Bacterial Infections in the Immunocompromised Host

Abstract

This chapter focuses on bacterial infections in specific settings where fundamental relationships relevant to the persistence of bacterial infections in the human host may be observed and studied. Neonates usually acquire bacterial pathogens transplacentally through the umbilical vein or by aspiration from amniotic fluid or cervical secretions. The complement system is able directly to lyse some gram-negative bacteria even in the absence of specific antibodies, but circulating levels of complement in the sera of neonates are lower than those in adults. Both the infected fetus and the neonate are able to produce protective IgM antibodies in response to bacterial antigens, but the levels in serum are lower than those in adults. The primary T-cell deficiencies produce defects in the cytokine production that is required to activate macrophages to kill intracellular bacteria. A primary defect of superoxide synthesis or adhesion of neutrophils is related to severe infection with pyogenic bacteria. The extreme example of acquired immune deficiency is human immunodeficiency virus (HIV) infection, which produces AIDS. Persistent infections modulate all aspects of immune response, including both adaptive and natural immune functions, and have long-term consequences for immune defense. Although encounters with bacteria are a normal aspect of neonatal life, infants are also more susceptible to bacterial infections than are adults.