Pubic symphysis osteomyelitis presenting as groin pain in a patient with rheumatoid arthritis: a case report

Abstract

Background

Osteomyelitis of the pubic symphysis is a rare entity, affecting less than 1% of all osteomyelitis cases. It most frequently occurs in individuals with predisposing conditions, including states of immunosuppression, a history of pelvic or urogenital surgery, and intravenous drug use. In patients with rheumatoid arthritis (RA), the diagnosis can be substantially delayed because clinical manifestations may mimic or overlap with those of inflammatory joint disease. We describe a case of presumed culture-negative osteomyelitis of the pubic symphysis in a patient with RA, emphasizing the diagnostic challenges and therapeutic considerations in this complex clinical setting.

Case presentation

A woman in her late 60s with long-standing seropositive RA, managed with methotrexate and prednisolone, and with comorbid type 2 diabetes mellitus, hypertension, and osteoporosis, presented with a two‑month history of progressively worsening right groin pain refractory to analgesic therapy, leading to significant functional limitation and gait impairment. On admission, she was afebrile with hemodynamically stable vital signs. Physical examination revealed suprapubic tenderness and a reduced range of motion of the right hip. Laboratory investigations showed leukocytosis (14.2 × 10⁹/L, 91% neutrophils), markedly elevated C‑reactive protein (149 mg/L), and an increased erythrocyte sedimentation rate (133 mm/h). Blood cultures remained sterile, whereas urine culture grew methicillin‑sensitive Staphylococcus aureus (MSSA). Serological testing for brucellosis and a tuberculin skin test were both negative. Contrast‑enhanced computed tomography (CT) of the pelvis demonstrated an abscess involving the pubic symphysis associated with reactive osteitis. Culture of aspirated abscess material was sterile, and histopathological examination of the biopsy specimen showed nonspecific inflammatory changes without granulomatous inflammation. Empirical antimicrobial therapy with intravenous cefazolin and ciprofloxacin was administered for 30 days, followed by oral ciprofloxacin and doxycycline for an additional two months. The patient achieved complete clinical and laboratory resolution without the need for surgical intervention. Follow‑up CT imaging confirmed resolution of the abscess, with residual diastasis of the pubic symphysis.

Conclusions

Pubic symphysis osteomyelitis should be included in the differential diagnosis of atypical pelvic pain in immunosuppressed patients with RA. Ongoing immunosuppressive therapy may obscure or attenuate systemic manifestations of infection, thereby contributing to delayed diagnosis. Early utilization of cross-sectional imaging modalities and the administration of prolonged, targeted antimicrobial therapy are critical to achieving favourable clinical outcomes.

Background

Osteomyelitis of the pubic symphysis (PS) is a rare clinical entity, representing less than 1% of all osteomyelitis cases [1]. It predominantly occurs in individuals with identifiable predisposing conditions, including states of immunosuppression, the postpartum period, high-level athletic activity, intravenous drug use, pelvic malignancies, and a history of pelvic or urological surgical interventions [2, 3]. The infection may arise either via haematogenous dissemination or by contiguous spread from adjacent infectious foci [3], with Staphylococcus aureus being the most commonly isolated pathogen [4].

The clinical presentation is typically non-specific and may include localised pelvic or suprapubic pain, groin discomfort, gait disturbances, fever, and lower urinary tract symptoms [5]. Osteomyelitis of the PS is exceedingly uncommon even among patients with established RA. In this setting, diagnostic evaluation is further complicated by the overlap of symptoms with inflammatory joint disease, as pelvic or hip pain may be misattributed to an RA flare, thereby delaying recognition of an underlying infectious process [6].

The risk of such infectious complications is markedly increased by prolonged immunosuppressive therapy, particularly regimens combining methotrexate (MTX) and corticosteroids, and is further exacerbated by concomitant diabetes mellitus (DM). The coexistence of these factors creates a synergistic impairment of host immune defenses that should warrant a low threshold for pursuing an infectious workup in this patient population [7, 8].

We describe a case of presumptive culture-negative PS osteomyelitis in a woman with RA receiving long-term immunosuppressive therapy and concomitant DM, underscoring the need to maintain a high index of clinical suspicion for this rare condition in immunocompromised patients presenting with atypical pelvic pain.

Case presentation

A woman in her late sixties presented with a two-month history of progressively worsening right groin and hip pain, which was exacerbated by weight-bearing activities. She had a ten-year history of severe, deforming, and erosive seropositive RA involving both large and small joints in a bilateral distribution, for which she was receiving MTX 15 mg once weekly and prednisolone 10 mg once daily. Her past medical history was significant for type 2 DM, diagnosed prior to the initiation of corticosteroid therapy and managed with oral hypoglycaemic agents, as well as coexisting hypertension and osteoporosis. Despite treatment with analgesic medications, her pain persisted and resulted in marked functional limitation and impaired ambulation. She denied any history of trauma, intravenous drug use, recent surgical interventions, urinary tract infections, or prior pelvic pathology.

On physical examination, the patient was afebrile with hemodynamically stable vital parameters. Musculoskeletal evaluation demonstrated suprapubic tenderness and a restricted range of motion of the right hip, with pain quantified as 8/10 on the visual analogue scale (VAS). Notably, systematic assessment of the joints typically affected in RA revealed no evidence of active synovitis, swelling, increased warmth, or effusion in any joint bilaterally. This absence of clinical signs of RA activity rendered the degree of inflammatory marker elevation incongruent with the expected RA disease activity, thereby raising concern for a concomitant infectious process.

Laboratory evaluation demonstrated leukocytosis, with a white blood cell (WBC) count of 14.2 × 10⁹ /L (reference range: 4.0–11.0 × 10⁹ /L), including 91% neutrophils. Inflammatory markers were markedly elevated, with a C-reactive protein (CRP) concentration of 149 mg/L (reference: <6 mg/L) and an erythrocyte sedimentation rate (ESR) of 133 mm/h (reference: <40 mm/h). Two sets of blood cultures remained sterile. In contrast, urine culture yielded methicillin-sensitive Staphylococcus aureus (MSSA), susceptible to oxacillin, cefazolin, clindamycin, and trimethoprim–sulfamethoxazole.

Given that the case occurred in Tunisia, a country in which both brucellosis and tuberculosis are endemic, and considering the patient’s residence in a rural setting with regular consumption of unpasteurised dairy products, a systematic infectious disease workup was performed. Serological testing for brucellosis, including Rose Bengal and Wright agglutination assays, was negative, and the Mantoux tuberculin skin test was non-reactive. Transthoracic echocardiography showed no evidence of valvular vegetations, thereby making infective endocarditis unlikely. Chest radiography was within normal limits.

Plain pelvic radiography demonstrated subtle marginal irregularities of the PS, findings suggestive of a subacute inflammatory or infectious process of several weeks’ duration (Fig. 1). Contrast-enhanced pelvic computed tomography (CT) confirmed a PS abscess with surrounding reactive osteitis, as well as an associated fluid collection adjacent to the right proximal hamstring tendon insertion (Fig. 2). Magnetic resonance imaging (MRI) was not performed because of limited availability at our institution, which represents a notable diagnostic constraint.

Fig. 1.

Plain pelvic radiography showing marginal irregularities of the pubic symphysis (arrow)

Fig. 2.

Axial contrast-enhanced computed tomography (CT) of the pelvis. (a) Soft tissue window demonstrating an abscess within the pubic symphysis and an adjacent fluid collection near the insertion of the right proximal hamstring muscle (arrow). (b) Bone window showing reactive osteitis of the pubic symphysis (arrowhead)

Ultrasound-guided aspiration of the abscess was undertaken; Gram staining showed no microorganisms, and both aerobic and anaerobic cultures remained sterile, most plausibly due to prior empirical antibiotic administration. Subsequently, a CT-guided biopsy of the PS was obtained for microbiological and histopathological evaluation. Standard aerobic and anaerobic bacterial cultures were not performed on the biopsy specimen because of laboratory limitations at our institution. Mycobacterial cultures on Löwenstein–Jensen medium yielded negative results. Broad-range 16S rRNA gene sequencing was unavailable and therefore not conducted. Histopathological assessment of the biopsy specimen demonstrated a dense polymorphonuclear infiltrate without granulomatous inflammation, a pattern consistent with acute pyogenic osteomyelitis.

The initial working diagnosis of RA-associated coxitis was revised in light of three key findings: a disproportionate elevation of inflammatory markers relative to the observed RA disease activity; cross-sectional imaging findings localising the primary pathological process to the PS; and a positive urine culture yielding S. aureus. Septic arthritis of the hip was deemed unlikely given the absence of joint effusion on imaging. Osteitis pubis was considered improbable in the context of a CT-demonstrated abscess. Tuberculous and brucellar osteomyelitis were effectively excluded on the basis of negative serological testing, a non-reactive Mantoux test, negative mycobacterial cultures, and the absence of granulomatous inflammation on histopathological examination.

Collectively, the clinical, laboratory, and radiological data supported a diagnosis of presumptive culture-negative osteomyelitis of the PS, with urinary methicillin-susceptible S. aureus (MSSA) considered a plausible, albeit microbiologically unconfirmed, source of haematogenous seeding. Management was directed by a multidisciplinary team including rheumatology, infectious diseases, and orthopaedic surgery. Methotrexate (MTX) was discontinued immediately upon establishment of the diagnosis, in view of its recognised capacity to impair host immune-mediated clearance of infection. Prednisolone was maintained at 10 mg daily throughout the treatment period to prevent adrenal insufficiency and to reduce the risk of an RA flare.

To optimise glycaemic control in the setting of active infection and concomitant corticosteroid therapy, oral hypoglycaemic agents were temporarily replaced with insulin for the duration of the intravenous antibiotic phase and subsequently reintroduced after its completion. Empirical intravenous antimicrobial therapy was initiated with cefazolin (1 g four times daily) and ciprofloxacin (400 mg twice daily), and continued for 30 days. Following documented clinical improvement and normalisation of inflammatory indices (C-reactive protein [CRP] <10 mg/L; white blood cell [WBC] count within the reference range), treatment was de-escalated to an oral consolidation regimen comprising ciprofloxacin (500 mg twice daily) and doxycycline (200 mg once daily) for an additional two months. The full course of antibiotic therapy was well tolerated, with no reported adverse events.

Supportive management included an initial period of bed rest, followed by a structured, progressively intensified mobilisation programme under physiotherapy supervision. At the six-week follow-up, the patient reported complete resolution of groin pain. Inflammatory markers had normalised (CRP 4 mg/L; WBC 7.8 × 10⁹ /L). Follow-up CT imaging demonstrated complete resolution of the abscess, with residual osseous lysis and persistent PS diastasis remaining (Fig. 3). At six months, after radiological and clinical confirmation of infection clearance, MTX was reintroduced at the previous dose, and the patient had resumed full engagement in usual daily activities.

Fig. 3.

Follow-up axial contrast-enhanced computed tomography (CT) of the pelvis, bone window, showing complete resolution of the abscess with residual bone lysis (asterisk) and pubic symphysis diastasis (double-headed arrow)

Discussion

Osteomyelitis of the PS is an uncommon infectious entity that predominantly occurs in individuals with established predisposing conditions, including immunosuppression, postpartum status, intravenous drug use, and a history of pelvic interventions [1, 2]. To our knowledge, only a single previous case of PS osteomyelitis in a patient with rheumatoid arthritis (RA) has been reported in the literature. In that report, Tsukahara et al. described a woman in her late seventies with RA and Felty syndrome who developed Staphylococcus aureus bacteraemia manifesting as groin pain, initially misinterpreted as an RA flare, and who was ultimately managed successfully with prolonged antibiotic therapy [6].

The present case shares several characteristics with the previously described patient, including female sex, advanced age, a urinary focus of methicillin-sensitive S. aureus (MSSA) as a possible, although microbiologically unconfirmed, source of haematogenous dissemination, a delay in diagnosis due to initial attribution of symptoms to underlying RA, and a favourable clinical outcome. However, our patient also had concomitant type 2 diabetes mellitus (DM), which constituted an additional, independent, and central predisposing factor. A detailed comparison of the two cases is provided in Table 1.

Table 1.

Summary of reported cases of pubic symphysis osteomyelitis in patients with rheumatoid arthritis

Feature	Tsukahara et al.	Present case
Age / Sex	77-year-old woman	Woman in her late 60s
Rheumatoid arthritis subtype	RA with felty syndrome	Seropositive RA
Immunosuppressive therapy	Prednisone	Methotrexate, prednisolone
Comorbidities	-	Type 2 diabetes mellitus, hypertension, osteoporosis
Presenting symptom	Groin and hip pain	Right hip/groin pain
Fever at presentation	Not reported	Absent
Causative organism	Staphylococcus aureus (blood culture)	Staphylococcus aureus (urine culture—possible but unconfirmed source of bone infection)
Suspected mechanism	Haematogenous	Haematogenous spread suspected; urinary focus possible but unconfirmed
Diagnostic imaging	Radiography, MRI	Radiography, computed tomography
Initial misdiagnosis	Rheumatoid arthritis flare	Rheumatoid arthritis-related coxitis
Treatment	Antibiotic therapy	Antibiotic therapy (3 months)
Surgical intervention	Surgical drainage and abscess resection	Not required
Outcome	Favourable	Complete clinical and radiological resolution

The diagnostic workup was significantly confounded by the patient’s underlying RA and its immunosuppressive treatment regimen. Methotrexate (MTX) and corticosteroids impair T-cell–mediated immunity and inhibit pro-inflammatory cytokine production, potentially blunting classical clinical manifestations of infection, most notably fever, as observed in this case despite markedly elevated inflammatory biomarkers, thereby contributing to the delay in diagnosis [9, 10]. The principal discriminating feature was the pronounced elevation of C-reactive protein (CRP) to 149 mg/L and erythrocyte sedimentation rate (ESR) to 133 mm/h in the complete absence of active synovitis in the small joints typically affected by RA. In patients with established, severe RA, inflammatory flares are usually accompanied by clear clinical evidence of synovitis in the involved joints; its absence at presentation, combined with the atypical localisation of pain at the PS—a joint not recognised as a typical target in RA—strongly argued against an isolated RA flare and prompted further evaluation for a superimposed infectious process.

Type 2 diabetes mellitus (DM) should be regarded as a primary and independent predisposing factor in this case, rather than as a secondary comorbidity. Type 2 DM compromises several components of innate immunity, including polymorphonuclear neutrophil chemotaxis, phagocytosis, oxidative burst activity, and macrophage-mediated bacterial clearance, and additionally impairs adaptive immune responses through reduced T‑cell proliferation and diminished natural killer cell activity [8]. In the present patient, these immunological defects were further exacerbated by the immunosuppressive effects of long‑term methotrexate (MTX) therapy and chronic corticosteroid exposure, culminating in a state of marked immune dysfunction. This immune milieu increased susceptibility to opportunistic staphylococcal infection at an atypical anatomical site, blunted the systemic inflammatory response, and provided a pathophysiological rationale for extending antimicrobial therapy beyond standard guideline‑based durations [8, 11].

The diagnosis of PS osteomyelitis in this case is supported by a concordant constellation of clinical, laboratory, cross‑sectional imaging, and histopathological findings, rather than by microbiological confirmation, and is therefore most appropriately classified as presumptive culture‑negative PS osteomyelitis. Several constraints precluded definitive pathogen identification. MRI, the reference imaging modality for detecting bone marrow oedema and soft‑tissue involvement in osteomyelitis [3, 4], was not available at our institution, representing a significant limitation in diagnostic refinement. Standard aerobic and anaerobic cultures could not be performed on the CT‑guided biopsy specimen because of laboratory restrictions, and broad‑range 16S rRNA gene polymerase chain reaction (PCR) and sequencing—techniques capable of identifying pathogens directly from tissue specimens irrespective of prior antibiotic exposure, with a reported sensitivity of up to 60–70% in culture‑negative osteomyelitis [12]—were likewise unavailable. The absence of growth from both abscess aspirate and biopsy cultures is most plausibly explained by prior empirical antibiotic administration, a well‑recognised cause of culture‑negative osteoarticular infection [13]. Culture‑negative osteomyelitis constitutes approximately 30–50% of reported cases [14], and the findings in this patient are consistent with this established clinical entity.

Histopathological analysis revealed polymorphonuclear leukocytic infiltration in the absence of granulomatous changes, a pattern compatible with acute pyogenic infection. However, this finding is not pathognomonic, as comparable histological features may also occur in osteitis pubis and active rheumatoid synovitis [15, 16]. Notably, the lack of pannus formation, plasma cell–rich infiltrates, and organized lymphocytic aggregates characteristic hallmarks of rheumatoid synovial pathology, combined with the computed tomography–confirmed, well-circumscribed abscess, supported an infectious rather than a primary inflammatory aetiology.

Although methicillin-sensitive Staphylococcus aureus (MSSA) was isolated from urine culture and regarded as the presumptive pathogen, definitive assignment of this organism as the aetiological agent of the osteoarticular infection cannot be made in the absence of corroborating positive blood or bone cultures. Three pathogenic mechanisms can be postulated: (i) haematogenous seeding of the pubic symphysis from a primary urinary tract source, which represents the classical pathway for S. aureus osteomyelitis [4] and appears most plausible in this case; (ii) descending or contiguous spread from a primary osseous focus to the adjacent urinary tract, facilitated by the intimate anatomical relationship between these structures; or (iii) the occurrence of two temporally overlapping but independent infectious processes in a profoundly immunocompromised host. The directionality of this association remains unresolved, and any causal linkage between the urinary MSSA isolate and the osteitic process must therefore be interpreted with considerable caution.

Collectively, these diagnostic uncertainties emphasize the critical importance of obtaining appropriate microbiological specimens, including bone biopsy, prior to the initiation of antimicrobial therapy whenever clinically permissible. Furthermore, they underscore the urgent need to expand access to advanced molecular diagnostic modalities in resource-constrained healthcare settings.

The geographic context of this case, Tunisia, a country in which both brucellosis and tuberculosis are endemic, necessitated systematic screening for these infections, each of which may closely simulate pyogenic osteomyelitis on clinical and radiological grounds, particularly in immunocompromised hosts [17]. Clinicians practising in endemic areas should maintain a low threshold for investigating these entities in any patient presenting with osteoarticular infection of uncertain aetiology.

Staphylococcus aureus remains the most frequently implicated pathogen in pubic symphysis (PS) osteomyelitis [4], and the empirical antimicrobial regimen in the present case was structured accordingly. Cefazolin was selected as the backbone of intravenous therapy, in accordance with IDSA guidelines, owing to its robust activity against methicillin-susceptible S. aureus (MSSA) and favourable bone tissue penetration [18, 19]. Ciprofloxacin was added on the basis of its excellent penetration into bone and joint tissues and its activity against Gram-negative bacilli (GNB), particularly Enterobacteriaceae, which are common uropathogens and plausible aetiological agents of secondary haematogenous bone infection in individuals with diabetes mellitus [20]. Although ciprofloxacin is not recommended as monotherapy for MSSA, its use in combination with a β-lactam has been described in polymicrobial infections or in scenarios with uncertain microbiological aetiology [21]. This dual regimen thus provided rational empirical coverage for both MSSA and potential Gram-negative co-pathogens in the context of a suspected urinary source.

After 30 days of intravenous therapy, the patient was transitioned to oral consolidation therapy once clinical improvement had been documented and inflammatory markers had normalised (C-reactive protein < 10 mg/L; white blood cell count within the reference range), in line with evidence supporting early switch to oral therapy in bone and joint infections [22]. Ciprofloxacin (500 mg twice daily) was continued because of its high oral bioavailability and its established role in the treatment of osteoarticular infections [23]. Doxycycline (200 mg once daily) was selected as the companion agent, as the urinary MSSA isolate was resistant to rifampicin and fusidic acid, and oral clindamycin, agents typically preferred for staphylococcal bone infections, was not available in our setting [24]. This combination provides complementary mechanisms of action (ciprofloxacin inhibition of DNA gyrase and topoisomerase IV; doxycycline inhibition of protein synthesis via binding to the 30S ribosomal subunit) and offers broad coverage in the context of a culture-negative infection [25]. Although formal pharmacodynamic synergy has not been demonstrated in randomised clinical trials, similar regimens have been successfully employed in other complex osteoarticular infection cases [26].

The total treatment duration of approximately three months exceeded the standard six‑week regimen recommended for haematogenous osteomyelitis [18]. This extension was deemed appropriate in view of a markedly immunocompromised background, comprising rheumatoid arthritis (RA)-related immunosuppression, long-term corticosteroid and methotrexate therapy, and type 2 diabetes mellitus (DM), the absence of microbiological confirmation from bone cultures, and radiological findings compatible with both chronic osteitis and residual changes of osteomyelitis.

The favourable clinical course, characterised by complete clinical and functional recovery at six‑month follow‑up without surgical intervention, may be partly explained by the absence of adverse prognostic factors such as underlying pelvic malignancy, fistula formation, polymicrobial infection, and multidrug‑resistant organisms, all of which have been associated with treatment failure rates of up to 44% in pubic symphysis (PS) osteomyelitis [2]. Persistent PS diastasis on follow‑up imaging represents a well‑recognised radiological sequela of this condition [27] and did not compromise the patient’s functional outcome.

This report has several limitations, most notably the lack of microbiological confirmation from bone biopsy due to institutional laboratory constraints, as well as the unavailability of magnetic resonance imaging (MRI) and broad‑range 16S rRNA gene sequencing. As a single case report, the observations may not be generalisable to the wider population of patients with similar comorbidities. Nonetheless, this case adds substantively to the emerging body of literature on PS osteomyelitis in immunocompromised hosts, underscoring the diagnostic complexity, the importance of a systematic multidisciplinary approach, and the necessity for heightened clinical vigilance in patients with coexistent RA‑related immunosuppression and type 2 DM. This synergistic immunocompromised state should consistently lower the threshold for an infectious work‑up when atypical musculoskeletal pain is present, even in the absence of classical clinical or laboratory features of systemic sepsis.

Conclusion

PS osteomyelitis should be included in the differential diagnosis of atypical pelvic pain in immunocompromised patients with RA, even when classical systemic signs of infection are absent. The coexistence of RA-related immunosuppressive therapy and type 2 DM constitutes a high‑risk immunological milieu that may blunt the systemic inflammatory response and contribute to substantial diagnostic delay. Markedly elevated inflammatory markers that are disproportionate to the degree of articular involvement, particularly in the absence of active synovitis, should prompt early cross‑sectional imaging and comprehensive microbiological assessment, incorporating molecular diagnostic modalities where available. Antimicrobial therapy should be individualised and extended in duration for high‑risk patients. When identified promptly and managed appropriately within a multidisciplinary framework, complete clinical and functional recovery without recourse to surgical intervention is achievable.

Abbreviations

RA

Rheumatoid arthritis

CT

Computed tomography

MRI

Magnetic resonance imaging

CRP

C-reactive protein

ESR

Erythrocyte sedimentation rate

WBC

White blood cell count

S. aureus

Staphylococcus aureus

MSSA

Methicillin-sensitive Staphylococcus aureus

DM

Diabetes mellitus

PS

Pubic symphysis

Author contributions

OJ: Conceptualization, clinical management of the patient, data collection, manuscript writing, and corresponding author. MB: Clinical management of the patient, data collection, and critical revision of the manuscript. RS: Clinical management of the patient, data collection, and critical revision of the manuscript. MA: Clinical management of the patient, data collection, and critical revision of the manuscript. ABM: Infectious disease consultation, clinical guidance on antimicrobial management, and critical revision of the manuscript. JC: Infectious disease consultation, clinical guidance on antimicrobial management, and critical revision of the manuscript; RB: Infectious disease consultation, clinical guidance on antimicrobial management, and critical revision of the manuscript.Sirine Abdellatif: Literature review, manuscript writing, and critical revision of the manuscript. MY: Supervision of clinical management, oversight of the manuscript, critical revision, and final approval of the version to be published. All authors read and approved the final manuscript.

Funding

No specific funding was received for this work.

Data availability

All data generated or analysed during this study are included in this published article.

Declarations

Ethics approval and consent to participate

Ethical approval was not required for this case report in accordance with local institutional regulations. The study was conducted in accordance with the Declaration of Helsinki. Written informed consent was obtained from the patient prior to publication.

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 no competing interests.