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.

Systemic illnesses caused by chronic Chl pneumoniae infection have common features whichever bodily system is affected; indeed, there is an astonishing overlap between diseases long considered unrelated. MRI scans on patients with Crohn’s disease may show large numbers of white-matter hyperintensities indistinguishable from those found in MS. Patients with reactive arthritis may develop uveitis, also seen in some patients with MS. Whichever system is involved, the disease often takes a relapsing/remitting course with recurrence of symptoms which tend to worsen; there is an increased lack of resolution. With time there is a destruction of the normal anatomy. Finally, the disease becomes ‘burned out’: there is the impression that infection has been vanquished, but with enormous collateral damage. At this stage bacteria may be few, and there may be little that antibiotics can do to help.

Here is an incomplete list of disorders in which vasculitis due to Chl pneumoniae may be implicated:

adult-onset asthma; refractory sinusitis, chronic obstructive pulmonary disease, uveitis, optic neuritis, radiculitis, nerve deafness, transverse myelitis, Alzheimer’s disease, multiple sclerosis, sarcoid, myocarditis, pericarditis, culture-negative endocarditis, atheromatous arterial disease, aneurysm, giant-cell (temporal) arteritis, polyarteritis nodosa, Wegener’s granuloma, inflammatory bowel disease, primary sclerosing cholangitis, reactive arthritis, Reiter’s syndrome, Behcet’s disease, interstitial cystitis, cutaneous vasculitides including pyoderma gangrenosa.

Conditions which may suggest the possibility of flare-ups of chronic Chl pneumoniae infection deserving serological investigation include the following — a multiplicity being more strongly suggestive:

recurrent sinusitis, recurrent chest infections, chronic fatigue (especially if following a respiratory infection), focal neurological deficits, myalgia, muscle fasciculations, recurrent episodes of bronchospasm, unexplained pleuritic pain, angina, recurrent arthralgia, unexplained recurrent abdominal pain, unexplained menorrhagia, recurrent fistula-in-ano, recurrent cutaneous vasculitides, achalasia, intestinal dysmotility.

Here is a link to a website dedicated to multisystem diseases caused by Chl pneumoniae; it is maintained by people who have the infection and who are undergoing treatment. It is very comprehensive and has many personal stories.

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.

A brief note on chronic fatigue and persistent infection with Chlamydia pneumoniae can be found here.

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