Clogging the arteries

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Atherosclerosis is a leading cause of mortality in North America and Europe. Several research groups have developed models of Chlamydia pneumoniae respiratory infection in rabbits and have observed pathological changes consistent with atherosclerotic vascular disease. Muhlestein et al.[1]now report the effects of C. pneumoniae respiratory infection followed by antibiotic (azithromycin) treatment on the development of atherosclerosis in rabbits. All the rabbits were fed a diet supplemented with small amounts of cholesterol, an established method of accelerating atherosclerosis. The degree of intimal atheromatous involvement was determined by the measure of maximal intimal thickness, the percentage of luminal circumference involved and the plaque area index. The average of these measurements was significantly higher in the infected untreated rabbits than in the infected antibiotic-treated rabbits and the uninfected controls. These results argue the causal nature of C. pneumoniae infection in the development of atherosclerosis, and thus heart disease, as well as the therapeutic role of antibiotic therapy. Interestingly, the response to infection was not uniform among the infected untreated rabbits (40% showed prominent atherogenesis, while 60% did not), suggesting that there is variability in the ability of the bacteria to establish an infection or in the host response to combat such an infection. Muhlestein et al.[1]point out the limitations of their study: they did not determine whether cholesterol supplementation was important or whether other doses or other antibiotics would have the same anti-atheromatous effect. They also note that, as with any model, this rabbit model is not identical to that of the human disease and any extrapolations must be made with caution.