During the period August-September 1986, CDC received four reports of disseminated gonococcal infection (DGI) caused by penicillinase-producing Neisseria gonorrhoeae (PPNG).

Cases 1 and 2: A 28-year-old woman (Patient 1) was admitted to a Racine hospital on August 4, 1986, with a 1-week history of arthritis of the left knee with effusion. Synovial and cervical cultures were both positive for PPNG. She was treated for 2 days with intravenous penicillin. When the culture results became known, her therapy was changed to ceftriaxone, 500 mg once daily. Despite the change in therapy, the knee remained swollen. Even though the dosage of ceftriaxone was increased to 1 g every 12 hours, the knee had to be surgically drained on August 14. The woman recovered rapidly and was discharged 1 week later.

The index patient's only recent sexual partner (Patient 2) was examined on August 8. He had had urethritis for 1 week and a swollen, painful left wrist for 2 weeks. Nine days earlier, he had been treated for the wrist symptoms with a non-steroidal, anti-inflammatory agent. Upon examination, the patient had purulent urethritis and a tender, slightly swollen wrist. Urethral culture was positive for PPNG. The wrist was not cultured. He was treated intramuscularly with 2 g of spectinomycin and recovered completely.

Case 3: A 20-year-old woman seen in an emergency room in Philadelphia had had wrist pain for 1 week and pain in the right knee, left ankle, and the dorsum of the left hand for 3 days. On physical examination, she was febrile, had tenosynovitis of the extensor tendons of the left hand, and had effusion of the right knee and ankle. Arthrocentesis of the knee yielded purulent fluid which grew PPNG. A cervical culture was also positive for PPNG. Initially, she was treated intravenously with penicillin; therapy was changed to cefotaxime when culture results became available. She recovered completely.

Case 4: A 52-year-old woman seen in a Philadelphia emergency room had had pain in the right wrist and third finger of the left hand for 2 days. She was febrile, and the right wrist and proximal interphalangeal joint of the left third finger were swollen and tender. Arthrocentesis of the wrist yielded purulent fluid that grew PPNG. She was treated intravenously with penicillin. Therapy was changed to intravenous ceftriaxone when culture results became available. She recovered completely.

Antibiotic-susceptibility testing, auxotype, protein I serovar determination, and plasmid analysis of isolates from all patients were performed at CDC. All isolates were resistant to penicillin (minimum inhibitory concentration (MIC) 1-8 ug/ml), and all demonstrated moderate chromosomally mediated resistance to tetracycline (MIC range: 0.5-4.0 ug/ml) and to cefoxitin (MIC range: 0.5-2.0 ug/ml). All were sensitive to spectinomycin and ceftriaxone. All isolates were auxotype/serovar class Pro-/IA-6, and all contained the 2.6 megaDalton (mDal) cryptic plasmid, the 3.2 mDal B-lactamase plasmid, and the 24.5 mDal conjugative plasmid. Despite the similarity of the isolates, suggestive of a clonal origin, no linkage could be demonstrated between the two Philadelphia patients or between either Philadelphia patient and the Wisconsin patients. Reported by: DW Miller, MD, GA Shove, MD, Racine; T Jones, E Jensen, JP Davis, MD, State Epidemiologist, Dept of Health and Social Svcs, Madison, Wisconsin. C Pritchard, MD, S Berney, MD, Temple University Hospital, Philadelphia; JA Boscia, MD, LM Bush, MD, Medical College of Pennsylvania, Philadelphia; M Goldberg, H Heineman, MD, D Green, R Sharrar, MD, Philadelphia Dept of Public Health; E Witte, VMD, MPH, State Epidemiologist, State Dept of Health, Harrisburg, Pennsylvania. Sexually Transmitted Disease Laboratory Program, Center for Infectious Diseases; Epidemiology Research Br, Program Svcs Br, Div of Sexually Transmitted Diseases, Center for Prevention Svcs, CDC.

Editorial Note

Editorial Note: DGI, a serious complication of gonorrhea, is estimated to occur in 0.5%-1.0% of all gonococcal infections. Tenosynovitis and septic arthritis are the two most common clinical syndromes (1).

Published reviews have reported that DGI is predominantly caused by organisms which are extremely susceptible to antibiotics and are more likely to be nutritionally fastidious, requiring arginine, hypoxanthine, and uracil for growth (A-H-U- auxotype) (2-4). This may have led to the mistaken impression that antibiotic-resistant strains of N. gonorrhoeae do not cause DGI.

Cases of DGI caused by PPNG are being reported more frequently (5-7). There have also been reports of DGI caused by gonococci with chromosomally mediated resistance to penicillin (8). Furthermore, in a recent, large prospective study, DGI isolates were no more susceptible to antibiotics than isolates from localized anogenital gonorrhea (9).

Patients with DGI caused by resistant gonococcal strains should be hospitalized and treated with ceftriaxone (1-2 g/day intravenously) until signs and symptoms resolve. Daily outpatient therapy with either ceftriaxone (250 mg intramuscularly) or an oral regimen defined either by in-vitro susceptibility tests should follow, for at least 1 week of antimicrobial therapy. When an infection does not respond to appropriate antimicrobial therapy, surgical drainage should be considered.

Less than 50% of synovial-fluid cultures in gonococcal arthritis are positive. Therefore, antibiotic-resistant N. gonorrhoeae should be considered in culture-negative, clinically diagnosed cases of gonococcal arthritis that do not respond to standard antimicrobial therapy.

In 1986, 16,608 PPNG infections were reported to CDC (10), a 90% increase from 1985. As the incidence of PPNG and other resistant strains increases, there is likely to be an increase in the incidence of DGI caused by antibiotic-resistant N. gonorrhoeae.

References

1. Masi AT, Eisenstein BI. Disseminated gonococcal infection and gonococcal arthritis--II: clinical manifestations, diagnosis, complications, treatment, and prevention. Semin Arthritis Rheum 1981;10:173-97.

2. Wiesner PJ, Handsfield HH, Holmes KK. Low antibiotic resistance of gonococci causing disseminated infection. New Engl J Med 1973;288:1221-2.

3. Thompson SE, Reynolds G, Short HB, et al. Auxotypes and antibiotic susceptibility patterns of Neisseria gonorrhoeae from disseminated and local infections. Sex Transm Dis 1978;5:127-31.

4. O'Brien JP, Goldenberg DL, Rice PA. Disseminated gonococcal infection: a prospective analysis of 49 patients and a review of pathophysiology and immune mechanisms. Medicine 1983;62:395-406.

5. Rinaldi RZ, Harrison WO, Fan PT. Penicillin-resistant gonococcal arthritis: a report of four cases. Ann Intern Med 1982;97:43-5.

6. Thompson J, Dunbar JM, VanGent A, VanFurth R. Disseminated gonococcal infection due to a B-lactamase-producing strain of Neisseria gonorrhoeae: a case report. Br J Vener Dis 1981;57:325-6.

7. Saraux J, Vigneron A, Berthelot G, Dombret M, Smejian J, Kahn M. Disseminated gonococcal infection caused by penicillinase-producing organisms in patients with unusual joint involvement. J Infect Dis 1987;155:154-5.

8. Strader KW, Wise CM, Wasilauskas BL, Salzer WL. Disseminated gonococcal infection caused by chromosomally mediated penicillin-resistant organisms. Ann Intern Med 1986;104:365-6.

9. Bohnoff M, Morello JA, Lerner SA. Auxotypes, penicillin susceptibility, and serogroups of Neisseria gonorrhoeae from disseminated and uncomplicated infections. J Infect Dis 1986;154:225-30.

10. CDC. Penicillinase-producing Neisseria gonorrhoeae--United States, 1986. MMWR 1987;36:107-8.

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