Possible role of streptococcal infection in flares of juvenile idiopathic arthritis

Barash, Judith; Goldzweig, Gil

doi:10.1002/art.22787

Cited by 21 publications

(10 citation statements)

References 6 publications

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“…Of these 33 cases, only 9 % was positive for a recent streptococcal infection [59]. Another study that examined all cases of JIA hospitalized during a period of 10 years found a high correlation between disease exacerbations and streptococcal infections, concluding that "arthritogenic" streptococci may cause flare-ups of chronic arthritides [60].…”

Section: The Potential Role Of Bacteria In Juvenile Idiopathic Arthritismentioning

confidence: 98%

The Etiology of Juvenile Idiopathic Arthritis

Rigante

Bosco

Esposito

2014

Clinic Rev Allerg Immunol

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Over the years, the commonly used term to describe juvenile idiopathic arthritis (JIA) has changed. By definition, JIA includes all types of arthritis with no apparent cause, lasting more than 6 weeks, in patients aged less than 16 years at onset. JIA pathogenesis is still poorly understood: the interaction between environmental factors and multiple genes has been proposed as the most relevant working mechanism to the development of JIA. The concept that various microbes that colonize or infect not only the mucosal surfaces, like the oral cavity, but also the airways and gut might trigger autoimmune processes, resulting in chronic arthritides, and JIA was first drafted at the outset of last century. JIA development might be initiated and sustained by the exposure to environmental factors, including infectious agents which affect people at a young age, depending on the underlying genetic predisposition to synovial inflammation. Many data from patients with JIA suggest a scenario in which different external antigens incite multiple antigen-specific pathways, cytotoxic T cell responses, activation of classical complement cascade, and production of proinflammatory cytokines. In this review, emphasis is paid not only to the potential role of parvovirus B19 and Epstein-Barr virus in primis but also to the general involvement of different bacteria as Salmonella spp., Shigella spp., Campylobacter spp., Mycoplasma pneumoniae, Chlamydophila pneumoniae, Bartonella henselae, and Streptococcus pyogenes for the development of immune-mediated arthritides during childhood. No unequivocal evidence favoring or refuting these associations has been clearly proved, and today, the strict definition of JIA etiology remains unknown. The infection can represent a random event in a susceptible individual, or it can be a necessary factor in JIA development, always in combination with a peculiar genetic background. Further studies are needed in order to address the unsolved questions concerning this issue.

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Section: The Potential Role Of Bacteria In Juvenile Idiopathic Arthritismentioning

confidence: 98%

The Etiology of Juvenile Idiopathic Arthritis

Rigante

Bosco

Esposito

2014

Clinic Rev Allerg Immunol

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“…Indeed, several studies reported that infections by various microbial agents occur more frequently in JIA and often precede the disease onset 20 . Indeed, several studies reported that infections by various microbial agents occur more frequently in JIA and often precede the disease onset 20 .…”

Section: Rheumatologymentioning

confidence: 99%

Structural Polymorphisms in the Mannose-Binding Lectin Gene Are Associated with Juvenile Idiopathic Arthritis

et al. 2009

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“…However, infections, especially of upper respiratory * Correspondence to: Disciplina tract, remain an important cause of morbidity in these patients, as they may contribute to JIA flares [2]. Pneumococcal vaccination is therefore recommended for all patients under immunosuppressive therapy, particularly, with anti-TNF blockage indication [3,4].…”

Section: Introductionmentioning

confidence: 99%