ME/CFS in the Department of Medicine

Chlamydia Pneumoniae

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Charles Stratton, MD

Charles W. Stratton, MD,
associate professor of pathology and director of clinical microbiology at Vanderbilt University Medical Center.

Chlamydia pneumoniae was initially recognized as a cause of acute lower respiratory tract infections such as pneumonia and bronchitis in both adults and children, hence the species name "pneumoniae". Moreover, C. pneumoniae has been noted in some individuals to cause a persistent respiratory tract infection following an acute infection, which is entirely consistent with the known chronic nature of all chlamydial infections.

The establishment of such a persistent low-grade infection in the lung by C. pneumoniae creates an important factor for the pathogenesis of this microorganism. The ability of C. pneumoniae to infect a wide variety of human cells including epithelial, endothelial, and smooth muscle cells as well as macrophages, monocytes, and lymphocytes has been well documented. The infection of macrophages, in particular, allows C. pneumoniae to enter into the circulation from pulmonary tissues and can thus cause systemic dissemination. The tendency for C. pneumoniae to disseminate from the initial site of infection in the lung has been described in the murine model of infection. Similar dissemination is presumed to occur in humans. Indeed, the presence of C. pneumoniae DNA in peripheral blood mononuclear cells (PBMCs) has been well documented. In addition, the viability of C. pneumoniae in circulating PBMCs has recently been established.

The ability of C. pneumoniae to cause persistent lung infections combined with its ability to disseminate via the vascular system has raised questions as to the role of this pathogen in a number of chronic diseases including infection-associated chronic fatigue syndrome.

It is not surprising that C. pneumoniae has been reported as a possible cause of infection-associated chronic fatigue syndrome. It is clear that any chronic infection would result in patients experiencing chronic fatigue, thus a chronic chlamydial infection would be expected to do the same. Fibromyalgia and other myalgia of unknown cause have been described in patients with chronic fatigue syndrome; C. pneumoniae antibodies have been linked with myalgia of unknown cause including fibromyalgia.

It is also recognized that Chlamydiae are energy parasites and depend on their host cell for ATP and other high-energy intermediates. It is clear that infection of eukaryotic cells with Chlamydiae results in an increase in the rate of glycolysis, and that this increase is not caused by chlamydial metabolic activity, but instead is a host cell response to the infection. It is not difficult to imagine that a chronic intracellular pathogen that steals the host cell ATP would result in chronic fatigue.

Finally, the fact that C. pneumoniae infects immune cells and steals ATP from these immune cells suggests that these cells would not function as well. In this regard, infection by C. pneumoniae would produce a chronic immunosuppressive disorder that could result in many different co-infections, mostly by viral pathogens. Some of these with pathogens such as EBV and HHV-6 may result in chronic co-infections. These co-infections, of course, would result in additional symptoms as well as additional fatigue.

In summary, there are many reasons that C. pneumoniae is likely to play an important role in infection-associated chronic fatigue syndrome. Well-designed clinical studies are now needed to establish the exact role of C. pneumoniae in chronic fatigue syndrome as well as to determine the effect of therapy. Fortunately, improved diagnostic testing is now available, and suitable treatment regimens are being established through multiple sclerosis studies.

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