Reactive Arthritis: Causes and Treatment – Part One

Katherine Poehlmann, PhD, discusses the causes and treatments of Reactive Arthritis in this first installment of a two-part series. The second installment, to be published in early January, will present nutritional methods to deal with Reactive Arthritis. Katherine, who has been a director of Road Back Foundation since 2012, continues to study infectious causes of RA and other inflammatory conditions, and has authored two books on the infectious connection between rheumatoid arthritis and other autoimmune diseases.



Katherine Poehlmann, PhD

The cause(s) of most of the 100+ distinct types of arthritis are still being studied, but the common denominator is inflammation and, in turn, the breakdown of cartilage and synovial tissue.

When inflammation is a reaction to infection, the condition is called Reactive Arthritis (ReA), formerly known as Reiter’s syndrome. ReA is also known as seronegative spondyloarthropothy, which includes the spine as well as the joints, and enthesitis-related Rheumatoid Arthritis where inflammation occurs at points where tendons or ligaments insert into the bone. Other disorders in the family of spondyloarthropathies are Psoriatic Arthritis, Ankylosing Spondylitis, and the type of arthritis that sometimes accompanies inflammatory bowel disease (IBS).

ReA usually begins one to four weeks after a genitourinary or gastrointestinal tract infection. The principal causative organisms have been found to include Chlamydia (both C. trachomatis and C. pneumoniae), Ureaplasmas, Mycoplasma pneumoniae (and other species), Shigella, Salmonella, Yersinia entercolytica, Mycobacterium paratuberculosis (Johne’s Disease), and Campylobacter species. Researchers tend to seek and study a single cause, when many infections may coexist symbiotically in nature.

Onset of infection is typically acute, with the inflammation affecting two to four joints within a few days. Enthesitis is often experienced in the heel. ReA affects the joints of the lower extremities but inflammatory back pain and swelling of fingers or toes (dactylitis) is common.

Treatment usually begins with nonsteroidal anti-inflammatory drugs (NSAIDs) and disease-modifying antirheumatic drugs (DMARDs) like sulfasalazine (a gut antibiotic) has been shown to be effective when the ReA is triggered by a respiratory infection, followed closely by a gastrointestinal infection. Research suggests that a prolonged course of two or more antibiotics (e.g., Doxycycline and Rifampin) could help patients with chronic Chlamydia- or Chlamydophila-induced Reactive Arthritis.

The HLA-B27 gene is found in 80 percent of patients diagnosed with ReA. Recent research has been looking for specific bacteria shown to cause arthritis, and methods to protect the immune system from overreacting to these bacteria.

Spinal arthritis is linked to gut infections, like Mycobacterium paratuberculosis (thought to cause Crohn’s disease), paramyxovirus (the measles viruses, both natural and vaccine strains, which also cause neural inflammation), Listeria monocytogenes (that causes diarrhea), and, similar to pathogenic E. coli, all reside in the intestines. Gut dysbiosis can be improved by using antibiotics followed a few hours later by probiotic formulations.

Fifty years ago, it was accepted that chronic infections could complicate arthritis and its accompanying inflammation. However, chronic arthritis without an obvious known severe infection was seen as a disease without a generally recognized cause.

Today we know there are as many causes of ReA as there are persistent infections, each microbe possessing a unique molecular DNA stamp, acting in combination with each other. With the development of a wide range of prescription and non-prescription anti-inflammatory and immune/histamine suppressant drugs, temporary relief is obtained, but the underlying infections and nutritional dependencies are left untreated, and there are few cures. What is too often missed is that some antibiotics, like the tetracycline family, can significantly improve pain relief when co-administered with NSAIDs, leading to a shorter, more effective treatment. The untreated persistent infection becomes encysted, walled off by calcium nodules, dormant, symptomless, or difficult to detect. Antibodies against the microbe are detectable, but the site of the infection colony often is not the location of the inflamed joint, thus it may be hard to discover. This dormant, biofilm-protected, or calcium-encysted site leads to new slow-growing, sometimes relocating, often inflamed colonies of the parasitic microbes.

These colonies generate toxins and shed bioactive molecules and enzymes that can upset the chemical balance of other nearby regions of the body, (especially associated with synovial tissue) such as the joints, tendons, sheaths (carpal tunnels), bursae, and the spine.  Viral co-infections from chronic to acute generate immune-suppressive molecules that facilitate streptococcal bacterial replication. More and more of these viral/bacterial co-infection pairs are being identified. Some strains are real killers.  Others, like human herpes viruses (HHVs) and dormant chronic obstructive pulmonary disease (COPD) viruses may be almost benign, but can progress to inflammation, arthritis, and flares when a new invader disables or excites the immune system defenses.

Treating bacterial infections can be ineffective for many reasons: some stages of the bacteria are highly resistant, biofilms shield colony members from antibiotics, the specific organism strains and their matching antibiotic susceptibilities are unknown. Multiple organisms and benign strains may be present, making it hard to discover precisely which strains were pathogenic. The usual short course, single antibiotic protocols may work well for acute invasion-stage microbe forms, but fail for multi-stage chronic infections, like Chlamydia pneumoniae.

Highly effective antibiotics like Ciproflaxin may kill the targeted microbe(s) but the resulting toxins and fragments trigger the immune system, causing a disabling inflammation flare, making the patient feel worse and converting a positive result into negative symptoms.  Thus, attacking the pathogens often leads to a worsening of inflammation before ultimately leading to a lowering of the immune response, called the Jarisch-Herxheimer reaction or “Herx” for short.  Practitioners have been taught to avoid this perverse situation, unfortunately, not by using appropriate antibiotics cyclically, along with suitable anti-inflammatory drugs, but by not using effective antibiotic combinations in proper sequences, or none at all. Suitable tetracycline family antibiotic medical protocols are found here: Pulsed and Daily Antibiotic Protocols.


Spondyloarthropathies: Am Fam Physician. 2004 Jun 15;69(12):2853-2860

Combination antibiotics as a treatment for chronic Chlamydia-induced reactive arthritis: a double-blind, placebo-controlled, prospective trial: Arthritis Rheum. 2010 May;62(5):1298-307. doi: 10.1002/art.27394.

American College of Rheumatology – Reactive Arthritis Patient/Caregiver Overview

Reactive Arthritis (Reiter’s Syndrome): Am Fam Physician. 1999 Aug 1;60(2):499-503.

RA Infection Connection Gut Health Case Histories – [#15. Gut Health]

Ankylosing Spondylitis (Reactive Arthritis of the Spine): Dr. Gabe Mirkin

Herpes Viruses: Patient Info

The influence of virus infections on the course of COPD: Eur J Microbiol Immunol (Bp). 2012 Sep; 2(3): 176–185.  

Effect of Prolonged Treatment with Azithromycin, Clarithromycin, or Levofloxacin on Chlamydia pneumoniae in a Continuous-Infection Model: Antimicrob Agents Chemother. 2002 Feb; 46(2): 409–412.


Be sure to check back in January to catch Part 2 of Katherine’s Reactive Arthritis (ReA) series that will cover supportive nutritional considerations.