CPn resistance in lymphocytes

Antimicrob Agents Chemother. 2003 June; 47(6): 1972–1975.
doi: 10.1128/AAC.47.6.1972-1975.2003.
Copyright © 2003, American Society for Microbiology

Chlamydia pneumoniae Resists Antibioticsi in Lymphocytes
Hiroyuki Yamaguchi,1 Herman Friedman,1 Mayumi Yamamoto,2 Keigo Yasuda,2 and Yoshimasa Yamamoto1,3*

Department of Medical Microbiology and Immunology, College of Medicine, University of South Florida, Tampa, Florida 33612,1 Third Department of Internal Medicine, School of Medicine, Gifu University, Gifu,2 Division of Molecular Microbiology, Department of Basic Laboratory Sciences, School of Allied Health Sciences, Faculty of Medicine, Osaka University, Osaka, Japan3

Chlamydia pneumoniae infection of lymphocytes in blood has been well documented, and it is apparent that control of this pathogen in these cells may be critical in the development of chronic inflammatory diseases associated with infection by this bacterium. The activity of antibiotics against C. pneumoniae in lymphocytes was assessed in this study by utilizing an in vitro infection model with lymphoid cells. The results obtained indicated that although all of the antibiotics tested showed remarkable activity against bacterial growth in epithelial cells, C. pneumoniae in lymphocytes was less susceptible to antibiotics than was bacterial growth in epithelial cells, which are widely used for the evaluation of anti-C. pneumoniae antibiotics.

The full text of this paper is HERE<.

The full paper has a lovely chart that compares various antibiotics in these cells. Unfortunately there are no bactericidals in the comparison. The best effect was had from azithromycin in this research. You might also note that in the discussion the author suggests that the antibiotics may have induced a persistant state and because this is non metabolizing perhaps that was why the poor effect from what otherwise was considered a CPn effective drug.

Well goodness, this aspect of CPn has already been taken into account by the researchers at VU and that is why we have the bactericidal (flagyl tinizadole)aspect to the protocol we use. Note also that it was single antibiotics used not combinations.

the whole point of the findings in this work is that different CPn infected cells have different responsiveness to antibiotics, and this may support the idea of tissue penetration often discussed here ie a person on treatment was fine last pulse but this time they had a bigger response and it seems that new cells must have been reached.
Good paper! reference three on the paper we already have in this same section (bacterial research)of the research pages. "Chlamydia pneumoniae infection in circulating human monocytes is refractory to antibiotic treatment"


It does not appear as if they used metronidazolei or tinidazole or any other Nitroimidazoles type antibioticsi, so hopefully this should not scare us too much.

Michele (UK) GFAi: Wheldon CAP1st May 2006 . 26th March 2007 continuous Flagyl at 400mg with 5 day pulses at 1200mg every three weeks. Spokesperson for Ella, RRMSi Wheldon CAP 16th March 2006

Michèle (UK) GFAi: Wheldon CAPi 1st May 2006. Daily Doxyi, Azi MWF, metroi pulse.

I would note that in the Vanderbilt studies, the most effective combination for clearing Cpni from macrophages i(in mice) was INHi/Flagyli/Amoxi. This would suggest that those of us with immunei system infectionsi (for example, CFSi) might do well to include INH in the mix. 

CAPi for Chlamydia pneumonia since 11/04. 25yrs CFS & FMSi- Currently: 150mg INH, 200 Doxycycline, 500mg MWF Azithromycin, 1000mg Flagyl daily (Continuous protocol)


CAPi for Cpni 11/04. Dxi: 25+yrs CFSi & FMSi. Currently: 250 aithromycin mwf, doxycycline 100mg BIDi, restarted Tinii pulses; Vit D2000 units, T4 & T3, 6mg Iodoral

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