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Cardiovascular risk factors cannot be ignored in vascular disease following C burnetii infection.
- Martin Wildman (16 August 1999)
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C burnetii is different from Rickettsia spp.
- Lars Wesslen (27 August 1999)
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Martin Wildman
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Editor - We read the paper by Lovey et al (1) on the potential for infection by C. burnetii to be a risk factor for cardiovascular disease. They suggest that the established mode of transmission of C. burnetii is unlikely to be associated with risk factors for cardiovascular disease and that the unavailability of baseline data of such risk is unlikely to influence their findings. However in an outbreak of Q fever pneumonia affecting 147 patients in the United Kingdom in 1989 not referred to by the authors (2,3,) we found that in 110 patients in whom smoking history was available for the time of the infection 60 (55%) were current smokers, 28 (25%) were ex-smokers and only 22 (20%) had never smoked. A subsequent case-control study in this cohort confirmed smoking to be a risk factor for Q fever (3). Follow-up of 87(59%) patients in clinic 9 years after the original outbreak identified 31(35%) to be current smokers (mean age 51.2 SD10.2) with a mean (SD) smoking burden of 33 (15.8) pack-years. Amongst this group 1 patient had had a CVA and 3 had ischaemic heart disease. 35 (40.2%) patients were ex-smokers (mean age 57.0 SD 13.4) with a mean (SD) smoking burden of 26.4 (18.8) pack years. In this group 1 had had a CVA and 6 had IHD. Only 17 (19.5%) patients (mean age 53.8 SD 9.1) had never smoked and none of these patients had vascular disease. These results suggest that smoking is a risk factor for Q fever and show that in our patients it has been the current or ex-smokers who have developed cardiovascular disease. It is therefore essential that current and past cigarette smoking are added to a re-analysis by the Geneva group before C burnetii can be taken as the explanation of the excess cardiovascular morbidity and mortality they have observed. References 1) Lovey P, Morabia A, Bleed D, Peter O, Dupuis G, Petite J. Long term vascular complications of Coxiella burnetii infection in Switzerland: cohort study. BMJ 1999;319:284-6 2) Smith D L, Ayres JG, Blair I, Burge PS, Carpenter MJ, Caul EO, et al. A large Q fever outbreak in the West Midlands: clinical aspects. Resp Med 1993;87:509-516 3) Hawker JI, Ayres JG, Blair I, Evans MR, Smith DL, Smith EG et al. A large outbreak of Q fever in the West Midlands: windborne spread into a metropolitan area? Commun Dis Public Health 1998;1:180-187 4) Ayres JG, Flint N, smith EG, Tunnicliffe WS, Fletcher TJ, Hammond K, et al. Post-infection fatigue syndrome following Q fever. Q J Med 1998; 91:105-123 Dr Martin Wildman, Jon G Ayres, Heartlands Research Institute, Lincoln House, Birmingham Heartlands Hospital, Bordesley Green East, B9 5SS 1st author and corresponding author -Martin Wildman |
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Lars Wesslen, Consultant in infectious diseases Department of Infectious Diseases, Uppsala University Hospital, SE-751 85 Uppsala, Sweden
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EDITOR - In Pierre-Yves Lovey et al's paper on the long term vascular complications of Coxiella burnetii infection in Switzerland (1), the fact that C burnetii belongs to the tribe of Rickettsiae is pointed out thereby drawing parallels to the patogenetic properties of other members in this group. Rickettsia spp. are known to cause vasculitis by proliferation of organisms in the endothelial lining of small arteries, veins and capillaries. There are only limited data on whether C burnetii may have similar properties. Initially rickettsiae encompassed all intracellular bacteria. However, C burnetii have since long been considered separate from other Rickettsiales when comparing phenotypic characteristics (2), but because of historical reasons, such as need for propagation in eukaryotic cells and risk for accidental infection of laboratory personnel, the organism has been studied by the few centres working with other Rickettsiales as well, thereby conserving the taxonomy. However, taxonomy is not a static art, but continuously in change, being constructed of man-made boundaries where nature has none. At present, genotypic phylogeny has emerged as the golden standard, thereby sometimes rewriting our paradigms considerably. The results of this may by courtesy of the National Center for Biotecnology Information, and all scientists contributing, be browsed at www.ncbi.nlm.nih.gov/Taxonomy/tax.html C. burnetii is a proteobacterium belonging to the gamma subdivision and is not closely related to Rickettsia spp., which are proteobacteria belonging to the alpha subdivision; the order Rickettsiales; the family Rickettsiaceae; the tribe Rickettsiae. More close relatives to C burnetii would be the Legionellaceae, also causing a more related clinical picture including pneumonia and endocarditis and sharing genotypic similarities. C burnetii is certainly associated with chronic endocarditis especially in the immunocompromised, and in patients with cardiovascular abnormalities such as valvulopathy, prosthesis or aneurysms, chronic infection may affect those sites. The report by Pierre-Yves Lovey et al is therefore welcome, and as they say, add evidence to the current research on the role of bacterial infections in causing vascular disease. Lars Wesslen, 1. Lovey P-Y, Morabia A, Bleed D, Péter O, Dupuis G, Petite J. Long term vascular complications of Coxiella burnetii infection in Switzerland: cohort study. BMJ 1999;319:284-6. 2. Lennette EH, Schmidt NJ, ed. Diagnostic procedures for viral, rickettsial and chlamydial infections. 15 ed. Washington: R.R. Donnelley & Sons Company, Crawfordsville IN, 1979:1061-1108. |
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