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Meningitis Clinical Presentation

Overview
Presentation
DDx
Workup
Treatment
Medication

Updated: Jan 28, 2015

History
Physical Examination
Complications
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References
History

Only about 44% of adults with bacterial meningitis exhibit the classic triad of
fever, headache, and neck stiffness.[12] These symptoms can develop over
several hours or over 1-2 days. In a large prospective study of 696 cases of
adults with bacterial meningitis, van de Beek et al reported that 95% of the
patients had 2 out of the following 4 symptoms: fever, headache, stiff neck,
and altered mental status.[12]

Other symptoms can include the following:

Nausea
Vomiting
Photalgia (photophobia) - Discomfort when the patient looks into bright
lights
Sleepiness
Confusion
Irritability
Delirium
Coma

Approximately 25% of patients with bacterial meningitis present acutely, well

within 24 hours of the onset of symptoms. Occasionally, if a patient has been
taking antibiotics for another infection, meningitis symptoms may take longer
to develop or may be less intense.

Approximately 25% of patients have concomitant sinusitis or otitis that could

predispose to S pneumoniae meningitis.[12] In contrast, patients with
subacute bacterial meningitis and most patients with viral meningitis present
with neurologic symptoms developing over 1-7 days. Chronic symptoms

lasting longer than 1 week suggest the presence of meningitis caused by

certain viruses or by tuberculosis, syphilis, fungi (especially cryptococci), or
carcinomatosis.

Patients with viral meningitis may have a history of preceding systemic

symptoms (eg, myalgias, fatigue, or anorexia). Patients with meningitis
caused by the mumps virus usually present with the triad of fever, vomiting,
and headache. This follows the onset of parotitis (salivary gland enlargement
occurs in 50% of patients), which clinically resolves in 7-10 days.

As bacterial meningitis progresses, patients of any age may have seizures

(30% of adults and children; 40% of newborns and infants). In patients who
have previously been treated with oral antibiotics, seizures may be the sole
presenting symptom; fever and changes in level of alertness or mental status
are less common in partially treated meningitis than in untreated meningitis.

Atypical presentation may be observed in certain groups. Elderly individuals,

especially those with underlying comorbidities (eg, diabetes, renal and liver
disease), may present with lethargy and an absence of meningeal symptoms.
Patients with neutropenia may present with subtle symptoms of meningeal
irritation.

Other immunocompromised hosts, including organ and tissue transplant

recipients and patients with HIV and AIDS, may also have an atypical
presentation. Immunosuppressed patients may not show dramatic signs of
fever or meningeal inflammation.

A less dramatic presentationheadache, nausea, minimal fever, and

malaisemay be found in patients with low-grade ventriculitis associated
with a ventriculoperitoneal shunt. Newborns and small infants also may not
present with the classic symptoms, or the symptoms may be difficult to
detect. An infant may appear only to be slow or inactive, or be irritable,
vomiting, or feeding poorly. Other symptoms in this age group include
temperature instability, high-pitched crying, respiratory distress, and bulging
fontanelles (a late sign in one third of neonates).

Epidemiologic factors and predisposing risks should be assessed in detail.

These may suggest the specific etiologic agent.
Exposures

A history of exposure to a patient with a similar illness is an important

diagnostic clue. It may point to the presence of epidemic disease, such as
viral or meningococcal meningitis.

Elicit any history of sexual contact or high-risk behavior from the patient.
Herpes simplex virus (HSV) meningitis is associated with primary genital HSV
infection and HIV infection. A history of recurrent bouts of benign aseptic
meningitis suggests Mollaret syndrome, which is caused by HSV.

Animal contacts should be elicited. Patients with rabies could present

atypically with aseptic meningitis; rabies should be suspected in a patient
with a history of animal bite (eg, from a skunk, raccoon, dog, fox, or bat).
Exposure to rodents suggests infection with lymphocytic choriomeningitis
virus (LCM) virus and Leptospira infection. Laboratory workers dealing with
these animals also are at increased risk of contracting LCM.

Brucellosis may be transmitted through contact with infected farm animals

(eg, cows or pigs). The intake of unpasteurized milk and cheese also
predisposes to brucellosis, as well as to L monocytogenes infection.
Previous medical treatment and existing conditions

A history of recent antibiotic use should be elicited. As many as 40% of

patients who present with acute or subacute bacterial meningitis have
previously been treated with oral antibiotics (presumably because of
misdiagnosis at the time of initial presentation).

The presence of a ventriculoperitoneal shunt or a history of recent cranial

surgery should be elicited. Patients with low-grade ventriculitis associated
with a ventriculoperitoneal shunt may have a less dramatic presentation than
those with acute bacterial meningitis, experiencing headache, nausea,

minimal fever, and malaise. The presence of cochlear implants with a

positioner has been associated with a higher risk of bacterial meningitis.

Alcoholism and cirrhosis are risk factors for meningitis. Unfortunately, the
multiple etiologies of fever and seizures in patients with alcoholism or
cirrhosis make meningitis challenging to diagnose.
Location and travel

Geographic location and travel history are important in the evaluation of

patients. Infection with H capsulatum or B dermatitidis is considered in
patients with exposure to endemic areas of the Mississippi and Ohio River
valleys; C immitis is considered in regions of the southwestern United States,
Mexico, and Central America. B burgdorferi is considered in regions of the
northeastern and northern central United States, if tick exposure is a
possibility.
Season and temperature

The time of year is an important variable because many infections are

seasonal. With enteroviruses (which are found worldwide), infections occur
during late summer and early fall in temperate climates and year-round in
tropical regions. In contrast, mumps, measles, and varicella-zoster virus
(VZV) are more common during winter and spring. Arthropod-borne viruses
(eg, West Nile virus, St Louis encephalitis, and California encephalitis virus)
are more common during the warmer months.
Physical Examination

The classic triad of meningitis consists of fever, nuchal rigidity, and altered
mental status, but not all patients have all 3, and almost all patients have
headache. Altered mental status can range from irritability to somnolence,
delirium, and coma. The examination reveals no focal neurologic deficits in
the majority of cases. Furthermore, the majority of patients with bacterial
meningitis have a stiff neck, but the meningeal signs are insensitive for
diagnosis of meningitis.[13]

Acute bacterial meningitis in otherwise healthy patients who are not at the

extremes of age presents in a clinically obvious fashion. In contrast, most

patients with subacute bacterial meningitis pose a diagnostic challenge.
Systemic examination occasionally reveals a pulmonary or otitis media
coinfection.

Systemic findings can also be present. Extracranial infection (eg, sinusitis,

otitis media, mastoiditis, pneumonia, or urinary tract infection [UTI]) may be
noted. Endotoxic shock with vascular collapse is characteristic of severe N
meningitidis (meningococcal) infection.

General physical findings in viral meningitis are common to all causative

agents, but some viruses produce unique clinical manifestations that help
focus the diagnostic approach. Enteroviral infection is suggested by the
presence of the following:

Exanthemas
Symptoms of pericarditis, myocarditis, or conjunctivitis
Syndromes of pleurodynia, herpangina, and hand-foot-and-mouth disease

Increased blood pressure with bradycardia can also be present. Vomiting

occurs in 35% of patients.

Nonblanching petechiae and cutaneous hemorrhages may be present in

meningitis caused by N meningitidis (50%), H influenzae, S pneumoniae, or S
aureus.[14] Arthritis is seen with meningococcal infection and with M
pneumoniae infection but is less common with other bacterial species.
Infants

Infants may have the following:

Bulging fontanelle (if euvolemic)

Paradoxic irritability (ie, remaining quiet when stationary and crying when
held)
High-pitched cry
Hypotonia

In infants, the clinicians should examine the skin over the entire spine for
dimples, sinuses, nevi, or tufts of hair. These may indicate a congenital
anomaly communicating with the subarachnoid space.
Focal neurologic signs

Focal neurologic signs include isolated cranial nerve abnormalities (principally

of cranial nerves III, IV, VI, and VII), which are present in 10-20% of patients.
These result from increased intracranial pressure (ICP) or the presence of
exudates encasing the nerve roots. Focal cerebral signs are present in 1020% of patients and may develop as a result of ischemia from vascular
inflammation and thrombosis.

Papilledema is a rare finding (< 1% of patients) that also indicates increased

ICP, but it is neither sensitive nor specific: it occurs in only one third of
meningitis patients with increased ICP and is present not only in meningitis
but also in brain abscess and other disorders.
Signs of meningeal irritation

For more than 100 years, clinicians have relied on meningeal signs (nuchal
rigidity, Kernig sign, and Brudzinski sign) to evaluate patients with suspected
meningitis and help determine who should undergo a lumbar puncture (LP).
However, a prospective study of 297 adults with suspected meningitis
documented very low sensitivities for these signs: 5% for the Kernig sign, 5%
for the Brudzinski sign, and 30% for nuchal rigidity.[13] Thus, the absence of
the meningeal signs should not defer the performance of the LP.
Systemic and extracranial findings

Systemic findings on physical examination may provide clues to the etiology

of a patients meningitis. Morbilliform rash with pharyngitis and adenopathy

may suggest a viral etiology (eg, Epstein-Barr virus [EBV], cytomegalovirus

[CMV], adenovirus, or HIV). Macules and petechiae that rapidly evolve into
purpura suggest meningococcemia (with or without meningitis). Vesicular
lesions in a dermatomal distribution suggest VZV. Genital vesicles suggest
HSV-2 meningitis.

Sinusitis or otitis suggests direct extension into the meninges, usually with S
pneumoniae or, less often, H influenzae. Rhinorrhea or otorrhea suggests a
cerebrospinal fluid (CSF) leak from a basilar skull fracture, with meningitis
most commonly caused by S pneumoniae.

Hepatosplenomegaly and lymphadenopathy suggest a systemic disease,

including viral (eg, mononucleosislike syndrome in EBV, CMV, and HIV) and
fungal (eg, disseminated histoplasmosis). The presence of a heart murmur
suggests infective endocarditis with secondary bacterial seeding of the
meninges.
Chronic meningitis

It is essential to perform careful general, systemic, and neurologic

examinations, looking especially for the following:

Lymphadenopathy
Papilledema and tuberculomas during funduscopy
Meningismus
Cranial nerve palsies

Tuberculous meningitis

The presentation of chronic tuberculous meningitis may be acute, but the

classic presentation is subacute and spans weeks. Patients generally have a
prodrome consisting of fever of varying degrees, malaise, and intermittent
headaches. Cranial nerve palsies (III, IV, V, VI, and VII) often develop,
suggesting basilar meningeal involvement.

Clinical staging of tuberculous meningitis is based on neurologic status, as

follows:

Stage 1 - No change in mental function, with no deficits and no

hydrocephalus
Stage 2 - Confusion and evidence of neurologic deficit
Stage 3 - Stupor and lethargy

Syphilitic meningitis

The median incubation period before the appearance of symptoms in chronic

syphilitic meningitis is 21 days (range, 3-90 days), during which time
spirochetemia develops. Syphilitic meningitis usually occurs during the
primary or secondary stage of syphilis, complicating 0.3-2.4% of primary
infections during the first 2 years. Its presentation is similar to those of other
types of aseptic meningitis, including headache, nausea, vomiting, and
meningismus.

Meningovascular syphilis occurs later in the course of untreated syphilis, and

the symptoms are dominated by focal syphilitic arteritis (ie, focal neurologic
symptoms associated with signs of meningeal irritation) that spans weeks to
months and results in stroke and irreversible damage if left untreated.
Patients with concomitant HIV infection have an increased risk of accelerated
progression.

Lyme meningitis

Although rare during stage 1 of Lyme disease, central nervous system (CNS)
involvement with meningitis may occur in Lyme diseaseassociated chronic
meningitis and is characterized by the concurrent appearance of erythema
migrans at the site of the tick bite. More commonly, aseptic meningitis
syndrome occurs 2-10 weeks after the erythema migrans rash. This
represents stage 2 of Lyme disease, or the borrelial hematogenous

dissemination stage.

Headache is the most common symptom of Lyme diseaseassociated chronic

meningitis, with photophobia, nausea, and neck stiffness occurring less
frequently. Somnolence, emotional lability, and impaired memory and
concentration may occur. Facial nerve palsy is the most common cranial
nerve deficit. These symptoms of meningitis usually fluctuate and may last
for months if left untreated.

Fungal meningitis

Meningitis from C neoformans usually develops in patients with defective cellmediated immunity (see CNS Cryptococcosis in HIV). It is characterized by
the gradual onset of symptoms, the most common of which is headache.

Coccidioidal meningitis is the most serious form of disseminated

coccidioidomycosis; it usually is fatal if left untreated. These patients may
present with headache, vomiting, and altered mental function associated with
pleocytosis, elevated protein levels, and decreased glucose levels.
Eosinophils may be a prominent finding on CSF analysis.

Patients infected with B dermatitidis may present with an abscess or

fulminant meningitis. Patients infected with H capsulatum may present with
headache, cranial nerve deficits, or changes in mental status months before
diagnosis.
Helminthic eosinophilic meningitis

After ingestion of A cantonensis larvae, which are found in raw or

undercooked mollusks, most patients with symptomatic disease present with
nonspecific and self-limited abdominal pain caused by larval migration into
the bowel wall. On rare occasions, the larvae can migrate into the CNS and
cause eosinophilic meningitis. Although A cantonensis is prevalent in
Southeast Asia and tropical Pacific islands, infestations from this parasitic
nematode have been reported in the United States and the Caribbean.[15]

Aseptic meningitis

In contrast to patients with bacterial meningitis, patients with aseptic

meningitis syndrome usually appear clinically nontoxic, with no vascular
instability. (See Aseptic Meningitis.) In many cases, a cause for meningitis is
not apparent after initial evaluation, and the condition 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.
Complications

Immediate complications of meningitis include the following:

Septic shock, including disseminated intravascular coagulation (DIC)

Coma with loss of protective airway reflexes
Seizures, which occur in 30-40% of children and 20-30% of adults
Cerebral edema
Septic arthritis
Pericardial effusion
Hemolytic anemia ( H influenzae)

Delayed complications include the following:

Decreased hearing or deafness

Other cranial nerve dysfunctions
Multiple seizures
Focal paralysis
Subdural effusions
Hydrocephalus

Intellectual deficits
Ataxia
Blindness
Waterhouse-Friderichsen syndrome
Peripheral gangrene

Cerebral edema, cranial nerve palsy, and cerebral infarction

Some degree of cerebral edema is common with bacterial meningitis. This

complication is an important cause of death.

Cranial nerve palsies and the effects of impaired cerebral blood flow, such as
cerebral infarction, are caused by increased ICP. In certain cases, repeated LP
or the insertion of a ventricular drain may be necessary to relieve the effects
of this increase.

In cerebral infarction, endothelial cells swell, proliferate, and crowd into the
lumen of the blood vessel, and inflammatory cells infiltrate the blood vessel
wall. Foci of necrosis develop in the arterial and venous walls and induce
arterial and venous thrombosis. Venous thrombosis is more frequent than
arterial thrombosis, but arterial and venous cerebral infarctions can be seen
in 30% of patients.
Brain parenchymal damage

Brain parenchymal damage is the most important and feared complication of

bacterial meningitis. It can lead to the following disorders:

Sensory and motor deficits

Cerebral palsy
Learning disabilities

Mental retardation
Cortical blindness
Seizures

Cerebritis

Inflammation often extends along the perivascular (Virchow-Robin) spaces

into the underlying brain parenchyma. Commonly, cerebritis results from
direct spread of infection, either from otorhinologic infection or meningitis
(including retrograde septic thrombophlebitis) or from hematogenous spread
from an extracranial focus of infection. Parenchymal involvement, with
edema and mass effect, may be localized or diffuse. Cerebritis can evolve to
frank abscess formation in the gray matterwhite matter junction.
Subdural effusion

In children with meningitis who are younger than 1 year, 20-50% of cases are
complicated by sterile subdural effusions. Most of these effusions are
transient and small to moderate in size. About 2% of them are infected
secondarily and become subdural empyemas. In the empyema, infection and
necrosis of the arachnoid membrane permit formation of a subdural
collection.

In addition to young age, risk factors include rapid onset of illness, low
peripheral white blood cell (WBC) count, and high CSF protein level. Seizures
occur more commonly during the acute course of the disease, though longterm sequelae of promptly treated subdural effusions are similar to those of
uncomplicated meningitis.
Ventriculitis

Ventriculitis may occur through the involvement of the ependymal lining of

the ventricles. This complication occurs in 30% of patients overall but is
especially common in neonates, with an incidence as high as 92%. The
organisms enter the ventricles via the choroid plexuses. As a result of
reduced CSF flow, and possibly of reduced secretion of CSF by the choroid

plexus, the infective organisms remain in the ventricles and multiply.

Ventriculomegaly

Ventriculomegaly can occur early or late in the course of meningitis and is

usually transient and mild to moderate in severity. As a result of the
subarachnoid inflammatory exudate, CSF pathways may become obstructed,
leading to hydrocephalus. Exudates in the foramina of Luschka and Magendie
can cause noncommunicating hydrocephalus, whereas exudates that
accumulate in the basilar cisterns or over the cerebral convexity can develop
into communicating hydrocephalus.
Differential Diagnoses
Read more about Meningitis on Medscape
Related Reference Topics

Aseptic Meningitis
Tuberculous Meningitis
Neonatal Meningitis

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