Leendert Kunst, Gijs J Jansen and Bertil R de Klyn
Since 2007 the Netherlands has been faced with serious public health issues resulting from an epidemic outbreak of Q-fever. Although acute Q-fever may etiologically be linked to Coxiella burnetii, there is currently no expert consensus on the primary cause of the pathogenic clinical manifestation in patients suffering from Q-fever fatigue syndrome (QFS). Scientists have been searching for the cause of QFS for many years. In the Netherlands, negative qPCR results and serology tests have led to the conclusion that there were no viable C. burnetii present in patients suffering from the Q-fever fatigue syndrome. In another study, infecting test animals with bacterial remnants taken from QFS patients did not result in a transfer of infection. The conclusion is that no viable bacteria are present and that the clinical condition should be attributed to an immuno-modulatory complex (IMC).
The QFS subjects in this study had been previously serologically diagnosed as having Q-fever. Using Fluorescence in situ Hybridization technology, the authors have found that QFS significantly correlated with the presence of viable large, cell variants (LCV) of C. burnetii. Other studies have shown that the host cells for these LCVs are macrophages, the part of the immune system designed to ingest and destroy pathogens. The cell wall of an LCV has a very limited amount of peptidoglycan and is, in fact, a cell wall deficient bacteria (CWDB). These CWDB hosted in the macrophages can multiply within the lysosome, and eventually revert back to the classical bacterial form given the right conditions.
This article demonstrates that automated Fluorescence in situ Hybridization technology can be used as a method to determine the presence of bacterial DNA of viable L-form bacteria in white blood cells derived from patients suffering from Q-fever Fatigue Syndrome.
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