Ureaplasma Septic Arthritis in an Immunosuppressed Patient With Juvenile Idiopathic Arthritis

Abstract

Mycoplasmas, including Ureaplasma and Mycoplasma species, are uncommon but important causes of septic arthritis, especially affecting immunosuppressed patients. Many of the reported cases have been associated with congenital immunodeficiency disorders, especially hypogammaglobulinemia. Mycoplasmas are difficult to grow in the laboratory, and these infections may be underdiagnosed using culture techniques. We report a case of a 21-year-old woman with juvenile idiopathic arthritis and hip arthroplasties treated with rituximab and adalimumab who developed urogenital infections and soft tissue abscesses followed by knee arthritis with negative routine cultures. Ureaplasma species was identified from synovial fluid on 2 separate occasions using a broad-range 16S ribosomal RNA gene polymerase chain reaction. Azithromycin led to rapid improvement in symptoms, but after completion of therapy, involvement of the hip prosthesis became apparent, and again, 16S rRNA gene polymerase chain reaction was positive for Ureaplasma species. The literature is reviewed with a discussion of risk factors for Mycoplasma septic arthritis, clinical presentation, methods of diagnosis, and treatment.

Ureaplasma urealyticum pyelonephritis presenting with progressive dysuria, renal failure, and neurologic symptoms in an immunocompromised patient

“…Rituximab may increase the risk of Ureaplasma infection by an unknown mechanism, given the five other reports of severe Ureaplasma infection in the context of recent or ongoing rituximab therapy . One hypothesis for the rituximab effect is by reducing immune globulins peripherally.…”

“…Ureaplasma infection in the context of recent or ongoing rituximab therapy. [7][8][9][10][11] One hypothesis for the rituximab effect is by reducing immune globulins peripherally. Indeed, many of these patients with severe U urealyticum infections were hypogammaglobulinemic from rituximab [7][8][9][10][11] or congenital absence of gammaglobulins.…”

“…[7][8][9][10][11] One hypothesis for the rituximab effect is by reducing immune globulins peripherally. Indeed, many of these patients with severe U urealyticum infections were hypogammaglobulinemic from rituximab [7][8][9][10][11] or congenital absence of gammaglobulins. 6,12 Our patient had normal immune globulins measured 3 months prior to her current presentation as did the patient identified in Gerber et al 5 Therefore, further research is necessary to determine the mechanism by which rituximab increases susceptibility to Ureaplasma infection.…”

More than just inflammation: Ureaplasma species induce apoptosis in human brain microvascular endothelial cells

“…Despite ongoing research, however, the implications of a postnatal Ureaplasma colonization or infection remain unresolved and appear to be underestimated so far [6]. As well as provoking invasive infections in immunocompromised adults [7–9], Ureaplasma spp. may cause pneumonia and sepsis in preterm and term neonates [10, 11].…”

Novel insights into neuroinflammation: bacterial lipopolysaccharide, tumor necrosis factor α, and Ureaplasma species differentially modulate atypical chemokine receptor 3 responses in human brain microvascular endothelial cells

“…Considered a significant co-factor in chorioamnionitis and premature birth [ 3 – 8 ], Ureaplasma spp. are also known to cause severe invasive infections in immunocompromised adults [ 9 – 11 ] as well as pneumonia, sepsis, and meningitis in preterm and term neonates [ 12 – 15 ].…”