CNS Macrophages and Infant Infections.

The central nervous system (CNS) harbors its own immune system composed of microglia in the parenchyma and CNS-associated macrophages (CAMs) in the perivascular space, leptomeninges, dura mater, and choroid plexus. Recent advances in understanding the CNS resident immune cells gave new insights into development, maturation and function of its immune guard. Microglia and CAMs undergo essential steps of differentiation and maturation triggered by environmental factors as well as intrinsic transcriptional programs throughout embryonic and postnatal development. These shaping steps allow the macrophages to adapt to their specific physiological function as first line of defense of the CNS and its interfaces. During infancy, the CNS might be targeted by a plethora of different pathogens which can cause severe tissue damage with potentially long reaching defects. Therefore, an efficient immune response of infant CNS macrophages is required even at these early stages to clear the infections but may also lead to detrimental consequences for the developing CNS. Here, we highlight the recent knowledge of the infant CNS immune system during embryonic and postnatal infections and the consequences for the developing CNS.

Fetal Candida sepsis at midgestation: a case report.

A patient presented with intrauterine fetal death at 21 weeks. A Candida vaginitis was treated at 18 weeks of gestation. Fatal fetal Candida sepsis caused by Candida albicans can occur in the absence of known risk factors such as prolonged rupture of membranes, the presence of an intrauterine contraceptive device or cervical cerclage.

Depression of bursal follicle formation by Candida albicans infections.

Sub-lethal i.v. inoculations of Candida albicans into 12-day-old chick embryos have been shown to cause a depression of follicle formation in the bursa of Fabricius. This depression occurred in the absence of any infection in the bursa, although candidal encephalitis was a frequent manifestation of the disseminated infection. A similar depression of bursal follicle formation was caused by the administration of viable C. albicans on to the embryonic chorio-allantoic membrane, in the absence of any disseminated infection. Non-viable extracts of disrupted C. albicans administered on to the chorioallantoic membrane also caused a depression of bursal follicle formation. This immunodeficiency produced by an endotoxin-like principle at a susceptible stage in the development of the chick has been considered in terms of human immunological development and the neonatal occurrence of C. albicans.