Örebro University
Clinical Epidemiology and Biostatistics, School of Medical Sciences

Author Of 1 Presentation

Epidemiology Oral Presentation

YI02.06 - Central nervous system infections in adolescence and MS risk after age 20 years

Speakers
Presentation Number
YI02.06
Presentation Topic
Epidemiology
Lecture Time
12:15 - 12:27

Abstract

Background

Infectious agents in MS etiology have been previously investigated. Theories of pathogenic mechanisms include molecular mimicry or activation of macrophages and natural killer cells with subsequent infiltration of the blood brain barrier. Epstein-Barr virus (EBV) infection often signaled by infectious mononucleosis (IM) is a notable MS risk factors, but other infections including Chlamydia pneumoniae, among others, are also associated with MS. Adolescence is a potentially critical period for susceptibility MS and associations with exposures in adolescence such as concussion, pneumonia, BMI, and EBV/IM have been found. No studies to our knowledge have examined CNS infection as a risk factor for MS.

Objectives

To determine if CNS infection in childhood (age 0-11 years) or adolescence (age 11-20) is associated with MS risk after age 20 years.

Methods

A cohort born in Sweden between 1970-1994 followed until 31 December 2014, was identified using the Total Population Register, excluding those diagnosed with MS before age 20 years (y) (N=2,422,969). ICD codes from the National Patient Register identified diagnoses of MS after age 20y (n=4,022) (two or more diagnoses), and CNS infection (bacterial and viral) before age 20y. Diagnoses of IM, pneumonia, and other bacterial or viral infections were identified. Infections were classified as present/absent at 0-10y or 11-20y. Cox regression was used to determine associations of CNS infection with MS, with follow-up from age 20y to first MS diagnosis, adjusting for gastrointestinal, genitourinary, respiratory, skin, other infections, sex and parental socioeconomic position.

Results

CNS infection before age 11y was not associated with MS. CNS infection in adolescence was statistically significantly associated with increased MS risk producing an adjusted hazard ratio of 2.80 (95%CI 1.90-4.12). Excluding encephalomyelitis (as this includes acute disseminated encephalitis, often a precursor of MS) the estimate was 1.85 (95%CI 1.11-3.07): an accurate estimate of risk lies between these two hazard ratios. Further adjustment for other infections did not alter the estimates notably.

Conclusions

This novel finding of CNS infection in adolescence associated with MS risk suggests such infections may cause cellular damage in the CNS triggering autoimmune processes pertinent to multiple sclerosis pathogenesis. It also adds to the evidence of a critical susceptibility period in adolescence for MS initiation.

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