Bacterial meningitis

Introduction:

It’s inflammation of the meninges affecting the pia, arachnoid, and

subarachnoid space that happens in response to bacteria. It’s a medical emergency
that requires immediate diagnosis and treatment. the untreated disease is virtually
100% lethal. Even after progress in medical care including vaccines and
antibiotics, meningitis still showed a high rate of morbidity and mortality,
especially in high-risk patients.

Therefore; proper and early diagnosis and treatment are critical for
recovery, and this will discuss below.
 Epidemiology:

Meningitis still has high morbidity and mortality in spite of the

introduction and widespread use of antibiotics and other advances in medical care.
(Mace, 2008)

The incidence of bacterial meningitis in Western countries (Finland,

Netherlands, and the United States) gradually declined by 3–4% per year to 0.7–
0.9 per 100 000 per year in the past 10–20 years. In African countries (Burkina
Faso and Malawi), incidence rates are still substantially higher at 10–40 per
100 000 persons per year. The introduction of pneumococcal conjugate vaccines
has not consistently decreased overall pneumococcal meningitis incidence because
of serotype replacement. (Brouwer & van de Beek, 2018)

Etiology:

1. Neisseria meningitidis:

Previously, it was the third most common cause of bacterial meningitis

but now it has moved to second place behind S. Pneumoniae and is common
among adolescents and young adults.

Properties:
 Diplococci, gram-negative "kidney-bean." Positive Oxidase. The large
capsule made of polysaccharides. One of three classic encapsulated pyogenic
bacteria (the other two are the Streptococcus pneumoniae and H. influenzae).

Prevention:
The vaccines contain the polysaccharide capsule as the immunogen
against groups A, C, Y, and W-135 meningococci, and Factor H binding protein
against group B meningococci. There are two forms of the polysaccharide vaccine:
the conjugate vaccine contains the polysaccharides coupled with a carrier protein
such as diphtheria toxoid and the non-conjugate vaccine contains only the
polysaccharides. Rifampin or ciprofloxacin administered to close contacts to
reduce the oropharyngeal carriage.

2. Streptococcus pneumoniae:

Overall, S. pneumoniae is the most common cause of bacterial

meningitis. Streptococcus agalactiae (group B Streptococcus) is however
predominate in neonates.

Properties:
Diplococci, gram-positive. α-Hemolytic colonies. Negative catalase-.
Optochin inhibits growth. Colonies are bile-soluble. The prominent capsule made
of polysaccharides.

Prevention:
There are 2 vaccines available. The one used in adults contains capsular
polysaccharide of the 23 serotypes that most usually cause bacteremia. The other,
which is mainly used in children younger than 2 years old, contains 13 serotypes of
capsular polysaccharide coupled with a carrier protein (diphtheria toxoid). Oral
penicillin is used in children who are immunocompromised.

3. Haemophilus influenzae:

Previously, H influenzae was the most common cause of bacterial

meningitis.

Features:
Small gram-negative rods. Requires growth factors V (NAD) and X
(hemin). There are six types of capsular polysaccharides, type b is responsible for
95% of invasive disease. Polyribitol phosphate is capsule type b.

Prevention:
Vaccine that contains the type b capsular polysaccharide conjugated with
diphtheria toxoid or other protein is administrated between the ages of 2 and 18
months. Close contact was given rifampin to prevent meningitis.

All organisms above are transmitted by respiratory droplets; it’s a habitat in

the upper respiratory tract.

4. Other organisms:
 Listeria monocytogenes is reasonably common in the very young, the
very old, and in immunocompromised patients. Less common pathogens include
Borrelia burgdorferi (Lyme disease) and Treponema pallidum (syphilis).

Pathophysiology:

The bacteria require access to the meninges. Entry mechanisms are

various. Bacteremia may cause bacteria to cross the blood-brain barrier. Only
certain bacteria can achieve this, most notably N. Meningitidis and S.
Pneumoniae. There may also be a direct extension of the otitis media or sinusitis
into the CNS. Dural defects, either congenital or acquired, facilitate bacteria to
enter the CNS. Neurosurgical manipulation of the meninges may result in
nosocomial bacterial meningitis. Meninges become inflamed when bacteria invade
into subarachnoid space. The breakdown of the blood-brain barrier occurs related
to infection and inflammatory response. This induces cerebral edema, rises
intracranial pressure, and reduces the flow of cerebral blood, resulting in altered
mental status, convulsions, and focal neurological deficits.

Clinical Manifestations:

Initial symptoms include the classic triad of headache, fever, and

neck stiffness. Symptoms can progress to convulsions, vomiting, photophobia, and
focal neurological deficits if untreated. Different bacteria can show different rates
of clinical progression, ranging from the sudden onset and rapid progression to the
subacute or chronic onset and slow progression. Infection with N. meningitidis can
be associated with meningococcemia and lead to petechial rash and purpura
fulminans. Signs are nuchal rigidity or positive signs of Kernig or Brudzinski. The
lack of these does not rule out the disease.

Investigations:

1. lumbar puncture:

Cerebrospinal fluid (CSF) analysis and culture remain the definitive

method for the diagnosis of meningitis. It will help in differentiating the causative
organism; CSF in bacterial meningitis is cloudy due to increased cell count (> 1000
x 106 cells/L) with neutrophils, elevated protein concentration (> 150mg/dl), and
low glucose concentration (<40mg/dl).

Gram stain of CSF allows identification of the organism in 60-90% of

cases, and culture is positive in 70-85%.

2. Cranial computed tomography (CT):

The main indication in meningitis is when the diagnosis is uncertain and

other possible causes of meningism are being considered, for example, if
complications of meningitis are suspected, e.g. cerebral abscess. (El Bashir, 2003)
Treatment:

Empirical therapy must include drugs with excellent CSF penetration, are
bactericidal, and are effective against the most common pathogenic organisms.
Cefotaxime, or ceftriaxone, plus vancomycin are a common empirical drug for
adults and older children. If Listeria is the cause, then ampicillin should be added.
Empirical therapy for neonatal bacterial meningitis includes ampicillin with or
without gentamicin, plus either ceftriaxone or cefotaxime. Infection with the HZV
and HSV is treated with acyclovir.

Conclusion:

Bacterial meningitis is a medical emergency requiring immediate

diagnosis and
immediate treatment. S. pneumoniae and N. meningitidis are the most common
and most aggressive pathogens of meningitis. Emerging antibiotic resistance is an
upcoming challenge. (Hoffman & Weber, 2009)

The critical step of management continues to be an early diagnosis with

the administration of appropriate antibiotics.