Geffers, C., Poets, C. F., & Gastmeier, P. (2007). Nosocomial infection in small for gestational age newborns with birth weight <1500 g: a multicentre analysis. Arch Dis Child Fetal Neonatal Ed, 92(6), F449-453.
Lopez Sastre, J. B., Coto Cotallo, D., & Fernandez Colomer, B. (2002). Neonatal sepsis of nosocomial origin: an epidemiological study from the "Grupo de Hospitales Castrillo". J Perinat Med, 30(2), 149-157.
Moro, M. L., De Toni, A., Stolfi, I., Carrieri, M. P., Braga, M., & Zunin, C. (1996). Risk factors for nosocomial sepsis in newborn intensive and intermediate care units. Eur J Pediatr, 155(4), 315-322.
Schelonka, R. L., Scruggs, S., Nichols, K., Dimmitt, R. A., & Carlo, W. A. (2006). Sustained reductions in neonatal nosocomial infection rates following a comprehensive infection control intervention. J Perinatol, 26(3), 176-179.









