J Pediatr Infect Dis 2010; 05(01): 001-007
DOI: 10.3233/JPI-2010-0217
Georg Thieme Verlag KG Stuttgart – New York

Chronic fatigue and infection

Philip R. Fischer
a   Division of General Pediatric and Adolescent Medicine, Mayo Clinic, Rochester, Minnesota, USA
,
Jonathan N. Johnson
b   Division of Pediatric Cardiology, Mayo Clinic, Rochester, Minnesota, USA
,
Thomas G. Boyce
c   Division of Pediatric Infectious Diseases, Mayo Clinic, Rochester, Minnesota, USA
› Author Affiliations

Subject Editor:
Further Information

Publication History

29 September 2008

28 April 2009

Publication Date:
28 July 2015 (online)

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.