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Clinical and Diagnostic Laboratory Immunology, November 1999, p. 891-894, Vol. 6, No. 6
1071-412X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Can an Antibiotic (Macrolide) Prevent Chlamydia pneumoniae-Induced Atherosclerosis in a Rabbit Model?

Ignatius W. Fong,1,* Brian Chiu,1 Esther Viira,1 Dan Jang,2 Michael W. Fong,1 Rosanna Peeling,3 and James B. Mahony2

Departments of Medicine, Laboratory Medicine and Pathology, St. Michael's Hospital, University of Toronto, Toronto,1 and Department of Pathology and Molecular Medicine, St. Joseph's Hospital, McMaster University, Hamilton,2 Ontario, and LCDC Chlamydia Laboratory, Winnipeg, Manitoba,3 Canada

Received 14 April 1999/Returned for modification 21 May 1999/Accepted 1 September 1999

There is increasing data implicating Chlamydia pneumoniae in the pathogenesis of atherosclerosis, and antibiotics may theoretically be useful to prevent secondary vascular complications. Three groups of New Zealand White specific-pathogen-free rabbits, fed cholesterol-free chow, were inoculated via the nasopharynx on three occasions, 2 weeks apart, with C. pneumoniae. Group I (n = 23) rabbits were untreated; group II (n = 24) rabbits were treated with azithromycin at 30 mg/kg of body weight daily for 3 days and then once every 6 days, starting 5 days after first inoculation and continuing until sacrifice (early treatment); and group III (n = 24) rabbits were treated with the same dose of azithromycin but initiated 2 weeks after the last inoculation. All animals were sacrificed at 10 to 11 weeks after initial inoculation 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 changes of the aorta and no significant reduction compared to untreated rabbits. Early treatment of C. pneumoniae-infected rabbits with azithromycin was highly effective (87%) in preventing atherosclerotic changes, but delayed treatment was ineffective. It is possible that longer or more aggressive antibiotic treatment may be needed to reverse preformed lesions or that antibiotics may not be of value once lesions have formed.

* Corresponding author. Mailing address: Division of Infectious Diseases, St. Michael's Hospital, 30 Bond St., Room 4-179V, Toronto, ON M5B 1W8, Canada. Phone: (416) 864-5746. Fax: (416) 864-5310. E-mail: fongi{at}smh.toronto.on.ca.

Clinical and Diagnostic Laboratory Immunology, November 1999, p. 891-894, Vol. 6, No. 6
1071-412X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:

  • Teig, N, Anders, A, Schmidt, C, Rieger, C, Gatermann, S (2005). Chlamydophilapneumoniae and Mycoplasma pneumoniae in respiratory specimens of children with chronic lung diseases. Thorax 60: 962-966 [Abstract] [Full Text]  
  • Tormakangas, L., Alakarppa, H., David, D. B., Leinonen, M., Saikku, P. (2004). Telithromycin Treatment of Chronic Chlamydia pneumoniae Infection in C57BL/6J mice. Antimicrob. Agents Chemother. 48: 3655-3661 [Abstract] [Full Text]  
  • Fong, I. W., Chiu, B., Viira, E., Jang, D., Mahony, J. B. (2002). Influence of Clarithromycin on Early Atherosclerotic Lesions after Chlamydia pneumoniae Infection in a Rabbit Model. Antimicrob. Agents Chemother. 46: 2321-2326 [Abstract] [Full Text]  
  • Boman, J., Hammerschlag, M. R. (2002). Chlamydia pneumoniae and Atherosclerosis: Critical Assessment of Diagnostic Methods and Relevance to Treatment Studies. Clin. Microbiol. Rev. 15: 1-20 [Abstract] [Full Text]  


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