Mycoplasmas are atypical bacteria that live as intra- or extracellular parasites.Mycoplasmas can be transmitted through aerosols (M. pneumoniae, M. fermentans, both of which are found in the saliva); sexual transmission is also frequent (M. genitalium). Acute M. pneumoniae infections cause pneumonia, bronchitis; chronic infection in the lungs can exacerbate other respiratory diseases such as asthma. Mycoplasmas can disseminate from their primary infection site to other organs. Central nervous system can be a target, resulting in encephalitis; attack on the joints and development of arthritis is also frequent.

Mycoplasma infections are particularly frequent in CFS patients. Using PCR detection, M. fermentans was found in 34% of CFS patients, versus 8% of healthy controls. Another study showed that more than two third of CFS patients (versus 5.6% of controls) were infected by at least one mycoplasma species (M. fermentans, M. pneumoniae, or M. hominis).

This high prevalence may result from the immunodepression typically observed in CFS (low NK activity); however persistent mycoplasma infections can in turn contribute to the etiology of the disease by eliciting a chronic inflammatory response.


Chlamydiae are bacterial intracellular pathogens which cause widespread infections in humans.

C. trachomatis is the world’s most common sexually transmitted bacterial pathogen. C. pneumoniae, which is transmitted via respiratory secretions, causes pneumonia.

The percentage of people displaying positive serology to C. pneumoniae is high, reaching 80% in adults.

Chlamydial organisms have the capacity to enter a particular growth stage characterized by reticulate bodies that divide very slowly and can persist in cells for a long time. This results in a chronic infection, which, by inducing a sustained inflammatory response, can lead to a number of serious pathologies.

Chlamydia pneumoniae

Acute C. pneumoniae infections cause pneumonitis; chronic persistence of the pathogen in the lungs has been linked to chronic obstructive pulmonary disease, asthma, and even lung cancer. In the lungs, C. pneumoniae can infect alveolar macrophages and spread to other organs via the blood. Infection can be directly transferred to vascular endothelial cells, leading to chronic endothelium inflammation that favors atherogenesis. Chlamydia infection stimulates the migration of monocytes through the blood-brain barrier, promoting inflammation of the central nervous system. An increased prevalence of C. pneumoniae infections has been reported in CFS patients.

Chlamydia trachomatis

C. trachomatis has a tropism for both conjunctival and urogenital epithelial cells. Ocular infections cause conjunctivitis, that frequently evolve to trachoma. Urogenital infections cause acute urethritis. Like C. pneumoniae, C. trachomatis can disseminate away from the site of primary infection. Several days after a genital infection, certain patients develop acute inflammatory arthritis; this is caused by C. trachomatis organisms that have reached the joint via circulating monocytes. A portion of these patients will then develop chronic arthritic disease. Persistent, chronic chlamydial infections may have little or no apparent symptoms. Though, they continue to elicit a chronic inflammation that will eventually cause disease. This of course strongly warrants screening for infections. Monocytes appear as common host cells for persistent organisms, and major effectors of systemic dissemination. PCR testing in whole blood is therefore an adequate approach for the detection of Chlamydia infections.


Borrelia burgdorferi are gram-negative spirochete bacteria that cause Lyme disease. 

Spirochetes are a group of phylogenetically distinct bacteria that have a unique mode of motility by means of axial filaments (endoflagella).

Borrelia are divided into “genospecies” including B. burgdorferi sensu strict, B. garinii and B. afzelii. The term used to collectively describe all these genospecies is B. burgdorferi sensu lato. B. burgdorferi invades the blood and tissues of various infected mammals and birds via the bite of ticks of genus Ixodes. The natural reservoir for B. burgdorferi is thought to be the white-footed mouse.

Ticks transfer the spirochetes to deer, humans, and other warm-blooded animals after a blood meal from an infected animal. In most mammals, including humans, infection by B. burgdorferi can result in Lyme disease.

Lyme disease exhibits a variety of symptoms that may be confused with immune and inflammatory disorders.

Inflammation around the tick bite causes skin lesions. Erythema (chronicum) migrans (ECM), a unique expanding skin lesion with central clearing that has a ring-like appearance, is typically the first stage of the disease. Arthritis, neurological disease, and cardiac disease may be later stage manifestations.



In Lyme disease concurrent infections frequently occur. The clinical and pathological impact of co-infections was first recognized in the 1990th. Their pathological synergism can exacerbate Lyme disease or induce similar disease manifestations. Co-infecting agents can be transmitted together with Borrelia burgdorferi by tick bite resulting in multiple infections but a fraction of co-infections occur independently of tick bite.

Clinically relevant co-infections are caused by Bartonella species, Yersinia enterocolitica, Chlamydophila pneumoniae, Chlamydia trachomatis and Mycoplasma pneumoniae. Infections caused by these pathogens in patients not infected by Borrelia burgdorferi can result in clinical symptoms similar to those occurring in Lyme disease. This applies particularly to infections caused by Bartonella henselae, Yersinia enterocolitica, and Mycoplasma pneumoniae.

Chlamydia trachomatis primarily causes polyarthritis. Chlamydophila pneumoniae not only causes arthritis but also affects the nervous system and the heart, which renders the differential diagnosis difficult.The diagnosis is even more complex when co-infections occur in association with Lyme disease. (from Berghoff W. Open Neurol J. 2012;6:158-78.)

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