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.
Keywords
Chronic fatigue - myalgic encephalomyelitis - adolescent - Epstein-Barr virus - autonomic
dysfunction - post-infectious fatigue