Reactive Arthritis Attributed to E. Coli, Enterococcus Faecalis GU Infection

While Chlamydia trachomatis is the most reported genitourinary pathogen causing ReA, other bacteria including E. coli and Enterococcus faecalis have been implicated in the pathogenesis of ReA.

Reactive arthritis (ReA) occurring following a genitourinary tract infection is typically described with Chlamydia trachomatis, Ureaplasma urealyticum, and Mycoplasma genitalium infection.1   A rarer case of ReA attributed to Escherichia coli and/or Enterococcus faecalis urinary tract infection (UTI) has been recently reported in a 58-year old man after undergoing percutaneous coronary intervention (PCI).

The patient, whose medical history was significant for hyperlipidemia, hypertension, and coronary artery disease, presented for PCI for a 99% occlusion of the left anterior descending coronary artery.  Three days after the uncomplicated placement of a bare metal stent, the patient presented with persistent fever >38℃, pain on micturition, and cloudy urine. 

Blood cultures were negative, but urine cultures grew E.coli (108 colony forming units/mL) and Enterococcus faecalis (105 colony forming units/mL) which were attributed to foley catheter insertion during PCI. Targeted, parenteral antimicrobial therapy was given over 9 days for presumptive catheter-associated UTI, after which patients was discharged from the hospital. 

Approximately 2 weeks after discharge, the patient developed difficulty walking secondary to right Achilles tendon enthesitis and left knee joint pain. Steroid pulses with prenisolone and treatment with methotrexate were initiated, for suspected connective tissue disease, with symptomatic improvement but with no definitive diagnosis.

The patient was later seen at an outpatient orthopedics clinic to be evaluated for persistent right shoulder joint, left knee joint, bilateral ankle joint, and Achilles enthesitis.  Radiographic examination revealed grade 3 sacroiliitis, and pertinent laboratory results included  HLA-B27 positivity (HLA-B*27:04/HLA-B*54:01) and negative rheumatoid factor and antinuclear antibodies.  Baseline axial spondyloarthritis was diagnosed, with presumptive superimposition of ReA. 

High-Yield Clinical Pearls

  • The bacterium most often associated with ReA is Chlamydia trachomatis
  • A case report reports that genitourinary infection with E. coli and Enterococcus faecalis may also cause ReA

The diagnosis of ReA was made upon excluding septic arthritis, crystal-induced arthritis, rheumatoid arthritis, and systemic lupus erythematosus, and noting the timing of arthritis onset 2 weeks after treatment for UTI. Methotrexate was discontinued and prednisolone was subsequently tapered by 1 mg every 2 weeks until complete discontinuation 8 months later.  

The presumptive diagnosis of ReA secondary to urinary catheter-associated E. coli and Enterococcus UTI was made.  It is thought that synovial tissue lipopolysaccharide may induce the secretion of inflammatory cytokines through activation of the nuclear factor-kB pathway and further production of monocyte and neutrophil chemotactic proteins. 

Summary and Clinical Applicability

While Chlamydia trachomatis is the most reported genitourinary pathogen causing ReA, other bacteria including E. coli and Enterococcus faecalis have been implicated in the pathogenesis of ReA. 

“Further accumulation of data and their analyses should be conducted because the data on the long-term prognosis of ReA caused by E.coli and/or Enterococcus faecalis as was shown in the present case are insufficient,” the authors caution.

Limitations and Disclosures

The reported case was not able to show definitive causality between pathogen and ReA. The diagnosis of ReA is often made only after excluding other probable diagnoses.  

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1. Hannu T. Reactive arthritis. Best Pract Res Clin Rheumatol. 2011;25(3):347-57.

2. Nishizaki Y, Yamagami S, Inoue H, Uehara Y, Kobayashi S, Daida H. Reactive Arthritis Caused by Urinary Tract Infection. Intern Med. 2016;55(9):1195-8.