Meningitis

Meningits
This is defined as the inflammation of the protective
membranes (meninges) covering the brain and spinal
cord.
A bacterial or viral infection of the fluid around the
brain and spinal cord usually results in inflammation
and swelling of the meninges.
This differs from an encephalitis, which is
inflammation of the brain parenchyma, presenting as
diffuse and/or focal neurological dysfunction.
Aetiology
Bacterial cause
Common cause: Neisseria meningitidis
(in children 1 month to 12 months)
Streptococcus pneumoniae and Haemophilus influenzae type b.
Less common pathogens such as Pseudomonas aeruginosa,
Staphylococcus aureus, coagulase negative staphylococci,
Salmonella spp., and Listeria monocytogenes.
Neonates: GBS and E. coli are common causes.
Tuberculous causes of meningitis are becoming less common.

(Due to alterations in host defence, anatomic defects or immune

deficits)
Neisseria meningitidis
Gram negative, non-motile, non-sporing diplococcus
Contains capsular antigens ( A, B, C, X, Y, W135)
responsible for immune complex formation.
Produces endotoxin responsible for circulatory
collapse and DIC.
Incubation period: 3-4 days (2-10 days on average)
Viral cause
Viral meningitis comprises most aseptic meningitis
syndromes. The viral agents of aseptic meningitis
include:
Enterovirus (polio virus, Echovirus, Coxsackievirus)
Herpes virus (HSV 1/2, Varicella z., EBV)
Paramyxovirus (Mumps, measles)
Togavirus (Rubella)
Rhabdovirus (Rabies)
Retrovirus (HIV)
Fungal cause
It is rare in healthy people, but is a higher risk in those
who have AIDS and other forms of immunodeficiency
or immunosuppression.
The most common agents:
Cryptococcus neoformans
Candida sp.
Histoplasma capsulatum
Acute Bacterial Meningitis
Acute Bacterial Meningitis
One of the most potentially serious infections
occuring in infants and older children.
The incidence of bacterial meningitis is sufficiently
high in febrile infants.
Epidemiology
Major risk factor for meningitis- lack of immunity to
specific pathogens associated with young age.
Additional risks:
Recent colonization with pathogenic bacteria from
close contact (household, daycare centres) with
individuals having invasive disease caused by N.
Meningitidis, and H. Influenzae type b, crowding,
poverty
Mode of transmission
Probably person-to-person contact trough respiratory
tract secretions or droplets.
Defects of complement (C5-C8) have been associated
with recurrent meningococcal infection.
Splenic dysfunction (sickle cell anaemia) and asplenia
(due to trauma, or congenital defect) is associated with
an increased risk of pneumococcal, H. influenzae type
b, and rarely meningococcal sepsis and meningitis.
Pathogenesis
Bacterial meningitis most commonly results from
haematogenous dissemination of microorganisms
from a distant site of infection; bacteremia usually
precedes meningitis or occurs concomitantly.
Usual source of bacteremia: bacterial colonisation of
the nasopharynx with potentially pathogenic
miroorganisms.
Clinical manifestations
Common presentation is:
Sudden onset
Rapidly progressive manifestations of shock
Purpura
Disseminated intravascular coagulation (DIC),
reduced levels of conciousness often resulting in
progression to coma or death in 24 hrs.
More often meningitis is preceded by several days of
fever accompanied by upper respiratory tract, or
gastrointestinal symptoms, followed my nonspecific
signs of CNS infection such as increasing lethargy and
irritability.
The signs and symptoms of meningitis are related to
the nonspecific findings associated with a systemic
infection and to manifestations of meningeal irritation.

Nonspecific signs include:

Fever
Anorexia
Poor feeding
Headache
Symptoms of upper respiratory tract infection
Myalgias
Arthralgias
Tachycardia
Hypotension
Various cutaneous signs, such as petechiae, purpura or
an erythematous macular rash
Meningeal irritation is manifested as:
Nuchal rigidity- impaired neck flexion resulting from
muscle spasm (not actual rigidity) of the extensor
muscles of the neck
Back pain
Kernig sign (flexion of the hip at 90 degrees with
subsequent pain with extension of the leg)
Brudzinski sign (involuntary flexion of the knees and
hips after passive flexion of the neck while supine)
Alterations of mental status are common among
patients with meningitis and may be a consequence of
increased ICP, cerebritis or hypotension
Manifestations include irritability, lethargy, stupor,
obtundation and coma.
Diagnosis
1. CSF study:
Confirmed by analysis of the CSF, which typically
reveals microorganisms on gram stain and culture
Lumbar puncture(LP) is done for CSF collection.

Contraindications to LP:
Evidence of raised ICP, HTN
In patients in whom positioning for the LP would
compromise cardiopulmonary function
Infection of skin overlying site of LP.
2. Blood cultures:
Blood cultures reveal the responsible bacteria in 80-
90% of cases of meningitis.
Elevations of C- reactive protein, erythrocyte
sedimentation rate and procalcitonin have been used
to differentiate bacterial (usually elevated) from viral
causes of meningitis.
3. CT scan
This is of limited use in acute bacterial meningitis.
CT in cerebral oedema may show slit-like lateral
ventricle and areas of low attenuation.
Role of Neuroimaging
Neuroimaging (with computed tomography [CT] or
magnetic resonance imaging [MRI]) may be indicated
during the course of treatment for acute bacterial
meningitis in the following circumstances :
●Focal neurologic signs, increasing head
circumference, or prolonged obtundation, irritability,
or seizures (>72 hours after the start of treatment).
●Persistently positive CSF cultures despite appropriate
antibiotic therapy.
●Persistent elevation of CSF neutrophils at the
completion of standard duration of therapy.
●Recurrent meningitis (to evaluate the possibility of a
communication between the nasal passage or ear and
the meninges). Sectional (2 mm) coronal cranial CT
has been reported to be a relatively easy, noninvasive
method of delineating anatomic abnormalities in
children with recurrent meningitis 
Differential Diagnosis
Acute viral meningoencephalitis ( can be confused
with bacterial meningitis)
Treatment
A child with rapidly progressive disease of less than 24
hr duration, in the absence of increased ICP, should
receive antibiotics as soon as possible after and LP is
performed.
If there are signs of increased ICP or focal neurological
findings, antibiotics should not be given without
performing an LP ands before obtaining a CT scan.
Immediate management of children with suspected bacterial
meningitis includes :
Assurance of adequate ventilation and cardiac perfusion
Initiation of hemodynamic monitoring and support at the same
time as obtaining appropriate laboratory studies (blood and
cerebrospinal fluid [CSF])
Establishment of venous access
Administration of fluids as necessary to treat septic shock, if
present
Administration of dexamethasone if warranted after assessment
of potential benefits and risks before or immediately after the
first dose of antimicrobial therapy
Administration of the first dose of empiric antibiotics
(vancomycin [15 mg/kg] plus either ceftriaxone
 [50 mg/kg] or cefotaxime[if available, 100 mg/kg]) 
Administration of glucose (0.25 g/kg) for documented
hypoglycemia (serum glucose concentration less than
40 mg/dL [2.2 mmol/L]) 
Treatment of acidosis and coagulopathy if present
Treatment of seizures if present.
Initial Empirical therapy
Vancomycin (60 mg/kg/24 hr, given every 6 hrs)
Because of the efficacy of the third generation
cephalosporins in the therapy of meningitis caused by
sensitive S. pneumoniae, N. Meningitidis and HIB:
Cefotaxime (300 mg/kg/24 hr, given every 6 hrs) OR
Ceftriaxone ( 100 mg/kg/24 hr, administered once per
day or 5o mg/kg/dose, given every 12 hrs)
Patients allergic to beta-lactam antibiotics and > 1 mo
of age can be treated with Chloramphenicol, 100
mg/kg/24 hr, given every 6 hrs.
Another option to beta-lactam antibiotics is a
combination of Vancomycin and Rifampin.
Duration of therapy
S. pneumoniae – 10 to 14 days
●N. meningitidis – 5 to 7 days
●H. influenzae type b (Hib) – 7 to 10 days
●L. monocytogenes – 14 to 21 days
●S. aureus – at least 2 weeks
●Gram-negative bacilli – 3 weeks or a minimum of 2
weeks beyond the first sterile cerebrospinal fluid (CSF)
culture, whichever is longer
Corticosteroids
Use of IV Dexamethasone
0.15 mg/kg/dose is given every 6 hrs for 2 days, in the
treatment of children older than 6 weeks with acute bacterial
meningitis caused by H. Influenzae type b, and pneumococcus
(new studies showing benefit of use for S. pneumoniae).
Dexamethasone should be initiated shortly before (15-20
mins) or at the same time as the first dose of antibiotics.
 
There is no proven benefit from dexamethasone therapy for
adult patients with meningitis due to other pathogens, mostly
meningococcus.
Among children with meningitis, corticosteroid
recipients have a shorter duration of fever
(inflammation reduced), lower CSF protein and lactate
levels, and a reduction in sensorineural hearing loss
(result of cochlear infection).
Complications
During the treatment of meningitis, acute CNS
complications include seizures, increased ICP, cranial
nerve palsies and stroke.
Subdural effusions are especially common in infants.
Prevention
Vaccination and antibiotic prophylaxis of susceptible at
risk contacts represent the 2 available means of reducing
the likelihood of bacterial meningitis.

Neisseria meningitidis :
Two quadrivalent (A, C, Y, W-135), conjugated vaccines
(MCV-4; Menactra and Menveo) are licensed by the FDA.
 Menactra is licensed for use in infants older than 9 mo
of age, and Menveo for use in children older than 2 yr of
age
Haemophilus influenzae Type B :
All children should be immunized with H. influenzae
type b conjugate vaccine beginning at 2 mo of age.
Streptococcus pneumoniae.
Routine administration of conjugate vaccine against S.
pneumoniae is recommended for children younger
than 5 yr of age. The initial dose is given at about 2 mo
of age.
Chemoprophylaxis for N. Meningitidis
Rifampin-Children aged <1 month5 mg/kg every 12
hours for two days
Children aged ≥1 month10 mg/kg every 12 hours for
two days
Adults-600 mg every 12 hours for two days
Ciprofloxacin –Adults: 500 mg Single dose
Ceftriaxone- Children age :<15 years125 mg Single IM
dose
Ceftriaxone-Adults: 250 mg Single IM dose
Prognosis
 Appropriate antibiotic therapy and supportive care have
reduced the mortality of bacterial meningitis after the neonatal
period to <10%.
The highest mortality rates are observed with pneumococcal
meningitis.
 Sensorineural hearing loss is the most common sequela of
bacterial meningitis and, usually, is already present at the time
of initial presentation.
It is a result of cochlear infection and occurs in as many as 30%
of patients with pneumococcal meningitis, 10% with
meningococcal, and 5-20% of those with H. influenzae type b
meningitis
Malnutrition is associated with increased morbidity
and mortality.
Hearing evaluation should be performed at the time
of or shortly after discharge from the hospital .
Young children who have been treated for meningitis
are at risk for developmental delay. Developmental
surveillance should continue throughout childhood. 
References
Nelson Textbook of Pediatrics, twentieth edition
Illustrated Textbook of Pediatrics 
https://www.uptodate.com/contents/bacterial-
meningitis-in-children-older-than-one-month-
treatment-and-prognosis?
search=meningitis&source=search_result&selectedTitl
e=5~150&usage_type=default&display_rank=5