In general, sign and symptoms of Reiter’s syndrome starts after 1 to 3 weeks from the initial primary infection. The following symptomatology are usually observed:

• Arthritis in joints – most commonly on the ankles, knees, feet, heels and lower back spine. Pain and swelling may lead to stiffness and disability.
• Conjunctivitis – Reactive arthritis is commonly associated with the inflammation of the conjunctiva.
• Urinary complains – There is an increased frequency of urination with or without pain in a number of patients. The prostate and the cervix may also inflame in some cases.
• Deformation of digits – In some cases of reactive arthritis, fingers and toes may swell and look deformed.

A complete physical examination will reveal the swelling of the joints in foot, arms and the back. Eye examination may reveal conjunctivitis as a herald sign of Reiter’s disease. Blood test may be conducted to determine signs of previous and ongoing infection, signs of inflammation, presence of antibodies, and genetic markers that points to Reiter’s syndrome.

Arthrocentesis to acquire joint fluids elucidating the presence of inflammatory cells, presence of specific bacterial infections and pathologic joint crystals may also be necessary. Radiographs with x-ray of the joints, back and pelvis may show signs of reactive arthritis.

The main goal in the treatment of Reiter’s syndrome is to relieve symptoms and control underlying infections. Specific antibiotics for the bacterial causative agents that were identified in the laboratory can be given.

The use of the NSAID indomethacin may relieve mild pain symptoms in Reiter’s syndrome. Direct corticosteroid injections on the affected joints may address the debilitation instantly.

Evidences were mounted that some anti-arthritic drugs like sulfasalazine and methotrexate can help control the pain in Reiter’s syndrome.

The natural history of Reiter’s syndrome is self-limiting even in patients that are suffering from acute forms of debility in the early onset. Cases of untreated reactive arthritis culminates significantly within 3 to 12 months from onset of symptoms. Serious outcomes that results in mortality are very rare and are usually due to the adverse effects of treatment. Scientific literature confers that post-dysenteric arthritis has a better prognosis than their post-venereal counterparts. Recurrence of disease happens in 15-50% of cases especially those found positive with HLA-B27 marker.

Complications

The self-limiting nature of reactive arthritis confers limited complications to patients also. The most common complication is recurrence of the disease in almost half of the patients which are usually triggered by an immune deficient period or chronic stress.

Among the recurring cases, 15 to 30% of which leads to destructive arthritis and spondylitis which may have permanent debilitation consequences. Chronic Reiter’s syndrome may rarely occur especially those with the hip joint involvement. These chronic forms can be very severe that symptoms may no longer respond to classic non-steroidal anti-inflammatory drugs (NSAID).

Reactive arthritis is a secondary reaction from a primary infection in the gastro-intestinal tract and genito-urinary tract. The primary infection are often caused by gram-negative, facultative, or obligate intracellular bacteria, and may present with very mild symptoms that may not be perceived by the patient [1].

Because of its usual origin in the gut and genitals, Reiter’s syndrome is sometimes classified as venereal or dysentery in nature. These are the most common etiologic agents that cause the primary disease in Reiter’s syndrome:

• Shigella flexneri which may present as bacillary dysentery.
• Neisseria gonorrhoeae that causes venereal gonorrhea.
• Ureaplasma urealyicum found in urinary tract infections.
• Chlamydia trachomatis which is one of the main cause of sexually transmitted disease, where the L2b serotype predispose to Reiter’s syndrome [2].
• Salmonellosis with Salmonella enteritica with serovars typhimurium and entiritidis are primary gut infection that initiates the immune response in reactive arthritis [3].
• Mycobacteria tuberculosis
• Cyclospora
• Yersinia enterocolytica causing dysentery.
• Clostridium defficile that cause pseudomembranous colitis.
• Beta-hemolytic Streptococcal veridans (A group) which possesses the highest immune response [4].

The general incidence of Reiter’s syndrome is rare because its arthritic signs are often mistaken with the more common arthritis symptoms [5]. The cases in the US are estimated at 3.5 to 5 cases per 100,000 population. Reactive arthritis has a higher penetrance on patients with Acquired immune deficiency syndrome (AIDS).

A shigellosis outbreak (HLA-B27 positive type) in Oregon recorded an increased incidence of Reiter's syndrome reaching a penetrance of 29% among those who had Shigella dysentery. In European countries like Norway and Finland, primary infections of Yersinia enterocolyitca are most common.

Men at the third decade are more predisposed to reactive arthritis while children beyond 9 years of age may manifest after an enteric episode [6].

The pathophysiology starts at the level of the primary infection with a bacteria in the level of the gastrointestinal tract (GIT) and the genitourinary tract (GUT). Respiratory infections like tonsillitis with streptococcal antigen may lead to Reiter’s syndrome but may be infrequent [7].

These bacterial antigen makes its way to the intrasynovial region where antibodies and the bacterial reactive T-cells causing an immune mediated synovitis and arthritis. In concert with the native T-cell response are various cytokines like the transforming growth factor (TGF-B) and Interleukin 6 and 17 (IL-6, IL-17) which mounts the antigen through time causing a more pronounced inflammation than the usual arthritis [8].

In AIDS patients, a severe immune response with generalized psoriasis-like rashes has been theorized to be mediated by the cytotoxic cells (CD4 and CD8).

Preventing Reiter’s syndrome involves the examination of the family tree for possible hereditary links with reactive arthritis. Those with familial predispositions should prevent infections from bacteria that may cause Reiter’s syndrome.

Proper food sanitation must be in place to prevent shigellosis, salmonellosis and Camphylobacter infections of the gut which may lead to reactive arthritis [9]. Sexual precaution should always be observed to prevent sexually transmitted diseases.

Reiter’s syndromes or reactive arthritis is a clinical disease characterized by an autoimmune joint inflammation in reaction to an infection in another part of the body. Inflammation symptoms may also affect the eyes and urethra completing the syndrome triad of arthritis, genito-urinary tract signs and conjunctivitis.

The most common joints affected are those of the ankles and knees with primary infection from the intestines, urinary tract and genitals. Symptoms usually occur 1 to 3 weeks from the primary infection.

Reiter’s syndrome is the old name of reactive arthritis which is sometimes referred to as Fiessinger-Leroy disease. Reiter’s syndrome is a rare disease with benign symptoms that usually resolves within a year.

It must be remembered that Reiter’s syndrome occurs in patients with poor health-related quality of life; thus, efforts should be made to alleviate poor health conditions and maintain proper functional status with proper and good hygiene all the time [10].

Patients diagnosed with the disease should be educated on the possible complications of disease and the importance of long term compliance to medications. Regular exercise can modify sedentary lifestyles that are more prone to have the disease. Adolescents and young adults should be involved in the active control of the spread of sexually transmitted diseases by promoting safer sex practices.

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2. El Karoui K, Mechai F, Ribadeau-Dumas F, Viard JP, Lecuit M, de Barbeyrac B, et al. Reactive arthritis associated with lymphogranuloma venereum proctitis L2b. Sex Transm Infect. June 2009, 85 (3): 180-1.
3. Dworkin MS, Shoemaker PC, Goldoft MJ, Kobayashi JM. Reactive arthritis and Reiter's syndrome outbreak of gastroenteritis Following on Caused by Salmonella enteritidis. Clin Infect Dis. Oct 1 2001, 33 (7): 1010-4.
4. van Bemmel JM, Delgado V, Holman ER, Allaart CF, Huizinga TW, Bax JJ, et al. Increased risk of valvular No heart disease in adult poststreptococcal reactive arthritis. Arthritis Rheum. April 2009, 60 (4): 987-93.
5. Braun J, Kingsley G, van der Heijde D, Sieper J. On the Difficulties of Establishing a consensus on the definition of and diagnostic Investigations for reactive arthritis. Results and discussion of a questionnaire prepared for the 4th International Workshop on Reactive Arthritis, Berlin, Germany, July 3-6, 1999 J Rheumatol. September 2000, 27 (9) :. 2185-92 
6. Macía Villa C, Sifuentes Giraldo W, Boteanu A, González Lanza M, Bachiller Corral J. Reactive arthritis after intravesical instillation of BCG the . Reumatol Clin Sep-Oct 2012, 8 (5): 284-6.
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8. Singh AK, Misra R, Aggarwal A. Th-17 associated cytokines in patients with reactive arthritis / undifferentiated spondyloarthropathy. Clin Rheumatol. 2011; 30 (6): 771-6 (ISSN: 1434-9949)
9. Ajene AN, Fischer Walker CL, Black RE. Enteric pathogens and reactive arthritis: a systematic review of campylobacter, salmonella and shigella-associated reactive arthritis. J Health Popul Nutr. , 2013, 31 (3): 299-307 (ISSN: 1606-0997)
10. Inman RD . Innate immunity of spondyloarthritis: the role of toll-like receptors Adv Exp Med Biol 2009; 649 300-9