Clinical Rheumatology (2018) 37:869–874

https://doi.org/10.1007/s10067-018-4022-5

REVIEW ARTICLE

Reactive arthritis: update 2018

A. García-Kutzbach 1 & J. Chacón-Súchite 1 & H. García-Ferrer 1 & I. Iraheta 1

Received: 27 November 2017 / Revised: 30 January 2018 / Accepted: 1 February 2018 / Published online: 17 February 2018
# International League of Associations for Rheumatology (ILAR) 2018

Abstract
At this time, reactive arthritis (ReA) is considered to be part of the spectrum of the spondyloarthritis, previously known as Reiter’s
syndrome, and refers to an infection induced systemic illness, characterized by a sterile synovitis occurring in a genetically
predisposed individual, secondary to an infection localized in a distant organ/system, but also accompanied with multiple extra
articular manifestations.

Keywords Gut microbiota . HLA-B27 . Reactive arthritis . Reiter’s syndrome . Spondyloarthritis

Introduction The first case of ReA in the American continent relates to

Reactive arthritis (ReA), previously known as Reiter’s syn-
drome [1, 2], is actually considered as part of the spectrum
of the spondyloarthritis. It refers to an infection-induced
systemic illness, characterized by a sterile synovitis occur-
ring in a genetically predisposed individual, secondary to a
bacterial infection localized in a distant organ/system, usu-
ally in the genitourinary (GU) or/and gastrointestinal (GI)
tract [3, 4].
ReA has been described in association with several patho-
gens and is present with a variety of other symptoms in many
organs. See Table 1.
History
Christopher Columbus, in his diary about his voyages on the
high seas between Puerto Rico and Santo Domingo, in
September 1494. He presented fever, mental confusion, and
severe arthritis of lower limbs. In 1498, he had a relapse with
fever and acute polyarthralgias. Six weeks later, he developed
arthritis and eye pain: BI have never had such affliction of my
eyes with hemorrhage and pain as in this time.^ In 1504, he
was Bparalyzed and bedridden^ because of Bgout^ and died in
1506 of unknown causes [8].
In 2007, Panush, Wallace, Dorff, and Engleman wrote a
letter to Arthritis & Rheumatism as a retraction for their sug-
gestion to use the term Reiter’s syndrome, 65 years later be-
cause of the previously unknown war criminal records of
Hans Reiter during World War II [1].

Perhaps, the first description of ReA was made by Epidemiology

Hippocrates, in the fourth century B.C. linking the presence
of arthritis and infection in the genitourinary tract, when he
described that BA youth does not suffer from gout until after
sexual intercourse.^ Gout was used to describe any acute ar-
thritis at that time, although it is not stated that the arthritis was
due to venereal disease [7].
* A. García-Kutzbach
abraham@garciakutzbach.org
1
AGAR, FM - UFM. Asociación Guatemalteca Anti-enfermedades
Reumáticas, Facultad de Medicina, Universidad Francisco
Marroquín, Guatemala City, CA, Guatemala
Epidemiological data in ReA varies around the world, due to
dissimilar criteria in diagnosis, variations in clinical presenta-
tions, lack of specific laboratory biomarkers, different geo-
graphical locations that predispose to multiple pathogens, dif-
ferent genetic backgrounds, different grades of infection, and
recently, changes observed in microbiome, among many other
factors [6, 9, 10].
According to Ehrenfeld, ReA usually manifests itself as
arthritis 2–4 weeks following GU or GI infections, sometimes
up to 6 months, often with HLA-B27 carriers [11].
It is commonly accepted that ReA is more frequent in
males under 40 years old, but our experience is somewhat
different, we observed more females than males [12, 13].
870 Clin Rheumatol (2018) 37:869–874

Etiopathogenesis and Chlamydia bacteria well documented as triggering re-

active arthritis [23–26].
The relationship between bacteria and genetics is very much Other HLA class 1 and class 2 alleles have been implicated
illustrated in ReA. Since 1973, HLA-B27 was found to be in AS susceptibility [HLA B-40/B-60 (B-40:01)].
highly associated to SpA [14, 15]. The best evidence is for MIC-A (complex class 1 chain-
related gene A), that controls activities of natural killer
Toll-like receptors cells γδ and αβ CD 8+ T cells, that are recognized by T
cells of the intestinal epithelia, also implicated in the path-
Toll-like receptors (TLRs) are able to recognize extracellular ogenesis of AS [17].
germs and produce cell responses of the innate immune sys- The relationship between HLA-B27 and ReA is less clear
tem. TLR-4 can recognize lipopolysaccharides and could have as in our cohort [20].
a role in ReA. TLR-2 has also been associated to ReA HLA B-27 association is stronger with ankylosing spondy-
[16–18]. litis (90%); the evidence of association with ReA is not clear
Others suggest that persistent urogenital organ infection (30%) [27] as in our population in Guatemala City; only one
may be the source of damage associated molecular patterns patient was HLA B-27 positive [28].
(DAMPS) and/or exogenous pathogens (PAMPS) [19]. It is not known the exact role of action of HLA B-27 in
These molecules are able to stimulate TLRs inducing im- Spondyloarthropathies; one theory postulates that HLA B-27
mune response in ReA. presents arthritogenic bacterial peptides to T cells, stimulating
an autoimmune response (molecular mimicry). Another theo-
Pathogens ry is that HLA-B-27 cells may act as an autoantigen that is
targeted by the immune system.
A long list of bacteria has been described as triggers of
ReA that can reach the joints through intestinal or genito-
urinary infections; these bacteria may reach the joints as a Table 1 Arthritogenic agents associated with the development of
complete form or as fragments. All these pathogens have in reactive arthritis
common that they are intracellular organisms. Chlamydia
trachomatis is proposed to be the most common cause of Enteric infections Urogenital infections
ReA genitourinary transmitted; Ureaplasma urealyticum Salmonella enterica Chlamydia trachomatis
and occasionally Neisseria gonorrohoeae have been de- Serovars: Typhimurium enteriditis Ureaplasma urealyticum
scribed [20]. paratyphi B, C, others Mycoplasma genitalium
Shigella: Neisseria gonorrhoeae
Genetics S. Flexneri Gardnerella vaginalis
S. dysenteriae Respiratory infections
It is well accepted the relationship between the mayor histo-
S. sonnei Chlamydia pneumoniae
compatibility complex (MHC) in spondyloarthropathies, par-
Yersinia Group A beta-hemolytic
ticularly HLA-B27 in ankylosing spondylitis, over 80% in Streptococcus
some populations [5, 21, 22]. Y. enterocolitica (O:3, O:8, and O:9) Miscellaneus
Such association was found in 1973 by two different Y. pseudotuberculosis HIV
groups: Schlosstein L, from La Joya, California, USA, and Campylobacter jejuni B-19 parvovirus
Brewerton DA, in London, England, who described the asso- C. jejuni Borrelia burgdorferi
ciation independently in the same year [14, 15]. C. coli Brucella abortus
HLA B-27 is a highly polymorphic molecule with more
Clostridium difficile Calmette-Guerin Bacillus
than 116 proteins subtypes, being HLA B27: 01 and B27:
Escherichia coli: diarrhogenic strains Chikungunya virus
117, the better known. HLA B-27 is associated with spon-
Bacillus cereus
taneous clearance of hepatitis C (HCV) infection as well as
Amoebae
viral evolution in HCV infection related to the CD8+ T
Cryptosporidium
cells [17, 22].
Giardia lamblia
Perhaps the best characterized relationship with HLA B-
Helicobacter pylori, cinaedi
27 is HLA B-40, specifically B40:01 [17]. Although HLA
Strongyloides spp
B-27 confers a survivor advantage in face of viral infec-
Tropheryma whippelii
tions such as HIV, HCV, and Influenza carriers of the gene
because they are defective in the killing of intracellular Modified from Colmegna I, Cuchacovich R, Espinoza L [5] and Gupta R,
bacterial species including Yersinia, Salmonella, Shigella, Misra R [6]
Clin Rheumatol (2018) 37:869–874 871

Microbiome In the intestinal lumen, we have all kinds of bacteria that

Very exciting new studies have found important association
between the microbiome and spondyloarthropahies and other
inflammatory arthritis [5, 10, 29].
For example, the intestinal microbiome in psoriasis and
psoriatic arthritis (PsA) patients has shown decreased abun-
dance of the coprococcus genus compared to healthy controls.
PsA group showed lower levels of the Akkermansia and
Ruminococcus [30].
Microbiome is an ecosystem that functions as a virtual
endocrine organ and encompasses about a hundred trillion of
bacterias (1–2 Kg). Over three million of bacterial genes, a
hundred times more than the human genoma, and ten times
more bacterial cells than that of human are in different loca-
tions inside and outside the human body. In other words, only
10% of our DNA is Bours^ and the other 90% is bacterial [31].
Despite this unthinkable number of bacteria, the human gut
microbiome is composed of about one thousand species, 12
divisions, and among those, two divisions are the most dom-
inant: Bacteroidettes and Firmicutes, which are 90% of the
total [32].
About 60 million years ago, an important evolutive muta-
tion occurred: the intestinal tube. This organ allowed nutrients
to go in and waste to go out.
During mammalians birth, bacteria and viruses colonize
the gut. From this moment on, a symbiosis between mamma-
lians and bacterial cells is created, which has evolved through
toll-like receptors 3 and 4 that modify the interexchange be-
tween gut and bacterial tolerance.
Microbiome is different in humans and changes according
to the following: age, diet (nutritional state), genetics, and
environment. Any disruption of this delicate equilibrium is
called dysbiosis, which has important repercussions in the
immune system [33].
It has been proposed that hydrogen sulphide produced by
sulphate-reducing bacteria (SRB) initiates mucosal injury
with a resulting increase in intestinal permeability [30].
are unable to penetrate the normal mucosal barrier. Under the
epithelial cell, we have the lamina propria, where we have
concentrated three fourths of the immune cells of the body:
B cells, T cells, dendritic cells (DC), macrophages, mono-
cytes, neutrophils, etc. [34]. Other very important cells, the
innate immune cells, that provide protection against foreign
bacterial invasion, serve as a bridge between microbiota and
adaptive immune system (T and B cells). Lamina propria-
derived antigen-presenting cells transport cells only to
mucosal-associated lymphoid tissue (MALT) and not beyond
to prevent potentially damaging systemic immune responses
against the microbiota [29]. See Table 2.
When this equilibrium is broken, foreign bacteria are able
to penetrate the epithelial cells. A group of bacteria known as
SFB (segmented fillamentous bacteria), gram positive anaer-
obic bacteria can penetrate the mucus layer lining intestinal
epithelial cells at the intercellular spaces [36]. When in the
circulation, activated immune cells can reach other tissues like
the synovia in joints producing inflammation.
Contrary to the popular belief, intestinal microbes are there
not only to help absorption of nutrients, but rather to produce
vitamin biosynthesis, short-chain fatty acid, modulation of
lipid metabolism, and glucose homeostasis of the host [37].
Our group in Guatemala, in association with Ogdie, A.
from U Penn and Scher, J. from NYU, found significant dif-
ferences between microbiome of patients with ReA, compared
to controls. Taxonomic differences including lower abun-
dance of Peptococcaceae and high abundance of Erwinia
and Pseudomonas. Erwinia is taxon with more than 97%
identity to various species of Salmonella, Shigella, and
Yersinia [10].
Therefore, the relation between microbiome changes in
spondyloarthropathies is becoming more and more evident.
Activation of the mucosal T cell by the microbiota is nec-
essary for the host to avoid infection.
Experimental studies have shown that mice colonized with
SFB increase production of IL-23 by dendritic cells and IL-1β

Table 2 Immune cells [35]

Effector cells Cytokines produced Stimulation pathways

Th17 cells IL 23, IL 6, IL 1β & TGF β STAT 3 y ROR-γT FoxP3 expression

Innate Lymphoid cells (ILCs) ILC1 IFN-γ, TNF T-bet
ILC2 IL-5, IL-13 GATA3
ILC3 IL-22, IL-17 ROR-γT
Mucosal-associated invariant T cells (MAITs) TNF-α, INF, and IL 17
Invariable cells natural killer (iNK-T) Th-1, Th-2, Th-17 ROR-γT
Th 9 cells IL-9, IL-7/9
Resident cells IL-23R ROR-γT
CD3+, CD4−, CD8 IL-6, IL17A, IL-22, BMP7
872 Clin Rheumatol (2018) 37:869–874

produced by macrophages inducing expression of IL-17A and Imagenology

IL-22 by SFB, specific T cells and innate lymphoid cells [38].
Despite the advances of technology and science, there are no
Interleukin-17 specific diagnostic tests that can help us to confirm this
disease.
Interleukin-17 was discovered in 1995, by Yao. In 2005, Th17 The imaging methods have improved across the timeline.
cells were described as the main source of IL-17 that also The first radiographic findings described are the following:
produces IL-22 [39]. sacroiliitis, periostitis, syndesmophytes, joint erosions, joint
The active form is the IL-17A, but IL-17F maintains 60% space narrowing, and bone marrow edema [9].
homology with IL-17A. More recently, there have been some groups that have ded-
icated their investigations on benefits of ultrasound in differ-
Clinical manifestations ent rheumatic diseases, including Spondyloarthritis. Related
to this, the experts have described findings in joints (effusion,
The clinical presentation of ReA is protean, from an asymp- sinovitis, bone erosions), tendons (tenosynovitis, tendinitis/
tomatic person to an acute asymmetrical olygoarthritis with or tendinosis, tendon rupture), and enthesis (enthesitis) [40].
without extraarticular manifestations. These findings have been described in different cohorts
(13–32%), especially for sacroiliitis and syndesmophytes
[41]. In Guatemala, we found 15% of bilateral sacroiliitis
Skeletal symptoms
and 39% of enthesitis of the Achilles tendon by ultrasound
[13].
Oligoarthritis of large joints, mainly lower limbs
Mild polyarthritis with dactylitis (sausage fingers) (16%)
Treatment
Axial skeletal involvement
Although there is an established link between pathogens and
Sacroiliitis (15–30%)
development of ReA, there is strong evidence against the ef-
Lumbar spine (up to half of patients)
ficacy of broad-spectrum antibiotic therapy [30].
Enthesitis (reported in literature 30%, but we found 67%)
Different than other rheumatic conditions, it is well
[10, 13]
established that NSAIDs are first-line drugs for the manage-
ment of spondyloarthropathies and reactive arthritis, not only
Extra-articular manifestations for the analgesic anti-inflammatory effects, but also because
they retard the development of syndesmophytes [9].
Ocular symptoms: conjunctivitis, uveitis, iritis DMARDs such as Sulfazalasine are effective for the pe-
Cardiac symptoms: aortic disease, rhythm abnormalities, ripheral manifestations, but not with the axial involvement,
pericarditis (rare) most experts consider glucocorticoids use in ReA contraindi-
GU symptoms: urethritis, cervicitis, prostatitis, and cated, except for an occasional intra-articular injection.
haemorrhagic cystitis Since IL-17 was discovered and found to be importantly
GI symptoms: diarrhea involved in the pathogenesis of spondyloarthropathies, despite
this anti-IL17A monoclonal antibodies have not been tried in
Skin manifestations ReA. At this moment, there are only three anti-interleukin-17
drugs commercially available: secukinumab, ixekizumab, and
Rash brodalumab. Good results have been reported in a small co-
Keratodermia blenorragicum hort of ten patients in ReA with anti-TNF, but there is no data
Circinate balanitis on anti-IL-17A in ReA.
Skin and mucosas: aphthous ulcers (up to 60%) Novel treatments include microbial ecosystem therapeutics
Erythema nodosum (rare) and fecal microbiota transplant (FMT), potentially useful es-
pecially in SpA [30, 42].

Laboratory
Unfortunately, there are no specific laboratory tests or bio-
markers to this date, except elevated CRP and ESR in acute
febrile cases.
Expert insights
The prevalence of ReA, we believe, has been underestimated
because of the multiple clinical manifestations, different
Clin Rheumatol (2018) 37:869–874
degrees of disease activity, geographical and genetical differ-
ences that make the diagnosis many times more difficult, but
we think that it is as common as rheumatoid arthritis; only one
third of patients develop a chronic phase, most of the patients
resolve in a few weeks, mainly in tropical areas. The partici-
pation of the microbiota in the pathogenesis of this type of
arthritis is being studied actively at the present.
New biologic agents such as secukinumab and others
monoclonal anti-IL-12 and 23 promise new venues for thera-
py for this disease.
Compliance with ethical standards
Conflicts of interest Abraham Garcia-Kutzbach: serve as Principal
Investigator for clinical studies of Merck, Abbie, Novartis, and Janssen
Helga Garcia: Medical Scientific Liaison for Novartis Pharma Central
America and Caribbean
Jose A. Chacon and Isa Iraheta do not report conflict of interest.
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