Case Rounds : Case 5

by Allan Gelber, M.D.


A 22 year old woman presented to The Emergency Department because of progressively severe unilateral wrist pain of 24 hours duration. She was triaged for surgical evaluation. No preceding injury or unusual physical activity was identified. Plain radiographs of the wrist were unremarkable. A splint was applied. Ibuprofen was prescribed at 600 mg po TID and she was discharged with a diagnosis of wrist sprain.

Over the next 12-18 hours, her condition worsened. Her sleep was frequently interrupted by wrist pain. Moreover, she developed a fever during the night. There followed progressive malaise and diminished appetite. Painful palms ensued. Inasmuch as her symptoms and overall condition worsened, she returned to The Emergency Department for reassessment.

At this juncture, she was triaged for medicine evaluation. Further inquiry revealed the absence of nausea, vomiting, diarrhea, bloody stool, swollen glands, photophobia or ocular irritation. Past medical and family histories were noncontributory.

Physical Examinination

The patient was a well-developed, well-nourished 22 year old woman. She was febrile, temperature 101oF, though hemodynamically stable. Articular examination was notable for swelling and warmth at the left wrist. The wrist joint was exquisitely tender to palpation and to manipulation. Swelling extended over the dorsal surface of the hand. The fingers were spared. Skin findings were notable for several tender bilateral palmar violaceous pustular eruptions. A diagnostic procedure was performed.

Differential Diagnosis

1.[ ]Acute rheumatic fever
2.[ ]Reiter’s syndrome
3.[ ]Post-setreptococcal reactive arthritis
4.[ ]Disseminated gonococcal infection
5.[ ]Systemic Lupus Erythematosus
6.[ ]Lyme arthritis

Diagnostic Procedure

Pelvic examination revealed a purulent cervical discharge. The presumptive diagnosis was gonococcal arthritis.

Antimicrobial therapy was administered, consisting of ceftriaxone 250 mg IM x1 dose. A 10 day course of oral ampicillin and doxycycline was prescribed.

Case Discussion

Gonococcal arthritis represents the most common cause of inflammatory monoarthritis in young adults (ref 1). The causative organism, Neisseria gonorrhoeae, a gram-negative diplococcus, is exclusively a human pathogen. It colonizes multiple mucosal surfaces in the human body and may lead to both localized and disseminated disease. Over the last 25 years, the number of reported cases of gonorrhea has been declining in the United States, from 468 cases per 100,000 population in 1975, to 150 cases per 100,000 in 1995, according to figures available from the Centers for Disease Control and Prevention. Among this volume of gonococcal disease, disseminated gonococcal infection occurs in up to 3% of cases (ref 2).

Both host and microbial factors play important roles in the potential for gonorrhea to disseminate. For example, gender is an important risk factor, in that disseminated gonococcal infection is four-fold more common among women than men (ref 2, 3). Women with gonococcal infection are at particular risk to develop disseminated disease during pregnancy and the perimenstrual period (ref 3). In addition, because of the important role played by complement in the control and containment of gonococcal infection in the otherwise healthy host, individuals with complement deficiency, particularly of the terminal components (C5-C8), are at increased risk to develop disseminated disease. There are also well defined microbial factors related to the pathogenesis of gonococcal infection. The Neisseria gonorrhoeae bacterium possesses pili, long-hair-like protein filaments, that extend from the bacterial cell surface to mediate attachment to epithelial cells. Though these pili initiate an antigenic response in the host, the gonococcus is able to undergo antigenic variation and phase variation of the pili, mechanisms involved in eluding the host immune response (ref 4). The gonococcus also contains outer-membrane proteins (I, II, and III) that mediate the interaction of the microbe with the neutrophil. Of note, pathogenic gonococci elaborate IgA proteases that neutralize IgA production by the host at mucosal sites.

Disseminated gonococcal infection is characterized by the classic triad of dermatitis, tenosynovitis, and migratory polyarthralgia. Disseminated disease may follow gonococcal infection at any one of various mucosal sites, including the genitourinary tract, rectum and oropharynx. Two clinical presentations of disseminated gonococcal infection are commonly described. One clinical scenario is that of tenosynovitis, associated with skin rash and fever, during which there is a high yield for a positive blood culture. This variant is alternately known as the arthritis-dermatitis syndrome. The arthralgia of gonococcal infection is most often an asymmetric polyarthralgia, though one-quarter of patients develop a monoarthralgia only. Asymmetric joint involvement frequently affects the knee, elbow, wrist, metacarpophalangeal and ankle joints. The other scenario represents a suppurative arthritis. Approximately, one-third of patients thus manifest an actual septic arthritis, yielding a synovial fluid white blood cell count in the range of 50,000 – 200,000 cells/mm3, with neutrophil predominance. Synovial fluid white blood cell counts are usually less elevated in patients with predominant tenosynovitis and dermatitis. The skin rash may be maculopapular, pustular, vesicular or necrotic, and often involves the torso, limbs, palms and soles. (see figures below) The tenosynovitis seen in two-thirds of patients typically involves the hands and fingers. Rarely, gonococcal infection can disseminate to other internal organs and result in pericarditis (ref 5, 6), endocarditis (ref 7), and meningitis, and can even result in fatality.

Figure 1 : Pustule with a Ncrotic center

Figure 2 - pustule with central petechia

Figure 3 - large hemorrhagic blister (less common)


Cervical culture was positive for Neisseria gonorrhoeae, sensitive to penicillin. Outpatient follow-up two days later revealed a substantially improved, comfortable appearing woman. The unilateral wrist pain and swelling, as well as the palmar eruption, had largely subsided. In addition, the fever and sense of malaise and anorexia had cleared.


1. Baker DG, Schumacher HR. Acute monoarthritis. N Engl J Med 329:1013-1020, 1993.

2. Cucurull E, Espinoza LR. Gonococcal arthritis. Rheum Dis Clin N Amer 24:305-322, 1998.

3. Holmes KK, Counts GW, Beaty HN. Disseminated gonococcal infection. Ann Intern Med 74:979-993, 1971.

4. Britigan BE, Cohen MS, Sparling PF. Gonococcal infection: A model of molecular pathogenesis. N Engl J Med 312:1683-1694, 1985.

5. Coe MD, Hamer DH, Levy CS, Milner MR, Nam MH, Barth WF. Gonococcal pericarditis with tamponade in a patient with systemic lupus erythematosus. Arthritis Rheum 33:1438-1441, 1990.

6. Wilson J, Zaman AG, Simmons AV. Gonococcal arthritis complicated by acute pericarditis and pericardial effusion. Br Heart J 63:134-135, 1990.

7. Wall TC, Peyton RB, Corey GR. Gonococcal endocarditis: A new look at an old disease. Medicine 68:375-380, 1989.

Updated: July 9, 2012


About agelber

Associate Professor of Medicine
Johns Hopkins University