Infections of the Fetus and Newborn
The usual 10-month period from conception through birth and the first 4 weeks ofextrauterine life is one of unusual susceptibility to infection but also a time at which special defenses acquired from the mother are operating.
• During normal development, the fetus is in a protected intrauterine environment, with fetal membranes serving as a physical barrier to external infection and the placenta contributing, with maternal immunity, to protection against many blood-borne infec-tions. Transplacental transmission of specific immunoglobulins, particularly of the IgG class (IgM does not normally cross the placental barrier), continues to provide some immunologic protection to the infant for weeks to months after birth, while cy-tokines from the mother can provide transient cell-mediated immune support. If the infant is breast-fed, specific immunoglobulins (predominantly of the IgA class) in ma-ternal colostrum afford some protection against pathogens that involve or invade through the infant’s gastrointestinal tract.
• On the other hand, the fetal immune system is immature, and there is relative suppres-sion of maternal cell-mediated immunity as pregnancy progresses. These immune de-ficiencies serve an important biological purpose; they protect fetus and mother from activation of specific immunologic recognition and response mechanisms to differ-ences in their histocompatibility locus antigens. If these processes did not occur nor-mally, the fetus could be immunologically rejected by the mother or the fetal immune mechanisms activated to respond against maternal antigens in a form of “graft versus host” disease.
• Specific and nonspecific immune responses begin to develop in early fetal life, perhaps as early as 8 weeks’ gestation; however, a nearly normal immunocompetent state is usu-ally not achieved until the infant is more than 2 years of age. Deficiencies commonly seen in the early period include poor antibody response to polysaccharide antigens, de-creased phagocytic capability and variability in intracellular killing of certain infectious agents, lower levels of complement components, and decreased opsonic capacity.
• Cell growth and organ differentiation are at their highest rates in the fetal – neonatal period, making the host especially susceptible to permanent damage when an infec-tious process intervenes.
The actual risk of infection and the types of pathogens encountered are influenced by a variety of interacting factors, including the state of maternal health and susceptibility to specific agents, adequacy of fetal and neonatal nutrition, integrity of fetal membranes, and degree of maturity at birth.
A number of terms are commonly used to describe the infections that can affect the fetus and newborn. Prenatal infections include those acquired by the mother and/or fetus at any time before birth. When fetal infection develops, it is usually blood-borne to the pla-centa with subsequent spread to the fetus (transplacental) or follows the ascending route from the vagina through torn or ruptured fetal membranes. Natal, or peripartum, infec-tions are those acquired during delivery. They are often caused by agents in the maternal genital tract but occasionally result from organisms introduced from exogenous sources through attendants, fetal monitors, or other instruments.Postnatal infections, which con-stitute the remainder of the group, include all infections acquired after delivery through-out the newborn (or neonatal) period, defined as the first 4 weeks of life.
Another commonly used term is congenital infection, which describes infection oc-curring at any time before or at birth (prenatal or natal). Consequently, the infection is usually still active in the newborn period and sometimes persists for months or years. Perinatal infection is often used to include a period extending from 20 to 28 weeks’ ges-tation to 7 to 28 days after birth.
Chorioamnionitis is an inflammatory response to infectious agents involving thechorionic and amniotic fetal membranes. It usually results from entry of pathogens from the vagina through tears or ruptures in the membranes, and it places the fetus at risk of di-rect exposure just before or at delivery. The risk of chorioamnionitis increases rapidly when membranes have been ruptured for longer than 12 hours before birth. When infec-tion is by the blood-borne maternal route, there may be evidence of infection of the pla-centa, termed placentitis. Endometritis may be observed occasionally if the infection is an extension from a maternal pelvic focus along venous or lymphatic pathways. Sepsis is a term used to indicate a severe systemic bacterial infection associated with bacteremia.
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