Chapter 8 : Bacterial Infections in the Immunocompromised Host

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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.

Citation: Cunningham-Rundles S, Nesin M. 2000. Bacterial Infections in the Immunocompromised Host, p 145-163. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch8
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Image of FIGURE 1

Neonatal NK cell activity in response to bacteria. The data show the effect of , prepared as ribosomal vesicles, and , prepared as whole inactivated cells, on neonatal NK effector cell function against the K562 target in the 4-h short-term Cr release assay following 18 h of pretreatment compared to endogenous activity at different effector-to-target ratios.

Citation: Cunningham-Rundles S, Nesin M. 2000. Bacterial Infections in the Immunocompromised Host, p 145-163. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch8
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Image of FIGURE 2

Production of IFN-γ in response to . The data show the production of IFN- γ by adult and neonatal mononuclear cells in response to after 18 h of culture.

Citation: Cunningham-Rundles S, Nesin M. 2000. Bacterial Infections in the Immunocompromised Host, p 145-163. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch8
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Image of FIGURE 3

Superoxide production in phagocytes. The data show a deficient monocyte respiratory burst in response to and phorbol myristate acetate in a child on two test dates compared with normal controls. The data are shown as percent activated cells detected by flow cytometry.

Citation: Cunningham-Rundles S, Nesin M. 2000. Bacterial Infections in the Immunocompromised Host, p 145-163. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch8
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Image of FIGURE 4

Lymphocyte response to lactobacilli in HIV-infected children. The data show mononuclear cell response to lactobacilli in vitro in HIV children with low CD4 T-cell numbers (mean, 7%) compared to children with better CD4 T-cell numbers (mean, 34%).

Citation: Cunningham-Rundles S, Nesin M. 2000. Bacterial Infections in the Immunocompromised Host, p 145-163. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch8
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Bacterial infections in primary immune deficiency

Citation: Cunningham-Rundles S, Nesin M. 2000. Bacterial Infections in the Immunocompromised Host, p 145-163. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch8

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