Meningococcemia presenting as septic arthritis, pericarditis, and tenosynovitis

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BRIEF REPORT

MENINGOCOCCEMIA PRESENTING AS SEPTIC ARTHRITIS, PERICARDITIS, AND TENOSYNOVITIS MICHAEL S. ROSEN, ALLEN R. MYERS, and BURTON DICKEY

There have been infrequent reports of meningococcemia mimicking gonococcemia (1-8). In this paper we extend such observations by reporting a case of tenosynovitis and septic arthritis in a young woman with meningococcemia. Case report. The patient, a 32-year-old black woman, was well until 1 day prior to admission, when she awoke with a temperature of 103"F, chills, myalgias, and pain in her left wrist, right ankle, and both knees. That evening she developed nausea and watery diarrhea. On the following day she presented to Germantown Hospital and Medical Center emergency room, with persistent arthralgias and myalgias and onset of severe anterior pleuritic chest pain. She denied having abdominal pain, vaginal discharge, rash, sore throat, dysuria, shortness of breath, cough, stiff neck, headache, or photophobia. She was sexually active, and her last known menstrual period was I month prior to admission. She denied contact with persons with meningococcal disease. Her medical history was significant for bilateral ectopic pregnancies, bilateral oophorectomy , and an appendectomy. She took no medications and had no allergies. Physical examination revealed a well-devel-

From the Departments of Medicine, Germantown Hospital Medical Center and Temple University Hospital, Philadelphia, Pennsylvania. Michael S. Rosen, MD: Chief Medical Resident, Temple University Hospital; Allen R. Myers, MD: Professor and Acting Chairman, Department of Medicine, Temple University School of Medicine; Burton Dickey, MD: Resident in Internal Medicine, Temple University Hospital. Address reprint requests to Allen R. Myers, MD, Professor and Acting Chairman, Department of Medicine, Temple University Hospital, 3400 N . Broad Street, Philadelphia, PA 19140. Submitted for publication August 15, 1984; accepted in revised form November 26. 1984. Arthritis and Rheumatism, Vol. 28, No. 5 (May 1985)

oped woman who appeared moderately ill. Her blood pressure was 80/50, pulse rate 132, temperature 100°F orally, and her respiratory rate was 24 and shallow. The skin was dry and there was no rash. Her pharynx was clear. There was no adenopathy and her neck was supple. The chest was clear to auscultation and percussion, and there were no rubs. Her chest wall was diffusely tender. The cardiac examination revealed a regular rate and rhythm with no murmurs, gallops, or rubs. Abdominal examination revealed tenderness in both lower quadrants, with guarding but no rebound. A pelvic examination showed a white vaginal discharge, tenderness on cervical motion, and bilateral lower quadrant tenderness. There were no palpable masses. Results of the rectal examination were negative. The joint examination revealed a tender left knee without obvious effusion, a tender right ankle, and warmth and tenderness along the dorsal aspect of her left hand following the course of the extensor tendon of her left wrist. The neurologic examination findings were within normal limits. Admission laboratory data revealed a white blood cell (WBC) count of 14,800/mm3 with 62% neutrophils, 30% bands, 6% lymphocytes, 4% monocytes; hemoglobin 11.2 gm/dl; hematocrit 33.2%; platelets 157,000/mm3; prothrombin time 10.9 seconds; partial thromboplastin time 3 1 seconds; sodium 140 mEq/liter; potassium 3.9 mEq/liter; HCO? 25 mEq/liter; chloride 105 mEq/liter; blood urea nitrogen 15 mg/dl; serum glucose 146 mg/dl. Results of a chest radiograph were within normal limits. Electrocardiogram (EKG) showed sinus tachycardia but otherwise normal findings. Urinalysis revealed trace ketones, 2+ protein, and no cells. Erythrocyte sedimentation rate was 87 m d h o u r . At admission a pelvic ultrasound was per-

BRIEF REPORTS formed, revealing no abnormality. Cultures were obtained from blood, urine, cervix, rectum, and throat, and she was started on a regimen of penicillin, 2 million units every 6 hours, for a presumed diagnosis of disseminated gonococcal infection. By the following day, she was afebrile and normotensive and felt much improved, with a decrease in her arthralgias and myalgias. However, she complained of persistent chest pain and increased pain and swelling of her right ankle. A right ankle effusion was noted on physical examination. Arthrocentesis of that ankle revealed purulent fluid with 117,000 WBC/mm’ with 98% neutrophils. Gram stain revealed many intracellular gramnegative diplococci. The next day her chest pain increased and a repeat EKG was performed, demonstrating diffuse S-T segment elevation. Subsequently, an echocardiogram showed a moderate-sized posterior pericardial effusion. Later that day, all of the initial 4 blood culture bottles were reported as showing positive results for Neisseria meningitidis, type C. All other cultures demonstrated no growth. A lumbar puncture was performed, revealing 22,000 WBC/mm’ with 85% neutrophils and 15% lymphocytes. Cerebrospinal fluid glucose was 26 mg% and protein was 71 mg%. Gram stain and cultures were negative. Over the ensuing days, her chest pain gradually improved with indomethacin therapy, and her ankle effusion slowly resolved with successive daily arthrocenteses. CH50 was 41 unitdm1 (normal 20-40). Immune complexes by Raji cell assay were negative. She received a I0-day course of antibiotics and was discharged in excellent condition. Discussion. Meningococcal arthritis is considered to be a reasonably common complication of meningococcal disease, occurring in 11% of adult patients (1). Only rarely, however, has it been clinically confused with disseminated gonococcemia (1-8). This presentation occurs predominantly in young patients without meningitis who develop a monarticular or oligoarticular arthritis involving mainly large joints, usually knees, but occasionally ankles, wrists, or elbows. It is frequently (79% of cases) associated with a rash. Our patient’s course was also initially misdiagnosed as gonococcemia, based on the finding5 of a vaginal discharge and pelvic pain, along with an oligoarticular polyarthritis. In addition, her condition was unique in its similarity to gonococcal arthritis in that she had an acute tenosynovitis of the left wrist. To the best of our knowledge, this has not been previously reported in meningococcal disease. The pathogenesis of this syndrome is unclear,

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although there may be similarities to disseminated gonococcemia. Direct invasion by bacteria may play a role in some patients, although in an extensive review of the literature, Schaad (1) noted that when evaluated, only 21.2% of patients had a positive joint fluid Gram stain or culture. Immune mechanisms have also been suspected in the etiology of the arthritis. Bryerson et al (9) investigated 4 patients with arthritis developing late in the course of meningococcal meningitis. Meningococcal antigen was detected in blood initially in all patients and was cleared from the circulation rapidly. One week later antibody was detected, along with a fall in C3. At that time meningococcal antigen, antibody, and C3 were detected in synoviial cells. Histologic examination of skin lesions also revealed meningococcal antigen, antibody, and C 3 . Furthermore, circulating immune complexes were detected by Davis et a1 (10) by C l q binding and polyethylene glycol methods in a patient with lateonset rnonarticular arthritis. It has been noted that the presumed allergic complications of meningococcal disease-arthritis, pericarditis, and cutaneous vasculitis-are seen more frequently with group C disease (9,11-13). I t is suspected that a bacterial cell wall polysaccharide antigen in group C meningococcus is responsible for the eventual formation of immune complexes. There has been a similar debate regarding the pathogenesis of gonococcal arthritis (14). Like gonococcal arthritis, meningococcal arthritis has an excellent prognosis with regard to joint function, with residua noted in only 0.7% of the patients (1). One feature helpful in distinguishing meningococceniia from gonococcemia is the presence of pericarditis, as seen in our patient. This is seen in 4-19% of cases of meningococcal disease (12,15-18). In contrast, although EKG changes are common in gonococcemia, documented pericarditis is rare (19). Although our patient had no skin lesions, they can be helpful in distinguishing between gonococcemia and meningococcemia. Skin lesions in gonococcemia, seen in 50% of patients (20), generally occur in the distal extremities (21) and consist of early petechial lesions which develop into papules or pustules on an erythematous or hemorrhagic base. Occasionally, bullae can be seen (19). Meningococcal skin lesions, seen in 79% of patients, are usually more generalized in distribution and consist of petechiae or maculopapular lesions. Eleven percent of patients develop more distal purpura or ecchymotic lesions, and this portends a more ominous prognosis (22). Another symptom which simulated gonococcal

BRIEF REPORTS

578 disease in our patient was abdominal pain. Although the etiology in her case was never proved, it might have been due to peritonitis from meningococcus, as described in 2 prior reports (23,24). In retrospect, meningococcal disease might have been suspected in our patient on the basis of hypotension (80/50) and tachycardia (136 beatdminute). These imply a picture of early septic shock, and are thus more consistent with meningococcus than with gonococcemia. In conclusion, although there have been other reports of meningococcemia resembling gonococcemia, this is the first case of meningococcemia presenting with tenosynovitis. In a patient with fever, polyarthritis, and tenosynovitis, meningococcemia may rarely be the cause of the syndrome, especially in the presence of clinical pericarditis. Acknowledgment. We appreciate the assistance of E. Lobb in preparation of the manuscript.

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Circulating immune complexes in a patient with meningococcal disease. Br Med J 1:1445-1446, 1976 11. Evans-Jones L, Whittle H, Onyewotu I, Egler L, Greenwood B: Comparative study of group A and group C meningococcal infection. Arch Dis Child 52:320-323, 1977 12. Morse J , Oretsky N , Hudson J: Pericarditis as a complication of meningococcal meningitis. Ann Intern Med 74~212-217, 1971 13. Edwards E: Immunological investigations of meningococcal disease. 11. Some characteristics of group C antigen of Neisseria meningitidis in the sera of patients with fulminant meningococcemia. J Infect Dis 129538544, 1974 14. O’Brien J , Goldenberg D, Rice P: Disseminated gonococcal infection: a prospective analysis of 49 patients and a review of pathophysiology and immune mechanisms. Medicine (Baltimore) 62:395-406, 1983 15. Pierce I, Cooper E: Meningococcal pericarditis. Arch Intern Med 129:918-922, 1972 16. Rao V, Rajashekaroiah K, Rice T, Riaz M, Towne W, Kallick C: Primary meningococcal pericarditis. South Med J 73: 1276-1278, 1980 17. Miller G, Witham C: Delayed febrile pleuropericarditis after sepsis. Ann Intern Med 79:194-197, 1973 18. Varriale P, Kumar R, Kwa R: Primary meningococcal pericarditis with tamponade. NY State J Med 81:79-81, 1981 19. Holmes K, Counts G, Beaty H: Disseminated gonococcal infection. Ann Intern Med 74:979-993, 1971 20. Brogadir S, Schimmer B, Myers A: Spectrum of gonococcal arthritis-dermatitis syndrome. Semin Arthritis Rheum 8:177-183, 1979 21. Myers AR: Septic arthritis, Textbook of Rheumatology. Vol. 2. Edited by WN Kelley, ED Harris Jr, S Ruddy, CB Sledge. Philadelphia, WB Saunders, 1981, pp 15511572 22. Toews W, Bass J: Skin manifestations of meningococcal infections: an immediate indicator of prognosis. Am J Dis Child 127:173-176, 1974 23. Bar-Meir S, Chojkier M, Groszmann R, Atterbury C, Conn A: Spontaneous meningococcal peritonitis: a report of two cases. Digestive Diseases 23:119-122, 1978 24. Bannatyne R, Lakdawalla N, Ein S: Primary meningococcal peritonitis (letter). Can Med Assoc J 117:436, 1977