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The Link Between Chlamydia pneumoniae and Atherosclerosis
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There is a growing body of evidence suggesting that coronary
artery disease is caused by an infectious agent. The leading
candidate is Chlamydia pneumoniae, based on seroepidemiologic
and histopathologic studies.
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When the representative articles on this topic are analyzed
surprising data and apparently contradictory can be found. A datum that
Saikku et al. considered fundamental and carries to them to establish
this association, is that the patients with acute myocardial infarction
or with coronary hearth disease were presenting geometric average of
IgG greater than control group (P. Saikku, 1998).
However, in 1993, Kuo et al demonstrate the presence of C.
pneumoniae through PCR and electron microscope in plaques of atheroma
from coronary. Precisely in those that previously to their death were
presenting low titles of IgG or absence (C.C. Kuo, 1993).
This apparent discrepancy seems very difficult to conciliating
through clinic experiment and perhaps alone could now to speculate as of
indirect data to explain these publications.
A possible explanation would be in the immune capacity of the
body against to the systemic infection by C. pneumoniae. A good immune
response to an infection by chlamydia can produce distortion of
membranes of chlamydia, losing its typical morphology and in a way
aberrant appearance with difficulty identificable to the optical
microscope. In this case certainly it will appear in blood antibodies in
microimmunofluorescence. If is not produced an adequate immune response
chlamydia maintains its morphology and antibodies can be not detected in
serum by microimmunofluorescence (R. Malinverni, 1996).
On the need noted by Muhlestein of infectious animal models of
appearance of atherosclerotic plaque by the infection by C. pneumoniae
to consider a causal relationship of C. pneumoniae already it has been
published by Fong et al. in Journal of Clinical Microbiology, January of
1997 (I.W. Fong, 1997).
On the other hand if we take as certain the causal association
of C. pneumoniae with the coronary pathology it should be of outlining
the boarding of this problem.
A first possibility would be the vaccine. But as occurs with the
trachoma and C. trachomatis there can not to solve the problem, since in
one moment of the evolution of trachoma, immune stimulation is
prejudicial in the evolution of the process.
Other possibility would be the antibiotic treatment. On this has
been said that upon trying a great infected population resistances can
be created to erythromycin or tetracyclines.
This phenomenon can not prevent its therapeutical use in this process
as either prevents it in trachoma.
Just as in trachoma, in advanced and very chronic injuries the
antibiotic treatment there can not to alter the evolution of the
coronary disease caused by this germ. For this is necessary to make an
early diagnosis of the chronicle infection by C. pneumoniae. Thus we
should develop a exact diagnostics technique for the diagnosis of the
chronicle infection by C. pneumoniae.
Malinverni R. 1996. The role of cytokines in chlamydial
infections. Curr Opin Infect Dis 9, 150-155.
Kuo CC, Shor A, Campbell LA, Fukushi H, Patton DL, Grayston JT.
1993. Demonstration of Chlamydia pneumoniae in atherosclerotic lesions
of coronary arteries. J. Infect. Dis. 167(4):841-9.
Saikku p, leinonen m, mattila k, ekman mr, nieminen ms, makela
ph, huttunen jk, valtonen v. 1988. Serological evidence of an
association of a novel Chlamydia, TWAR, with chronic coronary heart
disease and acute myocardial infarction. Lancet. 2(8618):983-6
Fong IW, Chiu B, Viira E, Fong MW, Jang D, Mahony J. 1997.
Rabbit model for Chlamydia pneumoniae infection. J. Clin. Microbiol.
1997;35:48-52
