1 Introduction

Fibromyalgia (FM) is a complex, chronic disorder characterized by widespread musculoskeletal pain, fatigue, sleep disturbances, and cognitive dysfunction [1]. Globally, its prevalence varies between 0.2% and 11.4%, depending on the diagnostic criteria and populations studied. Pain in FM patients is defined as central sensitization, but several works have now defined it as nociceptive. Epidemiological data indicate a higher prevalence in females, with a higher incidence typically noted in adulthood [1, 2]. Its pathogenesis remains incompletely understood but is thought to involve central sensitization, dysregulated pain processing, and neuroimmune interactions [2]. Various factors, including genetic predisposition, psychological stressors, and infectious triggers, have been implicated in the onset of FM [3]. Notably, human T-lymphotropic virus type 1 (HTLV-1) has been associated with a variety of neurological and rheumatological conditions [4]. Emerging evidence suggests that infections, including HTLV-1, may contribute to the pathogenesis of FM [5], supporting the hypothesis that infections may play a pivotal role in initiating FM symptoms. Parvovirus B19, a DNA virus primarily responsible for erythema infectiosum in children and arthropathy in adults, has also been linked to various rheumatologic manifestations [6, 7]. Some studies have indicated an increased seroprevalence of parvovirus B19 among patients with FM, suggesting a possible etiopathogenic or triggering role [8]. However, this association remains a matter of ongoing debate [9]. Here, we present a case in which parvovirus B19 infection appears to directly contribute to the onset of FM in a previously healthy young woman.

2 Case History/Examination

A 21-year-old Caucasian woman, non-smoker, and homemaker, presented with a 6-month history of widespread musculoskeletal pain and cognitive impairment, often described as “fibro fog.” She had a history of overall good health and was not taking any medications for significant medical conditions. The onset of her FM symptoms coincided with symptoms of a parvovirus B19 infection, which included fever and a skin rash. The diagnosis of parvovirus B19 infection was confirmed via serological testing, which demonstrated positive IgM antibodies. The patient had no prior history of musculoskeletal pain, joint symptoms, or cognitive difficulties. Additionally, her medical history was otherwise unremarkable, with no significant comorbidities or relevant health conditions. Physical examination during a rheumatology consultation demonstrated tenderness in 14 out of 18 tender points, consistent with the 2016 revised FM diagnostic criteria [10]. Specifically, the Widespread Pain Index (WPI) was 7, and the Symptom Severity Scale (SSS) score was 6, meeting the diagnostic thresholds. Neurological examination was unremarkable, with no focal deficits noted.

3 Differential Diagnosis, Investigations, and Treatment

Comprehensive laboratory evaluations, including complete blood count, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP), were within normal limits. Tests for antinuclear antibodies (ANA) and anti-cyclic citrullinated peptide (anti-CCP) antibodies were negative, and thyroid function tests were unremarkable. Differential diagnoses considered included rheumatic and inflammatory conditions such as rheumatoid arthritis, systemic lupus erythematosus, and other arthropathies. However, the absence of inflammatory markers, coupled with the presence of characteristic tender points, supported a diagnosis of FM. The patient was managed through a multidisciplinary approach involving physical therapy (Yoga), cognitive-behavioral therapy (CBT), and low-dose antidepressants (duloxetine 60 mg daily and amitriptyline 25 mg daily), specifically to mitigate chronic pain and address sleep disturbances.

4 Results (Outcome and Follow-Up)

Follow-up assessments indicated a significant improvement in both WPI, reduced from 7 to 5, and SSS, reduced from 6 to 4. The patient demonstrated partial symptom relief with a multidisciplinary treatment approach, incorporating both pharmacological and non-pharmacological interventions. She continues to be monitored for symptom evolution and response to ongoing therapy, including specific drug interventions such as low-dose antidepressants and non-drug therapies like physical and cognitive-behavioral therapies. The improvements in WPI and SSS are being tracked to evaluate the efficacy of these interventions.

5 Discussion

This case suggests a direct association between parvovirus B19 infection and the onset of FM symptoms. Viral infections are increasingly recognized as potential triggers for FM by precipitating immune activation, neuroinflammation, and central sensitization [3, 11]. The specific involvement of parvovirus B19, along with other viral agents, in the pathogenesis of FM remains an area of active investigation. Potential mechanisms include immune system activation, increased cytokine production, and neuroinflammatory processes that may lead to central sensitization. Previous studies have explored the relationship between HTLV-1 infection and FM. For example, Ablin et al. [5] reported higher rates of FM symptoms among HTLV-1-infected patients compared to noninfected individuals, supporting the premise that infections such as HTLV-1 may be implicated in the development of FM.

Recent findings have also pointed to an association between SARS-CoV-2 infection [12, 13] and the subsequent onset of FM symptoms. Khoja et al. [14] conducted a preliminary study involving patients with new-onset chronic musculoskeletal pain following COVID-19 infection and found that 72.2% of these individuals fulfilled the criteria for FM. This observation highlights the significant impact of viral infections on musculoskeletal health and supports the hypothesis that FM may develop as a long-term sequela of viral infections, thereby emphasizing the necessity for further research into post-viral syndromes.

Parvovirus B19 has been implicated in a variety of rheumatologic conditions, ranging from acute to chronic arthritis [7]. A study conducted by Sayed et al. [8] demonstrated significantly higher seroprevalence of parvovirus B19 IgG among patients with FM compared to healthy controls (81.3% vs. 64%, p = 0.027), suggesting that parvovirus B19 infection could contribute to the etiopathogenesis of FM or serve as a triggering factor in predisposed individuals. Conversely, other investigations have not found a significant link between parvovirus B19 exposure and FM. Narváez et al. [9] reported no serological evidence linking FM to parvovirus B19 exposure, underscoring the need for additional studies to resolve these inconsistencies. The absence of inflammatory markers and negative autoantibodies in the present case supports the notion that her symptoms are consistent with FM rather than with an underlying inflammatory arthropathy.

Parvovirus B19 infection may serve as a potential trigger for the onset of FM in predisposed individuals. This case report underscores a potential correlation between parvovirus B19 infection and the onset of FM symptoms, which persisted beyond the resolution of the initial viral infection. The patient demonstrated partial symptom relief with a multidisciplinary treatment approach, incorporating both pharmacological and non-pharmacological interventions. She continues to be monitored for symptom evolution and response to ongoing therapy. Clinicians should remain cognizant of the possibility that infections, including parvovirus B19, SARS-CoV-2, and HTLV-1, may act as triggers or exacerbating factors for FM, despite ongoing controversies regarding these associations. Early recognition and an integrated treatment strategy are essential for optimizing clinical outcomes in patients presenting with post-infectious FM.

6 Conclusion

This case report underscores a potential correlation between parvovirus B19 infection and the onset of FM symptoms, which persisted beyond the resolution of the initial viral infection. Strategies for preventing FM development following parvovirus B19 infection remain an area of interest; early intervention and monitoring of high-risk patients could potentially mitigate the onset of chronic symptoms. Clinicians should remain cognizant of the possibility that infections, including parvovirus B19, SARS-CoV-2, and HTLV-1, may act as triggers or exacerbating factors for fibromyalgia, despite ongoing controversies regarding these associations. Early recognition and an integrated treatment strategy are essential for optimizing clinical outcomes in patients presenting with post-infectious fibromyalgia.

Author Contributions

Angelo Nigro: conceptualization, writing – original draft, writing – review and editing.

Ethics Statement

The author has nothing to report.

Consent

Written informed consent was obtained from the patient for publication of this case report.

Conflicts of Interest

The author declares no conflicts of interest.