Rare Spiroplasma turonicum Bacteremia Presented as Knee Arthritis in an Immunocompromised Patient
A 61-year-old woman in southeast France arrived with 10 days of left knee pain and left the hospital with a diagnosis few clinicians would expect to encounter: Spiroplasma turonicum systemic infection. The organism was recovered from both blood and joint samples in a patient whose immune defenses were deeply compromised by IgA lambda multiple myeloma and ongoing teclistamab treatment. What began as monoarthritis with fever and skin erythema proved to be disseminated infection, not isolated joint disease.
The case matters because the first diagnostic impression could easily have pointed toward more familiar bacterial arthritis, inflammatory relapse, or even a malignant process. Instead, the microbiologic trail led to a fastidious intracellular gram-negative bacterium more often linked to plants, insects, and ticks than to human disease.
A Host Defense Failure Created Room for an Unusual Pathogen
The patient had multiple myeloma diagnosed in 2017 and had previously undergone autograft. Since 2024, she had been receiving teclistamab, a monoclonal antibody targeting B-cell maturation antigen. In practical terms, that type of therapy can strip away normal plasma cell function along with malignant clones, leaving patients with prolonged hypogammaglobulinemia and poor humoral defense. Her laboratory profile fit that vulnerability: C-reactive protein was 83 mg/L, serum protein electrophoresis showed severe hypogammaglobulinemia at 5.6 g/L, and both IgA and IgM were undetectable.
Clinically, her left knee was inflamed, painful, and functionally limiting. Positron emission tomography showed hyperfixation in the popliteal region of the left leg, suggesting active inflammatory or infectious involvement around the joint and adjacent soft tissue. Joint aspiration yielded inflammatory fluid with 16,800 white cells/mL, mostly polynuclear neutrophils. This was not a quiet synovial process.
Culture Grew Spiral-Shaped Gram-Negative Bacteria Before Identification Did
The first microbiologic clue appeared when knee aspirate was cultured in blood culture bottles and incubated at 35°C in a BacT/ALERT 3D system. After 48 hours, the cultures flagged positive. Gram stain showed tiny gram-negative spiral-shaped bacteria, and blood cultures drawn at the same time revealed the same morphology. Subculture on blood agar produced several small zones of β-hemolysis without macroscopic colony growth, a pattern that fits an organism with demanding growth requirements.
Conventional identification did not solve the case. Matrix-assisted laser desorption/time-of-flight mass spectrometry with MALDI Biotyper failed to identify the bacterium, a predictable limitation when the organism is rare and poorly represented in reference databases. PCR testing for Campylobacter and Helicobacter on the knee aspirate was negative, narrowing the differential but not ending it. Cytologic analysis of tissue collected during arthroscopic lavage and debridement showed numerous neutrophils, with no cancer cell infiltration.
One sentence captured the central diagnostic challenge: the pathogen was present, but routine laboratory tools could not name it.
Skin Erythema and Arthritis Pointed to Systemic Spread
After the first arthroscopic lavage and debridement of the popliteal nodular lesion, empirical carbapenem therapy was started. Blood inflammatory markers improved only partially, and the knee remained inflamed. A second arthroscopic lavage 3 weeks later again produced inflammatory joint fluid and the same unrecognized gram-negative spiral-shaped bacteria. Then the picture broadened further: large, asymptomatic annular erythematous lesions developed on the trunk, arms, and legs and lasted less than 48 hours.
Those transient skin findings matter because they suggest a systemic inflammatory or infectious response rather than a strictly localized joint infection. In the same bacterial family, Mycoplasma pneumoniae can trigger rash syndromes through immune-mediated mechanisms, and the parallel raises a plausible pathophysiologic explanation for the annular erythema seen here. The case also broadens the clinical phenotype of Spiroplasma infection, because arthritis had not previously been described for this genus.
16S rRNA Sequencing Solved the Diagnosis
Definitive identification came from 16S rRNA gene sequencing of the joint fluid, which identified the organism as S. turonicum. That result linked the blood culture, joint infection, and skin findings into a single systemic syndrome. Previous literature already associated this species with horseflies, and the patient later described a short stay in inland Nice that included a visit to a horse ranch. The exposure history offered a plausible ecological bridge between a vector-associated bacterium and human infection.
Antibiotic choice changed after the molecular diagnosis. The patient was started on doxycycline and levofloxacin, and both inflammatory markers and local signs progressively improved. After 6 days of this combination therapy, she was discharged and completed 6 weeks of antibiotics. At 4-month outpatient follow-up, blood inflammatory markers were within reference ranges and there was no clinical relapse.
The response fits the idea that delayed recognition of an unusual organism can prolong illness until treatment is aligned with the organism’s biology. Doxycycline and levofloxacin likely provided activity against the fastidious intracellular pathogen after carbapenem therapy had only partially restrained the inflammatory process.
Immunosuppression and Rare Zoonotic Infection Collided in One Case
Severe immune dysfunction shaped the entire presentation. Teclistamab is designed to target B-cell maturation antigen, but in doing so it can deplete both malignant and normal long-lived plasma cells. The resulting hypogammaglobulinemia creates a narrow margin of safety against uncommon and opportunistic pathogens. In that context, even an organism usually reserved for insects or environmental reservoirs can become a human pathogen.
This case also expands the clinical footprint of Spiroplasma infections in humans. Human disease remains extremely rare, but prior reports have already included S. ixodetis after tick exposure in Sweden, S. apis after an insect sting in France, and a first human systemic infection caused by Spiroplasma in Spain. The current case adds bacteremia with arthritis and transient annular erythema due to S. turonicum in an immunocompromised patient.
For clinicians, the bedside implication is direct. When an immunocompromised patient presents with culture-negative or hard-to-identify septic arthritis, unusual spiral-shaped gram-negative organisms deserve consideration, and molecular methods such as 16S rRNA sequencing may be essential for diagnosis. For microbiology laboratories, the case is a reminder that standard identification platforms can fail when the organism falls outside routine databases. For infectious diseases teams, it is evidence that rare vector-associated bacteria can present as systemic disease in profoundly immunosuppressed hosts and may require targeted dual therapy for resolution.