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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}

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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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