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Year : 2018  |  Volume : 15  |  Issue : 1  |  Page : 1-4

Acute bacterial meningitis in nigerian children beyond neonatal period: A review

1 Department of Paediatrics, ABU/ABUTH, Zaria, Nigeria
2 Department of Paediatrics, BUK/AKTH, Kano, Nigeria

Date of Web Publication23-Mar-2018

Correspondence Address:
Dr. Sani M Mado
Department of Paediatrics, ABU/ABUTH, Zaria
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/njbcs.njbcs_26_17

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Childhood acute bacterial meningitis remains a significant cause of morbidity and mortality especially in developing countries. The pattern of both sporadic and epidemic cases of meningitis has been known to change from place to place even in the same country or geographical region. Streptococcus pneumoniae, Haemophilus influenzae type b, and Neisseria meningitidis are the predominant causes of community-acquired bacterial meningitis beyond the neonatal period.

Keywords: ABM, children, Nigeria

How to cite this article:
Mado SM, Aliyu I. Acute bacterial meningitis in nigerian children beyond neonatal period: A review. Niger J Basic Clin Sci 2018;15:1-4

How to cite this URL:
Mado SM, Aliyu I. Acute bacterial meningitis in nigerian children beyond neonatal period: A review. Niger J Basic Clin Sci [serial online] 2018 [cited 2021 Jun 16];15:1-4. Available from: https://www.njbcs.net/text.asp?2018/15/1/1/228361

  Introduction Top

Acute bacterial meningitis (ABM) is an acute purulent infection of the cranial and spinal leptomeninges.[1] Despite advances in the medical treatment it remains a significant cause of morbidity and mortality especially in poor countries of the world where the problem is compounded by increasing level of poverty, overcrowding, low immunization coverage, and late presentation.[1] The causative organisms of meningitis may vary from place to place even in the same country or geographical region. Periodic validation of the changing pattern of the causative agents of ABM and their continuing sensitivity to antimicrobials in use is necessary.

  Etiology Top

Streptococcus pneumoniae, Haemophilus influenzae type b (Hib), and  Neisseria More Details meningitidis are the most common causes of community-acquired bacterial meningitis beyond the neonatal period.[2] Alteration of host defenses resulting from anatomic defects or immune deficits increase the risk of meningitis from the less common pathogens such as Pseudomonas aeruginosa, Staphylococcus aureus, S. epidermidis, Listeria monocytogenes, and  Salmonella More Details.[2]

S. pneumoniae is a Gram-positive encapsulated coccus (round shaped) organism more often found in the upper respiratory tract. There are more than 90 serotypes of S. pneumoniae but only smooth encapsulated strains cause disease in humans. Predominant pneumococcal serotypes causing invasive disease in temperate climates of the developed countries include type 4, 6B, 9V, 14, 18C, 19F, and 23F while types 1, 2, 3, 4, 5, 6, 8, 9, 10, 12, 14, 18, 19, 23, 25, 45, and 46 are the predominant serotypes in the West African sub-region.[1] In a very early study done in Zaria, Nigeria about 3 decades ago serotypes 1 and 3 were the predominant pneumococcal strains causing meningitis in children accounting for more than 70% of cases and was closely followed by types 2, 12, 5, 23, 25, 45, and 46.[3] In a more recent study on pneumococcal meningitis in Ibadan, the predominant strains were types 4, 5, and 19F.[4]H. influenzae is a fastidious, nonmotile Gram-negative coccobacillus consisting of two groups namely encapsulated and unencapsulated types. Based on the composition of the capsular polysaccharides encapsulated H. influenzae are divided into six antigenically distinct serologic types a, b, c, d, e, and f.[5] Encapsulated H. influenzae are responsible for almost all invasive disease and more than 90% are due to Hib.[5] Before the advent of conjugate Hib vaccine H. influenzae is responsible for bacterial meningitis in children between the ages of 2 months and 5 years worldwide. With inclusion of Hib vaccine into our routine immunization program, it is expected that the burden of Hib cases of bacterial meningitis will significantly reduce in Nigerian children under the age of 5 years.

Currently, N. meningitidis have been separated by seroagglutination into 13 serogroups.[6] The serogroups include A, B, C, D, 29E, X, Y, Z, and W135 which were the initial nine groups. To the initial nine groups four more are added namely H, I, K, and L. Groups B, C, Y, and W135 are the predominant serogroups associated with invasive disease in the United States of America and other developed countries whereas the group A and C strain account for epidemic disease in many other countries especially in sub-Saharan Africa.[1]

  Epidemiology Top

The exact incidence of ABM is not known but it was estimated that each year about 1.2 million people contract bacterial meningitis and 135,000 die from the disease.[1] The risk of a child developing meningitis by 5 years of age is between 1:400 and 1:2000.[1] In Nigeria, the prevalence of ABM in hospitalized children varies between studies done very early from 2.8% in Sagamu [7] through 3.5% in Maiduguri [8] and more recently 6.9% in Zaria.[9] In an extensive review by Peltola,[10] on the burden of meningitis and other severe bacterial infections of children in Africa, the annual incidence for all bacterial meningitis in the general population varied from 18 to 50 cases per 100,000 individuals in Senegal to 13.5 cases per 100,000 individuals in Swaziland.

The pattern of causative organisms of both sporadic and epidemic cases of meningitis has been known to change. In a study [11] from Enugu Nigeria, H. influenzae was the predominant cause of meningitis and closely followed by S. pneumoniae. However, later studies from other centers [9],[12],[13] showed that S. pneumoniae was the predominant cause of ABM replacing H. influenzae as the leading cause. The exact reason for the changing epidemiology is not known as Hib vaccine was not introduced in to the Nigerian routine immunization programme at the time of the later studies [9],[12],[13] as was observed in the developed countries of the world after introduction of the Hib vaccine. Large scale outbreaks of meningococcal meningitis occur every 5 to 10 years with varied severity from time to time. Major epidemiological changes of epidemic meningococcal meningitis have been observed in the last 3 decades as the intervals between epidemics have become shorter and more irregular.[1] Most epidemics in Nigeria [14],[15],[16],[17] were due to serogroups A but serogroups C have been documented in the past as well as the most recent epidemics of the year 2016–2017 that affected 24 states mostly in Northern Nigeria. A total of 14,513 cases were reported with a case fatality rate of 8.0% and serogroup C was the predominant (75.4%) cause of this outbreak. The states affected mostly were Zamfara, Sokoto, and Katsina which accounted for almost 89% of the total cases reported.[18]

Risk factors

Young age is a major risk factor for acquiring meningitis due to lack of immunity to specific pathogens. Specific host defense defects due to altered immunoglobulin production in response to encapsulated pathogens may be responsible for the increased risk of bacterial meningitis in some individuals. Individual with blunted immunologic response to vaccine, for example children with human immunodeficiency virus (HIV) infection, are at risk for Hib meningitis.[19] Opsonization defects such as seen in sickle anemia subjects increase the risk of pneumococcal meningitis. Terminal complement (C5-C9), properdin as well as acquired complements deficiencies predispose an individual child to recurrent meningococcal meningitis. Presence of cerebrospinal fluid (CSF) rhinorrhea (leakage of CSF from the nostrils) and otorrhea (leakage of CSF from the ears resulting from basilar skull fracture, erosion of the base of the skull by a malignant tumor, or presence of congenital meningoencephalocoeles also predispose the child to an increased risk of pneumococcal and Hib meningitis. Meningitis caused by Proteus, Pseudomonas, and Staphylococcus species is seen in individual with other congenital defects such as spinal dermoid cyst and ruptured meningomyelocoele.[19]

Pathogenesis of meningitis

Most of the common bacterial agents causing meningitis such as S. pneumoniae, N. meningitidis, and H. influenzae have the ability to colonize the host's mucosal epithelium especially of the nasopharynx, invade the intravascular space, cross the blood-brain-barrier (BBB) and finally enter into the subarachnoid space.[20] The micro-organisms penetrate the mucous sheet covering the nasopharyngeal epithelial cells using secretory immunoglobulin A (IgA) inhibitors and subsequently attach themselves to the nasopharyngeal epithelial cells.

The organisms enter the circulation through an endocytotic process in a phagocytic vacuole in the case of N. meningitidis while others are thought to breach the mucosa directly to reach the circulation.[19]H. influenzae enters the blood stream through the epithelium by opening the apical tight intercellular junctions.[5]

The capsular polyribose phosphate appears to be important in the virulence of the disease process. The sequelae of H. influenzae meningitis may be inversely related to the concentration of polyribose phosphate within the CSF and serum.[19],[20] Morbidity apparently correlates with the magnitude and duration of exposure to capsular polyribose phosphate.[19],[20] Antipolyribosephosphate antibodies to correlate with protection against the disease.[19],[20]

The capsular products of  Neisseria meningitidis More Details (capsular sialic acid) prevent binding of complement factor B to C3b and subsequent activation of the alternative pathway,[19] while C3b binds to factor B on the capsular surface inefficiently in case of Streptococcus pneumoniae. The polyribose phosphate capsule of Hib is incapable of serving as an acceptor for C3.[5]

The bacteria gain entry into the CSF through the choroid plexus of the lateral ventricles and the meninges and then circulate to the extra cerebral CSF and subarachnoid space.[19] After gaining entry into the CSF, there is rapid bacterial proliferation which is facilitated by the immunologically defective nature of the CSF. Large quantities of bacterial cell wall fragments are produced. The presence of endotoxin of Gram-negative bacteria and teichoic acid and peptidoglycan of Gram-positive bacteria stimulate local production of tumor necrosis factor, interlukin-1, prostaglandin E, and other cytokine inflammatory mediators.[19] The cytokines also activate neutrophils in the CSF to undergo degranulation thereby releasing proteolytic enzymes, cationic proteins, reactive oxygen species, and vasoactive lipid autocoids which further impair the blood-brain barrier.[19],[20] The overall effect of cytokines is initiation of intense inflammatory response causing local cell damage, damage to blood vessels, and increased vascular permeability.[1] The pathophysiologic consequences of cytokines induced damage include cerebral edema, vascular thrombosis, and focal inflammatory processes. Cerebral edema leads to raised intracranial pressure manifesting with headache, vomiting, or bulging anterior fontanelle in infants. The syndrome of inappropriate secretion of antidiuretic hormone causes water retention thereby worsening the cerebral edema.[19],[20] Papilledema when present highly suggests an underlying complication such as subdural effusion or brain abscess. The increased vascular permeability allows leakage of albumin into the CSF thereby raising the CSF protein content. The utilization of CSF glucose by the polymorphs and bacteria lead to low CSF glucose. The pleocytosis arise mainly from activation of adhesion-promoting receptors on cerebral vascular endothelial cells by cytokines thereby attracting neutrophils.[19]

Inflammation of the sheath of the meninges around the spinal nerve and nerve roots produces meningeal signs characterized by neck stiffness, Kernig's, and Brudzinski's signs. Focal inflammatory processes can lead to cerebritis, ventriculitis, and hydrocephalus. Focal inflammation around the cranial nerves causes craniopathies. The most common cranial nerves involved are the oculomotor, abducens, facial, and vestibule-cochlear nerves. Focal neurologic signs commonly result from vascular occlusion while focal or generalized seizures are usually due to cerebritis, infarction, or electrolyte disturbances.[19],[20]

  Clinical Features Top

The symptoms and signs of meningitis are variable and sometimes depend on the age of the patient.[21] Fever, change in affect, high pitch cry, listlessness, irritability, refusal to feed, vomiting, and temperature instability are frequent nonspecific manifestations of bacterial meningitis in young infants.[19] Meningeal irritation signs may be absent in the majority of infants and bulging fontanelle is a late feature.[19],[20] Signs of meningeal irritation is manifested by complaints of backache, nuchal rigidity (resistance to neck flection), Kernig's sign (difficulty and pain while extending the leg at knee when the thigh is flexed at the hip at 90o while patient is lying supine), and Brudzinski's sign (passive flexion of the neck is followed by spontaneous flexion of the knees and hips). Petechial and purpuric eruptions are usually indicative of meningococcemia, although they can be present in H. influenzae meningitis and are rarely seen with pneumococcal meningitis.[19] The rapid development of hemorrhagic eruptions with sudden onset and progressive manifestations of shock is almost pathognomonic of meningococcemia.[21] Affectation of the joints suggests infection with N. meningitidis or H. influenzae and can arise early (suppurative arthritis) or late (reactive arthritis) in the illness.[19] In a neutropenic patients, symptoms and signs may be subtle because of the impaired ability to mount a subarachnoid space inflammatory response. Therefore, in these patients, an altered mental status in the presence of fever warrants CSF examination to exclude meningitis.


Cerebrospinal fluid culture is the gold standard in the laboratory diagnosis of ABM but results are available only after 1–2 days.[21] The results of CSF Gram stain and culture can also be altered by prior use of antibiotics,[21] a common problem in developing countries.[1] Rapid immunologic tests have been developed to detect bacterial polysaccharide antigens in CSF and these tests are positive in about 80% of bacterial meningitis but sensitivity differs between tests. These tests include latex particle agglutination (LPA), counter immunoelectrophoresis (CIE), enzyme-linked immunosorbent assay (ELISA), and monoclonal antibody ELISA (Mab ELISA).[1] Nucleic acid amplification (NAA) is another promising, rapid, and specific test for the detection of all pathogens in the CSF but the test is very expensive and only available in research laboratories.[21]

Treatment of meningitis

The prompt initiation of appropriate empirical antimicrobial is an important determinant of the outcome of meningitis. The empirical antibiotics chosen should be effective against the probable pathogens and be able to attain adequate bactericidal activity in the CSF. The recommended treatment for bacterial meningitis in children beyond the neonatal period in developing countries is chloramphenicol (100 mg/kg/day given in four divided doses intravenously 6 hourly) combined with IV benzylpenicillin (400,000 IU/kg/day given in four divided doses 6 hourly) or ampicillin 200–300 mg/kg/day and chloramphenicol 100 mg/kg/day in four divided doses 6 hourly.[1] The advent of increasing resistance to ampicillin, chloramphenicol, and penicillin, a third generation cephalosporin such as ceftriaxone or cefotaxime is now recommended as part of initial empiric treatment of ABM together with vancomycin.[1],[19]

Supportive and adjunctive treatment of meningitis

Adequate oxygenation, prevention of hypoglycemia and hyponatremia, anticonvulsant treatment, and measures designed to decrease intracranial hypertension and to prevent fluctuation in cerebral blood flow are important in the management of patients with bacterial meningitis.[21]

Fluid restriction is no longer recommended unless there is an evidence of inappropriate antidiuretic hormone secretion for which 50–60% of normal maintenance is given until the serum sodium approaches normal. Many of the deleterious effects of meningitis are due to the inflammatory response evoked by bacterial lysis and steroids have been used to try to improve outcome by reducing this effect. A recent extensive review about the use of corticosteroids in the bacterial meningitis found that the use of steroids did not significantly reduce the mortality rates, but however significantly lower the rates of severe hearing loss and neurological sequelae.[22] The use of concentrates containing activated protein C (aPC) could potentially be useful in children with systemic meningococcemia and purpura fulminans.[1]

Outcome of bacterial meningitis

Childhood bacterial meningitis is responsible for much morbidity in children throughout the world, especially in developing countries.[23] With improved antibiotic therapy the mortality of children from bacterial meningitis has decreased in the last 2 decades. The overall mortality rate from childhood bacterial meningitis is still high in Nigerian children as rate of 12.1% was recently documented.[9] The highest mortality rates are observed with pneumococcal meningitis as shown in a study from Ibadan were eight of the nine (80.9%) children died. The most common neurologic sequelae include hearing loss, mental retardation, seizures, delay in acquisition of language, and visual and behavioral problems.[19]

Prevention of bacterial meningitis

Chemoprophylaxis is recommended for all close contacts of patients with meningococcal and Hib meningitis.[1],[5],[19] The advent of the conjugative vaccines during the last decade and a half is a remarkable achievement. In contrast to the purified polysaccharide vaccines the conjugate vaccines produce a T-dependent response and result in the development of an immunological memory leading to clinical protection even in children less than 2-year-old.[1],[19] Meningococcal quadrivalent vaccine against serogroups A, C, Y, and W135 is recommend for high-risk children older than 2 year. The vaccine may also be used during epidemics of meningococcal disease. Vaccination with groups A and C vaccines has been effective in controlling epidemic of cerebrospinal meningitis when undertaken very early.[2] Vaccination is also successful in preventing secondary infections in household contacts when given on the day after admission of the index case to hospital. High-risk patients aged 2 year or older should receive 23-valent pneumococcal vaccine.[19] The success achieved by Hib vaccine has stimulated the development of a pneumococcal heptavalent conjugate vaccine which has shown a high level of protection against invasive pneumococcal disease.[24]

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Conflicts of interest

There are no conflicts of interest.

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