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Background <p>Septic wrist arthritis is rare and usually due to Staphylococcus aureus. Gemella haemolysans is exceptionally involved in osteoarticular infection, mainly reported in prosthetic infections or spondylodiscitis.</p> Case presentation <p>A 45-year-old woman on haemodialysis, co-infected with HBV-HIV (CD4 152/µL) and untreated multiple myeloma, presented with 10-day fever (39.5&#xa0;°C) and right-wrist swelling. Synovial fluid and blood cultures grew G. haemolysans (MALDI-TOF score 2.31). MICs: amoxicillin 0.5&#xa0;mg/L, clindamycin 0.5&#xa0;mg/L, gentamicin 16&#xa0;mg/L. Echocardiography excluded endocarditis. Treatment by amoxicillin (3&#xa0;g/day IV, renal adjusted) alone failed to achieve clinical or biological improvement. The addition of clindamycin 600&#xa0;mg IV every 6&#xa0;h resulted in complete resolution of symptoms and normalization of inflammatory markers after five weeks of dual therapy.</p> Conclusion <p>This case illustrates the potential limits of monotherapy with beta-lactams in native joint infections caused by G. haemolysans, especially in immunocompromised patients. The failure of amoxicillin may be explained by factors such as limited diffusion into joint tissues, the absence of surgical debridement, and the use of pharmacokinetic and pharmacodynamic breakpoints not specifically validated for this rare species. Early reassessment and combination therapy may be warranted, particularly in immunocompromised individuals.</p>

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A case report of wrist arthritis caused by Gemella haemolysans

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月22日

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  • Camille Elbaz,
  • Y. Hamidou,
  • M. Choquet,
  • P-A. Bruy,
  • M. Doussiere,
  • J. P. Lanoix,
  • V. Goeb

摘要

Background

Septic wrist arthritis is rare and usually due to Staphylococcus aureus. Gemella haemolysans is exceptionally involved in osteoarticular infection, mainly reported in prosthetic infections or spondylodiscitis.

Case presentation

A 45-year-old woman on haemodialysis, co-infected with HBV-HIV (CD4 152/µL) and untreated multiple myeloma, presented with 10-day fever (39.5 °C) and right-wrist swelling. Synovial fluid and blood cultures grew G. haemolysans (MALDI-TOF score 2.31). MICs: amoxicillin 0.5 mg/L, clindamycin 0.5 mg/L, gentamicin 16 mg/L. Echocardiography excluded endocarditis. Treatment by amoxicillin (3 g/day IV, renal adjusted) alone failed to achieve clinical or biological improvement. The addition of clindamycin 600 mg IV every 6 h resulted in complete resolution of symptoms and normalization of inflammatory markers after five weeks of dual therapy.

Conclusion

This case illustrates the potential limits of monotherapy with beta-lactams in native joint infections caused by G. haemolysans, especially in immunocompromised patients. The failure of amoxicillin may be explained by factors such as limited diffusion into joint tissues, the absence of surgical debridement, and the use of pharmacokinetic and pharmacodynamic breakpoints not specifically validated for this rare species. Early reassessment and combination therapy may be warranted, particularly in immunocompromised individuals.