Mycoplasma hominis as Cause of Extragenital Infection in Patients with Hypogammaglobulinemia: Report of 2 Cases and Literature Review

Abstract

Mycoplasma hominis can be a part of human urogenital tract microbiome, and it is a frequent cause of urogenital infections. In rare cases, it can also cause extragenital infections, especially in immunocompromised patients. In this case series, we report two cases and provide a literature review of extragenital infections caused by M. hominis in patients with hypogammaglobulinemia. Patient 1 was a 61-year-old woman with diffuse large B-cell lymphoma who, after rituximab-containing chemotherapy and CAR-T therapy, developed M. hominis spondylodiscitis. Patient 2 was a 50-year-old woman with congenital hypogammaglobulinemia who developed disseminated M. hominis infection involving pleura, muscles, and right ankle. Antibiotic therapy with levofloxacin and doxycycline for 10 weeks in patient 1 and with levofloxacin alone for 6 weeks in patient 2 led to infection resolution. The literature review identified 14 additional cases reporting M. hominis extragenital infection in patients with hypogammaglobulinemia. M. hominis should also be suspected as an etiological agent of extragenital infection in patients with B-cell immunodeficiency with a clinical picture of persistent, standard-culture negative infection, particularly with arthritis or abscess formation. Even if M. hominis can grow on standard bacterial medium, in suspected cases molecular methods should be promptly used for correct diagnostic work-up and successful therapy.

Keywords: Mycoplasma hominis; Extragenital infection; Hypogammaglobulinemia.

Fig. 1

Baseline (A) and control (B) PET performed in the first patient. A FDG baseline PET performed before the start of antibiotic therapy; arrows mark tracer hyperaccumulation at the soma of the L1 and L2 vertebrae (SUV max 16.2). B control PET performed after 8 weeks of antibiotic therapy; tracer hyperaccumulation no longer evident at L2 soma level

Fig. 2

Baseline (A) and control (B) PET performed in the second patient. A Baseline PET performed before the start of antibiotic therapy. High tracer uptake in pelvis (A1), at internal obturator muscles of both sides (A2) and on the left extending to the external obturator muscle and great adductor muscle (A3) (SUV max 11). Concomitant high FDG uptake at the right tibio-calcaneal joint extending to the lateral aspect of the calcaneus and plantar region (A4) (SUV max 8). B Control PET performed after 6 weeks of antibiotic therapy. Marked reduction in size and hypermetabolism compared with previous control and suspicious for proportion of active disease at pelvis (B1). Residual modest tracer hyperaccumulation at the internal obturator muscles (B2) and external obturator muscle and great adductor muscle (B3) (SUV max 5). These findings are reported as borderline regarding diagnostic significance. No more significant accumulation evident at the right tibio-calcaneal joint (B4)