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FRI0198 The risk of chronic q fever in rheumatoid arthritis patients with and without anti-tnf 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. P. L. van Riel1,
  9. J. J. Oosterheert2,
  10. M. van Deuren1,
  11. M. C. Creemers3
  1. 1Radboud University Nijmegen Medical Centre, Nijmegen
  2. 2University Medical Center, Utrecht
  3. 3Jeroen Bosch Hospital, ‘s-Hertogenbosch
  4. 4Sint Maartenskliniek
  5. 5Canisius-Wilhelmina Ziekenhuis, Nijmegen, Netherlands


Background The Netherlands faced a large Q fever outbreak from 2007-2010, during which many individuals have been infected with Coxiella burnetii, the intracellular bacterium causing Q fever. Initial infection is often asymptomatic. Chronic Q fever, which develops in a minority of infected individuals (1-5%), presents months to years after primary infection, mostly as endocarditis or vascular infection. Immunosuppression, although not clearly defined, is a stated risk factor for chronic Q fever. Anti-TNF therapy is associated with increased risk of intracellular infections.

Objectives To examine whether rheumatoid arthritis (RA) patients on anti-TNF therapy are at increased risk of development of chronic Q fever, compared to TNF-naive RA patients using disease modifying drugs (DMARDs).

Methods RA patients, living in Q fever epidemic areas, were identified in rheumatology outpatient clinics in participating hospitals. We selected a cohort of patients on anti-TNF therapy (infliximab, etanercept, adalimumab) for at least three months during the epidemic and a cohort TNF-naive patients who were using DMARDs during the same period. Participants were screened for anti-C. burnetii antibodies, measuring IgG against C. burnetii phase I and II in serum. Patients with phase I and/or II IgG titres ≥1:32 were defined as seropositive, indicating previous exposure to C. burnetii. All seropositive individuals were referred for follow-up to the department of internal medicine. Chronic Q fever was diagnosed according to the Dutch guideline on chronic Q fever diagnostics,1 by a team of medical specialists.

Results From December 2011 to July 2012, 361 patients on anti-TNF therapy and 398 TNF-naive patients participated. The anti-TNF treated patients more frequently used systemic prednisone (at least three months during the epidemic) (P < 0.001). Of patients on anti-TNF therapy, 60/361 (16.6%) were seropositive, compared to 56/398 (14.1%) of TNF-naive patients (P=0.35). Overall, 10/116 (8.6%) seropositive patients were diagnosed with chronic Q fever, of which 7/60 (11.7%) patients on anti-TNF therapy compared to 3/56 (5.4%) TNF-naive patients (P=0.33). Univariate analysis in seropositive patients identified higher age, the use of systemic prednisone, valvulopathy/prosthetic valve and aneurysm/vascular prosthesis as significant risk factors for chronic Q fever.

Conclusions We did not find a significantly higher prevalence of chronic Q fever in patients on anti-TNF therapy compared to TNF-naive patients in this population. Nevertheless, the prevalence of chronic Q fever in seropositive RA patients, either on anti-TNF therapy or DMARD therapy, was substantially higher (8.6%) than reported in non-selected infected individuals (1-5%), suggesting that RA and anti-rheumatic treatment are a risk factor for development of chronic Q fever. Specifically, the use of systemic prednisone was identified as a risk factor in this population.


  1. Wegdam-Blans MC, Kampschreur LM, Delsing CE, et al. Chronic Q fever: review of the literature and a proposal of new diagnostic criteria. J Infect 2012; 64(3): 247-59.

Acknowledgements Investigators initiated study funded by Pfizer. This work was also supported by The Netherlands Organisation for Health Research and Development [grant number 205520002 to T.Schoffelen]

Disclosure of Interest None Declared

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