Reiter’s syndrome

Reiter’s syndrome is considered a rheumatic disease.  Named after the German doctor Hans Reiter, a prominent physiologist and linked to power experiments in Nazi concentration camps.  It is believed to result from the interaction of different genetic factors (such as HLA-B27) and environmental factors, that cause an abnormal immune responsiveness to certain bacterial pathogens, so many experts now describe it with the term ‘arthritis strip’.

Even when the terms Reiter’s syndrome and reactive arthritis are often used interchangeably, originally a description of Hans Reiter was a venereal infection.  Since there are other pathogens reactive arthritis (as is the case of rheumatic fever and Lyme disease), most experts agree reactive arthritis and inflammatory arthritis are secondary to infectious diseases.
They are a group of diseases sharing clinical features, pathogenesis and epidemiology.  The prototype disease of this group is ankylosing spondylitis.

Often begins with a genitourinary or gastrointestinal infection.  Some of the recognized pathogens are Chlamydia, Salmonella, Shigella, Yersinia and Campylobacter.  Its manifestation is nongonococcal urethritis, which sets the stage for Reiter’s syndrome.  The rest of the features are developed 1-5 weeks after the onset of urethritis.

Similarly, there can occur, infectious gastroenteritis.  The classic triad of clinical symptoms are inflammation of the urethra, conjunctivitis and arthritis, but one may also have enteritis, sacroiliitis, uveitis, and various mucocutaneous lesions (such as keratoderma blennorrhagic and balanitis circinata, etc).