Infectious Burden and Risk of Stroke

Abstract

To determine the association between a composite measure of serological test results for common infections (Chlamydia pneumoniae, Helicobacter pylori, cytomegalovirus, and herpes simplex virus 1 and 2) and stroke risk in a prospective cohort study. Design: Prospective cohort followed up longitudinally for median 8 years.Setting: Northern Manhattan Study.Patients: Randomly selected stroke-free participants from a multiethnic urban community.Main Outcome Measure: Incident stroke and other vascular events.Results: All 5 infectious serological results were available from baseline samples in 1625 participants (mean [SD] age, 68.4 [10.1] years; 64.9% women). Cox proportional hazards models were used to estimate associations of each positive serological test result with stroke.

Influenza‐like illness as a trigger for ischemic stroke

“…A composite measure of chronic infection assessed by serologies against several common bacterial and viral infections was associated with increased long‐term stroke risk in the Northern Manhattan Study 6. In case‐crossover analyses from both the Cardiovascular Health Study and the Atherosclerosis Risk in Cardiovascular Disease Study, recent hospitalization for infection was associated with increased risk of stroke 7, 8.…”

A case of bacterial meningitis complicated by venous sinus thrombosis

“…Cerebral infarction occurs in 15-20 % of adults with bacterial meningitis, typically in patients with pneumococcal meningitis [7,8]. Mechanisms for infarction in bacterial meningitis are septic arteritis or endarteritis obliterans, venous thrombophlebitis, or thromboembolic events [8].…”

Possible Pivotal Role of Latent Chronic T. gondii Infection in the Pathogenesis of Atherosclerosis

“…Another putative vascular pathogen, cytomegalovirus (CMV), encoded a chemokine receptor that rendered infected smooth muscle cells susceptible to CC chemokine-induced migration [96] . Several authors demonstrated the relationship between the seropositivity to CP, HSV-1 and 2, HCMV, HAV, HP, EBV, and atherosclerosis/coronary artery disease [97][98][99][100][101] . Recently, it was also suggested that more infectious agents rather than any single pathogen may be involved in the development of atherosclerosis and the subsequent cardiovascular events because the proatherogenic effect of each infectious organism might be amplified [1,102] .…”