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Cerebrovascular Complications of Infective Endocarditis

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1362 • CID 2008:47 (15 November) • CORRESPONDENCE layed-onset primary cytomegalovirus disease

and the risk of allograft failure and mortality after kidney transplantation. Clin Infect Dis

2008; 46:840–6.

5. Scemla A, Kreis H, Legendre C. Less pessimistic long-term results for patients with cytomega-lovirus disease. Clin Infect Dis 2008; 47:1360–1 (in this issue).

6. Paya C, Humar A, Dominguez E, et al. Efficacy and safety of valganciclovir vs. oral ganciclovir for prevention of cytomegalovirus disease in solid organ transplant recipients. Am J Trans-plant 2004; 4:611–20.

7. Limaye AP, Bakthavatsalam R, Kim HW, et al. Impact of cytomegalovirus in organ transplant recipients in the era of antiviral prophylaxis. Transplantation 2006; 81:1645–52.

Reprints or correspondence: Dr. Raymund R. Razonable, Div. of Infectious Diseases, Mayo Clinic, Marian Hall 5, 200 First St. SW, Rochester, Minnesota 55905 (Razonable.Raymund @mayo.edu).

Clinical Infectious Diseases 2008; 47:1361–2

 2008 by the Infectious Diseases Society of America. All rights reserved. 1058-4838/2008/4710-0020$15.00 DOI: 10.1086/592750

Cerebrovascular

Complications of Infective Endocarditis

To the Editor—We read with great in-terest the article by Snygg-Martin et al. [1] that was recently published in Clinical In-fectious Diseases, which analyzed the cer-ebrovascular complications of left-sided infective endocarditis using MRI and neu-rochemical brain damage markers. In that article, the authors found an elevated in-cidence of symptomatic and asymptom-atic cerebrovascular complications among patients with left-sided infective endocar-ditis. Among the factors associated with cerebrovascular complications, the size of valvular vegetation was identified as a risk factor for symptomatic and asymptomatic complications, and only Staphylococcus aureus infection was associated with symptomatic complications in the micro-biology analysis [1]. However, we feel that some of the issues raised in this article need to be addressed.

As noted in an article by Baddour and Bayer [2], the overall frequency of cebrovascular complications in the study re-ported by Snygg-Martin et al. [1] was very high. However, the number of patients in-cluded in the study was small (60

pa-tients), only 4 cases were due to gram-negative bacteria, and no cases were due to Candida species or other fungi (which are considered to be responsible for 1%– 2% of all cases of infective endocarditis) [3]. In an extensive revision of the liter-ature, Ellis et al. [4] found that 26% of patients with fungal endocarditis devel-oped symptomatic CNS involvement. In a recently published article [5], 33 (1.2%) of 2760 cases of infective endocarditis were due to Candida species. In this article, Boddley et al. [5] reported that infective endocarditis due to Candida species was associated with a similar incidence of cer-ebrovascular complications, compared with infective endocarditis due to all other causes. In a recent comparative analysis published by our group [6], we retro-spectively analyzed the medical literature on published cases of endocarditis due to Candida parapsilosis and endocarditis due to Candida albicans. We found that 17 (26.6%) of 64 patients with left-sided en-docarditis due to C. parapsilosis experi-enced symptomatic cerebrovascular com-plications. Seven patients had intracranial hemorrhage, and 10 patients experienced ischemic strokes [6].

In addition, we suspect that the asso-ciation reported by Snygg-Martin et al. [1] of symptomatic cerebrovascular compli-cations with S. aureus infection only, as well as their finding of a high number of cerebrovascular complications, might be attributable to the small number of pa-tients included in their study. It would be very interesting to perform a multicenter clinical trial to achieve a larger patient sample that would include more cases due to gram-negative bacteria and fungi. This could help us to better establish the re-lationship between the microbiological etiology of infective endocarditis and the risk of symptomatic and asymptomatic cerebrovascular complications.

Acknowledgments

Potential conflicts of interest. J.G. and J.A.: no conflicts.

Jorge Garbino and Juan Ambrosioni

Infectious Diseases Division, University Hospitals of Geneva, Geneva, Switzerland

References

1. Snygg-Martin U, Gustafsson L, Rosengren L, et al. Cerebrovascular complications in patients with left-sided infective endocarditis are com-mon: a prospective study using magnetic res-onance imaging and neurochemical brain dam-age markers. Clin Infect Dis 2008; 47:23–30. 2. Baddour LM, Bayer AS. Cerebrovascular

com-plications in patients with left-sided infective endocarditis: out of site, out of mind. Clin In-fect Dis 2008; 47:31–2.

3. Moreillon P, Que YA. Infective endocarditis. Lancet 2004; 363:139–49.

4. Ellis ME, Al-Abdely H, Sandridge A, Greer W, Ventura W. Fungal endocarditis: evidence in the world literature, 1965–1995. Clin Infect Dis

2001; 32:50–62.

5. Baddley JW, Benjamin DK Jr, Patel M, et al. Candida infective endocarditis. Eur J Clin Mi-crobiol Infect Dis 2008; 27:519–29.

6. Garzoni C, Nobre VA, Garbino J. Candida par-apsilosis endocarditis: a comparative review of the literature. Eur J Clin Microbiol Infect Dis

2007; 26:915–26.

Reprints or correspondence: Dr. Jorge Garbino, Infectious Dis-eases Div., University Hospitals of Geneva, Geneva, Swit-zerland ([email protected]).

Clinical Infectious Diseases 2008; 47:1362

 2008 by the Infectious Diseases Society of America. All rights reserved. 1058-4838/2008/4710-0021$15.00 DOI: 10.1086/592751

Reply to Garbino and Ambrosi

To the Editor—We thank Garbino and Ambrosioni [1] for their interest in our study of cerebrovascular complications (CVC) in left-sided infective endocarditis (IE) [2]. Our study is small, compared with some recent studies in this area [3– 5], but the patients in our study were ep-idemiologically well matched with patients in the National Swedish Endocarditis Reg-istry during the same period. Staphylococ-cus aureus was the only microorganism identified as a risk factor for symptomatic CVC in our study, which is in agreement with the findings of earlier studies [3–6]. As pointed out by Garbino and Ambro-sioni [1], there is a need to evaluate un-common microorganisms, such as Can-dida species or gram-negative bacilli, as potential risk factors for CVC. A much

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