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Table of Contents
CASE REPORT
Year : 2020  |  Volume : 6  |  Issue : 1  |  Page : 68-70

Reactive arthritis due to asymptomatic Escherichia coli bacteriuria in a young tuberculosis patient


Department of Respiratory Medicine, Kasturba Medical College Manipal, Manipal Academy of Higher Education, Manipal, Udupi, Karnataka, India

Date of Submission26-Sep-2019
Date of Decision06-Feb-2020
Date of Acceptance02-Apr-2020
Date of Web Publication5-Jun-2020

Correspondence Address:
Mohan K Manu
Department of Respiratory Medicine, Kasturba Medical College Manipal, Manipal Academy of Higher Education, Manipal, Udupi - 576 104, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/IJCFM.IJCFM_77_19

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  Abstract 


Reactive arthritis (ReA) is commonly associated with gastroenteritis by Yersinia, Salmonella, Shigella, Campylobacter, and Clostridium difficile and genitourinary infections by Chlamydia trachomatis and Neisseria gonorrhea. Urinary tract infection (UTI) with Escherichia coli is rarely associated with ReA. Failure to screen for UTI, especially in patients with asymptomatic bacteriuria, can lead to delayed diagnosis and inappropriate treatment. A 31-year-old homemaker, who had been diagnosed with pulmonary TB 1 month back and had completed 1 month of successful anti-TB therapy, presented with pain and swelling of the right knee and fever of 1-week duration. She had healing erythema nodosum on both her thighs. Her right knee had pain and swelling that lead to restriction of movements. X-ray of the right knee showed joint effusion with no joint destruction. Work up for autoimmune arthritis was negative. Synovial fluid studies ruled out septic arthritis, crystal arthropathies, and tuberculous arthritis. Urinalysis suggested UTI and urine culture isolated E. coli. Hence, we made the diagnosis of ReA due to UTI with E. coli. She received oral nonsteroidal anti-inflammatory drugs and a course of ciprofloxacin. She had a complete recovery.

Keywords: Asymptomatic bacteriuria, Escherichia coli, reactive arthritis, tuberculosis, urinary tract infection


How to cite this article:
Shahul HA, Manu MK, Mohapatra AK. Reactive arthritis due to asymptomatic Escherichia coli bacteriuria in a young tuberculosis patient. Indian J Community Fam Med 2020;6:68-70

How to cite this URL:
Shahul HA, Manu MK, Mohapatra AK. Reactive arthritis due to asymptomatic Escherichia coli bacteriuria in a young tuberculosis patient. Indian J Community Fam Med [serial online] 2020 [cited 2020 Oct 25];6:68-70. Available from: https://www.ijcfm.org/text.asp?2020/6/1/68/286035




  Introduction Top


Reactive arthritis (ReA) is a form of inflammatory arthritis that develops following an infection elsewhere in the body. It is a sterile form of arthritis, mainly affecting young adults.[1] ReA is most commonly postvenereal or postenteric, and symptoms begin 1–6 weeks after the inciting infection.[2] In the literature, the reports of ReA following a urinary tract infection (UTI) are limited. A few case reports are available depicting the link between Escherichia coli and ReA.[3]


  Case Report Top


A 31-year-old homemaker presented with pain and swelling of the right knee and fever of 1 week. The onset of pain preceded swelling by 2 days and had progressed ever since. She had pulmonary tuberculosis (TB) 1 month ago. She was on regular first-line antitubercular therapy (ATT). There was no history suggestive of upper respiratory, gastrointestinal, or urogenital infections preceding the joint symptoms. She denied any joint ailments in the past and any family history of arthritis. General physical examination revealed brownish, bruise-like rashes (healing erythema nodosum) over the lower thighs on both sides that were not tender. She had swelling of the right knee joint suggestive of effusion [Figure 1]. Joint movements were restricted and painful. The examination of other joints did not reveal any abnormality. There were bilateral inspiratory crepitations on chest auscultation. There were no focal neurological deficits.
Figure 1: Photograph showing swelling of the right knee joint with healing erythema nodosum over lower thighs on both sides

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Routine blood investigations revealed a raised erythrocyte sedimentation rate of 118 mm/h. The radiograph of the right knee showed effusion with no joint destruction [Figure 2]. Serum uric acid, C-reactive protein, and anti-streptolysin O levels were within the normal range. Rheumatoid factor and anti-cyclic citrullinated peptide were negative. Levels of serum anti-nuclear antibody, anti-double-stranded DNA, and anti-neutrophil cytoplasmic antibodies were normal. Synovial fluid aspiration revealed a straw-colored, nonturbid fluid. Polarized light microscopy revealed no crystals. Synovial fluid culture did not isolate any bacterial growth; staining for acid-fast bacilli and polymerase chain reaction (PCR) for Mycobacterium tuberculosis complex 1S6110 gene was negative. Fluid cytology did not reveal any malignant cells. The tests for human immunodeficiency virus, brucellosis, infectious mononucleosis, cytomegalovirus, toxoplasmosis, Salmonella, and Yersinia were negative. The patient was not willing for HLA–B27 studies. Stool culture and urogenital swab culture did not isolate any pathogen. Urinalysis showed numerous pus cells, and urine culture isolated E. coli. We diagnosed ReA due to E. coli UTI. She received oral nonsteroidal anti-inflammatory drugs (NSAIDs) along with a course of ciprofloxacin as per urine culture and sensitivity report. She recovered completely in 1 week.
Figure 2: X-ray of the right knee showing no evidence of joint destruction

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  Discussion Top


Arthritis in a young TB patient who is on ATT can be due to various reasons. TB affects the musculoskeletal system in around 15% of extrapulmonary cases. Tuberculous septic arthritis is a differential diagnosis; strengthened by the fact that only one joint was involved. Since the patient was clinically improving while on ATT, TB septic arthritis was unlikely. We ruled out TB septic arthritis by negative acid-fast staining as well as TB-PCR of the synovial fluid. As the patient developed joint symptoms after 1 month of initiation of ATT, we considered the possibility of pyrazinamide or ethambutol induced gout and pseudogout. However, we precluded it since polarized light microscopy of the synovial fluid showed no urate or pyrophosphate crystals. Poncet's disease is a form of ReA in patients with active TB, where the synovial fluid is sterile. It usually manifests as polyarthritis or oligoarthritis; monoarthritis is quite rare. Such patients respond well after starting ATT.[4] The joint problem began while the patient was on ATT, thereby making the possibility of Poncet's disease unlikely. We ruled out autoimmune arthritis by appropriate serological tests. The patient did not meet the revised Jones criteria for rheumatic fever. Viral and arthropod-borne arthritis tends to affect the small joints of the hands and feet mainly, and patients tend to have active itchy rashes, which were not present in our case. Synovial fluid cultures were sterile, ruling out septic arthritis as a cause.

ReA most commonly occurs following an episode of gastroenteritis by Yersinia, Salmonella, Shigella, Campylobacter, and Clostridium difficile or a genitourinary infection by Chlamydia trachomatis and Neisseria gonorrhea. However, specific serological tests, stool culture, and urogenital swab culture failed to identify any of these agents. We found very few cases of ReA after UTI with E. coli described in the literature. Renou et al. reported a case of ReA in a 25-year-old female following an episode of E. coli UTI.[3] In a mini case-series based review of the overlap between rheumatoid arthritis and seronegative spondyloarthritis, Sangha et al. described a case of ReA which developed after E. coli-positive UTI,[5] This correlation was also signified in a prospective, a comparative study from Kosovo, wherein Lahu et al. found E. coli to be the predominantly isolated bacterial causative agent in ReA.[6] Hence, it is important that clinicians are aware of this rare cause of ReA. The diagnosis is comparatively easier when there is a history of recent UTI or active symptomatic UTI. Urine analysis and urine culture can be done to confirm the diagnosis in suspected cases. However, our patient had asymptomatic bacteriuria, which was detected when urine analysis was done as a part of arthritis workup after we ruled out common causes of ReA. In most cases, the general condition of the patient is good and can be managed even in resource-limited settings. Adequate rest and proper analgesia is the mainstay of treatment. NSAIDs are highly effective and provide analgesic and anti-inflammatory benefits. Intra-articular steroid injections also result in rapid relief of joint inflammation.[7] Any active infection has to be treated with appropriate antibiotics.


  Conclusion Top


To conclude, UTI with E. coli, even if asymptomatic, can lead to ReA. Hence, caregivers should consider the possibility of UTI as a cause in all cases of ReA and should judiciously employ urine analysis and urine culture for the diagnosis in indicated cases.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that name and initials will not be published and due efforts will be made to conceal the identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Mukherjee S, Kar M. Reactive arthritis: Current perspectives. J Indian Acad Clin Med 2000;1:234-8.  Back to cited text no. 1
    
2.
Carter JD, Hudson AP. Reactive arthritis: Clinical aspects and medical management. Rheum Dis Clin North Am 2009;35:21-44.  Back to cited text no. 2
    
3.
Renou F, Wartel G, Raffray L, Kuli B, Fayeulle S, Yvin JL. Reactive arthritis due to Escherichia coli urinary tract infection. Rev Med Interne 2011;32:e4-5.  Back to cited text no. 3
    
4.
Kroot EJ, Hazes JM, Colin EM, Dolhain RJ. Poncet's disease: Reactive arthritis accompanying tuberculosis. Two case reports and a review of the literature. Rheumatology (Oxford) 2007;46:484-9.  Back to cited text no. 4
    
5.
Sangha MS, Wright ML, Ciurtin C. Strongly positive anti-CCP antibodies in patients with sacroiliitis or reactive arthritis post-E. coli infection: A mini case-series based review. Int J Rheum Dis 2018;21:315-21.  Back to cited text no. 5
    
6.
Lahu A, Bajraktari IH, Lahu S, Saiti V, Kryeziu A, Sherifi F, et al. The source of infection and the most frequent causes of reactive arthritis in Kosovo. Mater Sociomed 2016;28:201-4.  Back to cited text no. 6
    
7.
Toivanen A. Managing reactive arthritis. Rheumatology (Oxford) 2000;39:117-9.  Back to cited text no. 7
    


    Figures

  [Figure 1], [Figure 2]



 

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