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Disseminated Gonococcal Infections and Meningitis -- Pennsylvania

Between January 9, and January 31, 1984, two cases of disseminated gonococcal infection (DGI) associated with meningitis occurred in the Philadelphia, Pennsylvania, area. The patients did not have a common sexual contact. One patient died.

Case 1: A 15-year-old female, previously well, was admitted to a Philadelphia-area hospital on January 9, with less than 1 day of malaise, sore throat, and progressive mental confusion. Her previous medical history was unremarkable for repeated or unusual infections. During July 1983, she had been treated for a culture-proven Neisseria gonorrhoeae cervical infection with oral ampicillin 3.5 g/probenicid 1 g; her test-of-cure was negative. The patient was seen again at an area clinic during November 1983 as a suspected contact of gonorrhea and was treated with oral ampicillin 3.5 g/probenicid 1 g; the cervical culture submitted was negative for N. gonorrhoeae. No sexual partners were identified at these visits or at the current admission.

Clinical and laboratory findings on admission supported a diagnosis of hypovolemic shock and sepsis, with acute renal failure, disseminated intravascular coagulation, and meningitis. Intravenous ampicillin and chloramphenicol were administered, along with other supportive measures. Two blood cultures and a cervical culture obtained on admission were positive for N. gonorrhoeae. Although cerebrospinal fluid (CSF) cultures were negative for bacterial pathogens, large numbers of polymorphonuclear leukocytes were present. Despite intense supportive measures, including intubation with ventilator support, the patient succumbed to overwhelming sepsis, shock, and noncardiogenic pulmonary edema on January 13.

Case 2: A 19-year-old female, previously well, was admitted to a second area hospital on January 24, with a 2-day history of nausea, vomiting, headache, and neck stiffness. Following admission, she was treated with intravenous penicillin, to which she gradually responded. Specimens obtained from the cervix and CSF were culture-positive for N. gonorrhoeae. She was discharged following an uneventful recovery. Two male sexual contacts were identified, with symptoms localized to the genitourinary tract.

Laboratory investigation: Isolates were submitted to CDC for further confirmation and evaluation. The identities of the isolates were confirmed by carbohydrate utilization and commercial coagglutination; each isolate was tested for production of B-lactamase (penicillinase). Serogrouping based on major outer membrane proteins was determined using experimental monoclonal antibodies (1). Nutritional requirements were identified by auxotyping (2). Antibiotic susceptibilities were determined by agar dilution, and plasmid content was identified for each gonococcal isolate. Gonococci were incubated with normal human sera and the patients' sera to determine serum bactericidal activity. Major complement component levels were determined for each patient.

Isolates from the blood and cervix of the first patient were N. gonorrhoeae, nonpenicillinase-producing, serogroup IA, proline auxotype, plasmid content of 2.6 megadaltons, with susceptibility to penicillin, tetracycline, chloramphenicol, erythromycin, trimethoprim/sulfamethoxazole, spectinomycin, and cefoxitin. Incubation of gonococci with normal human serum (NHS) showed resistance to killing, but there was bactericidal activity with the patient's serum (PS). Quantitation of complement components for the first patient revealed a moderate depression of C-3 and C-4 components.

Isolates from the CSF and cervix of the second patient were confirmed as N. gonorrhoeae, nonpenicillinase-producing, serogroup IA, proline auxotype, plasmid content of 2.6 megadaltons, with a similar antibiotic susceptibility pattern to the isolates from the first patient. Incubation of gonococci with NHS and PS demonstrated resistance to NHS and bactericidal activity with PS. No serum complement deficiencies were demonstrated. Reported by S Plotkin, MD, C Pasquareillo, MD, E Charney, MD, J Campos, PhD, The Children's Hospital of Philadelphia, R Swenson, MD, N Pullman, MD, E Burkhardt, Temple University Hospitals, S Shapiro, MD, L Polk, MD, R Sharrar, MD, B Cassens, MD, M Goldberg, City of Philadelphia Dept of Health, CW Hays, MD, State Epidemiologist, Pennsylvania State Dept of Health; Sexually Transmitted Diseases Laboratory Program, Center for Infectious Diseases, Div of Sexually Transmitted Diseases, Center for Prevention Svcs, CDC.

Editorial Note

Editorial Note: The occurrence of two cases of DGI associated with meningitis within a 1-month period in the same area is extremely unusual. Both patients were similar by age group (15-19 years), sex, race, and geographic area. The isolates from the patients were identical with regard to serogrouping, auxotyping, and plasmid content. There were no complement deficiencies, except a moderate depression of C-3 and C-4 components in the first patient, which may have been attributable to overwhelming sepsis. However, C-3 deficiency has been associated with recurrent infections caused by other pyogenic organisms (3,4).

DGI is most commonly associated with clinically diagnosed arthritis or tenosynovitis and typical skin lesions. However, a microbiologic diagnosis based on positive blood, synovial fluid, or skin-lesion cultures may be difficult to confirm.

DGI causing meningitis, septic shock, and death is very rare to virtually unknown. Only 20 gonococcal meningitis cases were reported between 1922 and 1972 (5,6). Among 49 DGI patients from a recent report, none had meningitis; most of these organisms were serogroup IA (7).

The unusual clinical presentation of DGI with meningitis supports the necessity for the differentiation of N. gonorrhoeae from N. meningitidis among patients with Gram-negative diplococcal bacteremia and meningitis.

There have been no additional cases of DGI with meningitis reported from the Philadelphia area. Recommendations have been made to increase surveillance for DGI and complications of gonococcal infection, particularly among hospitalized patients. A survey is being conducted to sample representative N. gonorrhoeae among the Philadelphia population.


  1. Sandstrom EG, Chen KCS, Buchanan TM. Serology of Neisseria gonorrhoeae: Coagglutination serogroup WI and WII/III correspond to different outer membrane protein molecules. Infect Immunity 1982;38:462-70.

  2. Knapp JS, Holmes KK. Disseminated gonococcal infections caused by Neisseria gonorrhoeae with unique nutritional requirements. J Infect Dis 1975;132:204-8.

  3. Alper CA, Abramson N, Johnson RB, Jr, Jandi JH, Rosen FS. Increased susceptibility to infection associated with abnormalities of complement-mediated functions and of the third component of complement (C3). N Engl J Med 1970;282:349-53.

  4. Ballow M, Shira JE, Harden L, Yang SY, Day NK. Complete absence of the third component of complement in man. J Clin Invest 1975;56:703-10.

  5. Sayeed ZA, Bharudi U, Howell E, Meyers HL, Jr. Gonococcal meningitis, JAMA 1972;219:1730-1.

  6. Holmes KK, Counts GW, Beaty HN. Disseminated gonococcal infection. Ann Intern Med 1971;74:979-93.

  7. O'Brien JP, Goldberg 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.

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