Iw. Fong et al., Can an antibiotic (macrolide) prevent Chlamydia pneumoniae-induced atherosclerosis in a rabbit model?, CL DIAG LAB, 6(6), 1999, pp. 891-894
There is increasing data implicating Chlamydia pneumoniae in the pathogenes
is of atherosclerosis, and antibiotics may theoretically be useful to preve
nt secondary vascular complications. Three groups of New Zealand White spec
ific-pathogen-free rabbits, fed cholesterol-free chow, were inoculated via
the nasopharynx on three occasions, 2 weeks apart, with C. pneumoniae. Grou
p I (n = 23) rabbits mere untreated; group II (n = 24) rabbits were treated
with azithromycin at 30 mg/kg of body weight daily for 3 days and then onc
e every 6 days, starting 5 days after first inoculation and continuing unti
l sacrifice (early treatment); and group III (n = 24) rabbits were treated
with the same dose of azithromycin but initiated 2 weeks after the last ino
culation. AII animals were sacrificed at 10 to 11 weeks after initial inocu
lation and examined for signs of atherosclerosis of the aorta. Eight (34.8%
) untreated rabbits developed early signs of atherosclerosis, whereas only
one (4.2%) in the early-treatment group had such signs (P = 0.02). However,
eight rabbits (33.3%) of the delayed-treatment group had atherosclerotic c
hanges of the aorta and no significant reduction compared to untreated rabb
its. Early treatment of C. pneumoniae-infected rabbits with azithromycin wa
s highly effective (87%) in preventing atherosclerotic changes, but delayed
treatment was ineffective. It is possible that longer or more aggressive a
ntibiotic treatment may be needed to reverse preformed lesions or that anti
biotics may not be of value once lesions have formed.