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Lymphogranuloma venereum (LGV) occurs mainly in tropical and subtropical countries and is caused by C. trachomatis serotypes L1 - 3. It is acquired by sexual intercourse and can result in fibrosis and destruction of the inguinal lymph nodes with subsequent genital elephantiasis. In the 1940’s, a South American researcher [May, 1943] noted that there were similarities between the pathological processes of atherosclerosis [lay reader: hardening of the arteries] and the fibrotic and inflammatory destruction of lymph nodes in LGV. [We now know that C. trachomatis LGV organisms share many common antigens with C. pneumoniae]. It was noted that subjects with atherosclerosis were more likely to have a positive result when tested by a skin test [the Frei test, based on delayed hypersensitivity responses] for prior infection with LGV [May 1943; Quiroga & Ambrosetti 1943; Coutts & Davila, 1945].

Two major groups have been outstanding in modern C. pneumoniae research. Dr Pekka Saikku's group in Finland drew modern attention to a possible link between C. pneumoniae heart disease and other chronic conditions. Dr Tom Grayston's group in the USA, having achieved the promotion of the TWAR atypical isolates to species status, uncovered much of the epidemiology of the organism and further developed studies on its possible role in chronic diseases.

In the 1980’s, it was found that 68% of Finnish subjects presenting with myocardial infarction (MI) had at least a three-fold rise in antibody titres against genus specific chlamydial lipopolysaccharide antigen compared with only 2.4% of controls. This initial observation [Saikku et al., 1988] was subsequently followed by a prospective study based on the Helsinki heart study [Saikku et al., 1992]. The only known chlamydial species common enough to be the candidate was the then recently described C. pneumoniae [Mattila, 1989; Saikku et al., 1988]. MI is an acute event, which in most cases, is due to rupture of atherosclerotic plaques [Davies, 1996]. However, the causes of plaque rupture are unknown. One interpretation of the Finnish data  is that acute C. pneumoniae infection might contribute to plaque rupture.

Despite this impressive and unexpected result, only a few inconclusive studies have looked at acute C. pneumoniae infection as a cause of MI  [Leinonen et al., 1990; Blasi et al., 1997]. Instead, the main focus of interest has been whether chronic C. pneumoniae infection is a cause of the atherosclerotic process itself. In fact, the Finnish researchers played down the high seroconversion rate. Apart from genus specific antibodies, they also measured specific antibodies to C. pneumoniae. It was found that specific antibodies were also more likely to be found in cases than controls (85 vs. 61% for IgG titre ≥ 32). However, because seroconversion of specific antibodies [lay reader: dynamically rising antibody in response to current infection] was not seen, this was interpreted as showing that chronic, rather than acute infection was associated with coronary heart disease. The significance as to why such a high seroconversion rate was seen with genus specific but not with species-specific antibody was not addressed.

[YW] Updated by MEW March 2002

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References

Blasi, F., Cosentini, R., Raccanelli, R., Massari, F. M., Arosio, C., Tarsia, P. et al. (1997). A possible association of Chlamydia pneumoniae infection and acute myocardial infarction in patients younger than 65 years of age. Chest 112, 309 - 312. Full article

Coutts WE, Davila M. (1945). Lymphogranuloma venereum as a possible cause of arteriosclerosis and other arterial conditions. Journal of Tropical Medicine and Hygiene 48, 46 - 51.

Davies, M. J. (1996). Stability and instability: Two faces of coronary atherosclerosis - The Paul Dudley White Lecture 1995. Circulation 94, 2013 - 2020. [Excellent review]. Full article 

Leinonen, M., Linnanmaki, E., Mattila, K., Nieminen, M. S., Valtonen, V., Leirisalorepo, M. et al. (1990). Circulating immune complexes containing Chlamydial lipopolysaccharide in acute myocardial infarction. Microbial Pathogenesis 9, 67 - 73.

Mattila, K. J. (1989). Viral and bacterial infections in patients with acute myocardial infarction. Journal of Internal Medicine 225, 293 - 296.

May, J. (1943). La intradermoreaccion de Frei en las arteropatias. Revista Argentina Dermatosifilis 27, 581-2. [In Spanish].

Quiroga, M. & Ambrosetti, F. E. (1943). La reaccion de Frei en las endoarteritis obliterantes. Revista Argentina Dermatosifilis 27, 624 - 625.[In Spanish].

Saikku, P., Mattila, K., Nieminen, M. S., Huttunen, J. K., Leinonen, M., Ekman, M. R. et al. (1988). Serological evidence of an association of a novel Chlamydia, TWAR, with chronic coronary heart disease and acute myocardial infarction. Lancet 1988 vol 2, 983 - 986. [The paper that started the modern spate of interest].

Saikku,P., Leinonen, M., Tenkanen, L., Linnanmaki, E., Ekman, M. R., Manninen, V., Manttari, M., Frick, M.H. &  Huttunen, J. K. (1992). Chronic Chlamydia pneumoniae infection as a risk factor for coronary heart disease in the Helsinki heart study. Annals of Internal Medicine 116, 273 - 278.

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