Chronic fatigue and infection

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.