Campylobacter jejuni-Associated Lumbar Vertebral Osteomyelitis with Cauda Equina Syndrome in the Absence of Gastrointes Symptoms: A Rare Case Report

Qi Xiao, Jiabin Chen, Zunying Xu, Qingquan Wu, Huixiang Jiang, JingJie Zhang, Huiyun Deng, Hui Liu

Department of Orthopaedics, The 909th Hospital, School of Medicine, Xiamen University, Zhangzhou, People’s Republic of China

Correspondence: Hui Liu, Department of Orthopaedics, The 909th Hospital, School of Medicine, Xiamen University, No. 269, Zhanghua Central Road, Xiangcheng District, Zhangzhou, Fujian, 363000, People’s Republic of China, Email [email protected]

Background: Campylobacter jejuni (C. jejuni) is a common cause of self-limiting gastroenteritis but rarely causes extraintestinal infections. Vertebral osteomyelitis due to this pathogen is exceptionally uncommon, and cases presenting without gastrointestinal symptoms are even rarer. To our knowledge, no previous case has described lumbar osteomyelitis with a spinal extradural abscess leading to cauda equina syndrome in the absence of enteric symptoms. Diagnosing and managing this infection remains clinically challenging.
Case Presentation: A 65-year-old man presented with a two-month history of intermittent low back pain, bilateral lower limb numbness and pain, urinary frequency, and constipation. He had one episode of fever before admission but no gastrointestinal symptoms. Magnetic resonance imaging (MRI) showed lumbar (L4/5) osteomyelitis with an epidural abscess compressing the cauda equina. The patient underwent L4/5 partial laminectomy and debridement of the spinal canal abscess. Conventional cultures of preoperative blood and intraoperative specimens were negative. Metagenomic next-generation sequencing (mNGS) of both blood and surgical samples identified C. jejuni as the causative pathogen. Antibiotic susceptibility testing was not available. The patient initially received empirical antibiotics but developed recurrent fever. Treatment was switched to intravenous meropenem and levofloxacin, followed by oral levofloxacin for six weeks, completing a nine-week course. At two-year follow-up, MRI confirmed complete resolution of the infection and the patient made a full recovery.
Conclusion: C. jejuni should be considered in spinal infections even without gastrointestinal symptoms. mNGS is useful when cultures are negative. For cases failing initial antibiotics, meropenem plus levofloxacin may be an option, though further data are needed.

Keywords: Campylobacter jejuni, vertebral osteomyelitis, lumbar infection, spinal extradural abscess, cauda equina syndrome, metagenomic next-generation sequencing

Introduction

Campylobacteriosis is a leading cause of infectious diarrhea and foodborne disease worldwide. Among the genus Campylobacter, which comprises 57 recognized species, Campylobacter jejuni (C. jejuni) is the most clinically significant.1 It is a motile, non-spore-forming, microaerophilic, Gram-negative bacterium with a characteristic curved shape.2

Transmission occurs primarily through contaminated food, especially poultry.3 In humans, C. jejuni most commonly causes self-limiting acute gastroenteritis, although severe cases may require intervention.4 Extraintestinal manifestations—including soft tissue infection, myocarditis, osteomyelitis, meningitis, and Guillain-Barré syndrome—are uncommon but well documented.5–8

Vertebral osteomyelitis caused by C. jejuni is exceptionally rare. More importantly, cases occurring in patients without antecedent gastrointestinal symptoms are even less common, making early clinical recognition difficult. To date, no such case has been reported in China.9 The diagnostic challenge is compounded by the frequent failure of conventional cultures to identify the pathogen, particularly when patients have no enteric symptoms to suggest Campylobacter infection.

This report presents a case of C. jejuni-induced lumbar osteomyelitis with epidural abscess and cauda equina compression in an adult patient who had no gastrointestinal symptoms. The patient’s clinical course, imaging findings, treatment, and outcome are described. The crucial role of metagenomic next-generation sequencing (mNGS) in establishing diagnoses when conventional methods fail is emphasized, and similar cases from the literature are reviewed to raise clinical awareness of this rare condition.

Case Presentation

A 65-year-old male presented with a 2-month history of intermittent low back pain, accompanied by numbness and pain in both lower limbs (right side more severe), as well as urinary frequency and constipation. Ten days before admission, he developed a fever (peak axillary temperature 38.7°C; Figure 1) that resolved with self-administered antipyretics. He reported no gastrointestinal or respiratory symptoms. Physical examination revealed tenderness and restricted mobility of the lower lumbar spine, radiating pain and sensory deficits in both lower limbs, and muscle strength graded at IV. The visual analog scale (VAS) score was 7.

A line graph showing axillary temperature changes over time from admission through discharge.

Figure 1 Record of the patient’s axillary temperature (36–39°C) changes and follow-up.

Laboratory findings on admission showed elevated ESR (96 mm/h) and CRP (54.29 mg/L), with IL-6 also increased (25.82 pg/mL). White blood cell count, neutrophil count, PCT, and hemoglobin were within normal limits. Serum albumin was slightly reduced (35 g/L) (Table 1 and Figure 2). Urinalysis and stool microscopy were unremarkable, and anti-TB antibody testing was negative. Imaging studies revealed reduced L4/L5 disc height on radiography, and osteolytic destruction with gas in the disc space and spinal canal on CT. MRI confirmed L4/L5 discitis and osteomyelitis with epidural abscesses causing cauda equina compression (Figure 3).

Table 1 Longitudinal Changes in Laboratory Parameters During Hospitalization and Follow-Up

A multi-line graph showing trends in IL-6, Neutrophil, ESR, CRP, Hemoglobin and ALB over time.

Figure 2 Longitudinal trends in the patient’s laboratory parameters.

Abbreviations: IL-6, Interleukin-6; ESR, erythrocyte sedimentation rate; CRP, C-reactive protein; ALB, serum albumin.

Composite of 9 spine images: radiographs, CT, MRI with red arrows on lower lumbar levels.

Figure 3 Preoperative imaging. (a and b) X-ray shows L4–L5 disc narrowing (arrows). (c) Sagittal CT reveals gas within the collapsed disc and spinal canal (arrows). (d and e) Coronal and transverse CT demonstrate moth-eaten destruction of L4–L5 vertebrae (arrows). (f and g) Axial and sagittal MRI show discitis, osteomyelitis, and paravertebral edema (arrows). (h and i) Sagittal T2WI and contrast-enhanced T1WI MRI reveal multiple epidural abscesses and cauda equina compression (arrows). (Arrows in red online).

Given progressive cauda equina syndrome, the patient underwent surgical evacuation via a posterior unilateral interlaminar approach with partial laminectomy on April 26, 2024. The purulent material, granulation tissue, and infected disc tissue were completely debrided, which achieved adequate decompression of the cauda equina. Intraoperative specimens were submitted for conventional culture and PACEseq-based metagenomic next-generation sequencing (mNGS; Hugobiotech, Beijing, China). Empirical intravenous ceftriaxone was started postoperatively.

All cultures remained negative, but mNGS of surgical samples identified C. jejuni on April 29 (Table 2 and Figure 4). Therapy was adjusted to ceftriaxone plus oral azithromycin. However, the patient developed recurrent fever (38.5°C) on May 1 with elevated inflammatory markers. After switching to levofloxacin plus azithromycin, fever recurred (39.0°C) on May 3. Blood mNGS then confirmed C. jejuni bacteremia on May 6 (Table 3 and Figure 5). The regimen was finally changed to intravenous meropenem plus levofloxacin. Following this, fever resolved and inflammatory markers gradually normalized (Figures 1 and 2).

Table 2 Comprehensive Pathogen Profile Identified by mNGS in Operative Specimens

Table 3 Comprehensive Pathogen Profile Identified by mNGS in Venous Blood Specimen

A bar chart and a pie chart showing microbial reads and Campylobacter jejuni coverage and composition.

Figure 4 Surgical Specimen (L4–L5 Lesion) metagenomic next-generation sequencing of the patient revealed a total of 197 specific reads of Campylobacter jejuni were detected, accounting for 45.71%.

A bar chart and pie chart showing Campylobacter jejuni read positions and microbe read composition.

Figure 5 Venous blood metagenomic next-generation sequencing of the patient revealed a total of 9 specific reads of Campylobacter jejuni were detected, accounting for 0.64%.

A follow-up MRI on May 22 showed resolution of discitis and spinal canal abscess, with residual vertebral edema only (Figure 6). The patient was discharged after 3 weeks of intravenous therapy and prescribed oral levofloxacin for 4 additional weeks.

Composite image: two sagittal spine scans (a, b) and one axial scan (c) on dark background.

Figure 6 Post-operative MRI at 4 weeks (May 22, 2024). (a–c) T2-weighted, fat-suppressed T2-weighted (sagittal and axial) images demonstrate resolution of the L4–5 discitis and abscess, with residual edema in the vertebrae and posterior paraspinal musculature.

At first follow-up (June 30, 2024), MRI showed persistent edema signals in L4/5 vertebral bodies and posterior paraspinal soft tissues (Figure 7). Inflammatory markers trended downward but remained slightly above normal reference ranges (Figure 2). VAS score was 2. He was advised to continue a lumbar brace for 3 more weeks and oral antibiotics for 2 more weeks. At second follow-up (February 27, 2025), he reported complete resolution of pain. MRI confirmed resolution of edema (Figure 8), inflammatory markers normalized, and he had resumed all daily activities. A telephone follow-up at 2 years postoperatively reported no recurrence.

Composite MRI image: 2 sagittal and 1 axial lumbar spine views on dark background.

Figure 7 First follow-up MRI (Jun 30, 2024). (a–c) T2-weighted, fat-suppressed T2-weighted (sagittal and axial) images demonstrate edema signals in the L4/5 vertebral bodies, accompanied by edema in the posterior paraspinal soft tissues.

MRI of lumbar spine: sagittal views (a, b) and axial view (c) on dark background.

Figure 8 Second follow-up MRI (February 27, 2025). (a–c) T2-weighted and fat-suppressed T2-weighted (sagittal and axial) images demonstrate complete resolution of the L4/5 lesion and surrounding edema.

Discussion

Following a literature search, only nine cases of spinal infection caused by extraintestinal C. jejuni have been reported to date: eight in English, one in French, eight from European countries, and one from Japan (Table 4). In China, the predominant pathogens causing vertebral osteomyelitis are Mycobacterium, Brucella, and Staphylococcus.9 However, in elderly patients presenting with fever and spinal pain without gastrointestinal symptoms, C. jejuni should still be considered, particularly when routine workup is unrevealing, although risk factors such as diabetes, immunosuppression, and malignancy are commonly associated with spinal infections.10,11 Among the ten documented cases, only three had a suspected source of infection,12–14 and only four presented with gastrointestinal symptoms,13,15–17 highlighting that the absence of enteric symptoms does not exclude C. jejuni spinal infection.

Table 4 Identified Cases of Campylobacter jejuni Spondylodiscitis in Literature Review and Our Case

Laboratory findings in this case showed a distinctive pattern: markedly elevated ESR, CRP, and IL-6 with normal WBC and PCT. This pattern—normal WBC/PCT with elevated acute-phase reactants—likely reflects a predominantly localized inflammatory response rather than systemic bacteremia, consistent with the high bacterial load detected in surgical tissue (197 reads, 45.71%) versus low blood load (9 reads, 0.64%). Imaging features (disc space narrowing, vertebral osteolysis, and epidural abscess) were typical of pyogenic spondylodiscitis and, combined with negative anti-TB antibody and stool cultures, guided the decision to pursue advanced molecular diagnostics. The key diagnostic challenge was the failure of conventional methods: blood cultures, intraoperative tissue cultures, and stool cultures all remained negative. This is not surprising—traditional culture is time-consuming, has low positivity rates for Campylobacter due to its microaerophilic requirements, and relies on targeted detection that may miss fastidious organisms.21 In contrast, mNGS offers a more comprehensive approach to pathogen detection, enabling faster and more accurate identification, guiding appropriate treatment, and facilitating disease surveillance and control.22,23 However, mNGS is costly and cannot provide susceptibility data. It is most useful when clinical suspicion is high despite negative cultures, and results must be interpreted in clinical context.

The treatment strategy for spinal infection is guided by the extent and severity of the disease. Surgical intervention is indicated in cases involving extensive abscess formation, spinal instability, neurological impairment, rapid progression, or poor response to antimicrobial therapy.22 In this patient, a spinal epidural abscess developed within the spinal canal, resulting in cauda equina compression and neurological deficits. Decompressive debridement was performed. Spinal stability was carefully assessed using preoperative X-rays, CT and intraoperative findings. As no instability was detected, and given the active infection, internal fixation was avoided to reduce the risk of implant-related complications. This surgical strategy aligns with the principle that intervention in spinal infections should prioritize decompression and pathogen acquisition while preserving stability whenever feasible.

The resistance patterns of C. jejuni vary globally;24–27 fluoroquinolone resistance has been reported in approximately 29% of US isolates, with higher rates in certain parts of Asia. Multidrug resistance is most commonly observed against fluoroquinolones, macrolides, and tetracyclines.28 Antimicrobial management was challenging due to the lack of susceptibility data. The patient did not respond to initial ceftriaxone, with recurrent high fever and confirmed bacteremia. After switching to meropenem plus levofloxacin, the infection resolved. Reduced susceptibility to the initial agents was suspected, but multidrug resistance could not be confirmed without formal susceptibility testing. The clinical response to the final regimen may reflect improved coverage, synergistic effects, or both. The choice of antibiotic regimen for vertebral osteomyelitis varies and is individualized based on comorbidities, infection severity, concomitant infections, and treatment response.29 Treatment regimens among the nine previously reported cases were heterogeneous, with durations ranging from 4 to 36 weeks (mean, 11 weeks).12–20 The patient received a 9-week course of antimicrobial therapy and achieved full recovery without any adverse events.

Several limitations should be acknowledged. First, antimicrobial susceptibility testing was not available because standard culture failed to isolate the organism, and the resistance profile could therefore not be determined. Second, as this is a single case report, the treatment experience may not be generalizable to other patients.

Conclusion

This case highlights that C. jejuni should be considered in spinal infections even without gastrointestinal symptoms, that mNGS is useful when cultures are negative, and that imaging evidence of epidural abscess with neural compression may guide surgical decision-making. For cases failing initial antibiotics, meropenem plus levofloxacin may be an option, though further data are needed given the lack of susceptibility testing and the single-case nature of this report.

Abbreviations

C. jejuni, Campylobacter jejuni; MRI, Magnetic resonance imaging; mNGS, Metagenomics next generation sequencing; VAS, Visual analog scale; ESR, Erythrocyte sedimentation rate; CRP, C-reactive protein; IL-6, Interleukin-6; ALB, Serum albumin; TBAb, Anti-tuberculosis antibody; CT, Computed tomography; WBC, white blood cell count; PCT, Procalcitonin; PCR, Polymerase chain reaction; MIC, Minimal inhibitory concentration.

Ethics Approval and Consent to Participate

All treatments complied with relevant laws and institutional regulations. The study and the publication of this case report were approved by the Human Ethics Committee of the 909th Hospital, School of Medicine, Xiamen University. Written informed consent for participation and for the publication of clinical details was obtained from the patient.

Consent for Publication

Written informed consent was obtained from the patient for publication of this case report and any accompanying images.

Acknowledgments

The authors thank all staff who assisted us with this study.

Author Contributions

All authors made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis and interpretation, or in all these areas; took part in drafting, revising or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.

Funding

There is no funding to report.

Disclosure

The authors report no conflicts of interest in this work.

References

1. Veronese P, Dodi I. Campylobacter jejuni/coli infection: is it still a concern? Microorganisms. 2024;12(12):2669. doi:10.3390/microorganisms12122669

2. Best EL, Fox AJ, Frost JA, Bolton FJ. Real-time single-nucleotide polymorphism profiling using Taqman technology for rapid recognition of Campylobacter jejuni clonal complexes. J Med Microbiol. 2005;54(Pt 10):919–11. doi:10.1099/jmm.0.45971-0

3. Tikhomirova A, McNabb ER, Petterlin L, et al. Campylobacter jejuni virulence factors: update on emerging issues and trends. J Biomed Sci. 2024;31(1):45. doi:10.1186/s12929-024-01033-6

4. Young KT, Davis LM, Dirita VJ. Campylobacter jejuni: molecular biology and pathogenesis. Nat Rev Microbiol. 2007;5(9):665–679. doi:10.1038/nrmicro1718

5. Kaakoush NO, Castaño-Rodríguez N, Mitchell HM, Man SM. Global epidemiology of Campylobacter infection. Clin Microbiol Rev. 2015;28(3):687–720. doi:10.1128/CMR.00006-15

6. Same RG, Tamma PD. Campylobacter infections in children. Pediatr Rev. 2018;39(11):533–541. doi:10.1542/pir.2017-0285

7. Katsuno S, Itamoto C, Hase I. Pericarditis due to Campylobacter coli infection: a case report. BMC Infect Dis. 2023;23(1):316. doi:10.1186/s12879-023-08293-x

8. Latov N. Campylobacter jejuni infection, anti-ganglioside antibodies, and neuropathy. Microorganisms. 2022;10(11):2139. doi:10.3390/microorganisms10112139

9. Gao Q, Liu Q, Zhang G, et al. Identification of pathogen composition in a Chinese population with iatrogenic and native vertebral osteomyelitis by using mNGS. Ann Med. 2024;56(1):2337738. doi:10.1080/07853890.2024.2337738

10. Heuer A, Strahl A, Viezens L, Koepke LG, Stangenberg M, Dreimann M. The hamburg spondylodiscitis assessment score (HSAS) for immediate evaluation of mortality risk on hospital admission. J Clin Med. 2022;11(3):660. doi:10.3390/jcm11030660

11. Henry MW, Dowdell JE, Miller AO. Pyogenic Vertebral Osteomyelitis. Infect Dis Clin North Am. 2025;39(3):419–435. doi:10.1016/j.idc.2025.02.011

12. Nakatani N, Miyazaki R, Nagata Y, Nozato T, Ashikaga T, Kutsuna S. Cervical spine osteomyelitis caused by Campylobacter jejuni without gastrointestinal symptoms. Am J Med. 2022;135(1):e9–e10. doi:10.1016/j.amjmed.2021.08.006

13. Kirk KF, Boel J, Nielsen HL. Vertebral osteomyelitis caused by Campylobacter jejuni in an immunocompetent patient. Gut Pathog. 2023;15(1):61. doi:10.1186/s13099-023-00589-2

14. Yabe H, Inoue R, Yanai R, Nishimi S. Spinal epidural abscess caused by Campylobacter jejuni without gastrointestinal symptoms. Cureus. 2024;16(9):e68408. doi:10.7759/cureus.68408

15. Feodoroff B, Lauhio A, Ellström P, Rautelin H. A nationwide study of Campylobacter jejuni and Campylobacter coli bacteremia in Finland over a 10-year period, 1998-2007, with special reference to clinical characteristics and antimicrobial susceptibility. Clin Infect Dis. 2011;53(8):e99–e106. doi:10.1093/cid/cir509

16. Puljiz I, Topic A. Campylobacter jejuni vertebral osteomyelitis. Lancet Infect Dis. 2017;17(9):1002. doi:10.1016/S1473-3099(17)30466-8

17. Greminger S, Strahm C, Notter J, et al. Vertebral osteomyelitis with Campylobacter jejuni - a case report and review of the literature of a very rare disease. J Bone Jt Infect. 2024;9(1):59–65. doi:10.5194/jbji-9-59-2024

18. Ajili F, Labidi J, Ben Abdelhafith N, Battikh R, Othmani S. Candida albicans: une étiologie rare de pyélonéphrite emphysémateuse [Candida albicans: a rare cause of emphymatous pyelonephritis]. Med Mal Infect. 2011;41(10):560–562. doi:10.1016/j.medmal.2011.05.004

19. Tappe D, Schulze MH, Oesterlein A, et al. Molecular detection of Campylobacter jejuni as a cause of culture-negative spondylodiscitis. J Clin Microbiol. 2012;50(4):1499–1500. doi:10.1128/JCM.06275-11

20. Langereis JD, Henriet SS, Kuipers S, et al. IgM augments complement bactericidal activity with serum from a patient with a novel CD79a mutation. J Clin Immunol. 2018;38(2):185–192. doi:10.1007/s10875-017-0474-7

21. Berbari EF, Kanj SS, Kowalski TJ, et al. Executive summary: 2015 infectious diseases society of America (IDSA) clinical practice guidelines for the diagnosis and treatment of native vertebral osteomyelitis in adults. Clin Infect Dis. 2015;61(6):859–863. doi:10.1093/cid/civ633

22. Li N, Cai Q, Miao Q, Song Z, Fang Y, Hu B. High-throughput metagenomics for identification of pathogens in the clinical settings. Small Methods. 2021;5(1):2000792. doi:10.1002/smtd.202000792

23. Wang G, Long J, Zhuang Y, et al. Application of metagenomic next-generation sequencing in the detection of pathogens in spinal infections. Spine J. 2023;23(6):859–867. doi:10.1016/j.spinee.2023.02.001

24. Centers for Disease Control and Prevention (CDC). Antibiotic resistance threats in the United States, 2019. Atlanta, GA: US Department of Health and Human Services, CDC; 2019. doi:10.15620/cdc:82532.

25. Russo TP, Pace A, Varriale L, et al. Prevalence and antimicrobial resistance of enteropathogenic bacteria in yellow-legged gulls (Larus michahellis) in Southern Italy. Animals. 2021;11(2):275. doi:10.3390/ani11020275

26. Shin E, Oh Y, Kim M, Jung J, Lee Y. Antimicrobial resistance patterns and corresponding multilocus sequence types of the Campylobacter jejuni isolates from human diarrheal samples. Microb Drug Resist. 2013;19(2):110–116. doi:10.1089/mdr.2012.0099

27. Thomrongsuwannakij T, Blackall PJ, Chansiripornchai N. A study on Campylobacter jejuni and Campylobacter coli through commercial broiler production chains in Thailand: antimicrobial resistance, the characterization of DNA gyrase subunit A mutation, and genetic diversity by flagellin A gene restriction fragment length polymorphism. Avian Dis. 2017;61(2):186–197. doi:10.1637/11546-120116-Reg.1

28. Szczepanska B, Andrzejewska M, Spica D, Klawe JJ. Prevalence and antimicrobial resistance of Campylobacter jejuni and Campylobacter coli isolated from children and environmental sources in urban and suburban areas. BMC Microbiol. 2017;17(1):80. doi:10.1186/s12866-017-0991-9

29. Matsuo T, Borgonovo F, Lahr BD, et al. Clinical manifestations, long-term trends, and risk factors for treatment failure in native vertebral osteomyelitis: a 26-year mayo clinic experience. Clin Infect Dis. 2026;82(6):e1171–e1180. doi:10.1093/cid/ciag048

Comments (0)

No login
gif