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African Health Sciences
Makerere University Medical School
ISSN: 1680-6905 EISSN: 1729-0503
Vol. 4, Num. 2, 2004, pp. 136-138

African Health Sciences, Vol. 4, No. 2, August, 2004, pp. 136-138


Reiters syndrome - a case report and review of literature

Alebiosu C.O, Raimi T.H, Badru A.I, Amore O.O, Ogunkoya J.O. Odusan O.

Department of Medicine, Olabisi Onabanjo University Teaching Hospital Sagamu, Nigeria
Correspondence: Alebiosu C.O FWACP. POBOX 4622 Dugbe Post Office, Ibadan, Oyo State, Nigeria. E-mail: Dralechristo@Yahoo.Com

Code Number: hs04024


The occurrence of Reiter’s Syndrome is rare and not commonly reported in Nigeria. This paper reports a case of a 35yr old male Nigerian with Reiter’s Syndrome, occurring 1-2 weeks after a bout of a dysenteric illness. The patient presented with fever, conjunctivitis, dysentery, urethritis and arthralgia. The joint pains involved the left wrist (which was swollen), the right knee and ankle joints. The patient was managed conservatively. The case is presented with a view to documenting the occurrence of Reiter’s Syndrome in an African Nigerian.

Key words: Reiters syndrome Nigerian

Running title: Reiters syndrome in African Nigerian


In 1916, Hans Reiter described the classic triad of arthritis, nongonococcal urethritis, and conjunctivitis (Reiters syndrome, RS) in a Prussian soldier with diarrhea, during the first world war1,2. More recently, RS has been defined as a peripheral arthritis lasting longer than 1 month, associated with urethritis, cervicitis, or diarrhea2. Symptoms generally appear within 1-3 weeks but can range from 4-35 days from onset of inciting episode of urethritis/ cervicitis or diarrhea3. Signs and symptoms usually remit within 6 months. However, a significant percentage of patients have recurrent episodes of arthritis (15-50%), and some patients develop chronic arthritis (15-30%)3. Cardiac signs such as aortic regurgitation caused by inflammation of aortic wall and valve are rare. Other rare manifestations are central or peripheral nervous system lesions and pleuropulmonary infiltrates 2,4.

RS is triggered by bacterial infection that enters via mucosal surfaces usually, (but not always) associated with human leukocyte antigen (HLA)-B271,2,4. Nongonococcal venereal disease (most often Chlamydia) and infectious diarrhea usually precede RS. These include infections with: Shigella flexneri, Shigella dysenteriae, Salmonella typhimurium,Salmonella enteritidis, Streptococcus viridans, Mycoplasma pneumonia, Cyclospora, Chlamydia trachomatis, Yersinia enterocolitica, and Yersinia pseudotuberculosis. Campylobacter jejuni 1,2,4. Others include Chlamydia pneumoniae and Ureaplasma urealiticum1,2,4.

The syndrome was the first rheumatologic disease noted in association with Human Immunodeficiency Virus2. RS is most common in individuals aged between 15-35 years; and it is rarely seen in children1,2,5. The male-to-female post venereal ratio is 5-10:1,while the post-enteric ratio is1:1. The incidence is estimated at 3.5 per 100,000, and is uncommon among Negroes2.

This paper reports a case of RS with a view to documenting the occurrence of an uncommon disease in an African Nigerian.


Mr. S.L was a 35-year-old Nigerian driver who presented at the emergency unit of the Olabisi Onabanjo University Teaching Hospital Sagamu Nigeria, with two weeks onset of fever, dysentery, dysuria and joint pains. The joint pains involved the left wrist, (which was also swollen), the right knee and the ankle joints. There was no urethral discharge, hematuria or genital ulcer. There was associated discharging of both eyes with redness but no chest symptoms. He had not been transfused with blood in the past and there was no history of multiple sexual partners.

Physical examination revealed a middle aged man who was not pale but febrile to touch and was dehydrated. He had a swollen, tender left wrist and tenderness over the right knee and ankle joints (especially at tendon insertions -local enthesopathy). Other joints were normal. Apart from tachycardia of 114 beats / min, other systemic examinations were normal. Cardiac auscultation was normal.

Laboratory investigation revealed a haematocrit of 45% and a total white cell count of 14,500/mm3, neutrophils 80% and 20% lymphocytes. The erythrocyte sedimentation rate was 36 mm first hour (Winthrobe method). Urinalysis was normal while urine, stool and urethral swab cultures were negative. Rheumatoid factor and retroviral screening (HIV 1 and 2) were negative.

He was rehydrated with intravenous fluids and placed on Ibuprofen, intravenous ciprofloxacin (later changed to tetracycline) and metronidazole. The patient made marginal clinical improvement but discharged himself against medical advice within few days of admission, possibly due to financial constraints.


RS is reported most frequently among whites, occurrence appears to be related to HLA-B27 prevalence in the population. It is uncommon in the Negroid race, when it is frequently HLA-B27 negative2.

The age and gender of this patient are in keeping with the pattern among other population, that is, male preponderance and age range of between 15-35 years. The patient presented with urethritis, arthritis and conjunctivitis about 2 weeks after the onset of dysentery. This is in agreement with documentation that most cases of RS usually follow an infection (1-3 weeks after)1,2,3,4,5. The classic triad of RS was present in this patient. The arthritis was asymmetrical, oligoarticular and mainly involved the joints of the lower extremities. Tenderness was remarkable at tendon insertions rather than in the synovium, typical of RS1,2. Furthermore, the conjunctivitis was transient and resolved without specific treatment. These are all typical findings in RS.

Features suggestive of cardiovascular, nervous and pulmonary involvement were not present in the patient. Such dermatologic manifestations as balanitis circinata, keratoderma, nail changes (onycholysis, ridging and hyperkeratosis) and superficial oral ulcers were absent in the case presented. These are known to be rare in RS1,2.

Generally, the diagnosis of RS is clinical; there are no definite diagnostic laboratory test or radiographic findings. Apart from the elevated erythrocyte sedimentation rate (ESR) and neutrophilic leucocytosis that suggested a bacterial infection, all the laboratory investigations were negative. Elevated ESR and acute phase reactants are usually found in cases of RS commonly. Although anemia is commonly found in RS, the haemaocrit of 45% in our patient must have been due to the effects of dehydration. The negative report obtained for urine, stool and urethral swab cultures in the patient does not negate a diagnosis of RS. The test may only be positive for organisms occasionally; in a sizeable minority no laboratory evidence of infection is found2. There were no facilities to carry out antinuclear antibody screening and HLA genotype of the patient. Immunohistochemistry, polymerase chain reaction and molecular hybridization may be useful in further assessment1,2.

The patient was managed conservatively with ibuprofen and antibiotics. These are the recommended medications in the management of RS 1,2. It has been shown that prolonged administration of long acting tetracycline may accelerate recovery from Chlamydia induced RS, although therapy for other bacterial triggers of RS has shown little or no benefit. Other drugs that may be used are sulfasalazine, methotrexate, Azathioprine, and intra-articular steroid injection. 2,3,6

Long term follow - up studies suggest that some joint symptoms persist in 30 to 60% of patients with RS2. Recurrences of the acute syndrome are common, and as many as 25% cases evolve into chronic illness leading to disability which may make the patient unable to work or forced to change occupation2,4,6. We do not know the outcome in this patient because he discharged himself against medical advice.

In conclusion, this case is reported to document that RS, though rare, does occur in African Nigerians. Clinicians in developing countries of Africa should have a high index of suspicion, and make attempts at proper documentation of cases seen.

  1. Tauros JD, Lipsky PE. Ankylosing Spondylitis, Reactive arthritis and Undifferentiated Spondiloarthropathy. In Harrison’s Principles of Internal Medicine. 14th Edition. Editors- Braunwald E, Isselbacher KJ, Petersdorf RG, Wilson JD, Martin JB, Fauci AS. Publishers - McGraw - Hill Book Company. 1998 Chapter 317; pages 1906-1909.
  2. Thomas Scoggins, MD : Igor Boyarsky, DO . Reiter’s syndrome. Available at Assessed, November 02, 2003.
  3. Amor B: Reiter’s syndrome. Diagnosis and clinical features. Rheum Dis Clin North Am 1998 Nov; 24(4): 677-95, vii
  4. Fan PT, Yu DTY: Reiter’s syndrome. In: Rudd: Kelley’s Textbook of Rheumatology. 6th Edition. WB Saunders; 2001:1039-1067.
  5. Cuttica RJ, Scheines EJ, Garay SM, et al: Juvenile onset Reiter’s syndrome. A retrospective study of 26 patients. Clin Exp Rheumatol 1992 May-Jun; 10(3): 285-8.
  6. Hughes RA, Keat AC: Reiter’s syndrome and reactive arthritis: a current view. Semin Arthritis Rheum 1994 Dec; 24(3): 190- 210.

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