A 61-year-old woman with IgA lambda multiple myeloma presented to Cannes Hospital in November 2025 with a 10-day history of left knee pain and functional impairment. She had been receiving teclistamab since 2024. On admission the team documented fever and pronounced local inflammation of the left knee. Laboratory testing showed marked systemic inflammation with C-reactive protein at 83 mg/L and severe hypogammaglobulinemia (total gammaglobulin 5.6 g/L) with undetectable IgA and IgM. Knee aspiration produced inflammatory fluid containing 16,800 white cells/mL, mostly polynuclear neutrophils. The clinical picture combined local septic-appearing arthritis and systemic inflammatory response in a patient with profound humoral immunodeficiency.
Arthrocentesis fluid was inoculated into blood culture bottles and incubated in a BacT/ALERT 3D system; cultures flagged positive after 48 hours. Gram stain of the positive blood culture revealed tiny gram-negative spiral-shaped bacteria. Subcultures on blood agar incubated 48 hours produced small β-hemolytic zones without visible macroscopic colonies. Blood cultures drawn concurrently yielded an identical Gram-stain appearance. The laboratory attempted organism identification by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF), which did not generate an identification. The treating team then pursued molecular sequencing; 16S rRNA gene sequencing on joint fluid identified the organism as Spiroplasma turonicum.
Positron emission tomography identified focal hyperfixation in the left popliteal region, correlating with the clinical site of inflammation. Arthroscopic biopsy and lavage provided tissue for histology. Hematoxylin and eosin staining showed polymorphous synovial inflammatory infiltrates dominated by neutrophils and inflammatory granulomas without malignant cell infiltration. Cytologic analysis reproduced the neutrophil-predominant inflammatory profile seen on joint fluid aspirate. Targeted PCRs for Campylobacter and Helicobacter species on the joint fluid were negative.
Initial management included arthroscopic lavage with debridement and empiric broad-spectrum carbapenem therapy. Blood inflammatory markers partially improved but local inflammatory signs persisted, prompting a second arthroscopic lavage three weeks after the first. After 16S rRNA sequencing identified Spiroplasma turonicum, the patient was started on doxycycline plus levofloxacin, as referenced in prior literature for related infections. Following the switch to dual therapy, blood markers and local signs progressively improved. The patient completed a six-week antibiotic course as an outpatient; at four-month follow-up she had normalized inflammatory markers and no clinical relapse.
Investigators reviewed exposure history for potential arthropod contact. The patient reported a short stay in an inland area near Nice that included a visit to a horse ranch. The authors referenced prior work identifying S. turonicum as a parasite of Haematopota spp. horseflies, and thus suggested this exposure as a plausible source. The report does not document a witnessed insect bite or a direct vector specimen; the source article did not provide entomologic confirmation.
After surgery the patient developed several large, asymptomatic annular erythematous lesions on her trunk, arms, and legs that resolved within 48 hours. The authors compared these transient erythematous lesions to known skin manifestations associated with Mycoplasma pneumoniae infections—erythema multiforme being a recognized presentation—and noted that Spiroplasma and Mycoplasma belong to the same bacterial family (Mollicutes). The source article proposes shared pathophysiologic mechanisms as a possible explanation for the cutaneous findings, but it does not provide mechanistic data.
This case documents systemic Spiroplasma turonicum infection with bacteremia, knee arthritis, and transient annular erythema in a profoundly immunocompromised patient. Clinicians should consider rare Mollicutes organisms in immunosuppressed hosts who present with culture-positive inflammatory syndromes that elude routine identification. The laboratory team in this report required 16S rRNA gene sequencing to establish the species; standard culture and MALDI-TOF were insufficient for identification. The patient improved after targeted treatment with doxycycline plus levofloxacin following molecular diagnosis.
Limitations and unresolved questions are explicit in the source: the report is a single case, entomologic source attribution was inferred by exposure history rather than confirmed by vector testing, and the optimal antibiotic regimen and duration for human S. turonicum infections remain based on limited prior reports rather than randomized data. The authors emphasize that severely immunosuppressed patients, particularly those receiving agents such as teclistamab that induce prolonged hypogammaglobulinemia, face increased susceptibility and that identification of these organisms may require specific molecular methods and tailored antimicrobial therapy.