CHLAMYDIA PNEUMONIAE AS A RESPIRATORY PATHOGEN

David L. Hahn¹, Anthony A. Azenabor², Wandy L. Beatty³ and Gerald I. Byrne³

1Arcand Park Clinic, Dean Medical Center, Madison WI 53704, ²Department of Medical Microbiology and Immunology, University of Wisconsin Medical School, Madison. WI 53706, ³ Department of Medical Microbiology and Immunology, University of Wisconsin - Madison, WI

FIGURES

Figure 1. Transmission electron micrograph of Chlamydia pneumoniae associated with macrophages (RAW cells). A. Typical pear shaped EBs (arrows) are shown at the macrophage surface. B. Intracellular EBs display the typical pear shaped morphology and a large periplasmic space containing round electron-dense bodies (arrowheads). Scale bar = 0.5µm.

Figure 2. Chlamydial life cycle. Chlamydiae adhere to the host cell and are endocytosed (A). The pathogen prevents phagosome-lysosome fusion (B), differentiates into the reticulate body (C), and begins replicating within the inclusion (D). Replicating reticulate bodies may re-differentiate back into elementary bodies (E, F) and lyse the host cell to begin a new round of infection. In addition, under conditions of immune stress, such as the presence of immune-regulated cytokines (e.g. IFN-gamma), the pathogen may enter a non-infectious, non-replicating persistent state (G); when the stress is removed, the pathogen can re-differentiate into infectious EB and begin a new cycle of replication. In certain host cells (e.g. alveolar macrophages, circulating monocytes, C. pneumoniae may be rendered permanently persistent, but still capable of pathogenic potential).