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In what other conditions may chlamydial vasculitis be implicated? Chl pneumoniae is a common pathogen and almost everyone encounters it. It is quite likely that a considerable proportion of the population is chronically but asymptomatically parasitized by this organism. Indeed, a trivial infection caught in childhood may remain dormant for life, or it may take decades to develop into a disease form. And, if it does the latter, the window of opportunity for treatment may be quite narrow. Can pathologies be additive? The organism tends to render the host cells it invades less effective. Complex derangements of host systems may take place, often with harmful feedback. Consider one dynamic, mechanical example. It is known that chronic Chl pneumoniae infection (as evidenced by elevated specific IgA serology) is associated with stiffening of the walls of the great arteries in young men (as evidenced by an increase in brachio-pedal pulse velocity); see this neat study: [Tasaki N, Nakajima M, Yamamoto H, Imazu M, Okimoto T, Otsuka M, Shimizu Y, Kohno N. Influence of Chlamydia pneumoniae infection on aortic stiffness in healthy young men. Atherosclerosis. 2003; 171(1): 117-22.] Baroreceptors in the aortic arch and carotid body are sensitive to the stretching of the arterial wall, and stiffening of the elastic wall of the great arteries may be expected to make these receptors less sensitive: an increase in blood-pressure would result. Paradoxically, the tone of parasitized smooth muscle in the more distant arteries may decrease, causing a fall in peripheral resistance. This might well account for the widening of pulse-pressure which is now known to be so dangerous. The danger comes because the coronary arteries are capable of being filled only as the cardiac muscle relaxes and the aortic valve closes; that is to say, during the approach towards diastole. In health, a return pulse to the heart — a haemodynamic echo, if you will — both softens the final closure of the leaflets of the aortic valve and fills the coronary arteries. If the great arteries are stiffened the return pulse comes back to the heart before the main pulse has subsided. Because the pulse-pressure is now wide there is insufficient pressure to fill the coronary arteries. Angina develops. Three other pathologies might make this chain of events catastrophic; a narrowed and irregular coronary lumen which no longer allows a laminar flow, hypercoagulable blood, and cardiac conduction defects. It is likely, though unproven, that all these may have a Chl pneumoniae input. 
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