A nurse is creating a plan of care for a newly admitted adolescent who has bacterial meningitis

Bacterial meningitis consists of pyogenic inflammation of the meninges and the underlying subarachnoid CSF, with a bacterial cause of this syndrome. This is usually characterized by an acute onset of meningeal symptoms and neutrophilic pleocytosis. If not treated, it may lead to lifelong disability or death. [2, 5, 6]  Depending on age and general condition, patients with acute bacterial meningitis present acutely with signs and symptoms of meningeal inflammation and systemic infection of less than 24 hours’ (and usually >12 hours’) duration.

Bacterial seeding of the meninges usually occurs through hematogenous spread. In patients without an identifiable source of infection, local tissue and bloodstream invasion by bacteria that have colonized the nasopharynx may be a common source. Many meningitis-causing bacteria are carried in the nose and throat, often asymptomatically. Most meningeal pathogens are transmitted through the respiratory route, including Neisseria meningitidis (meningococcus) and S pneumoniae (pneumococcus).

Certain respiratory viruses are thought to enhance the entry of bacterial agents into the intravascular compartment, presumably by damaging mucosal defenses. Once in the bloodstream, the infectious agent must escape immune surveillance (eg, antibodies, complement-mediated bacterial killing, and neutrophil phagocytosis).

Subsequently, hematogenous seeding into distant sites, including the CNS, occurs. The specific pathophysiologic mechanisms by which the infectious agents gain access to the subarachnoid space remain unclear. Once inside the CNS, the infectious agents likely survive because host defenses (eg, immunoglobulins, neutrophils, and complement components) appear to be limited in this body compartment. The presence and replication of infectious agents remain uncontrolled and incite the cascade of meningeal inflammation described above.

With almost 4100 cases and 500 deaths occurring annually in the United States, bacterial meningitis continues to be a significant source of morbidity and mortality. The annual incidence in the United States is 1.33 cases per 100,000 population. [7]

The specific infectious agents that are involved in bacterial meningitis vary among different patient age groups, and the meningeal  inflammation may evolve into the following conditions:

• Ventriculitis

• Empyema

• Cerebritis

• Abscess formation

Some of the bacteria associated with bacterial meningitis include the following [2] : 

Streptococcus pneumoniae

Staphylococcus aureus

Coagulase negative Staphylococcus

Streptococcus pyogenes

Streptococcus agalactiae

Viridans streptococci

Enterococcus spp

Haemophilus influenzae

Listeria monocytogens

Cutibacterium acnes

Escherichia coli

Klebsiella pneumoniae

Pseudomonas aeruginosa

Salmonella spp

Acinetobacter spp

Stenotrophomonas maltophilia

Fusobacterium necrophorum

Pasteurella multocida

Capnocytophaga canimorsus 

Table 1. Most Common Bacterial Pathogens on Basis of Age and Predisposing Risks (Open Table in a new window)

Some of the more common bacterial pathogens causing meningitis are elaborated below, but any bacteria is capable of causing meningitis

H influenzae meningitis

H influenzae is a small, pleomorphic, gram-negative coccobacillus that is frequently found as part of the normal flora in the upper respiratory tract. The organism can spread from one individual to another in airborne droplets or by direct contact with secretions. Meningitis is the most serious acute manifestation of systemic infection with H influenzae. 

In the past, H influenzae was a major cause of meningitis, and the encapsulated type b strain of the organism (Hib) accounted for the majority of cases. Since the introduction of Hib vaccine in the United States in 1990, the overall incidence of H influenzae meningitis has decreased by 35%, with Hib accounting for fewer than 9.4% of H influenzae cases. [5, 2]

The isolation of H influenzae in adults suggests the presence of an underlying medical disorder, such as the following:

• Paranasal sinusitis

• Otitis media

• Alcoholism

• CSF leak after head trauma

• Functional or anatomic asplenia

• Hypogammaglobulinemia

Pneumococcal meningitis

S pneumoniae, a gram-positive coccus, is the most common bacterial cause of meningitis. [2] In addition, it is the most common bacterial agent in meningitis associated with basilar skull fracture and CSF leak. It may be associated with other focal infections, such as pneumonia, sinusitis, or endocarditis (as, for example, in Austrian syndrome, which is the triad of pneumococcal meningitis, endocarditis, and pneumonia).

S pneumoniae is a common colonizer of the human nasopharynx; it is present in 5% to 10% of healthy adults and 20% to 40% of healthy children. It causes meningitis by escaping local host defenses and phagocytic mechanisms, either through choroid plexus seeding from bacteremia or through direct extension from sinusitis or otitis media.

Patients with the following conditions are at increased risk for S pneumoniae meningitis:

• Hyposplenism

• Hypogammaglobulinemia

• Multiple myeloma

• Glucocorticoid treatment

• Defective complement (C1-C4)

• Diabetes mellitus

• Renal insufficiency

• Alcoholism

• Malnutrition

• Chronic liver disease

Streptococcus agalactiae meningitis

Streptococcus agalactiae (group B streptococcus [GBS]) is a gram-positive coccus that inhabits the lower GI tract. It also colonizes the female genital tract at a rate of 5% to 40%, which explains why it is the most common agent of neonatal meningitis (associated with 70% of cases). Routine testing and treatment of pregnant females for GBS has led to a decrease in neonatal meningitis with this organism.

Predisposing risks in adults include the following:

• Diabetes mellitus

• Pregnancy

• Alcoholism

• Hepatic failure

• Renal failure

• Corticosteroid treatment

In 43% of adult cases, however, no underlying disease is present.

Meningococcal meningitis

N meningitidis is a gram-negative diplococcus that is carried in the nasopharynx of otherwise healthy individuals. It initiates invasion by penetrating the airway epithelial surface. The precise mechanism by which this occurs is unclear, but recent viral or mycoplasmal infection has been reported to disrupt the epithelial surface and facilitate invasion by meningococcus.

Most sporadic cases of meningococcal meningitis (95-97%) are caused by serogroups B, C, and Y, whereas the A and C strains are observed in epidemics (< 3% of cases). Currently, N meningitidis is one of the leading causes of bacterial meningitis in children and young adults, but the incidence has decreased with use of the conjugate meningococcal vaccine. [8]

Risk factors for meningococcal meningitis include the following:

• Deficiencies in terminal complement components (eg, membrane attack complex, C5-C9), which increases attack rates but is associated with surprisingly lower mortality rates

• Properdin defects that increase the risk of invasive disease

• Antecedent viral infection, chronic medical illness, corticosteroid use, and active or passive smoking

• Crowded living conditions, as is observed in college dormitories (college freshmen living in dormitories are at highest risk) and military facilities, which has been reported in clustering of cases

Listeria monocytogenes meningitis

Listeria monocytogenes is a small gram-positive bacillus that causes 3% of bacterial meningitis cases and is associated with one of the highest mortalities (20%). [5]  The organism is widespread in nature and has been isolated in the stool of 5% of healthy adults. Most human cases appear to be food-borne.

L monocytogenes is a common food contaminant, with a recovery rate of up to 70% from raw meat, vegetables, and meats. Outbreaks have been associated with consumption of contaminated coleslaw, milk, cheese, and alfalfa tablets.

Groups at risk include the following:

• Pregnant women

• Infants and children

• Elderly individuals (>60 years)

• Patients with alcoholism

• Adults who are immunosuppressed (eg, steroid users, transplant recipients, or persons with AIDS)

• Individuals with chronic liver and renal disease

• Individuals with diabetes

• Persons with iron-overload conditions (eg, hemochromatosis or transfusion-induced iron overload)

Meningitis caused by gram-negative bacilli

Aerobic gram-negative bacilli include the following:

• Escherichia coli

• Klebsiella pneumoniae

• Serratia marcescens

• P aeruginosa

• Salmonella species

Gram-negative bacilli can cause meningitis in certain groups of patients. E coli is a common agent of meningitis among neonates. Other predisposing risk factors for meningitis associated with gram-negative bacilli include the following:

• Neurosurgical procedures or intracranial manipulation

• Old age

• Immunosuppression

• High-grade gram-negative bacillary bacteremia

• Disseminated strongyloidiasis

Disseminated strongyloidiasis has been reported as a classic cause of gram-negative bacillary bacteremia, as a result of the translocation of gut microflora with the Strongyloides stercoralis larvae during hyperinfection syndrome.

Staphylococcal meningitis

Staphylococci are gram-positive cocci that are part of the normal skin flora. Meningitis caused by staphylococci is associated with the following risk factors:

• Neurosurgery

• Head trauma

• Presence of CSF shunts

• Infective endocarditis and paraspinal infection

S epidermidis is the most common cause of meningitis in patients with CNS (ie, ventriculoperitoneal) shunts.

Aseptic meningitis

Aseptic meningitis is one of the most common infections of the meninges. Although viruses are the most common cause of aseptic meningitis, however, aseptic meningitis can also be caused by bacteria, fungi, and parasites. It is noteworthy that partially treated bacterial meningitis accounts for a large number of meningitis cases with a negative microbiologic workup. 

In many cases, a cause of meningitis is not apparent after initial evaluation, and the disease is therefore classified as aseptic meningitis. These patients characteristically have an acute onset of meningeal symptoms, fever, and CSF pleocytosis that is usually prominently lymphocytic.

When the cause of aseptic meningitis is discovered, the disease can be reclassified according to its etiology. If appropriate diagnostic methods are performed, a specific viral etiology is identified in 55% to 70% of cases of aseptic meningitis. However, the condition can also be caused by bacterial, fungal, mycobacterial, and parasitic agents.

If, after an extensive workup, aseptic meningitis is found to have a viral etiology, it can be reclassified as a form of acute viral meningitis (eg, enteroviral meningitis or herpes simplex virus [HSV] meningitis).

Table 2. Infectious Agents Causing Aseptic Meningitis (Open Table in a new window)

Enteroviruses account for of the majority of cases of aseptic meningitis in children. Enteroviruses belong to the family Picornaviridae and are further classified as follows:

• Poliovirus (3 serotypes)

• Coxsackievirus A (23 serotypes)

• Coxsackievirus B (6 serotypes)

• Echovirus (31 serotypes)

• Newly recognized enterovirus serotypes 68-71

Enteroviruses are usually spread by fecal-oral or respiratory routes. Infection occurs during summer and fall in temperate climates and year-round in tropical regions.

The nonpolio enteroviruses (NPEVs) account for approximately 90% of cases of viral meningitis in which a specific pathogen can be identified.

Echovirus 30 was reported as the cause of an epidemic in Japan in 1991. It was also reported as the cause of 20% of cases of aseptic meningitis reported to the Centers for Disease Control and Prevention (CDC) in 1991.

The Herpesviridae family consists of large, DNA-containing enveloped viruses. Eight members are known to cause human infections, and all have been implicated in meningitis syndromes, with the exception of HHV-8 or Kaposi sarcoma–associated virus.

HSV accounts for 0.5% to 3% of cases of aseptic meningitis; it is most commonly associated with primary genital infection and is less likely during recurrences. HSV-1 is a cause of encephalitis, whereas HSV-2 more commonly causes meningitis. Although Mollaret syndrome (a recurrent, but benign, aseptic meningitis syndrome) is more frequently associated with HSV-2, HSV-1 has also been implicated as a cause.

Epstein-Barr virus (EBV, or HHV-4) and cytomegalovirus (CMV, or HHV-5) infection may manifest as meningitis in patients with the mononucleosis syndrome. Varicella-zoster virus (VZV, or HHV-3) and CMV cause meningitis in immunocompromised hosts, especially patients with AIDS and transplant recipients. HHV-6 and HHV-7 have been reported to cause meningitis in transplant recipients.

The most common arthropod-borne viruses are West Nile virus, St Louis encephalitis virus (a flavivirus), Colorado tick fever virus, and California encephalitis virus (bunyavirus group, including La Crosse encephalitis virus). St Louis encephalitis virus is a mosquito-borne flavivirus that may cause a febrile syndrome, aseptic meningitis syndrome, and encephalitis. Other members of the flavivirus group that may cause aseptic meningitis include tick-borne encephalitis virus, Powassan encephalitis, and Japanese encephalitis virus. [9]

California encephalitis is a common childhood disease of the CNS that is caused by a virus in the genus Bunyavirus. Most of the cases of California encephalitis are probably caused by mosquito-borne La Crosse encephalitis virus.

LCM virus is a member of the arenaviruses, a family of single-stranded, RNA-containing viruses in which rodents are the animal reservoir. The modes of transmission include aerosols and direct contact with rodents. Outbreaks have also been traced to infected laboratory mice and hamsters.

The mumps virus is the most common cause of aseptic meningitis in unimmunized populations, occurring in 30% of all patients with mumps. Upon exposure, an incubation period of approximately 5 to 10 days ensues, followed by a nonspecific febrile illness and an acute onset of aseptic meningitis. This may be associated with orchitis, arthritis, myocarditis, and alopecia.

Patients with acute HIV infection may present with aseptic meningitis syndrome, usually as part of the mononucleosis like acute seroconversion phenomenon. HIV should always be suspected as a cause of aseptic meningitis in a patient with risk factors such as IV drug use or high-risk sexual behaviors. These patients will have negative results on HIV serologic tests (eg, enzyme-linked immunosorbent assay [ELISA] and Western blot); the diagnosis is made by the detection of serum HIV RNA on polymerase chain reaction (PCR) testing or of HIV p24 antigen.

Adenovirus (serotypes 1, 6, 7, and 12) has been associated with cases of meningoencephalitis. Chronic meningoencephalitis has been reported with serotypes 7, 12, and 32. The infection is usually acquired through a respiratory route.

Toscana virus meningitis or encephalitis should be considered in travelers returning from a Mediterranean country (eg, Italy, Spain, or Greece) during the summer. Toscana viruses are transmitted by the bite of a sandfly. Toscana virus infection can be diagnosed by performing paired serologies and CSF PCR, which in the United States is available only through the CDC. [9]

Astrovirus MLB2, usually a gastrointestinal virus, and Cache Valley virus in an immunosuppressed individual are newly identified as causes of meningitis. [10, 11]

Chronic meningitis

Chronic meningitis is a constellation of signs and symptoms of meningeal irritation associated with CSF pleocytosis that persists for longer than 4 weeks.

Chronic meningitis can be caused by a wide range of infectious and noninfectious etiologies (see Table 3 below).

Table 3. Causes of Chronic Meningitis  (Open Table in a new window)

Brucellae are small gram-negative coccobacilli that cause zoonoses as a result of infection with Brucella abortus, Brucella melitensis, Brucella suis, or Brucella canis. Transmission to humans occurs after direct or indirect exposure to infected animals (eg, sheep, goats, or cattle). Direct infection of the CNS occurs in fewer than 5% of cases, with most patients presenting with acute or chronic meningitis.

Persons at risk for brucellosis include individuals who had contact with infected animals or their products (eg, through intake of unpasteurized milk products). Veterinarians, abattoir workers, and laboratory workers dealing with these animals are also at risk.

M tuberculosis is an acid-fast bacillus that causes a broad range of clinical illnesses that can affect virtually any organ of the body. It is spread through airborne droplet nuclei, and it infects one third of the world’s population. Involvement of the CNS with tuberculous meningitis is usually caused by rupture of a tubercle into the subarachnoid space

Tuberculous meningitis should always be considered in the differential diagnosis of patients with aseptic meningitis or chronic meningitis syndromes, especially those with basilar meningitis, symptoms of more than 5 days’ duration, or cranial nerve palsies. If tuberculous meningitis is suspected, antituberculosis therapy, with or without steroids, should be empirically started.

Treponema pallidum is a slender, tightly coiled spirochete that is usually acquired by sexual contact. Other modes of transmission include direct contact with an active lesion, passage through the placenta, and blood transfusion (rare).

Borrelia burgdorferi, a tick-borne spirochete, is the agent of Lyme disease, the most common vector-borne disease in the United States. Meningitis may be part of a triad of neurologic manifestations of Lyme disease that also includes cranial neuritis and radiculoneuritis. Lyme disease meningitis is typically associated with a facial palsy that can sometimes be bilateral.

Cryptococcus neoformans is an encapsulated, yeastlike fungus that is ubiquitous. It has been found in high concentrations in aged pigeon droppings and pigeon nesting places. The 4 serotypes are designated A through D, with the A serotype causing most human infections. Onset of cryptococcal meningitis may be acute, especially among patients with AIDS.

Numerous cases occur in healthy hosts (eg, persons with no known T-cell defect); however, approximately 50-80% of cases occur in immunocompromised hosts. At particular risk are individuals with defects of T-cell–mediated immunity, such as persons with AIDS, organ transplant recipients, and other patients who use steroids, cyclosporine, and other immunosuppressants. Cryptococcal meningitis has also been reported in patients with idiopathic CD-4 lymphopenia, Hodgkin disease, sarcoidosis, and cirrhosis.

Coccidioides immitis is a soil-based, dimorphic fungus that exists in mycelial and yeast (spherule) forms. Persons at risk for coccidioidal meningitis include individuals exposed to the endemic regions (eg, tourists and local populations) and those with immune deficiency (eg, persons with AIDS and organ transplant recipients).

Blastomyces dermatitidis is a dimorphic fungus that has been reported to be endemic in North America (eg, in the Mississippi and Ohio River basins). It has also been isolated from parts of Central America, South America, the Middle East, and India. Its natural habitat is not well defined. Soil that is rich in decaying matter and environments around riverbanks and waterways have been demonstrated to harbor B dermatitidis during outbreaks and are thought to be risk factors for acquiring the infection.

Inhalation of the conidia establishes a pulmonary infection. Dissemination may occur in certain individuals, including those with underlying immune deficiency (eg, from HIV or pharmaceutical agents) and extremes of age, and may involve the skin, bones and joints, genitourinary tract, and CNS. Involvement of the CNS occurs in fewer than 5% of cases.

Histoplasma capsulatum is one of the dimorphic fungi that exist in mycelial and yeast forms. It is usually found in soil and can occasionally cause a chronic meningitis. The preferred means of making the diagnosis is CSF histoplasma antigen detection.

Candida species are ubiquitous in nature. They are normal commensals in humans and are found in the skin, the GI tract, and the female genital tract. The most common species is Candida albicans, but the incidence of non-albicans candidal infections (eg, Candida tropicalis) is increasing, including species with antifungal resistance (eg, Candida krusei and Candida glabrata).

Involvement of the CNS usually follows hematogenous dissemination. The most important predisposing risks for acquiring disseminated candidal infection appear to be iatrogenic (eg, the administration of broad-spectrum antibiotics and the use of indwelling devices such as urinary and vascular catheters). Prematurity in neonates is considered a predisposing risk factor as well. Infection may also follow neurosurgical procedures, such as placement of ventricular shunts.

Sporothrix schenckii is an endemic dimorphic fungus that is often isolated from soil, plants, and plant products. Human infections are characteristically lymphocutaneous. Extracutaneous manifestations of sporotrichosis may occur, though meningeal sporotrichosis, which is the most severe form, is a rare complication. AIDS is a reported underlying risk factor in many described cases and is associated with a poor outcome.

Infection with free-living amoebas is an infrequent but often life-threatening human illness, even in immunocompetent individuals. N fowleri is the only species of Naegleria recognized to be pathogenic in humans, and it is the agent of primary amebic meningoencephalitis (PAM). The parasite has been isolated in lakes, pools, ponds, rivers, tap water, and soil.

Infection occurs when a person is swimming or playing in contaminated water sources (eg, inadequately chlorinated water and sources associated with poor decontamination techniques). The N fowleri amebas invade the CNS through the nasal mucosa and cribriform plate.

PAM occurs in two forms. The first is characterized by an acute onset of high fever, photophobia, headache, and altered mental status, similar to bacterial meningitis, occurring within 1 week after exposure. Because it is acquired via the nasal area, olfactory nerve involvement may manifest as abnormal smell sensation. Death occurs in 3 days in patients who are not treated. The second form, the subacute or chronic form, consists of an insidious onset of low-grade fever, headache, and focal neurologic signs. Duration of illness is weeks to few months.

Acanthamoeba and Balamuthia cause granulomatous amebic encephalitis, which is a subacute opportunistic infection that spreads hematogenously from the primary site of infection (skin or lungs) to the CNS and causes an encephalitis syndrome. These cases can be difficult to distinguish from culture-negative meningitis.

Angiostrongylus cantonensis, the rat lungworm, can cause eosinophilic meningitis (pleocytosis with more than 10% eosinophils) in humans. The adult parasite resides in the lungs of rats. Its eggs hatch, and the larval stages are expelled in the feces. The larvae develop in the intermediate host, usually land snails, freshwater prawns, and crabs. Humans acquire the infection by ingesting raw mollusks.

Gnathostoma spinigerum, a GI parasite of wild and domestic dogs and cats, may cause eosinophilic meningoencephalitis. Humans acquire the infection after ingesting undercooked infected fish and poultry.

Baylisascaris procyonis is an ascarid parasite that is prevalent in the raccoon populations in the United States and rarely causes human eosinophilic meningoencephalitis. Human infections occur after accidental ingestion of food products contaminated with raccoon feces.

Additional causes of meningitis

Congenital malformation of the stapedial footplate has been implicated in the development of meningitis. Head and neck surgery, penetrating head injury, comminuted skull fracture, and osteomyelitic erosion may infrequently result in direct implantation of bacteria into the meninges. Skull fractures can tear the dura and cause a CSF fistula, especially in the region of the frontal ethmoid sinuses. Patients with any of these conditions are at risk for bacterial meningitis.