Long-head biceps tendon rupture as a complication of brucellar tenosynovitis: a rare manifestation of multifocal osteoarticular brucellosis

INTRODUCTION

Brucellosis is one of the most important zoonotic infections worldwide and remains a major public health problem in endemic regions, including the Middle East, Mediterranean basin, Latin America, and parts of Asia and Africa. It is caused by intracellular gram-negative coccobacilli of the genus Brucella, with B. melitensis, B. abortus, B. suis, and B. canis being the main species associated with human disease. Among these, B. melitensis is generally considered the most virulent and clinically significant species in humans.^1-3 Human infection usually occurs through direct contact with infected animals or ingestion of unpasteurized animal products. Raw milk and dairy products from goats, sheep, cattle, and camels remain important transmission routes in endemic communities. In Oman and the wider Middle East, B. melitensis is an important cause of human brucellosis, and raw camel milk consumption remains a relevant cultural exposure, particularly in rural communities.^4-6 Osteoarticular involvement is the most common focal complication of brucellosis. The spine and sacroiliac joints are most frequently affected, whereas peripheral septic arthritis, bursitis, and tenosynovitis are less common. Shoulder involvement is unusual, and tendon-sheath infection complicated by tendon rupture is exceedingly rare.^7-10 We report a rare case of multifocal osteoarticular brucellosis presenting with simultaneous L5-S1 spondylodiscitis and right glenohumeral septic arthritis complicated by long-head biceps tenosynovitis and proximal long-head biceps tendon rupture. The case emphasizes diagnostic pitfalls, imaging findings, and the need for multidisciplinary management in endemic settings.

CASE REPORT

A 69-year-old man with no significant known comorbidities presented with severe low back pain and right shoulder pain. There was no history of trauma. On initial assessment, he was clinically stable, afebrile, and not septic.

Physical examination showed marked tenderness over the lower lumbar spine and painful but initially full range of motion of the right shoulder. No motor or sensory neurological deficit was detected. Plain radiographs showed lumbar spondylosis, and lumbar CT demonstrated advanced spondylodegenerative changes with reduced L5-S1 disc height. He was treated conservatively with physiotherapy and analgesics.

One week later, he returned with anorexia, fever, night sweats, severe constant pain unresponsive to treatment, restricted right shoulder motion, and newly developed bilateral sciatica. Neurological examination showed no motor or sensory deficit; however, the right ankle reflex was absent, and straight-leg raise testing was positive bilaterally at 20°. There were no bowel or urinary symptoms. Laboratory investigations showed mildly impaired renal function, ESR of 74 mm/h, and CRP of 121 mg/l.

Right shoulder ultrasound demonstrated a lobulated heterogeneously hypoechoic collection with internal hyperechoic debris anterior to the humerus along the long-head biceps tendon sheath, extending intra- and extra-articularly. There was associated turbid septated fluid tracking along the tendon sheath, minimal turbid glenohumeral joint effusion, thick irregular capsular thickening, and irregularity of the supraspinatus footprint with altered fibrillar pattern. Because infection was suspected, blood cultures were obtained, and empirical amoxicillin-clavulanate was started (Figure 1).

Two days later, aerobic blood culture grew B. melitensis, and Brucella serology titre was 1:320. After further discussion, the patient reported drinking raw camel milk in a rural area one month before presentation.

Urgent MRI of the right shoulder and lumbosacral spine was performed. Shoulder MRI showed moderate glenohumeral joint effusion, synovial thickening, articular cartilage thinning, subchondral marrow signal abnormality of the humeral head, a severely thinned and frayed glenoid labrum, and an anterosuperior labral tear involving the biceps-labral complex remnant. Loculated septated fluid was seen within the long-head biceps tendon sheath, associated with complete proximal-third rupture of the long-head biceps tendon. Severe supraspinatus tendinopathy with a partial-thickness tear was also noted (Figures 2 and 3).

Lumbosacral MRI demonstrated abnormal fluid signal within the L5-S1 disc, adjacent end-plate marrow oedema, anterior paravertebral inflammatory fluid signal, severe L5-S1 disc-height loss, and posterior disc bulge causing moderate bilateral foraminal narrowing with nerve-root impingement (Figure 4). There was no epidural abscess, paraspinal abscess, psoas abscess, spinal canal compromise, or radiological spinal instability. These findings were consistent with L5-S1 spondylodiscitis in the context of confirmed systemic brucellosis.

Following discussion with the spine surgery team, conservative management was chosen for the spondylodiscitis because there was no objective neurological deficit, spinal instability, or abscess requiring drainage. Arthroscopic debridement of the right shoulder was subsequently performed. Intraoperatively, a collection was found over the long-head biceps tendon, and 12 ml of yellowish fluid was aspirated and sent for culture and sensitivity. Diagnostic arthroscopy demonstrated synovitis, mild arthritic changes of the glenoid and humeral head, a frayed labrum, and complete rupture of the long-head biceps tendon with capsular retraction.

The patient was treated with intravenous gentamicin 360 mg once daily and ceftriaxone 2 g once daily for seven days, in addition to oral rifampicin 300 mg twice daily and doxycycline 100 mg twice daily. The aspirated shoulder fluid culture showed no growth after two weeks. The postoperative period was uneventful, with significant improvement in shoulder pain. He was discharged one week after surgery with oral antibiotics, regular follow-up, and physiotherapy. Completion of antimicrobial therapy was transferred to an external infectious disease team.

At two months after surgery, he was pain-free in the right shoulder, shoulder range of motion was almost full, back pain had improved, CRP had normalized, and no recurrence was documented.

DISCUSSION

Osteoarticular disease is the most frequent focal complication of brucellosis, with reported prevalence varying across studies depending on region, case definition, and diagnostic method. A systematic review found that patients with brucellosis have at least a 27% risk of osteoarticular involvement, while other reviews report broader ranges in endemic settings.^8,9 The present case illustrates a common diagnostic pitfall: the patient initially presented with low back pain and imaging evidence of degenerative lumbar disease, which delayed recognition of an infective process. This is particularly relevant in older patients, where spondylosis and disc-height loss may coexist with early infectious spondylodiscitis.¹⁰

Brucellar spondylodiscitis is one of the most serious skeletal manifestations of brucellosis and commonly affects the lumbar spine. It may mimic pyogenic or tuberculous spondylodiscitis clinically and radiologically. MRI is the imaging modality of choice because it can detect disc-space fluid, end-plate oedema, paravertebral inflammation, epidural extension, and abscess formation.^11-13 In this patient, MRI demonstrated L5-S1 disc fluid signal, adjacent end-plate marrow oedema, anterior paravertebral inflammatory fluid signal, and severe disc-height loss, supporting the diagnosis of brucellar spondylodiscitis in the context of positive blood culture, positive serology, and compatible exposure history.

Conservative management is appropriate in brucellar spondylodiscitis when there is no progressive neurological deficit, spinal instability, or abscess requiring drainage.¹¹ In this case, the spine team opted for non-operative management because there was no motor or sensory deficit, no epidural or paraspinal abscess, no significant spinal canal compromise, and no radiological instability. The patient’s back pain improved with antimicrobial therapy and follow-up care.

Peripheral septic arthritis is a recognized but less common manifestation of brucellosis compared with axial skeletal disease. Large joints such as the knee, hip, and ankle are more frequently involved, while glenohumeral involvement is uncommon.^14-16 Shoulder brucellosis may be misdiagnosed as degenerative rotator cuff disease, bursitis, adhesive capsulitis, or non-specific inflammatory arthritis, particularly in elderly patients with coexisting degenerative shoulder pathology. In this case, the shoulder findings were clinically significant because the patient had severe pain, restricted motion, ultrasound evidence of septated fluid, MRI evidence of glenohumeral effusion and synovial thickening, tendon-sheath fluid around the long-head biceps tendon, and operative confirmation of yellowish fluid and synovitis. Although shoulder fluid culture was negative, the diagnosis of presumed brucellar glenohumeral septic arthritis and long-head biceps infective tenosynovitis was supported by positive blood culture, positive Brucella serology, raw camel milk exposure, compatible imaging, intraoperative findings, and clinical response to brucellosis-directed therapy.

Tenosynovitis is a rare manifestation of brucellosis. Published reports mainly describe tendon-sheath infection in the hand and wrist, with very limited literature describing larger tendon sheaths or tendon rupture.^14-18 The most distinctive feature in this case is involvement of the long-head biceps tendon sheath with complete proximal-third tendon rupture, directly confirmed arthroscopically.

The relationship between infection and tendon rupture warrants cautious interpretation. In a 69-year-old patient, proximal long-head biceps rupture may occur due to chronic degenerative tendinopathy, commonly associated with rotator cuff disease, labral degeneration, and age-related tendon attrition. However, Brucella infection likely contributed through infective synovitis within the tendon sheath, inflammatory degradation of tendon collagen, increased local pressure, and mechanical attrition within the inflamed bicipital groove.¹⁸ Because histopathological analysis of the tendon and synovium was not performed, direct causation cannot be proven. The most accurate interpretation is that Brucella infection likely contributed to proximal long-head biceps tendon rupture through infective tenosynovitis superimposed on pre-existing degenerative shoulder disease.

The absence of histopathological analysis of the resected synovium and long-head biceps tendon stump represents the most significant limitation of this case. Tissue-level confirmation of Brucella invasion of the tendon sheath was not obtained, as synovial and tendon biopsy were not part of the routine arthroscopic protocol at our institution. Consequently, a definitive causal link between Brucella infective tenosynovitis and tendon rupture cannot be established with certainty, and the contribution of pre-existing degenerative tendinopathy well documented on preoperative MRI cannot be excluded. However, the diagnosis of brucellar glenohumeral septic arthritis and long-head biceps infective tenosynovitis rests on the convergence of six independent criteria: positive aerobic blood culture for Brucella spp.; Brucella serology titre of 1:320, consistent with active systemic infection; epidemiologically relevant exposure through raw camel milk; MRI evidence of glenohumeral joint effusion, synovial thickening, and loculated long-head biceps tendon sheath fluid; intraoperative confirmation of synovitis and turbid intra-articular fluid on arthroscopy; and favourable clinical and biochemical response to brucellosis-directed antimicrobial therapy. This integrative diagnostic approach is consistent with established frameworks for focal brucellosis, in which tissue culture sensitivity from joint fluid is reported as low as 4.5%, and histopathological confirmation is frequently absent in published case reports of brucellar tenosynovitis and septic arthritis. Furthermore, the mechanism of tendon rupture in this context is biologically plausible: infective tenosynovitis within the bicipital groove likely promoted mechanical friction and increased local compartment pressure, while infection-driven pro-inflammatory cytokines including interleukin-1β, tumour necrosis factor-α, and matrix metalloproteinases accelerated degradation of type I tendon collagen. This inflammatory collagenolytic mechanism, superimposed on a substrate of pre-existing degenerative tendinopathy, represents the most probable explanation for the complete proximal rupture observed. This "two-hit" model degenerative attrition compounded by infective collagenolysis best reconciles the clinical, imaging, and operative findings in this case.¹⁹

The management strategy was clinically reasonable and individualized. The spinal disease was treated conservatively because there was no neurological deficit, instability, or drainable abscess. By contrast, the shoulder had loculated fluid, synovitis, severe pain, restricted motion, and functional limitation, making arthroscopic washout and debridement appropriate. Arthroscopic management of septic shoulder arthritis allows lavage, drainage, debridement, microbiological sampling, and assessment of intra-articular pathology while limiting surgical morbidity.²⁰

The negative shoulder aspirate culture is an important diagnostic limitation but does not exclude brucellar septic arthritis. Brucella is a fastidious organism, and culture yield may be limited, particularly after antibiotics have already been administered. In this patient, empirical antibiotics were started before shoulder aspiration, which likely reduced culture sensitivity. Culture-negative focal infection is a recognized challenge in brucellosis, and diagnosis often depends on integrating exposure history, serology, blood culture, imaging, operative findings, and treatment response rather than relying solely on isolation from the affected site.⁷

The antibiotic regimen for brucellosis typically uses a doxycycline and rifampicin backbone, often supplemented by an aminoglycoside such as streptomycin or gentamicin in complicated disease.^21,22 Osteoarticular brucellosis and spondylodiscitis generally require prolonged treatment to reduce relapse risk. In this case, gentamicin and ceftriaxone were used during the inpatient period, while doxycycline and rifampicin were continued orally after discharge. Ceftriaxone was used as empirical adjunctive coverage for suspected septic arthritis while awaiting microbiological clarification, rather than as a primary anti-brucellosis agent. The total duration of therapy was completed under the care of an external infectious disease team. At two months, the patient showed clinical and biochemical improvement, with resolved shoulder pain, almost full shoulder range of motion, improved back pain, normalized CRP, and no recurrence.

This case has several limitations. First, the shoulder fluid culture was negative, most likely because antibiotics had already been given before aspiration. Second, histopathological assessment of the tendon and synovium was not performed, so direct proof of Brucella invasion of the tendon sheath or tendon tissue was not available. Third, antimicrobial treatment completion occurred under an external infectious disease team, limiting detailed reporting of total treatment duration. Despite these limitations, the combination of positive blood culture, positive serology, raw camel milk exposure, multifocal MRI findings, operative evidence of shoulder infection, and favourable response to brucellosis-directed treatment supports the final diagnosis.

CONCLUSION

This case demonstrates a rare and clinically important presentation of multifocal osteoarticular brucellosis involving simultaneous L5-S1 spondylodiscitis, presumed culture-negative glenohumeral septic arthritis, long-head biceps infective tenosynovitis, and proximal long-head biceps tendon rupture after raw camel milk exposure. It emphasizes the need to consider brucellosis in endemic regions when severe back or shoulder pain is associated with fever, night sweats, elevated inflammatory markers, and raw milk exposure. MRI is essential for defining multifocal disease, and management should be individualized through multidisciplinary discussion. The contribution of infection to biceps tendon rupture is biologically plausible but cannot be proven without tissue histopathology.

Funding: No funding sources

Conflict of interest: None declared

Ethical approval: Not required

REFERENCES

1. 1. Corbel MJ. Brucellosis in humans and animals. Geneva: World Health Organization, 2006. Available at: https://iris.who.int/handle/10665/43597?. Accessed on 09 April 2026.
2. 2. Franco MP, Mulder M, Gilman RH, Smits HL. Human brucellosis. Lancet Infect Dis. 2007;7(12):775-86.
3. 3. Pappas G, Papadimitriou P, Akritidis N, Christou L, Tsianos EV. The new global map of human brucellosis. Lancet Infect Dis. 2006;6(2):91-9.
4. 4. Dadar M, Al-Khaza’leh J, Fakhri Y, Akar K, Ali S, Shahali Y. Human brucellosis and associated risk factors in the Middle East region: a comprehensive systematic review, meta-analysis, and meta-regression. Heliyon. 2024;10(14):e34324.
5. 5. Al-Ani F, Al Ghenaimi S, Hussein E, Al Mawly J, Al Mushaiki K, Al Kathery S. Human and animal brucellosis in the Sultanate of Oman: an epidemiological study. J Infect Dev Ctries. 2023;17(1):52-8.
6. 6. Holloway P, Gibson M, Holloway T, Pickett I, Crook B, Cardwell JM, et al. Camel milk is a neglected source of brucellosis among rural Arab communities. Nat Commun. 2025;16:624.
7. 7. Yagupsky P, Morata P, Colmenero JD. Laboratory diagnosis of human brucellosis. Clin Microbiol Rev. 2019;33(1):e00073-19.
8. 8. Adetunji SA, Ramirez G, Foster MJ, Arenas-Gamboa AM. A systematic review and meta-analysis of the prevalence of osteoarticular brucellosis. PLoS Negl Trop Dis. 2019;13(1):e0007112.
9. 9. Esmaeilnejad-Ganji SM, Esmaeilnejad-Ganji SMR. Osteoarticular manifestations of human brucellosis: a review. World J Orthop. 2019;10(2):54-62.
10. 10. Pourbagher A, Pourbagher MA, Savas L, Turunc T, Demiroglu YZ, Erol I, et al. Epidemiologic, clinical, and imaging findings in brucellosis patients with osteoarticular involvement. AJR Am J Roentgenol. 2006;187(4):873-80.
11. 11. Colmenero JD, Ruiz-Mesa JD, Plata A, Bermudez P, Martin-Rico P, Queipo-Ortuño MI, et al. Clinical findings, therapeutic approach, and outcome of brucellar vertebral osteomyelitis. Clin Infect Dis. 2008;46(3):426-33.
12. 12. Oztekin O, Calli C, Adibelli ZH, Kantarci F, Aydinlioglu A, Sener RN. Brucellar spondylodiscitis: magnetic resonance imaging features with conventional sequences and diffusion-weighted imaging. Radiol Med. 2010;115(5):794-803.
13. 13. Bozgeyik Z, Ozdemir H, Demirdag K, Ozden M, Sonmezgoz F, Ozgocmen S. Clinical and MRI findings of brucellar spondylodiscitis. Eur J Radiol. 2008;67(1):153-8.
14. 14. Horiuchi K, Asakura T, Bessho Y, Saito F. Infectious tenosynovitis of the long head of the biceps caused by methicillin-resistant Staphylococcus aureus in a patient with diabetes and small cell lung cancer. BMJ Case Rep. 2019;12(3):e229040.
15. 15. Elzein FE, Sherbeeni N, Alomari A, Alhazzani W, Alsaeed M, Almuneef M. Brucella septic arthritis: case reports and review of the literature. Case Rep Infect Dis. 2016;2016:4687840.
16. 16. Chernchujit B, Srimongkolpitak S, Kintarak J, Pornmeechai Y. The role of shoulder arthroplasty after chronic brucellosis of glenohumeral joint septic arthritis: a case report and literature review. Int J Surg Case Rep. 2022;97:107467.
17. 17. Tekin R, Ceylan TF, Cevik R. Brucellosis as a primary cause of tenosynovitis of the extensor tendons. Infez Med. 2015;23(3):257-60.
18. 18. Zangeneh M, Rezvanfar K, Khosravani-Nejad Y, Faghani Y, Dezfulinejad M, Saadat Fakhr M, et al. Infection of tendon sheaths, joints, bursae, soft tissue, and tendon rapture by brucella: a case report. Clin Case Rep. 2023;11(11):e8157.
19. 19. Riley GP. The pathogenesis of tendinopathy. A molecular perspective. Rheumatology (Oxford). 2004;43(2):131-42.
20. 20. Chun YM. Arthroscopic treatment of septic arthritis of the shoulder: decision-making for reoperation. Clin Shoulder Elb. 2020;23(1):1-2.
21. 21. Skalsky K, Yahav D, Bishara J, Pitlik S, Leibovici L, Paul M. Treatment of human brucellosis: systematic review and meta-analysis of randomised controlled trials. BMJ. 2008;336(7646):701-4.
22. 22. Hasanjani Roushan MR, Soleimani Amiri MJ, Janmohammadi N, Sadeghi Hadad M, Javanian M, Baiani M, et al. Comparison of the efficacy of gentamicin for 5 days plus doxycycline for 8 weeks versus streptomycin for 2 weeks plus doxycycline for 45 days in the treatment of human brucellosis: a randomized clinical trial. J Antimicrob Chemother. 2010;65(5):1028-35.