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Coxiella burnetii infection (Q fever) in rheumatoid arthritis patients with and without anti-TNFα therapy
  1. T Schoffelen1,
  2. L M Kampschreur2,
  3. S E van Roeden2,
  4. P C Wever3,
  5. A A den Broeder4,
  6. M H Nabuurs-Franssen5,
  7. T Sprong5,
  8. L A B Joosten1,
  9. P L C M van Riel6,
  10. J J Oosterheert2,
  11. M van Deuren1,
  12. M C W Creemers7
  1. 1 Department of Internal Medicine, Radboud University Medical Center, Nijmegen, The Netherlands
  2. 2 Department of Internal Medicine and Infectious Diseases, University Medical Centre Utrecht, Utrecht, The Netherlands
  3. 3 Department of Medical Microbiology and Infection Control, Jeroen Bosch Hospital, 's-Hertogenbosch, The Netherlands
  4. 4 Department of Rheumatology, Sint Maartenskliniek, Nijmegen, The Netherlands
  5. 5 Department of Medical Microbiology and Infectious Diseases, Canisius-Wilhelmina Hospital, Nijmegen, The Netherlands
  6. 6 Department of Rheumatology, Radboud University Medical Center, Nijmegen, The Netherlands
  7. 7 Department of Rheumatology, Jeroen Bosch Hospital, 's-Hertogenbosch, The Netherlands
  1. Correspondence to Teske Schoffelen, Department of Internal Medicine, Radboud University Medical Center, P.O. Box 9101, Nijmegen 6500 HB, The Netherlands; Teske.Schoffelen{at}radboudumc.nl

https://doi.org/10.1136/annrheumdis-2014-205455

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    Q fever is a zoonosis caused by the intracellular bacterium Coxiella burnetii. The Netherlands experienced a major Q fever outbreak between 2007 and 2010, with an estimate of more than 40 000 infected individuals.1 Initial infection is asymptomatic in over 50% of the infected individuals or causes a mostly self-limiting febrile disease.2 However, chronic Q fever may develop months to years after initial infection. This serious, life-threatening condition presents mostly as endocarditis or infection of an aortic aneurysm or vascular prosthesis, and is accompanied by high IgG antibody titres against phase I C burnetii.3 Individuals most at risk for chronic Q fever are those with pre-existing valvulopathy, vascular aneurysm or prosthesis and yet undefined types of immune suppression.4 ,5 Tumour necrosis factor-α (TNFα) plays an important role in the defence against intracellular bacteria such as C burnetii. In vitro studies show that TNFα is involved in internalisation and intracellular killing of C burnetii in monocytes.6 ,7 In addition, C burnetii-infected TNFα knockout mice develop early bacteraemia and severe …

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    Footnotes

    • Contributors All authors were involved in drafting the article or revising it critically for important intellectual content, and all authors approved the final version to be published. TS and LMK had full access to all the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.

    • Funding This investigator-initiated study was supported by grants of Pfizer BV and The Netherlands Organisation for Health Research and Development (grant number 205520002 to TS).

    • Competing interests PLCMvR received speaker honoraria and/or consulting fees from Abbvie, UCB, Pfizer, Roch and MSD. All other authors declare that they have no competing interests.

    • Patient consent Obtained.

    • Ethics approval Medical Ethical Committee Arnhem-Nijmegen (CMO regio Arnhem-Nijmegen).

    • Provenance and peer review Not commissioned; externally peer reviewed.