Gonococcemia Clinical Presentation

  • Author: Robert A Schwartz, MD, MPH; Chief Editor: Dirk M Elston, MD   more...
 
Updated: Apr 18, 2012
 

History

History reflects the classic clinical manifestations of gonococcemia—cutaneous lesions, arthritis, and, possibly, pericarditis, discussed in Physical. A dramatic increase in the incidence of gonorrhea has been observed, emphasizing the increasing importance of its complications, particularly in pregnancy.[7] Disseminated gonococcal infection has been estimated to occur in less than 5% of those with Neisseria gonorrhoeae, with most first seen with arthritis, tenosynovitis, polyarthralgia, or dermatitis.[14]

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Physical

The clinical evolution of DGI is biphasic consisting of a bacteremic phase and a localized, suppurative phase.

Bacteremic phase

In this phase, which occurs during the first 2-3 days of gonococcemia, the patient experiences polyarthralgias and constitutional symptoms, such as malaise, fever, and weakness. The classic skin lesions are acral hemorrhagic pustules.[15] Note the image below.

Disseminated gonococcemia, acral pustules. Disseminated gonococcemia, acral pustules.

This phase is associated with a clinical picture of polyarthritis, dermatitis, and tenosynovitis. The joints most commonly involved include those of the extremities, including the wrists, the fingers, the elbows, the knees, and the ankles, with 70% of patients experiencing a migratory polyarthralgia of 1-3 joints and the remaining 30% having involvement of more than 3 joints. This arthritis is believed to be a sterile arthritis with negative culture results. Certain patient populations, such as patients infected with HIV, can experience involvement of unusual joints, such as the sternoclavicular joint and the hips, and the arthritis may have a more aggressive course, with potential destruction of the joint.

About 75% of patients experience a dermatitis that can vary from macular/papular to vesicular/pustular to necrotic or hemorrhagic erythema. The dermatitis is nonscarring. Vasculitis has also been reported.

Skin lesions are often in multiple stages of development, and 5-50 individual lesions can be present. They are mostly located on the distal extremities. The face, the scalp, the palms, the soles, and the trunk are classically spared, but not always.[16] Lesions can be painful but are usually asymptomatic, and they resolve in 4-7 days even without treatment.

In this bacteremic phase, the possibility of pericarditis, endocarditis, perihepatitis (Fitz-Hugh-Curtis syndrome), osteomyelitis, glomerulonephritis, as well as other end-organ involvement must be considered, but the occurrence of these conditions is rare and continues to decrease with effective treatment and earlier diagnosis of disease.

Localized, suppurative phase

This phase usually occurs on days 3-6 of the infection and consists of mainly arthritis. In contrast to the arthritis/arthralgia of the bacteremic phase, this arthritis is a septic arthritis with purulent joint fluid and a positive culture result in 50% of patients. WBC counts in aspirated joint fluid are typically 50-100,000 cells/μL and consist of more than 90% neutrophils.

Skin findings in this phase are minimal; only 15-20% of patients have active skin lesions, and the remaining 80-85% of patients have resolved dermatitis or resolving dermatitis.

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Causes

Risk factors for both mucosal infection and disseminated infection include sexual activity/promiscuity, lower socioeconomic status, ethnic minority, male homosexuality, drug use, lower educational level, and past history of other STDs. See Pathophysiology.

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Contributor Information and Disclosures
Author

Robert A Schwartz, MD, MPH  Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, University of Medicine and Dentistry of New Jersey-New Jersey Medical School

Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi

Disclosure: Nothing to disclose.

Coauthor(s)

Rajendra Kapila, MD, MBBS  Associate Professor, Department of Medicine, University of Medicine and Dentistry of New Jersey-New Jersey Medical School

Rajendra Kapila, MD, MBBS is a member of the following medical societies: American College of Physicians, American Medical Association, Infectious Diseases Society of America, and Infectious Diseases Society of New Jersey

Disclosure: Nothing to disclose.

Specialty Editor Board

Gregory J Raugi, MD, PhD  Professor, Department of Internal Medicine, Division of Dermatology, University of Washington at Seattle School of Medicine; Chief, Dermatology Section, Primary and Specialty Care Service, Veterans Administration Medical Center of Seattle

Gregory J Raugi, MD, PhD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

David F Butler, MD  Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic, Northside Clinic

David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Jeffrey Meffert, MD  Assistant Clinical Professor of Dermatology, University of Texas School of Medicine at San Antonio

Jeffrey Meffert, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, Association of Military Dermatologists, and Texas Dermatological Society

Disclosure: Nothing to disclose.

Joel M Gelfand, MD, MSCE  Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania

Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology

Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds Investigator; Genentech Grant/research funds investigator; Centocor Consulting fee Consulting; Abbott Grant/research funds investigator; Abbott Consulting fee Consulting; Novartis investigator; Pfizer Grant/research funds investigator; Celgene Consulting fee DMC Chair; NIAMS and NHLBI Grant/research funds investigator

Chief Editor

Dirk M Elston, MD  Director, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author, Dr. Neal Ammar, to the development and writing of this article.

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Disseminated gonococcemia, acral pustules.
Cytologic smear of cutaneous acral pustule showing gram-negative intracellular diplococci.
 
 
 
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