Affiliations: Division of General Pediatric and Adolescent Medicine,
Mayo Clinic, Rochester, Minnesota, USA | Division of Pediatric Cardiology, Mayo Clinic,
Rochester, Minnesota, USA | Division of Pediatric Infectious Diseases, Mayo
Clinic, Rochester, Minnesota, USA
Note: [] Correspondence: Philip R. Fischer, MD, Division of General
Pediatric and Adolescent Medicine, Mayo Clinic, 200 First Street SW, Rochester,
Minnesota 55905, USA. Tel.: +1 507 538 0127; Fax: +1 507 284 0727; E-mail:
fischer.phil@mayo.edu
Abstract: Chronic fatigue is common during adolescence, and up to 1% of the
adolescent population is unable to participate in normal activities due to
persisting tiredness. The onset and perpetuation of chronic fatigue are
multifactorial, and infection has often been postulated to be an important
aspect of the etiology. While some infections persist for many months or even
years and can be accompanied by fatigue, acute infection more frequently serves
as a trigger for subsequent pathophysiologic mechanisms, which are associated
with fatigue that persists much longer than the initial, inciting infection.
Altered gene expression might mediate some of these ongoing processes. Chronic
fatigue is often associated with altered cytokine and natural killer cell
patterns and is sometimes associated with the development of autoimmunity, even
to specific neurologic receptors. Autonomic dysfunction in the form of the
postural orthostatic tachycardia syndrome is frequently linked to adolescent
chronic fatigue, as is cardiovascular deconditioning. Psychologic profiles both
prior to and after the inciting infection have also been associated with
ongoing fatigue. Thus, infectious illnesses can interact with immune,
neurologic, cardiovascular, and psychologic factors to stimulate the
development of chronic fatigue in adolescents.
