Manifestations of tuberculosis possibly associated with rituximab in a patient with diagnosed multiple sclerosis: a case report

Abstract

Background

Multiple sclerosis (MS) is an autoimmune disease affecting the central nervous system. Following the elucidation of the role of B cells in MS pathogenesis, B-cell-depleting agents such as Rituximab have become increasingly utilized. However, the relationship between rituximab therapy and susceptibility to tuberculosis (TB) remains a subject of ongoing investigation, with conflicting evidence in the literature.

Case presentation

A 55-year-old Iranian woman with multiple sclerosis who had received rituximab for five years presented with high-grade fever, chills, and suprapubic pain. One year before admission, she had developed lower-extremity skin lesions initially diagnosed as eosinophilic fasciitis and later revised to erythema nodosum. Computed tomography revealed a left ovarian mass, a right ovarian cyst, ascites, pulmonary involvement, and bilateral pleural effusions, raising concern for malignancy. Bronchoalveolar lavage polymerase chain reaction confirmed tuberculosis. The patient was treated with the World Health Organization standard anti-TB regimen (isoniazid, rifampin, pyrazinamide, and ethambutol). Rituximab was discontinued; dimethyl fumarate was introduced after four months of therapy and rituximab was reintroduced at six months. At one-year follow-up, there was no TB reactivation and no worsening of MS.

Conclusion

This case demonstrates an atypical multisystem presentation of tuberculosis in an immunocompromised patient receiving long-term anti-CD20 therapy. Susceptibility was likely multifactorial, including immunosuppression, occupational exposure, MS-related immune dysregulation, and prior corticosteroid use. Clinicians should maintain a high index of suspicion for atypical tuberculosis in immunocompromised patients receiving biologic therapies.

Supplementary Information

The online version contains supplementary material available at https://doi.org/10.1186/s13256-026-06325-z.

Background

Tuberculosis (TB) remains one of the most lethal infectious diseases globally, imposing a significant social and economic burden on humanity [1]. Pulmonary manifestations are the most characteristic feature of TB; however, extrapulmonary and atypical presentations—particularly in immunocompromised hosts—are well recognized and may substantially delay diagnosis [2–4].

Previous studies have indicated that individuals with multiple sclerosis (MS) are at a heightened risk of developing latent tuberculosis infections (LTBI). The prevalence of LTBI in MS patients has been reported to be 3–5% in the United States, 3.95% in Germany, and 1.8% in Israel [5]. Accordingly, screening for LTBI in patients with MS is recommended, particularly prior to initiation of immunomodulatory therapies. It should be noted, however, that MS itself may contribute to immune dysregulation through inflammatory and autoimmune mechanisms, which may, in addition to the effects of disease-modifying therapy, alter susceptibility to infections such as TB.

In a review by Pourcher et al., the infectious risks associated with disease-modifying drugs for MS were investigated. Fingolimod, teriflunomide, dimethyl fumarate (DMF), natalizumab, anti-CD20 drugs, and cladribine were discussed as potentially increasing susceptibility to opportunistic infections including TB. The review reported cases of gastrointestinal and pulmonary TB linked to the administration of teriflunomide [6].

Rituximab is a chimeric monoclonal antibody targeting the CD20 antigen on B-lymphocytes. It is utilized in the treatment of rheumatoid arthritis, MS, B-cell lymphoma, leukemia, and systemic vasculitis [7, 8]. The mechanism of action of rituximab is primarily directed at humoral immunity through B-cell depletion; cell-mediated immunity, which is considered the principal defense against TB, is theoretically preserved [9]. Nevertheless, only a limited number of studies have examined the risk of TB in patients receiving rituximab [10, 11], and the evidence remains conflicting. Given these uncertainties, further investigation into the appropriate screening protocols and risk stratification for TB in rituximab-treated patients is warranted [12–14].

Herein, we report the case of a 55-year-old woman who developed an atypical, multisystem presentation of TB during long-term rituximab therapy for MS. This case may serve to illustrate the complexity of TB susceptibility in immunocompromised patients and the diagnostic challenges posed by non-classical presentations.

Case presentation

Patient history and disease-modifying therapy timeline

The patient is a 55-year-old Iranian woman with a diagnosis of relapsing–remitting multiple sclerosis established 15 years prior to admission. Her MS treatment history proceeded as follows: she was initially managed with dimethyl fumarate (DMF). Approximately five years before the index admission, rituximab (1 g every 6 months) was introduced as her primary disease-modifying therapy. The last dose of rituximab prior to hospitalization was administered two months before admission. The patient had an occupational history as a healthcare worker involved in TB patient care and supervision; however, she reported no direct contact with confirmed TB patients for at least two years preceding hospitalization. The patient had no significant family history of TB or autoimmune disease. No relevant psychosocial stressors or risk factors were reported.

Prodromal skin manifestation

Approximately one year before the index admission, the patient presented with a nodular, erythematous skin lesion located on her lower extremities. A skin biopsy was performed, and the initial histopathological diagnosis was eosinophilic fasciitis. Rheumatological and infectious workups at that time were negative. Her serum IgG level was measured at 750 mg/dL (reference range: 700–1600 mg/dL), which was within normal limits. Topical corticosteroid treatment and a short course of low-dose oral prednisolone were initiated by the dermatologist, resulting in partial improvement. Upon subsequent hospitalization for the systemic illness described below, the validity of the initial skin biopsy was questioned. Re-evaluation of the histopathological specimen confirmed a revised diagnosis of erythema nodosum (Fig. 1), a recognized cutaneous manifestation of extrapulmonary TB, supporting the diagnosis.

Fig. 1.

Histopathological findings of the skin lesion. Histopathological microscopic examination of the skin biopsy specimen reveals septal panniculitis with lymphocytic vasculitis, characterized by perivascular lymphocytic infiltration. Scattered eosinophils and histiocytes are identified within the inflammatory infiltrate. Prominent fibrosis is observed between fat lobules, with associated hemosiderin deposition. These findings are consistent with erythema nodosum, a recognized cutaneous manifestation of extrapulmonary tuberculosis

TB screening history

A purified protein derivative (PPD) intradermal test was performed prior to the initiation of rituximab therapy and returned a negative result. It is important to note that PPD testing may yield false-negative results in immunocompromised individuals due to impaired cell-mediated immune responses, and this limitation should be considered when interpreting negative screening in patients receiving B-cell-depleting agents.

MS disease activity prior to admission

Over the two years preceding admission, the patient's Expanded Disability Status Scale (EDSS) score increased from 5.5 to 6.0 despite ongoing rituximab therapy. Magnetic resonance imaging (MRI) of the brain and spinal cord demonstrated no new T2-weighted lesions or gadolinium-enhancing activity, suggesting that the observed clinical deterioration may not have been attributable solely to active MS disease. In retrospect, the progressive disability observed over this period may have been, at least in part, a consequence of the undiagnosed systemic infection.

Index admission and initial presentation

The patient was admitted to hospital in July 2023 with chief complaints of high-grade fever, chills, and suprapubic pain. On physical examination, abdominal distension and mild tenderness in the lower abdomen were noted. Auscultation of the chest revealed diminished breath sounds at both lung bases bilaterally, without adventitious sounds. The cardiovascular and neurological examinations were unremarkable.

Initial laboratory investigations and preliminary diagnosis

Initial blood investigations demonstrated marked leukocytosis with a white blood cell (WBC) count of 33.8 × 10³/µL (reference: 4.5–11.0 × 10³/µL), with a polymorphonuclear neutrophil (PMN) count of 80% and 10% band cells, indicating a significant neutrophilic response with left shift. The erythrocyte sedimentation rate (ESR) was elevated at 75 mm/hour (reference: 0–20 mm/hour for females of this age). C-reactive protein and procalcitonin levels were measured; procalcitonin was within normal limits (< 0.25 ng/mL), which, in conjunction with negative blood cultures (obtained prior to antibiotic administration), argued against a primary bacterial sepsis as the etiology of the systemic inflammatory response. Urinalysis revealed 4–6 white blood cells per high-power field, and a urine culture with antimicrobial susceptibility testing was obtained prior to the initiation of empirical antibiotic therapy; this culture subsequently returned negative. An initial working diagnosis of urinary tract infection (UTI) was made, and imipenem was prescribed empirically.

Clinical course and escalation of investigations

The following day, the patient demonstrated transient clinical improvement, with a reduction in WBC count to 22.4 × 10³/µL. An abdominal ultrasound at this time revealed normal renal parenchyma and bladder without evidence of obstructive uropathy. Despite this initial improvement, the patient subsequently developed recurrent fever and rising inflammatory markers, with the WBC count returning to 33 × 10³/µL and ESR increasing to 90 mm/hour. The negative urine culture confirmed that UTI was not the source of the ongoing systemic inflammatory response.

Repeated abdominal ultrasound imaging detected free fluid in the hepatorenal space (Morrison's pouch), bilateral pleural effusions, free fluid in the pelvis, and increasing ascites. A hypoechoic mass with cystic components, measuring approximately 45 × 40 mm, was identified in the left adnexa, along with a 29 mm cyst in the right ovary.

Cross-sectional imaging

Computed tomography (CT) of the abdomen and pelvis with intravenous contrast confirmed a larger heterogeneous mass measuring 75 × 46 mm in the left ovary, a 24 mm cyst in the right ovary, free fluid in the abdominal and pelvic cavity, and involvement of the lung bases (Fig. 2C–F). In the context of confirmed TB and ascites, these adnexal findings raise the possibility of tuberculous peritonitis or pelvic/genitourinary TB and warrant further investigation. Pulmonary CT imaging demonstrated bilateral pleural effusions and consolidation at both lung bases, initially raising the differential diagnosis of pneumonia (Fig. 2A, B). Upon confirmation of TB, we identified these findings as indicative of extrapulmonary TB. Echocardiography was negative for endocarditis. Blood cultures were negative. Serological testing for autoimmune conditions and brucellosis returned negative results.

Fig. 2.

Pulmonary and abdominopelvic findings on computed tomography. A and B Axial computed tomography images of the chest demonstrating bilateral pleural effusions and consolidation at the lung bases, representing pulmonary involvement without associated respiratory symptoms. C and D Axial computed tomography images of the pelvis demonstrating a heterogeneous mass measuring 75 × 46 mm in the left ovary and a cystic lesion measuring 24 mm in diameter in the right ovary. In the context of confirmed tuberculosis and ascites, these adnexal findings raise the possibility of tuberculosis peritonitis or pelvic/genitourinary tuberculosis and warrant further investigation. E Axial computed tomography image demonstrating free fluid in the abdominal cavity. F Axial computed tomography image demonstrating free fluid in the pelvic cavity

Pleural fluid and microbiological investigations

Thoracentesis was performed. The pleural fluid was noted to be serous in character, and the procedure was atraumatic, with no evidence of a hemothorax. Pleural fluid analysis demonstrated the following: red blood cell (RBC) count 48,000/mm³ (which, in the context of an atraumatic tap, may reflect a modest degree of hemorrhagic effusion, and should be interpreted accordingly); WBC count 400/mm³ (47% neutrophils, 53% lymphocytes; reference for pleural fluid: < 100/mm³); glucose 81 mg/dL (reference: > 60 mg/dL or > 60% of serum glucose); protein 2.5 g/dL (reference: < 3 g/dL); and lactate dehydrogenase (LDH) 1186 U/L (reference: < 200 U/L in pleural fluid), consistent with an exudative effusion by Light's criteria. Adenosine deaminase (ADA) was elevated at 71 U/L (reference: < 40 U/L), a finding suggestive of tuberculous etiology.

Pleural fluid cytology was negative for malignant cells. Pleural fluid polymerase chain reaction (PCR) for Mycobacterium tuberculosis was performed and returned negative. A bronchoscopy was subsequently performed. The bronchoscopic findings were notable for mucous plugging and reactive airway changes at the lung bases, which were considered secondary to the underlying systemic inflammatory and possibly infectious process. Bronchoalveolar lavage (BAL) was performed, and BAL PCR for Mycobacterium tuberculosis returned positive, thereby confirming the diagnosis of TB.

Treatment and follow-up

Anti-TB therapy

Upon microbiological confirmation of TB, the patient was commenced on the WHO standard anti-TB regimen comprising isoniazid, rifampin, pyrazinamide, and ethambutol for an intensive phase of eight weeks, followed by a continuation phase of isoniazid and rifampin for four months (total six months of therapy). One week after initiation of anti-TB treatment, the patient became afebrile, her overall clinical condition improved, and leukocyte counts normalized. She was subsequently discharged from hospital.

Disease-modifying therapy management

Rituximab was discontinued upon the diagnosis of TB. The decision to manage MS during the TB treatment period was made through multidisciplinary consultation involving the neurology, infectious disease, and rheumatology teams. The risk of MS relapse during a prolonged period without disease-modifying therapy was carefully weighed against the risk of TB relapse or reactivation. After four months of anti-TB therapy, when the patient had demonstrated sustained clinical improvement and microbiological response, dimethyl fumarate (DMF) was introduced as an interim immunomodulatory agent to mitigate the risk of MS relapse. Rituximab was then reintroduced at six months, coinciding with the completion of the anti-TB regimen. Throughout the treatment period, the patient was monitored with serial liver function tests and complete blood count (CBC) to assess for drug toxicity and treatment response.

Clinical outcome

Following completion of the six-month anti-TB regimen, the patient was confirmed to be microbiologically and clinically cured. Resolution of TB was verified by repeat abdominal ultrasonography, chest CT imaging, and clinical assessment, all of which demonstrated normalization. Notably, during the treatment period, the patient experienced no clinical features of a new MS relapse, and no increase in EDSS was observed. At six-month and one-year follow-up assessments, there was no evidence of TB reactivation, and MS symptomatology remained stable. The patient reported a return to her everyday activities without abdominal pain or other sequelae related to the TB illness.

To improve clarity, a concise timeline of the clinical course is as follows:

Time points are expressed relative to the index admission (T0). At T–15 years, the patient was diagnosed with multiple sclerosis. At T–5 years, rituximab therapy (1 g every 6 months) was initiated following a negative PPD screening test. At T–2 years, the patient experienced neurological deterioration, with an increase in EDSS from 5.5 to 6, although brain MRI showed no new T2 lesions or contrast enhancement. At T–1 year, a skin lesion developed and was initially diagnosed as eosinophilic fasciitis, for which low-dose prednisolone was prescribed, resulting in mild improvement. At T0 (July 2023), the patient was admitted with high fever, chills, suprapubic pain, and abdominal distention. Initial laboratory evaluation revealed leukocytosis (WBC 33.8 × 10³/μL) and elevated ESR (75 mm/hour), and urinalysis showed 4–6 WBCs/high power field. A presumptive diagnosis of urinary tract infection was made, and imipenem was initiated. At T + 2 days, the patient showed temporary clinical improvement; however, by T + 3 days, fever and leukocytosis recurred (WBC 33 × 10³/μL, ESR 90 mm/hour) with negative urine cultures. Subsequent imaging (T + ~ 1 week) revealed a 75 × 46 mm left ovarian mass, a right ovarian cyst, ascites, bilateral pleural effusion, and basal lung consolidation. Pleural fluid analysis showed elevated ADA (71 U/L) and LDH (1186 U/L). Initial BK PCR was negative. Further evaluation with bronchoscopy and bronchoalveolar lavage (BAL) was performed, and BAL PCR returned positive for Mycobacterium tuberculosis, confirming the diagnosis. Following diagnosis (T + ~ 1 week), rituximab was discontinued and standard four-drug anti-tuberculosis therapy (isoniazid, rifampin, pyrazinamide, and ethambutol) was initiated. At T + 1 week after treatment initiation, the patient became afebrile and leukocyte counts normalized. At T + 4 months, multiple sclerosis therapy was modified, and dimethyl fumarate was initiated. At T + 6 months, anti-tuberculosis treatment was completed with full clinical recovery. At T + 1 year follow-up, there was no evidence of tuberculosis reactivation, and the patient’s multiple sclerosis remained stable.

Discussion and conclusions

Atypical presentation of TB

Atypical manifestations of TB may substantially delay diagnosis, a challenge that is compounded in immunosuppressed patients receiving immunomodulatory therapies [15]. The classical presentation of pulmonary TB includes cough, fever, weight loss, and characteristic radiological findings such as upper-lobe infiltrates, nodules, and consolidations [16]. However, a range of uncommon manifestations has been reported in the literature, including pancytopenia, chyluria, atypical skin nodules, and multiple swellings [3].

The present case is notable for the multisystem and atypical nature of the TB presentation. Three features in particular merit detailed discussion. First, the dermatological manifestation: erythema nodosum was observed approximately one year before the onset of systemic symptoms. Erythema nodosum is a recognized, albeit uncommon, cutaneous manifestation of extrapulmonary TB, and in this clinical context may have represented the earliest clinical sign of the disease. Second, the abdominal and pelvic findings: the initial presentation with suprapubic pain, followed by the identification of ovarian masses, ascites, and free pelvic fluid, is not a typical feature of pulmonary TB. These findings raise the possibility of concomitant tuberculous peritonitis or pelvic/genitourinary TB. Ovarian TB, while rare, is a recognized entity, particularly in endemic regions, and the presence of adnexal masses in the context of confirmed TB and ascites warrants consideration of this diagnosis. Whether additional investigations—such as fine-needle aspiration or histopathological examination of the ovarian lesion—were performed to further characterize the mass should be clarified by the authors. In the present case, histopathological evaluation of the ovarian lesion was not performed, and the diagnosis was based on clinical, radiological, and microbiological findings. Although tissue sampling could have provided additional diagnostic certainty, follow-up imaging and clinical assessment demonstrated complete resolution of the adnexal findings after anti-tuberculosis therapy, supporting a tuberculous etiology. Third, the absence of respiratory symptoms: despite radiological evidence of lung base involvement and pleural effusions, the patient did not present with cough, dyspnea, or hemoptysis, which are hallmark features of pulmonary TB.

Multifactorial TB susceptibility and causal attribution

The question of TB susceptibility in this patient is likely multifactorial, and any attribution of causality to a single factor should be made with caution. Several contributing factors may have increased the patient's risk of developing active TB. Rituximab induces profound B-cell depletion, and while TB is primarily controlled by T-cell-mediated immunity, there is growing recognition that B cells may play a more significant role in mycobacterial immunity than previously appreciated [10, 11]. Long-term B-cell depletion may also indirectly impair T-cell function or alter other aspects of the adaptive immune response. Furthermore, the patient had an occupational history involving the care of TB patients, representing a potential source of exogenous infection or reactivation of previously acquired latent infection. The presence of MS itself is associated with immune dysregulation, and prior exposure to corticosteroids (a short course of prednisolone was administered for the skin lesion) may have transiently augmented immunosuppression. In view of these considerations, it is more appropriate to describe the relationship between rituximab and TB in this case as a probable contributory association, rather than to imply direct causation.

In a retrospective cohort study by Alkaldi et al., the risk of TB reactivation under rituximab therapy was assessed. The authors followed 53 patients receiving rituximab for rheumatoid arthritis over a period of six months and found no cases of TB flare-up, concluding that rituximab therapy may be relatively safe in TB-endemic regions when appropriately monitored [10]. In another study by Parikh et al., two cases of TB arising during rituximab therapy were described: the first in a 45-year-old male with systemic lupus erythematosus receiving rituximab in combination with mycophenolate sodium, prednisolone, and hydroxychloroquine, who presented with high-grade fever, chills, and pleural effusion; the second in a 19-year-old male with dilated cardiomyopathy and dermatomyositis, who developed TB symptoms within ten days of rituximab infusion [17]. Notably, in both previously reported cases, concomitant immunosuppressive medications were also being administered, further supporting the view that TB susceptibility in rituximab-treated patients is likely polypharmacological and multifactorial in nature.

Distinction between TB reactivation and new infection

An important consideration in this case is whether the patient's TB represents reactivation of a previously acquired latent infection or a new infection acquired during the course of rituximab therapy. The patient had a negative PPD test prior to the initiation of rituximab, which, if accurate, would argue against pre-existing latent TB at that time. However, as noted above, PPD testing is known to yield false-negative results in immunocompromised individuals. The patient's occupational exposure to TB patients—though she reported no direct contact for at least two years before hospitalization—raises the possibility that latent infection may have been acquired during earlier occupational exposure and subsequently reactivated in the setting of immunosuppression. Alternatively, a new infection acquired from an unidentified environmental or occupational source cannot be excluded. Genotyping or molecular epidemiological studies, if available, could have helped to clarify this distinction.

Diagnostic challenges and pitfalls

This case illustrates several important diagnostic pitfalls. The initial misdiagnosis as a urinary tract infection highlights how nonspecific symptoms—fever, suprapubic pain, and pyuria—can lead to incorrect preliminary diagnoses in immunocompromised patients. The markedly elevated WBC count (33.8 × 10³/µL) with left shift is atypical for TB alone and would ordinarily raise concern for a bacterial superinfection or sepsis. In this case, the negative blood cultures (obtained prior to antibiotic administration), normal procalcitonin, and negative urine culture collectively support the conclusion that no concurrent bacterial infection was present, and that the systemic inflammatory response was driven by the TB process itself. Nonetheless, this degree of leukocytosis in the context of TB warrants careful consideration of the possibility of a superimposed bacterial infection, and clinicians should remain vigilant for this in similar presentations. Although tuberculosis is not typically associated with such marked leukocytosis, similar findings have been reported in severe or disseminated forms of the disease, particularly in immunocompromised patients [18].

The negative PPD test prior to rituximab initiation and the initially negative pleural fluid PCR for Mycobacterium tuberculosis further underline the potential for false-negative results in TB screening and diagnostic testing in immunocompromised hosts. Ultimately, the definitive diagnosis was established by BAL PCR, underscoring the value of bronchoalveolar lavage as a diagnostic modality in patients with atypical or extrapulmonary TB presentations when initial investigations are inconclusive.

Rationale for resumption of rituximab during TB therapy

The decision to reintroduce rituximab at six months, concurrent with the completion of anti-TB therapy, was made following multidisciplinary discussion and a careful assessment of the balance between the risk of MS relapse and the risk of TB reactivation. The patient had demonstrated sustained clinical and microbiological improvement over the preceding months, and the six-month anti-TB regimen had been completed. Dimethyl fumarate had been introduced at four months as a lower-risk interim agent to reduce the risk of MS relapse during the period of rituximab cessation. It must be emphasized, however, that the decision to resume rituximab during or immediately following TB therapy is complex, and the findings of this single case should not be generalized to suggest that such resumption is broadly safe. Each clinical decision in this context should be individualized, guided by multidisciplinary input, and informed by the patient’s specific risk profile.

Impact on MS disease activity

The patient's EDSS increased from 5.5 to 6.0 over the two years preceding admission, a period during which she was receiving rituximab therapy. Notably, MRI demonstrated no new inflammatory lesions or gadolinium enhancement during this interval. This dissociation between clinical deterioration and radiological stability raises the possibility that the progressive disability observed may have been influenced, at least in part, by the presence of undiagnosed chronic TB, which may have contributed to fatigue, reduced functional capacity, and general deconditioning. Following the successful treatment and eradication of TB, the patient reported improvement in gait and overall well-being, lending further support to this hypothesis. The complex interplay between chronic infection, systemic inflammation, and neurological symptoms in MS represents an area warranting further research.

Limitation

While this case provides valuable insights into atypical tuberculosis in immunocompromised patients, several limitations should be considered. First, histopathologic confirmation of the ovarian mass was not obtained, and the diagnosis relied on clinical, radiologic, and microbiologic findings. Second, distinguishing between tuberculosis reactivation and a newly acquired infection was not possible. Finally, as a single-case report, these findings may not be generalizable. Future systematic studies and tissue-based investigations are warranted to better define the spectrum of extrapulmonary TB in patients receiving anti-CD20 therapy.

Clinical learning points

• Atypical presentations of TB: extrapulmonary TB may manifest with dermatologic lesions (for example, erythema nodosum), ovarian/adnexal masses, ascites, or minimal respiratory symptoms, especially in immunocompromised patients.

• Limitations of TB screening: standard screening tests (for example, PPD) may yield false-negative results in patients receiving B-cell-depleting therapies such as rituximab; repeated or alternative diagnostic approaches (for example, BAL PCR) may be necessary.

• Multifactorial susceptibility: TB risk in patients receiving anti-CD20 therapy is influenced by immunosuppression, underlying autoimmune disease, prior corticosteroid use, and environmental/occupational exposure, rather than by a single factor.

• High index of suspicion: clinicians should maintain vigilance for TB in immunocompromised patients presenting with nonspecific systemic symptoms, even in the absence of classical respiratory signs.

Conclusion

This case report serves as an important illustration of the complex interactions between chronic autoimmune diseases such as MS, immunomodulatory therapies including anti-CD20 agents, and opportunistic infections such as TB. The TB susceptibility observed in this patient was likely the result of a convergence of risk factors—including rituximab-induced B-cell depletion, occupational exposure, MS-associated immune dysregulation, and prior corticosteroid use—rather than a consequence of any single factor. The case reinforces the importance of vigilant monitoring, comprehensive and repeated TB screening (with awareness of the limitations of standard screening modalities in immunocompromised patients), and a high index of suspicion for atypical presentations of common infections in this population. Prospective studies examining TB risk, optimal screening strategies, and safe management protocols in patients receiving long-term rituximab therapy are needed to further inform clinical practice.

Abbreviations

ADA

Adenosine deaminase

BAL

Bronchoalveolar lavage

CBC

Complete blood count

CT

Computed tomography

DMF

Dimethyl fumarate

DST

Drug-susceptibility testing

EDSS

Expanded Disability Status Scale

ESR

Erythrocyte sedimentation rate

LDH

Lactate dehydrogenase

LTBI

Latent tuberculosis infection

MRI

Magnetic resonance imaging

MS

Multiple sclerosis

PCR

Polymerase chain reaction

PMN

Polymorphonuclear neutrophils

PPD

Purified protein derivative

RBC

Red blood cell

TB

Tuberculosis

UTI

Urinary tract infection

WBC

White blood cell

WHO

World Health Organization

Author contributions

Conceptualization: LP. Drafting of the manuscript: LP, RM, PK. Critical revision and review: LP, MS. Investigation and data collection: LP, RM, MS. All authors have read and approved the final manuscript for publication.

Funding

This study received no external funding.

Data availability

Data sharing is not applicable to this article, as no datasets were generated or analyzed in the course of the present study.

Declarations

Ethics approval and consent to participate

Written informed consent was obtained from the patient for the publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal. This study has received approval from the Arak University of Medical Science Ethics Committee IR.ARAKMU.REC.1404.056.

Consent for publication

Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

Competing interests

The authors declare that they have no conflicts of interest.