Infections and the Immune System

The interactions between the fetal and the maternal immune systems during pregnancy are complex (Taeusch et al., 2005). Carefully regulated changes in the fetal immune system are programmed to retain the pregnancy and reduce the likelihood of being attacked by the maternal immune system (i.e., as in an allogeneic graft) yet to prepare the fetus for birth and survival in the extrauterine environment. Many of the mother's antibodies cross the placenta to protect the growing fetus beginning at 20 weeks of gestation, but most transfer during the third trimester.

Abnormalities of this delicate and complex interplay between the fetal and the maternal immune systems and infections can result in fetal compromise, maternal or fetal death, or pre-term birth. Although the mechanism is not well understood, many data support the association between subclinical infection and preterm birth (see Chapter 9). Infections with the rubella virus, cytomegalovirus, Toxoplasma, the syphilis spirochete, the malaria parasite, and human immunodeficiency virus during pregnancy can have devastating consequences for the fetus and infant (Beckerman, 2005; Pan et al., 2005; Sanchez and Ahmed, 2005). Other maternal infections and subsequent inflammation in the fetus have been implicated as causes of fetal brain injury (including white matter injury, neuronal cell disruption, and programmed neuronal cell death) and, later, neurodevelopmental disabilities (Dammann et al., 2002; Hagberg et al., 2005; Walther et al., 2000).

Preterm infants have immature immune systems that are inefficient at fighting off the bacteria, viruses, and other organisms that can cause infections. The most serious manifestations of infections with these agents commonly seen in preterm infants include pneumonia, sepsis, meningitis, and urinary tract infections. As many as 65 percent of infants with birth weights of less than 1,000 grams have at least one infection during their initial hospitalization (Stoll et al., 2004). Neonates contract these infections at birth from their mothers or after birth through their immature skin, lungs, or GI tract, which lack fully developed immunoprotective functions. They have difficulty confining infections to where they arise and forming abscesses, so sepsis (i.e., a blood-borne infection) frequently develops. Septic infants are generally critically ill, and infection can spread to other parts of the body (resulting in, for example, meningitis, an infection of the membranes that surround the brain). In addition to intravenous antibiotics, septic infants often require support for other organ systems that break down (e.g., respiratory and blood pressure support). Neonates with birth weights of less than 1,000 gram and infections have been found to have poorer head growth, more cognitive impairment, and higher rates of cerebral palsy than those who did not have infections as neonates (Stoll et al., 2004).

Invasive fungal infections occur in 6 to 7 percent of infants in a NICU, and the rates of such infections increase with decreasing gestational age and birth weight (Hofstetter, 2005; Stoll et al., 1996). Candida is the most common fungal species that causes infections in preterm infants and colonizes approximately 20 percent of infants with birth weights of less than 1,000 grams (Kaufman et al., 2001). Disseminated fungal infection, in which the infection is spread throughout the body, has a mortality rate of 30 percent. Prompt treatment with antifungal medication can prevent dissemination and improve survival, but side effects are frequent. Intravenous administration of the antifungal fluconazole as prophylaxis against fungal infections in infants with birth weights of less than 1,000 grams can reduce the rates of colonization and fungal infection (Kaufman et al., 2001).

The immune system has many component parts, and there are significant differences between the immune systems of neonates and adults and their responses to inflammation and infec tions with pathogens. Inflammation is implicated in many of the complications of prematurity, including BPD/CLD, NEC, intracranial and especially white matter injury, and ROP. The complex relationships among pathogens, stress, the cytokine system, tissue injury, hormones, and multiple gene-environment interactions in producing or reducing inflammation have important implications for preterm birth, survival, health, brain injury, and neurodevelopmental outcomes (see Chapter 6).

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