Brucellar spondylodiscitis mimicking lumbar discectomy with cauda equina syndrome: A case report

Abstract

Brucellar spondylodiscitis frequently poses diagnostic challenges due to its atypical early clinical manifestations, which may mimic degenerative spinal diseases. This report described a 42-year-old male patient who initially presented with severe low back pain and acute cauda equina syndrome and was preoperatively diagnosed with lumbar disc herniation. Emergency lumbar decompression was performed; however, the patient later developed fever and systemic symptoms. Repeated serological testing confirmed brucellosis. The early clinical, laboratory, and imaging features were nonspecific, and initial inflammatory markers and bacterial cultures were negative. Empirical levofloxacin may have masked inflammatory responses. This case highlights the importance of maintaining high index of suspicion for brucellar spondylodiscitis in endemic regions, even in the absence of systemic signs of infection. Repeat serologic testing, careful radiological evaluation, and attention to epidemiological exposure are critical for early and accurate diagnosis.

Introduction

Brucellosis is a globally prevalent zoonotic infectious disease caused by Gram-negative, facultative intracellular Brucella spp., with the spine being one of the most frequently involved sites.^1,2 Spinal brucellosis accounts for a considerable proportion of cases and may present with insidious and nonspecific symptoms, particularly in the early stages. Clinical manifestations typically include back pain, fever, night sweats, and elevated inflammatory markers; however, atypical presentations without systemic signs are common, which can lead to misdiagnosis as degenerative spinal disorders.^3,4 Such mimicking presentations may lead to delayed treatment and potentially result in severe complications, including vertebral destruction, spinal instability, or neurological deficits. ⁵ This report presents a highly atypical case of brucellar spondylodiscitis that initially mimicked lumbar disc herniation (LDH) with acute cauda equina syndrome (CES), without fever or elevated inflammatory markers. We analyzed the diagnostic pitfalls, radiological clues, laboratory false-negative results, and therapeutic lessons to improve clinical awareness among clinicians in endemic regions.

Case report

A middle-aged male patient, previously healthy and with no history of trauma, presented to the Affiliated Hospital of Jining Medical University, Jining, Shandong, China, on 20 April 2025 with a 7-day history of severe low back pain radiating to the left lower limb. Within 3 h of admission, he developed new-onset perineal hypoesthesia and dysuria, consistent with CES. Physical examination revealed a body temperature of 36.8°C (afebrile), marked tenderness over the left lumbar paravertebral muscles with radiation to the left leg, a positive left straight leg raise test at 30° (Lasegue sign), and decreased perineal tactile sensation. Laboratory investigations showed a white blood cell (WBC) count of 8.81 × 10⁹/L (normal range: 4.0–10.0 × 10⁹/L), C-reactive protein (CRP) <0.20 mg/L (normal range: <10.0 mg/L), and erythrocyte sedimentation rate (ESR) of 8 mm/h (normal range: 0–20 mm/h). Lumbar magnetic resonance imaging (MRI) demonstrated a posterior L4–L5 disc herniation with direct compression of the cauda equina.

Based on clinical and imaging findings, the initial diagnosis of LDH with CES was reasonably established. Emergency posterior lumbar decompression was performed. Intraoperatively, a small quantity of grayish-white serous fluid was identified surrounding the herniated nucleus pulposus, raising suspicion for an underlying infectious process.

The abnormal intervertebral disc tissue was resected, and the disc space was meticulously irrigated sequentially with hydrogen peroxide solution and normal saline to ensure thorough decontamination. Intraoperative specimens of the herniated disc tissue were promptly submitted for bacterial culture and histopathological examination to confirm the diagnosis. Postoperatively, the patient received empirical anti-infective therapy with levofloxacin (500 mg once daily, intravenously). On postoperative day 1, his neurological symptoms (perineal hypoesthesia and dysuria) improved significantly. Repeat laboratory tests showed a WBC count of 9.46 × 10⁹/L and CRP of 1.39 mg/L. On postoperative day 7, lumbar computed tomography (CT) confirmed adequate decompression of the cauda equina Figure 1(f), and follow-up laboratory tests revealed a WBC count of 12.81 × 10⁹/L and CRP of 0.20 mg/L. Both pathological examination (revealing degenerative disc tissue without inflammatory infiltrates) and bacterial culture (no growth after 5 days of incubation) failed to confirm an infectious etiology. Given that the patient resided in a brucellosis-endemic region (northern China), a tube agglutination test (TAT) for Brucella antibodies was performed; however, the result was negative (titer, <1:20). The patient was discharged on postoperative day 8 with resolution of most symptoms. One week after discharge, the patient developed acute-onset high fever (peak temperature 39°C), chills, arthralgia, and myalgia. Laboratory tests showed an elevated WBC count of 15.85 × 10⁹/L and CRP of 10.89 mg/L. Empirical treatment with third-generation cephalosporins (2 g ceftriaxone once daily, intravenously) for 3 days yielded no clinical improvement. He was subsequently transferred to a local hospital, where a repeat TAT was positive for Brucella antibodies (titer, 1:320), confirming the diagnosis of brucellosis. Combined targeted antibiotic therapy with doxycycline and rifampicin was then initiated, and the patient’s febrile symptoms resolved within 48 h. The patient completed a 6-month course of treatment. Follow-up CT at 3 months revealed focal bone destruction at the inferior endplate of L4, consistent with brucellar spondylodiscitis Figure 1(g). At 6 months, CT showed complete resolution of bone destruction and solid interbody fusion Figure 1(h).

Figure 1.

MRI and CT data of a 42-year-old male patient with brucellar spondylodiscitis. (a, b, c, d) shows the patient’s MRI findings on admission. On sagittal views, the herniated intervertebral disc tissue exhibits hypointensity on T1-weighted imaging (T1WI) and hyperintensity on T2-weighted imaging (T2WI) (red arrows; (a) and (b), respectively). On coronal T2WI, severe compression of the cauda equina is indicated (red arrow, (d)). Notably, the posterior superior margin of the L5 vertebral body demonstrates hypointensity on T1WI and hyperintensity on T2-weighted fat-saturated imaging, which may serve as an indicator to early brucellar spondylodiscitis (white arrows; (a) and (c)). (e, f, g, h) presents the patient’s CT findings. Preoperative (pre-op) CT reveals narrowing of the intervertebral space and compression of the dural sac (e). Seven days postoperatively (PO 7d), CT confirms resolution of dural sac compression (f). At 3 months postoperatively (PO 3 m), focal bony destruction in the region of the inferior endplate of the L4 vertebral body is observed, consistent with radiological features of brucellar spondylodiscitis ((g), white arrow). At 6 months postoperatively (PO 6 m), CT demonstrates satisfactory interbody fusion at the L4–L5 level and complete resolution of the bony destruction in the L4 vertebral body (h). CT: computed tomography; MRI: magnetic resonance imaging.

Epidemiological exposure history

The patient resided in a brucellosis-endemic region of northern China. He had a long-term history of contact with sheep and cattle and occasionally consumed unpasteurized dairy products. No recent travel history was reported.

Radiological findings

The radiological findings were as follows:

Initial sagittal MRI showed that the herniated disc exhibited hypointensity on T1-weighted imaging (T1WI) and hyperintensity on T2-weighted imaging (T2WI). The posterior superior margin of the L5 vertebral body showed bone marrow edema, suggestive of early inflammatory change.

CT on postoperative day 7 showed adequate decompression. At 3 months, focal osteolytic changes at the inferior endplate of L4 were visible, consistent with brucellar spondylodiscitis. At 6 months, bony fusion was achieved.

The T2WI hyperintensity of the disc is a nonspecific finding; however, it may serve as a subtle indicator of early infection. Degenerative discs typically demonstrate low or intermediate signal intensity. The signal change at the posterior superior corner of L5 is consistent with the Pedro Pons sign, an early erosion suggestive of brucellar spondylodiscitis.

Discussion

This case is not rare; however, it represents a highly atypical early form of brucellar spondylodiscitis that lacks systemic inflammation and mimics degenerative disease, making it particularly prone to misdiagnosis. It demonstrates that early brucellar spondylodiscitis can closely mimic LDH with CES. The absence of fever, night sweats, and elevated inflammatory markers at initial presentation contributed to diagnostic challenges. ⁶ Nevertheless, the initial diagnosis was clinically reasonable and consistent with the acute neurological presentation.

First, the patient’s initial presentation with low back pain, radiculopathy, and CES was highly suggestive of LDH, which is one of the most common degenerative spinal disorders in middle-aged adults. Notably, he lacked classic systemic manifestations of brucellosis (e.g. prolonged fever and night sweats) during the initial hospitalization, and routine inflammatory markers (CRP and ESR) were within normal limits. This absence of overt infectious indicators contributed to the initial diagnostic difficulty. A striking finding in this case was the persistently low CRP levels during the first hospitalization, which contrasts with the typically elevated CRP observed in most cases of infectious spondylodiscitides. ⁷ This phenomenon may be explained by two potential mechanisms: (a) intraoperative thorough debridement of the infected disc tissue and irrigation with hydrogen peroxide, which may have significantly reduced the local bacterial load and (b) empirical use of levofloxacin, which has moderate activity against Brucella, potentially suppressing local and systemic inflammation, thereby resulting in falsely normal laboratory markers and delayed diagnosis. ⁸ Collectively, these factors represent an important clinical pitfall.

Second, MRI is valuable for detecting early inflammatory changes.^9,10 However, T2WI hyperintensity of the disc is nonspecific and cannot be regarded as pathognomonic. ¹¹ In this case, the signal intensity differed from those of typical degenerative discs, and the early bone marrow edema at the posterior superior corner of L5 suggested the Pedro Pons sign, supporting the possibility of early brucellar infection.^12,13 Meticulous radiological evaluation is critical for distinguishing rare infectious lesions from common degenerative conditions. Radiological parameters also play an important role in assessing spinal stability and postoperative outcomes.

Third, serological testing, particularly TAT, is a commonly used screening tool for brucellosis, with a sensitivity of 80%–95% in established infections. ¹⁴ However, false-negative results may occur in the early stage of infection, as observed in this case. The initial negative TAT may be attributed to the early immunological window period (within 2 weeks of symptom onset), during which specific immunoglobulin M (IgM) antibodies have not reached detectable levels. ¹⁵ In addition, a prozone phenomenon, resulting from high antibody concentration, cannot be excluded as a cause of false-negative results.^16,17 Variation in laboratory cutoff titers may also have contributed to the initial negative result. Repeat serological testing is essential in suspected cases. Bacterial culture of disc tissue was negative, which is not uncommon in brucellosis.^18,19 Blood culture and polymerase chain reaction (PCR) were not performed initially because infection was not suspected. The diagnosis was established retrospectively based on seroconversion, typical imaging progression, and a favorable response to targeted antibiotics.

Finally, the treatment of brucellar spondylodiscitis requires a prolonged course of combination antibiotic therapy to eradicate the intracellular pathogen and prevent recurrence. In this case, the patient received 6 months of combined therapy with doxycycline and rifampicin, resulting in complete resolution of infection and satisfactory spinal fusion. Moreover, assessment of spinal alignment and stability after surgical intervention is essential for postoperative recovery and fusion. Meticulous radiological evaluation helps distinguish rare pathological lesions from common degenerative diseases.^20,21

Conclusion

This case highlights the diagnostic challenges posed by atypical early brucellar spondylodiscitis, which may mimic degenerative spinal disease in the absence of typical infectious manifestations. The key takeaways from this report include the following. (1) A high index of suspicion for brucellar spondylodiscitis should be maintained in patients from endemic regions, even in the absence of systemic infectious symptoms or elevated inflammatory markers. (2) Early negative serological results do not exclude brucellosis; repeat testing after 2–4 weeks is strongly recommended. (3) Subtle MRI findings, including disc T2WI hyperintensity and the Pedro Pons sign, may provide auxiliary clues, although they are not pathognomonic. (4) Empirical use of levofloxacin may mask inflammatory signs and delay the diagnosis of brucellar spondylodiscitis. (5) When conditions permit, genetic testing can be used to improve the detection rate of early infection, particularly when bacterial culture is negative. Early recognition and initiation of targeted antibiotic therapy are crucial to prevent progressive vertebral destruction, spinal instability, and neurological sequelae.