Chronic fatigue syndrome following infections in adolescents

aDivision of Infectious Diseases, Ann and Robert H. Lurie Children's Hospital of Chicago, Northwestern University Feinberg School of Medicine bCenter for Community Research, DePaul University, Chicago, Illinois, USA.
Current opinion in pediatrics (Impact Factor: 2.53). 12/2012; 25(1). DOI: 10.1097/MOP.0b013e32835c1108
Source: PubMed


Purpose of review:
To review the recent epidemiology, pathophysiology, and treatment of postinfectious chronic fatigue syndrome (CFS) in adolescents.

Recent findings:
Thirteen percent of adolescents (mainly women) met the criteria for CFS 6 months following infectious mononucleosis; the figure was 7% at 12 months and 4% at 24 months. Peak work capacity, activity level, orthostatic intolerance, salivary cortisol, and natural killer cell number and function were similar between adolescents with CFS following infectious mononucleosis and recovered controls. Autonomic system, oxygen consumption, peak oxygen pulse, psychological and cytokine network differences were documented between those who recovered and those who did not.

The prognosis of CFS is better in adolescents than in adults. Activity level, exercise tolerance, and orthostatic testing could not distinguish patients with CFS from adolescents who have recovered from infectious mononucleosis (controls), while certain cytokine network analyses, life stress factors, and autonomic symptoms could.

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Available from: Ben Z Katz, Apr 01, 2015
    • "Alterations in both the innate and acquired immune systems have been reported [12] [13] [14] [15] [16] [17]. Disease clustering and even small epidemics have been described [18] [19] [20] [21] [22] [23] [24]. It has been proposed that autoimmune mechanisms may play a role [25] [26] [27], and that, in addition to infections, immunizations could be involved in the onset or continuation of the pathophysiological process. "
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    ABSTRACT: Background: Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is associated to infections and it has been suggested that vaccination can trigger the disease. However, little is known about the specific association between clinically manifest influenza/influenza vaccine and CFS/ME. As part of a registry surveillance of adverse effects after mass vaccination in Norway during the 2009 influenza A (H1N1) pandemic, we had the opportunity to estimate and contrast the risk of CFS/ME after infection and vaccination. Methods: Using the unique personal identification number assigned to everybody who is registered as resident in Norway, we followed the complete Norwegian population as of October 1, 2009, through national registries of vaccination, communicable diseases, primary health, and specialist health care until December 31, 2012. Hazard ratios (HRs) of CFS/ME, as diagnosed in the specialist health care services (diagnostic code G93.3 in the International Classification of Diseases, Version 10), after influenza infection and/or vaccination were estimated using Cox proportional-hazards regression. Results: The incidence rate of CFS/ME was 2.08 per 100,000 person-months at risk. The adjusted HR of CFS/ME after pandemic vaccination was 0.97 (95% confidence interval [CI]: 0.91-1.04), while it was 2.04 (95% CI: 1.78-2.33) after being diagnosed with influenza infection during the peak pandemic period. Conclusions: Pandemic influenza A (H1N1) infection was associated with a more than two-fold increased risk of CFS/ME. We found no indication of increased risk of CFS/ME after vaccination. Our findings are consistent with a model whereby symptomatic infection, rather than antigenic stimulation may trigger CFS/ME.
    No preview · Article · Oct 2015 · Vaccine
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    • "It also has been shown that cumulative life stress is involved in the pathophysiology of CFS [69] [70] and depression [71]. For example, in a cohort study, it was reported that perceived stress and stressful life events at baseline were associated with postinfectious CFS following infectious mononucleosis at 6 months [20]. Therefore, the present findings shed light on our understanding on the pathophysiological role of psychological stress in CFS or depression, i.e. there is a possibility that stress-induced GCs and microglia play a role in the pathogenesis of post-infectious functional syndromes such as post-infectious CFS and post-viral depression. "
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    ABSTRACT: When animals suffer from viral infections, they develop a set of symptoms known as the "sickness response." Recent studies suggest that psychological stress can modulate the sickness response. However, it remains uncertain whether acute and chronic psychosocial stress have the same effect on viral infection-induced sickness responses. To address this question, we compared changes in polyI:C-induced sickness responses, such as fever, change of body weight and food intake, mechanical allodynia, and depressive-like behavior, in rats that had been pre-exposed to single and repeated social defeat stress. Intraperitoneal injection of polyI:C induced a maximal fever of 38.0 °C 3 h after injection. Rats exposed to prior social defeat stress exhibited blunted febrile responses, which were more pronounced in the repeated stress group. Furthermore, only the repeated stress group showed late-onset and prolonged mechanical allodynia lasting until 8 days after injection in the von Frey test and prolonged immobility time in the forced swim test 9 days post-injection. To assess the role of glucocorticoids and microglia in the delayed and persistent development of these sickness responses in rats exposed to repeated stress, we investigated the effect of pretreatment with RU486, a glucocorticoid receptor antagonist, and minocycline, an inhibitor of microglial activation, on polyI:C-induced allodynia and depressive-like behavior. Pretreatment with either drug inhibited both the delayed allodynia and depressive-like behavior. The present study demonstrates that repeated, but not single, social defeat stress followed by systemic polyI:C administration induced prolonged allodynia and depressive-like behavior in rats. Our results show that even though a single-event psychosocial stress does not have any effect by itself, animals may develop persistent allodynia and depressive-like behavior when they suffer from an infectious disease if they are pre-exposed to repeated or chronic psychosocial stress. Furthermore, this study suggests that stress-induced corticosterone and microglial activation play a pivotal role in this phenomenon. Copyright © 2015. Published by Elsevier Inc.
    Full-text · Article · Apr 2015 · Physiology & Behavior
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    ABSTRACT: Summary Background: Lyme neuroborreliosis (LNB) is a nervous system infection due to Borrelia burgdorferi sensu lato (Bb). Objectives: To present evidence-based recommendations for diagnosis and treatment. Methods: Data were analysed according to levels of evidence as suggested by EFNS. Recommendations: The following three criteria should be fulfilled for definite LNB, and two for possible LNB: (1) neurological symptoms; (2) CSF pleocytosis; (3) Bb specific antibodies produced intathecally. PCR and CSF culture may be corroborative if symptom duration is less than 6 weeks, when Bb antibodies may be absent. PCR is otherwise not recommended. There is insufficient evidence to recommend the following tests for diagnostic purposes: microscope-based assays, chemokine CXCL13, antigen detection, immune complexes, lymphocyte transformation test, cyst formation and lymphocyte markers. Adult patients with definite or possible acute LNB (symptom duration < 6 months) should be offered a single, 14-day course of antibiotic treatment. Oral doxycycline (200 mg daily) and intravenous (IV) ceftriaxone (2 g daily) are equally effective in patients with symptoms confined to the peripheral nervous system, including meningitis (Level A). Patients with CNS manifestations should be treated with IV ceftriaxone (2 g daily) for 14 days, and late LNB (symptom duration > 6 months) for 3 weeks (good practice points). Children should be treated as adults, however doxycycline is contraindicated in children under 8 years of age (9 years in some countries). If symptoms persist for more than 6 months after standard treatment, the condition is often termed post-Lyme disease syndrome (PLDS). Antibiotic therapy has no impact on PLDS (Level A).
    No preview · Chapter · Sep 2011
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