Meningococcal Infections 

  • Author: Darvin Scott Smith, MD, MSc, DTM&H; Chief Editor: Burke A Cunha, MD   more...
 
Updated: Oct 17, 2011
 

Background

Meningococcal (Neisseria meningitidis) bloodstream infections (known as meningococcemia) can range in severity from a transient bacteremia that is relatively benign to an overwhelming infection that is rapidly fatal. Meningitis commonly occurs during the course of meningococcemia. In rare cases, N meningitidis organisms can spread hematogenously to other sites, such as the pericardium, the joints, and the eyes.

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Pathophysiology

The human nasopharynx is the only known reservoir for N meningitidis. Meningococci spread from person to person by airborne droplets of infected nasopharyngeal secretions. Meningococcal organisms attach to mucosal surfaces, where they produce few symptoms. Concomitant viral respiratory infections, particularly those involving influenza viruses, appear to enhance the spread of meningococcal infection and the likelihood of nasopharyngeal carriage after exposure to meningococci.

Nasopharyngeal meningococcal infection is usually subclinical. Asymptomatic nasopharyngeal carriage of meningococci is transient and resolves within several weeks. In very rare cases, N meningitidis organisms invade the bloodstream and cause clinical disease. Clinical meningococcal disease can be arbitrarily classified into 3 general forms: (1) an uncomplicated bacteremic process, (2) a metastatic infection that commonly involves the meninges, or (3) an overwhelming systemic infection with circulatory collapse and evidence of disseminated intravascular coagulation (DIC).

The fundamental pathologic change in meningococcemia is widespread vascular injury characterized by endothelial necrosis, intraluminal thrombosis, and perivascular hemorrhage. Skin lesions usually contain numerous meningococci undergoing phagocytosis by neutrophils. Occlusive thrombi composed of platelets, red blood cells, and fibrin are most prominent in deep dermal vessels. Serous surfaces and other organs incur the same vascular injury, although N meningitidis bacteria are difficult to find in tissues other than the skin.

Patients with fulminant meningococcemia develop thrombosis and hemorrhage in the skin, the mucous membranes, the serosal surfaces, the adrenal sinusoids, and the renal glomeruli. Adrenal hemorrhage is rarely extensive. Thrombosis of the glomerular capillaries may cause renal cortical necrosis, the chief characteristic of the generalized Shwartzman reaction. Thrombi containing numerous leukocytes are occasionally found in the lungs, and extensive intra-alveolar hemorrhage can occur. Myocarditis has been observed in adults with fatal meningococcal infections.

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Epidemiology

Frequency

United States

During the past 6 decades, the occurrence of meningococcal disease has been mostly sporadic, and no widespread outbreaks have occurred. The prevalence has been approximately 1-2 cases per 100,000 population, although it has shown variation from year to year.

Limited outbreaks of meningococcal disease have occurred in some populations. Public health officials arbitrarily define an outbreak of meningococcal disease as the occurrence of 3 or more cases during a 3-month period, with a primary attack rate of at least 10 cases per 100,000 population, which is approximately 10 times greater than normal. Outbreaks may be restricted to a closed population or may involve a larger community. In a Los Angeles County outbreak of meningococcal disease, nearly one half of community residents with the disease had had contact with persons who had been incarcerated.[1]

Recently, the incidence of meningococcal disease in adolescents and college-aged young adults appears to have increased. College students living in dormitories seemed to be the population at an increased risk (see Deterrence/Prevention).

Meningococcal disease is also a relatively common problem in military recruit populations.[2]

International

Meningococcal disease occurs sporadically or in episodic epidemics worldwide. Massive outbreaks of meningococcal disease have occurred in many parts of the world. Large-scale outbreaks have spread at cyclic intervals through Central African countries, with attack rates as high as 400-500 cases per 100,000 population, as shown in the image below.

Areas with frequent epidemics of meningococcal disAreas with frequent epidemics of meningococcal disease. This is known as the Meningitis Belt of Africa, and visitors to these locales may benefit from meningitis vaccine. Image courtesy of CDC.

Outbreaks of meningococcal disease have also occurred in Mecca, Saudi Arabia, and in visitors returning from that city.

Mortality/Morbidity

The case-fatality rate of meningococcal infections varies depending on the prevalence of disease, the clinical form of disease, and the socioeconomic conditions of the society in which the infections occur. In the United States, the case-fatality rate is approximately 10%.

During endemic situations in industrialized countries, the case-fatality rate can be as low as 3% for meningitis and as high as 50% for fulminant meningococcemia. The mortality rate of meningococcal disease may be lower during epidemic situations because heightened diagnostic awareness may result in detection and treatment of greater numbers of cases before the disease progresses to a more lethal form.

Fulminant meningococcemia carries the highest mortality rate; it can exceed 50% despite the use of appropriate antibiotic therapy. It can be as high as 70% in developing countries. Survivors of fulminant meningococcemia may have ischemic complications.

Meningococcal meningitis without antibiotic therapy is uniformly fatal.

Race

One population-based study in the United States found that the incidence of meningococcal disease was significantly higher among African Americans (1.5 cases per 100,000 population) than among Anglo Americans (1.1 cases per 100,000 population). The relative risk (RR) was 1.4 (95% confidence interval [CI], 1.1-1.8).

Sex

Males accounted for 55% of all cases, with an incidence of 1.2 cases per 100,000 population, compared to 1 case per 100,000 population among females (RR, 1.3; 95% CI, 1.0-1.6).

Age

Age is a major determinant of susceptibility to meningococcal disease; however, most infected individuals experience a period of asymptomatic carriage rather than symptomatic disease.[3]

The age-specific incidence of meningococcal disease is highest in young children, although maternal antibodies usually protect infants in the first few months of life. A multicenter study evaluating the serogroups in children with N meningitis infection found that meningococcal disease continues to result in substantial morbidity and mortality in children. The study found that, overall, 55 (44%) of isolates were serogroup B, 32 (26%) were serogroup C, and 27 (22%) were serogroup Y. All but one isolate (intermediate) were susceptible to penicillin. The overall mortality rate in this pediatric population was 8%.[4]

A 1995 study in the United States found that the incidence of meningococcal disease among infants aged 1-23 months was 11.1 cases per 100,000 population. The age-specific rate was 1.5 per 100,000 population among individuals aged 2-29 year, 0.6 among individuals aged 30-50 years, and 1.3 among individuals aged 60 years and older. See the image below.

A 9-month-old baby in septic shock with purpuric NA 9-month-old baby in septic shock with purpuric Neisseria meningitis skin lesions. Photo by D. Scott Smith, MD, taken at Stanford University Hospital.

About one third of meningococcal disease cases occur in adults.

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Contributor Information and Disclosures
Author

Darvin Scott Smith, MD, MSc, DTM&H  Adjunct Assistant Professor, Department of Microbiology and Immunology, Stanford University School of Medicine; Chief of Infectious Diseases and Geographic Medicine, Department of Internal Medicine, Kaiser Redwood City Hospital

Darvin Scott Smith, MD, MSc, DTM&H is a member of the following medical societies: American Medical Association, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, and International Society of Travel Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Thomas A Hoffman, MD  Professor, Department of Internal Medicine, Division of Infectious Diseases, Jackson Memorial Hospital, University of Miami

Thomas A Hoffman, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Joanna L Chan, MD  Mohs Fellow, California Skin Institute

Joanna L Chan, MD is a member of the following medical societies: American Academy of Dermatology and American Society for Dermatologic Surgery

Disclosure: Nothing to disclose.

Specialty Editor Board

Joseph Richard Masci, MD  Professor of Medicine, Professor of Preventive Medicine, Mount Sinai School of Medicine; Director of Medicine, Elmhurst Hospital Center

Joseph Richard Masci, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, Association of Professors of Medicine, and Royal Society of Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Aaron Glatt, MD  Professor of Clinical Medicine, New York Medical College; President and CEO, Former Chief Medical Officer, Departments of Medicine and Infectious Diseases, St Joseph Hospital (formerly New Island Hospital)

Aaron Glatt, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physician Executives, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Medical Association, American Society for Microbiology, American Thoracic Society, American Venereal Disease Association, Infectious Diseases Society of America, International AIDS Society, and Society for Healthcare Epidemiology of America

Disclosure: Nothing to disclose.

Eleftherios Mylonakis, MD  Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital

Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD  Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital

Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

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Scattered petechial lesions in a patient with acute meningococcemia.
Purpuric lesions in a young adult with fulminant meningococcemia.
The legs of a 22-year-old woman in septic shock with a rapidly evolving purpuric rash. Photo by D. Scott Smith, MD, taken at Stanford University Hospital.
A 9-month-old baby in septic shock with purpuric Neisseria meningitis skin lesions. Photo by D. Scott Smith, MD, taken at Stanford University Hospital.
The leg of a 9-month-old infant in septic shock with a rapidly evolving purpuric rash. Photo by D. Scott Smith, MD, taken at Stanford University Hospital.
Neisseria meningitis purpuric lesions on the ear and cheek of a 9-month-old infant who is in septic shock. Photo by D. Scott Smith, MD, taken at Stanford University Hospital.
Lesions caused by Neisseria meningitis bacteremia on the palm of the hand of a 9-month-old infant. Photo by D. Scott Smith, MD, taken at Stanford University Hospital.
Areas with frequent epidemics of meningococcal disease. This is known as the Meningitis Belt of Africa, and visitors to these locales may benefit from meningitis vaccine. Image courtesy of CDC.
 
 
 
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