Epidemiology of community-acquired bacterial meningitis in adults

INTRODUCTION — In the pre-antibiotic era, bacterial meningitis due to Streptococcus pneumoniae and Haemophilus influenzae was virtually 100 percent fatal. With the advent of antibiotics, the mortality for H. influenzae and Neisseria meningitidis infections decreased to <10 percent, and that of S. pneumoniae to 30 percent [1]. Mortality due to S. pneumoniae meningitis in high-income countries has further decreased with the use of adjunctive steroids [2]. Meningitis remains an important global health disease despite the effectiveness of current antibiotics as well as the availability of conjugate vaccines for the three most common meningeal pathogens [3,4].

The epidemiology of community-acquired bacterial meningitis in adults will be reviewed here. The pathogenesis, clinical features, treatment, prognosis, and prevention of bacterial meningitis in adults and children and issues related to chronic and recurrent meningitis are discussed separately. (See "Pathogenesis and pathophysiology of bacterial meningitis" and "Clinical features and diagnosis of acute bacterial meningitis in adults" and "Initial therapy and prognosis of community-acquired bacterial meningitis in adults" and "Treatment of bacterial meningitis caused by specific pathogens in adults" and "Bacterial meningitis in children older than one month: Clinical features and diagnosis" and "Bacterial meningitis in children older than one month: Treatment and prognosis" and "Approach to the patient with chronic meningitis" and "Approach to the adult with recurrent infections", section on 'Meningitis'.)

The epidemiology of health care-associated meningitis and ventriculitis is discussed elsewhere. (See "Health care-associated meningitis and ventriculitis in adults: Clinical features and diagnosis", section on 'Incidence and risk factors'.)

INCIDENCE

United States — S. pneumoniae and N. meningitidis are the two major organisms causing community-acquired meningitis (table 1) [5-7]. The high frequency of pneumococcal meningitis in adults reflects the relatively high rate of pneumococcal infection in the community.

In the United States and other countries, following the institution of routine infant immunization with the conjugate H. influenzae type b vaccine in 1990 and the 7-valent S. pneumoniae (pneumococcus) conjugate vaccine in 2000, followed by the 13-valent pneumococcal vaccine (PCV13) in 2010, bacterial meningitis decreased in frequency, and the peak incidence of bacterial meningitis has shifted from children under five years of age to adults (figure 1) [5,8,9]. The frequency with which various bacteria cause meningitis in children is discussed separately [6,7]. (See "Bacterial meningitis in children older than one month: Clinical features and diagnosis", section on 'Epidemiology'.)

It has been estimated that meningitis occurs in only 4 percent of invasive pneumococcal infections, compared with 48 percent of invasive N. meningitidis infections, 30 percent of invasive listeriosis, 10 percent of invasive H. influenzae infections, and 4 percent of invasive group B streptococcal infections [10]. (See "Pneumococcal pneumonia in patients requiring hospitalization" and "Clinical manifestations of meningococcal infection" and "Clinical manifestations and diagnosis of Listeria monocytogenes infection".)

●S. pneumoniae – In a population-based observational study between 1997 and 2010 in the United States, the most common identifiable pathogen was S. pneumoniae (21,858 cases) with an incidence of 0.306 cases per 100,000 people [6]. With the introduction of the PCV13 in 2010, the number of cases in the United States remained unchanged, although the proportion of cases caused by serotypes in the vaccine decreased significantly [11]. A subsequent 16-year prospective study in France showed a reduction in the incidence of pneumococcal meningitis in children after the implementation of PCV13, but with a sharp increase in cases in the last two years of the study due to serotype 24F, which is not present in the current vaccine [12]. The impact of PCV on invasive pneumococcal disease in adults is discussed in greater detail separately. (See "Pneumococcal vaccination in adults", section on 'Rationale for vaccination' and "Invasive pneumococcal (Streptococcus pneumoniae) infections and bacteremia in adults", section on 'Epidemiology'.)

Another important trend has been the increase in incidence of penicillin-resistant S. pneumoniae meningitis worldwide. This is discussed in detail separately. (See "Treatment of bacterial meningitis caused by specific pathogens in adults", section on 'Streptococcus pneumoniae' and "Resistance of Streptococcus pneumoniae to beta-lactam antibiotics" and "Streptococcus pneumoniae: Microbiology and pathogenesis of infection".)

●N. meningitidis – The incidence of Neisseria meningitidis infection has decreased likely associated with meningococcal vaccination in the United States and now occurs at rates close to common bacterial causes of nosocomial meningitis such as staphylococcus, gram-negative bacteria, and H. influenzae [6]. In 2018, the incidence of meningococcal disease was 0.10 per 100,000 persons [7].

●H. influenzae type b – In a population-based observational study in the United States (1997 to 2010), the incidence of H. influenzae meningitis decreased from 0.10 to 0.058 per 100,000 people [6]. A more recent study of 694 infants with meningitis admitted to a large pediatric hospital between 2010 and 2017 found only one case of H. influenzae [13]. This marked decrease is presumed due to widespread vaccination of infants. Strains other than type b continue to cause occasional invasive infection (including meningitis) in children and adults. In an epidemiologic study of H. influenzae disease in children, an increase of invasive H. influenzae disease was noted and mainly caused by nontypeable and type a strains [14]

Global — S. pneumoniae remains the most common etiology globally, accounting for approximately 25 to 41 percent of cases [4]. In a prospective review of 1412 episodes of community-acquired bacterial meningitis in the Netherlands from 2006 to 2014, S. pneumoniae was responsible for 51 percent, N. meningitidis for 37 percent, and L. monocytogenes for 4 percent of cases [9]. The remaining cases were primarily due to H. influenzae, streptococci, Staphylococcus aureus, and gram-negative bacilli.

The distribution of pathogens depends upon the region of the world. As an example, large epidemics of meningitis due to N. meningitidis serogroup A used to occur in sub-Saharan Africa. Although the implementation of the meningococcal group A conjugate vaccine has virtually eliminated meningococcal group A, epidemics due to non-group A meningococcal and other meningeal pathogens continue to occur [15]. In Ghana, pneumococcal meningitis is still common despite introduction of PCV13 into the routine infant immunization program, predominantly due to meningitis caused by serotype 1 [16].

Streptococcus suis is an emerging zoonosis that causes meningitis in Asia and has been linked to exposure to pigs [17]. It is the most frequent cause of bacterial meningitis in adults in southern Vietnam and has caused outbreaks in China.

RISK FACTORS — In community-acquired meningitis, the organism responsible for acute bacterial meningitis depends in part upon the route of acquisition and underlying host factors (table 1). There are three major mechanisms for developing meningitis:

●Colonization of the nasopharynx, with subsequent bloodstream invasion followed by central nervous system (CNS) invasion.

●Invasion of the CNS following bacteremia due to a localized source, such as infective endocarditis.

●Direct entry of organisms into the CNS from a contiguous infection (eg, sinuses, mastoid), trauma, or a cerebrospinal fluid (CSF) leak [18].

Risk factors for recurrent bacterial meningitis are similar to risk factors for initial episodes and include anatomic defects of the spinal cord, brain or inner ear, acquired defects due basilar skull fractures or surgery, parameningeal infections, or immunodeficiency [19]. (See "Approach to the adult with recurrent infections", section on 'Meningitis'.)

Host factors that can predispose to meningitis include asplenia, complement deficiency, glucocorticoid excess, diabetes mellitus, alcoholism, hypogammaglobulinemia, and HIV infection (table 2). Patients with suspected meningitis should also be questioned for other predisposing factors, such as:

●Recent infection (especially respiratory or ear infection)

●Recent exposure to someone with meningitis

●Injection drug use

●Recent head trauma

●Otorrhea or rhinorrhea

●Recent travel (eg, Hajj pilgrimage) [20]

The frequency of underlying host risk factors in patients with bacterial meningitis was illustrated in a series of 1412 patients in the Netherlands [9]. Almost one-half had a predisposing condition such as otitis or sinusitis (34 percent), pneumonia (9 percent), or an immunocompromised state (11 percent).

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topic (see "Patient education: Bacterial meningitis (The Basics)")

SUMMARY

●In the pre-antibiotic era bacterial meningitis was virtually 100 percent fatal. Despite the effectiveness of current antibiotics in clearing bacteria from the cerebrospinal fluid (CSF), bacterial meningitis continues to cause significant morbidity and mortality worldwide. (See 'Introduction' above.)

●In the United States, following the institution of routine infant immunization with the conjugate Haemophilus influenzae type b vaccine in 1990 and the 7-valent Streptococcus pneumoniae (pneumococcus) conjugate vaccine in 2000 (PCV7) followed by the 13-valent pneumococcal vaccine (PCV13) in 2010, bacterial meningitis has decreased in frequency, and the peak incidence of bacterial meningitis has shifted from children under five years of age to adults (figure 1). (See 'Incidence' above.)

●S. pneumoniae remains the leading pathogen of community-acquired bacterial meningitis globally and continues to be associated with a high mortality rate. (See 'Global' above.)

●Large epidemics of meningitis due to serogroup A Neisseria meningitidis in sub-Saharan Africa have been eliminated by mass vaccination using the meningococcal A conjugate vaccine, but epidemics due to non-group A meningococcal and other meningeal pathogens continue to occur. (See 'Global' above.)

●Streptococcus suis is an emerging zoonosis that causes meningitis in Asia and has been linked to exposure to pigs or pork. (See 'Global' above.)

●Despite the decreased mortality of meningitis with the advent of effective antibiotics, mortality from meningitis still remains significant. The use of adjunctive dexamethasone in pneumococcal meningitis has been shown in clinical trials and observational studies to decrease mortality in high-income countries. (See "Dexamethasone to prevent neurologic complications of bacterial meningitis in adults".)

●The organism responsible for acute bacterial meningitis depends in part upon the route of acquisition and underlying host factors (table 1). There are three major mechanisms for developing meningitis:

•Colonization of the nasopharynx, with subsequent bloodstream invasion followed by central nervous system (CNS) invasion

•Invasion of the CNS following bacteremia due to a localized source, such as infective endocarditis

•Direct entry of organisms into the CNS from a contiguous infection (eg, sinuses, mastoid), trauma, or a CSF leak (see 'Risk factors' above)