Viral and parasitic pathogen burden and the association with stroke in a population-based cohort

• Type of Material: Article
• Authors: Bradley Pearce, Emory University; Anna Bracher, Emory University; Jeffrey L. Jones, Centers for Disease Control and Prevention; Deanna Kruszon-Moran, Centers for Disease Control and Prevention
• Language: English
• Date: 2018-07-01
• Publisher: SAGE PUBLICATIONS LTD
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: 2017
• Final Published Version (URL): http://dx.doi.org/10.1177/1747493017729269
• Title of Journal or Parent Work: INTERNATIONAL JOURNAL OF STROKE
• Volume: 13
• Issue: 5
• Start Page: 481
• End Page: 495
• Grant/Funding Information: The author(s) disclosed receipt of the following financial support for the research, authorship and/or publication of this article: National Institute of Mental Health (Award Number: 1R01MH092512-01).
• Keywords: Neurosciences & Neurology; Epidemiology; Toxoplasma gondii; infection; Science & Technology; Toxocara; Peripheral Vascular Disease; Cardiovascular System & Cardiology; VIRUS-INFECTION; SEROPREVALENCE; NATIONAL-HEALTH; HELICOBACTER-PYLORI; Life Sciences & Biomedicine; TOXOPLASMA-GONDII INFECTION; CYTOMEGALOVIRUS; DISEASE; cytomegalovirus; PREVENTION; RISK; hepatitis virus; UNITED-STATES; Clinical Neurology
• Research Categories: Biology, Virology; Health Sciences, Epidemiology; Biology, Neuroscience

Abstract

Background: Higher cumulative burden of viral and bacterial pathogens may increase the risk of stroke, but the contribution of parasitic infections in relation to cumulative pathogen burden and risk of stroke has rarely been examined. Aim: To estimate the association of multiple persistent viral and parasitic infections with stroke in a representative sample of adults in the United States. Methods: Serological evidence of prior infection was categorized as positive for 0–1, 2, 3, or 4–5 infections based on immunoglobulin G seropositivity to cytomegalovirus, hepatitis A virus, hepatitis B virus, Toxoplasma gondii, and Toxocara spp. in 13,904 respondents from the National Health and Nutrition Examination Survey III. Regression analysis was used to estimate the cross-sectional association between serological evidence of prior infection and history of stroke adjusting for demographic risk factors, and potential mediators of stroke. Results: Age-adjusted models that included serological evidence of prior infection to cytomegalovirus, hepatitis A virus, hepatitis B virus, Toxoplasma gondii, and Toxocara spp. showed that adults in the highest serological evidence of prior infection category (4–5 infections) had a higher prevalence of stroke (5.50%, 95% confidence interval 2.44–10.46%) than those in the lowest serological evidence of prior infection categories (1.49%, 95% confidence interval 1.01–2.11%), and a trend test suggested a graded association between serological evidence of prior infection and stroke (p = 0.02). In multivariable logistic regression models, the positive association of serological evidence of prior infection with stroke prevalence remained significant after adjustment for other significant risk factors (odds ratio = 1.4, p = 0.01) but was only significant among those aged 20–59 (odds ratio = 2.0, p = 0.005) and not among those aged 60–69 (p = 0.78) or 70 and older (p = 0.43). Conclusion: We found support for a connection between serological evidence of prior infection to cytomegalovirus, hepatitis A virus, hepatitis B virus, Toxoplasma gondii, and Toxocara spp. and stroke among those aged 20–59. There may be a need to consider common parasitic infections in addition to viral and bacterial pathogens when calculating serological evidence of prior infection in relation to cerebrovascular disease.