Chlamydia pneumoniae infection in circulating human monocytes is refractory to antibiotic treatment
Circulation. 2001 Sep 25;104(13):E75.
Chlamydia pneumoniae infection in circulating human monocytes is refractory to antibiotic treatment.
Gieffers J, Fullgraf H, Jahn J, Klinger M, Dalhoff K, Katus HA, Solbach W, Maass M.
Institute of Medical Microbiology and Hygiene, Medical University of Lubeck, Lubeck, Germany.
BACKGROUND: Recovery of the intracellulari bacterium Chlamydia pneumoniae from atherosclerotic plaques has initiated large studies on antimicrobial therapy in coronary artery disease. The basic concept that antibiotic therapy may eliminate and prevent vascular infection was evaluated in vitro and in vivo by examining the antibiotic susceptibility of C pneumoniae in circulating human monocytes, which are thought to transport chlamydiae from the respiratory tract to the vascular wall. METHODS AND RESULTS: Blood monocytes (CD14+) from 2 healthy volunteers were obtained before and after oral treatment with azithromycin or rifampin and then inoculated with a vascular C pneumoniae strain and continuously cultured in the presence of the respective antibiotic. Progress of infection and chlamydial viability was assessed by immunogold-labeling and detection of C pneumoniae-specific mRNA transcripts. Circulating monocytes from patients undergoing treatment with experimental azithromycin for coronary artery disease were examined for C pneumoniae infection by cell culture. Antibiotics did not inhibit chlamydial growth within monocytes. Electron microscopy showed development of chlamydial inclusion bodies. Reverse transcription-polymerase chain reaction demonstrated continuous synthesis of chlamydial mRNA for 10 days without lysis of the monocytes. The in vivo presence of viable pathogen not eliminated by azithromycin was shown by cultural recovery of C pneumoniae from the circulating monocytes of 2 patients with coronary artery disease. CONCLUSIONS: C pneumoniae uses monocytes as a transport system for systemic dissemination and enters a persistent state not covered by an otherwise effective antichlamydial treatment. Prevention of vascular infection by antichlamydial treatment may be problematic: circulating monocytes carrying a pathogen with reduced antimicrobial susceptibility might initiate reinfection or promote atherosclerosis by the release of proinflammatory mediators.
PMID: 11157684 [PubMed - indexed for MEDLINE]
What's it mean:
vocabulary: in vivo means in the body or organism as opposed to in a petri dish in the lab, in vitro means in the lab
What happened here is that people have noticed that CPn is present in atherosclerotic plaques yet studies seem not to find abxi helpful. The researchers wanted to know if persistence was at fault. What they found was that monocytes (a white blood cell which is part of your immune system) carried CPn inside where it stayed inside an inclusion body (a bubble if you will inside the cell where in it is protected) and that after 10 days of treatment the ey were still able to find CPn evidence with PCRi analysis and immunogold labeling. The conclusion is that CPn is able to resist abxi considered to be effective against CPn and that treatment of CPn with abx is going to be problematic due to this issue. This explains some of the problems with culturing CPn and treating it in illness. Unless you account for this and have a thoughtful antimicrobial plan, then this is the outcome: insufficient treatment, reinfection, and treatment failure. The Wheldon and VU protocols use multiple agents to beat the bacteria at every stage and lifeform. Once again we see how it can be that people in medicine struggle with the new concepts of a bacteria that has multiple innovative ways of resisting treatment. These people are still discussing how it can be that 10 days of a single antibiotic is not effective and demonstrating how it can be that CPN is still culturable at that point. This kind of academic argument is useful to establish the facts about things, but do know that he VU and Wheldon protocls already accounts for this by using several agents and using flagyl to kill the bacteria outright. This is more support for the approach we are using