Figure 1Clinical presentation and intraoperative findings. A: Visible fistula over the olecranon region. B, C: Intraoperative views showing macerated skin and the inflamed bursa.
DOI: https://doi.org/https://doi.org/10.57187/5110
Bursitis is a common musculoskeletal condition. The olecranon bursa and prepatellar bursa are the most commonly affected sites because of their superficial anatomical location, which makes them more susceptible to trauma and infection [1]. Approximately one-third of cases of olecranon or prepatellar bursitis have a septic origin, with an annual incidence of 1 in 10,000 individuals [2, 3]. Septic olecranon or prepatellar bursitis can account for up to 0.1% of all hospital admissions [2]. In approximately 80% of septic bursitis cases, Staphylococcus aureus is identified as the causative pathogen [2]. However, opportunistic pathogens can also play a significant role, particularly in immunocompromised patients [4, 5]. The treatment of bursitis generally involves a combination of surgical intervention and antibiotic therapy [6]. There is no standardised approach to antibiotic therapy or the timing of surgical treatment. In current clinical practice, a multidisciplinary approach is often preferred. To facilitate targeted antibiotic therapy, intraoperative samples are routinely collected for microbiological analysis. This strategy allows for personalised treatment, improving patient outcomes while minimising the risks associated with broad-spectrum antibiotic use.
Here, we present a rare case of septic bursitis with Nocardia farcinica in an immunocompromised patient and provide a literature review of reported cases.
Although musculoskeletal nocardiosis has been described, isolated septic bursitis caused by Nocardia farcinica remains exceedingly rare. In contrast to most reported musculoskeletal cases, which frequently involve dissemination or severe systemic illness, our patient presented with a localised infection despite ongoing immunosuppressive therapy. Moreover, molecular characterisation was performed using whole-genome sequencing to further assess resistance and virulence determinants, providing additional microbiological insight. This case therefore adds clinically relevant information regarding the diagnostic evaluation and management of atypical bursitis in immunosuppressed patients.
The following case description outlines the chronological course of events from the initial symptoms through diagnosis, treatment, and follow-up.
A male patient in his mid-70s presented to his primary care physician with community-acquired left-sided traumatic olecranon bursitis that developed following a fall on the stairs outside his home. The patient reported progressive local pain and swelling over two weeks, with increasing discomfort during elbow movement. Initially, the overlying skin remained intact, but the lesion subsequently opened and began draining cloudy fluid (figure 1A). He denied fever, chills, or other systemic symptoms, but the skin lesion had progressively worsened. Examination showed local warmth and redness, with no involvement of other joints. The patient had a medical history of seronegative rheumatoid arthritis managed with immunosuppressive therapy consisting of methotrexate (10 mg weekly), golimumab (50 mg subcutaneously monthly), and low-dose prednisone (2.5 mg daily). He had no relevant family history of infectious or autoimmune diseases and no known genetic disorders. The patient reported no psychosocial factors or environmental exposures of clinical relevance.
Cultures of a bursal puncture obtained in the outpatient setting revealed Nocardia farcinica, prompting referral to our clinic for further evaluation, and surgical bursectomy was indicated. Preoperative laboratory tests were within normal limits. Surgery included excision of the macerated skin around the tip of the olecranon and removal of the affected bursa. Intraoperatively, the bursa appeared markedly inflamed and enlarged, resembling a pannus (figure 1B, C). Following excision, extensive irrigation, and haemostasis, the skin was closed in a standard manner.
Figure 1Clinical presentation and intraoperative findings. A: Visible fistula over the olecranon region. B, C: Intraoperative views showing macerated skin and the inflamed bursa.
Gram stain revealed the characteristic star-shaped growth and branching patterns of Nocardia (figure 2A). The colonies presented the typical yellow pigmentation and dry colony morphology (figure 2B). Matrix-assisted laser desorption ionisation–time-of-flight (MALDI-TOF) confirmed the species to be Nocardia farcinica. Histological sections of the biopsy displayed a nonspecific, florid inflammatory response marked by haemorrhage and a dense infiltrate of neutrophils (figure 2 C/D). Furthermore, whole-genome sequencing (WGS) of the isolate was performed to gain more molecular insight into this rare case. WGS also identified the isolate as Nocardia farcinica based on the digital DNA–DNA hybridisation values (figures S1 and S2 in the appendix). However, no previously reported virulence genes were detected, potentially underscoring the relevance of host immunosuppression, rather than pathogen-derived virulence factors, to the development of infection caused by this pathogen. A chest CT as well as a cranial MRI performed to check for systemic spread and potential pulmonary or cranial nocardial lesions were unremarkable.
Figure 2Microbiological and histopathological findings. A: Gram stain showing filamentous, branching structures typical of Nocardia spp. B: Nocardia colonies on blood agar. C, D: Histology of a retrieved biopsy demonstrating a florid inflammatory response with a dense neutrophilic infiltrate.
After surgery, empirical intravenous imipenem/cilastatin (500 mg four times daily) was initiated. After exclusion of disseminated infection and confirmation of antimicrobial susceptibility results, therapy was de-escalated after four days to oral trimethoprim/sulfamethoxazole (1600/320 mg twice daily). The wound healed well, and the patient was discharged home on the sixth day. After two weeks, the patient developed dyspnoea, fever, and a generalised rash, prompting re-hospitalisation. Elevated inflammatory markers and findings indicating hepatopathy suggested a drug reaction, which was supported by the findings of a skin biopsy of the exanthema. The treatment was switched to oral amoxicillin/clavulanic acid (875/125 mg three times daily), guided by susceptibility testing. The temporal relationship to trimethoprim/sulfamethoxazole exposure and clinical improvement after discontinuation further supported a probable adverse drug reaction.
Antibiotic treatment was stopped after three months. At the one-year follow-up (figure 3), the patient remained asymptomatic with full functional recovery of the elbow and no signs of recurrence.
Figure 3Postoperative clinical course. A, B: Two weeks post-surgery, showing progressive wound healing. C: Six weeks post-surgery, with resolution of local inflammation.
We conducted a systematic literature search using the keywords “Nocardia” and “bursitis” in PubMed. We identified only five case reports and compared patient characteristics and treatment approaches (table S1 in the appendix). The locations of the bursitis included olecranon, prepatellar, and malleolar sites. Interestingly, none of the patients were immunosuppressed (information was missing for two patients), and no cases of systemic infection were observed. Antibiotic treatment mostly consisted of a sulfonamide, and the treatment duration varied from one to six months. Two patients were managed conservatively without surgery, yet all achieved a good outcome.
To further evaluate the relevance of the subspecies Nocardia farcinica as identified in our case, we conducted an additional literature review focusing on musculoskeletal infections caused by Nocardia farcinica. A PubMed search using the keyword "Nocardia farcinica" yielded 503 papers. Of these, 12 papers primarily involved musculoskeletal manifestations (see figure S3 in the appendix for the selection workflow). Table S2 in the appendix summarises the screened papers.
These case reports illustrate the diverse manifestations of Nocardia farcinica musculoskeletal infections, which often occur in immunocompromised patients with comorbidities such as diabetes, chronic lung disease, lymphoma, or conditions requiring steroid therapy. The infection affected multiple anatomical sites in seven of the twelve patients, including the lungs, limbs, joints, and soft tissues.
Most cases required a combination of surgical intervention and long-term antibiotic treatment, with trimethoprim-sulfamethoxazole being the most commonly used antibiotic. In cases of adverse reactions, alternative antibiotics such as imipenem, moxifloxacin, and amoxicillin-clavulanic acid were successfully used. The reports highlight successful outcomes in the majority of patients treated using a multidisciplinary approach including both surgery and prolonged antibiotic treatment. However, patients with severe underlying disease sometimes experienced adverse outcomes or fatal complications, highlighting the important contribution of comorbidities to prognosis.
Here, we presented a rare case of Nocardia bursitis of the olecranon in an immunosuppressed patient. The combined surgical and targeted antibiotic treatment led to complete resolution of the infection. The literature review identified only five other cases of Nocardia bursitis, none of which showed documented immunosuppression or systemic spread. On the other hand, the more general literature review covering all types of musculoskeletal infections caused by Nocardia farcinica showed that these infections mostly occur in immunocompromised patients, with a propensity for systemic spread.
Nocardia are aerobic, Gram-positive bacteria commonly found in soil and organic matter [7–9]. They primarily cause opportunistic infections in immunocompromised hosts, with the potential for haematogenous dissemination, particularly to the central nervous system. However, more than one-third of reported cases have been documented in immunocompetent patients, suggesting that the pathogen can overcome certain host defences in healthy individuals as well [5, 10]. Nocardia most commonly causes localised infections at the primary site of entry, typically the lungs or skin, where it can produce granulomatous lesions resembling tuberculosis. Nocardia is capable of spreading haematogenously to distant organs, causing disseminated infection that may involve the central nervous system, kidneys, or joints. This dissemination often occurs in immunosuppressed patients but has also been observed in otherwise healthy individuals, underscoring the pathogen's potential for systemic involvement [11, 12].
Among the numerous Nocardia species, Nocardia farcinica is one of the more frequently isolated species in clinical infections and is known for its high virulence and multidrug resistance [13, 14]. Nocardia farcinica exhibits increased virulence compared to other Nocardia species, driven by genetic factors such as the virulence genes relA, icl, and mbtH, which enhance survival and proliferation within the host. Resistance-related genes such as RbpA, mtrA, FAR-1, blaFAR-1, and rox further complicate treatment by conferring resistance to multiple antibiotics [15]. In our isolate, whole-genome sequencing revealed the presence of the intrinsic FAR-1 and rox genes, while no acquired resistance mutations were detected. This supports the clinical observation of a good treatment response and indicates that the infection was driven primarily by host immunosuppression rather than by enhanced bacterial resistance.
Diagnosing nocardial infections is challenging due to the slow-growing nature of the organism. Standard diagnostic methods include culture and microscopy, using Gram and modified Ziehl-Neelsen stains. Advanced molecular techniques, such as MALDI-TOF mass spectrometry and 16S rRNA sequencing, have improved the speed and accuracy of Nocardia identification [11, 16]. In cases in which culture fails to yield results, whole-genome sequencing can provide or confirm a definitive diagnosis [5, 17].
Nocardia infections typically require prolonged antibiotic therapy, often lasting 6–12 months depending on the severity and extent of the infection. However, in cases of localised infections without systemic dissemination, shorter treatment durations may also be effective and should be considered on a case-by-case basis. In this case, the decision to continue antibiotic therapy for three months was based on an individualised risk–benefit assessment, taking into account the patient’s immunosuppression and the known virulence of Nocardia farcinica. Shorter durations (e.g., 4–8 weeks) may be sufficient after complete surgical excision [8]. The duration was defined according to the clinical course, and therapy was discontinued after three months in the absence of signs of relapse. Although trimethoprim-sulfamethoxazole remains the first-line therapy, alternative agents such as imipenem, moxifloxacin, linezolid, or amoxicillin-clavulanic acid may be required in cases of resistance or adverse drug reactions. Surgical intervention, such as abscess drainage or debridement, may be appropriate depending on the location, especially in severe cases. Interdisciplinary management involving infectious disease specialists and surgeons is crucial to optimise outcomes.
The clinical presentation of our patient was atypical, lacking prominent systemic signs such as fever or elevated inflammatory markers, which are commonly observed in classic bacterial bursitis caused by pathogens such as Staphylococcus aureus. In immunosuppressed individuals, this constellation should prompt consideration of unusual or opportunistic pathogens such as mycobacteria, fungal organisms, or other rare bacteria (e.g. Actinomyces or Rhodococcus).
In cases of non-staphylococcal or non-streptococcal musculoskeletal infections, particularly in immunosuppressed patients, clinicians should consider rare or opportunistic pathogens and involve infectious diseases specialists early to guide targeted microbiological diagnostics and antimicrobial management. Given the potential for resistance and adverse drug reactions, individualised treatment strategies guided by microbiological data are essential. Multidisciplinary collaboration involving infectious disease specialists, microbiologists, and surgeons plays a pivotal role in achieving favourable clinical outcomes.
Written informed consent was obtained from the patient for the publication of the case report and the accompanying images.
The authors did not receive any financial support for the preparation of this manuscript.
All authors have completed and submitted the International Committee of Medical Journal Editors form for disclosure of potential conflicts of interest. No potential conflict of interest related to the content of this manuscript was disclosed.
1. McAfee J, Smith D. Olecranon and prepatellar bursitis. Diagnosis and treatment. Western Journal of Medicine. 1988;149(5) doi: 607.
2. Baumbach SF, Lobo CM, Badyine I, Mutschler W, Kanz KG. Prepatellar and olecranon bursitis: literature review and development of a treatment algorithm. Arch Orthop Trauma Surg. 2014 Mar;134(3):359–70. doi: https://doi.org/10.1007/s00402-013-1882-7
3. Reilly D, Kamineni S. Olecranon bursitis. J Shoulder Elbow Surg. 2016 Jan;25(1):158–67. doi: https://doi.org/10.1016/j.jse.2015.08.032
4. Dutertre M, Delobel P, Marchou B, Boyer JF, Mougari F, Martin-Blondel G. Olecranon bursitis secondary to Mycobacterium europaeum infection in a patient receiving immunosuppressive drugs for rheumatoid arthritis. Med Mal Infect. 2019 Aug;49(5):358–9. doi: https://doi.org/10.1016/j.medmal.2019.03.002
5. Traxler RM, Bell ME, Lasker B, Headd B, Shieh WJ, McQuiston JR. Updated review on Nocardia species: 2006–2021. Clin Microbiol Rev. 2022 Dec;35(4):e0002721. doi: https://doi.org/10.1128/cmr.00027-21
6. Sayegh ET, Strauch RJ. Treatment of olecranon bursitis: a systematic review. Arch Orthop Trauma Surg. 2014 Nov;134(11):1517–36. doi: https://doi.org/10.1007/s00402-014-2088-3
7. Fatahi-Bafghi M. Nocardiosis from 1888 to 2017. Microb Pathog. 2018 Jan;114:369–84. doi: https://doi.org/10.1016/j.micpath.2017.11.012
8. Wilson JW, editor. Nocardiosis: updates and clinical overview. Mayo Clinic Proceedings. Elsevier; 2012.
9. Nocard E. Note sur la maladie des boeufs de Guadeloupe connue sous le nom de farcin. Ann Inst Pasteur (Paris). 1888;2: 293-302.
10. Beaman BL, Beaman L. Nocardia species: host-parasite relationships. Clin Microbiol Rev. 1994 Apr;7(2):213–64. doi: https://doi.org/10.1128/CMR.7.2.213
11. Brown-Elliott BA, Brown JM, Conville PS, Wallace RJ Jr. Clinical and laboratory features of the Nocardia spp. based on current molecular taxonomy. Clin Microbiol Rev. 2006 Apr;19(2):259–82. doi: https://doi.org/10.1128/CMR.19.2.259-282.2006
12. Steinbrink J, Leavens J, Kauffman CA, Miceli MH. Manifestations and outcomes of nocardia infections: comparison of immunocompromised and nonimmunocompromised adult patients. Medicine (Baltimore). 2018 Oct;97(40):e12436. doi: https://doi.org/10.1097/MD.0000000000012436
13. Toyokawa M, Ohana N, Ueda A, Imai M, Tanno D, Honda M, et al. Identification and antimicrobial susceptibility profiles of Nocardia species clinically isolated in Japan. Sci Rep. 2021 Aug;11(1):16742. doi: https://doi.org/10.1038/s41598-021-95870-2
14. Wang H, Zhu Y, Cui Q, Wu W, Li G, Chen D, et al. Epidemiology and Antimicrobial Resistance Profiles of the Nocardia Species in China, 2009 to 2021. Microbiol Spectr. 2022 Apr;10(2):e0156021. doi: https://doi.org/10.1128/spectrum.01560-21
15. Nathar S, Rajmichael R, Jeyaraj Pandian C, Nagarajan H, Mathimaran A, Kingsley JD, et al. Exploring Nocardia’s ecological spectrum and novel therapeutic frontiers through whole-genome sequencing: unraveling drug resistance and virulence factors. Arch Microbiol. 2024 Jan;206(2):76. doi: https://doi.org/10.1007/s00203-023-03799-z
16. Liu Y, Wu SY, Deng J, Zhuang KW, Tang Y, Wu N, et al. Application of MALDI-TOF mass spectrometry for identification of Nocardia species. BMC Microbiol. 2024 Sep;24(1):358. doi: https://doi.org/10.1186/s12866-024-03483-2
17. Schlaberg R, Chiu CY, Miller S, Procop GW, Weinstock G; Professional Practice Committee and Committee on Laboratory Practices of the American Society for Microbiology; Microbiology Resource Committee of the College of American Pathologists. Validation of Metagenomic Next-Generation Sequencing Tests for Universal Pathogen Detection. Arch Pathol Lab Med. 2017 Jun;141(6):776–86. doi: https://doi.org/10.5858/arpa.2016-0539-RA
The appendix is available in the pdf version of the article at https://doi.org/10.57187/5110.