The Journal of Maternal-Fetal & Neonatal Medicine

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Neonatal meningococcal disease: an update

Dimitrios Filippakis, Despoina Gkentzi, Gabriel Dimitriou & Ageliki Karatza

To cite this article: Dimitrios Filippakis, Despoina Gkentzi, Gabriel Dimitriou & Ageliki Karatza
(2022) Neonatal meningococcal disease: an update, The Journal of Maternal-Fetal & Neonatal
Medicine, 35:21, 4190-4195, DOI: 10.1080/14767058.2020.1849092

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THE JOURNAL OF MATERNAL-FETAL & NEONATAL MEDICINE
2022, VOL. 35, NO. 21, 4190–4195
https://doi.org/10.1080/14767058.2020.1849092

REVIEW ARTICLE

Neonatal meningococcal disease: an update

Dimitrios Filippakis
, Despoina Gkentzi
, Gabriel Dimitriou and Ageliki Karatza
Department of Paediatrics, Patras Medical School, University of Patras, Patras, Greece

ABSTRACT ARTICLE HISTORY

Purpose of the review: Neisseria meningitidis is a common cause of sepsis in the pediatric Received 2 February 2020
population but is only rarely observed in neonates. The true incidence of the disease in that Revised 21 October 2020
age group remains undefined. The purpose of this review is to summarize the published data Accepted 4 November 2020
on meningococcal disease in the neonatal period.
KEYWORDS
Materials and methods: All published studies reporting data on neonatal meningococcal dis- Neonate; neisseria;
ease were included for data extraction. meningitidis
Results: Published cases from around the world show that, while rare, neonatal meningococcal
disease is characterized by a high mortality rate and serious neurodevelopmental complications.
The initial clinical presentation is atypical and there is a rapid clinical deterioration. Predisposing
factors have been described and they include immune deficiencies and maternal genitourinary
tract colonization by the pathogen. Transmission can be intrauterine, intrapartum or postpartum.
Intrapartum transmission has been linked to conjunctivitis, which serves as a point of entry for
the pathogen.
Conclusions: Neonatal meningococcal disease remains a rare but potentially fatal disease,
whose true incidence is not known. Genitourinary colonization of the mother and nasopharyn-
geal carriage of both parents should be assessed, especially in early onset cases. N. meningitidis
should be suspected in cases of neonatal sepsis and seizures, even in the absence of typical
symptoms associated with meningococcemia. A high level of clinical suspicion and quick initi-
ation of therapy are needed to improve the clinical outcome, and patients who survive require
long term follow-up to detect possible neurodevelopmental sequelae. Transmission can be intra-
uterine, intrapartum or postpartum. Intrapartum transmission has been linked to conjunctivitis,
which serves as a point of entry for the pathogen. Published case reports from around the
world show that, while rare, neonatal meningococcal disease is characterized by a high mortality
rate and serious neurodevelopmental complications. The initial clinical presentation is atypical
and there is a rapid clinical deterioration within less than 12 h. The objective of this review is to
summarize the latest literature on N. meningitidis infections in the neonatal period.

Introduction less than 1 year have been attributed to immaturity of

Neisseria meningitidis is a gram negative, encapsulated,
fastidious, oxidase positive, aerobic diplococcus [1,2].
It is primarily transmitted via aerosol droplets, respira-
tory secretions and, notably in neonatal cases, via
vaginal secretions [1,2]. It only affects humans, there is
no animal reservoir, and while infections occur world-
wide the highest rates are in Sub-Saharan Africa [3,4].
The pathogen colonizes the nasopharynx of approxi-
mately 10% of the population and from there it rarely
enters the blood stream (meningococcemia) to cause
generalized disease (invasive meningococcal disease)
[1]. There are 13 capsule types, of which, only 6 (A, B,
C, W-135, X, Y) cause the majority of infections world-
wide [5]. The high rates of disease amongst children
the immune system and complement pathways [1]. In
general, there are numerous factors associated with a
higher risk of infection such as the low level of bac-
tericidal antibodies in the host’s serum, prematurity,
nasopharyngeal carriage, acute viral infections, age
less than 2 years, complement C3 and C5 deficiencies,
properdin deficiency, anatomic or functional asplenia,
HIV infection, crowded living conditions such as mili-
tary camps or university dormitories, and active or
passive smoking [1,5–7]. Routine vaccinations against
Neisseria meningitidis are recommended as part of a
variety of immunization schedules worldwide [4].
N.meningitidis is considered as the leading cause of
bacterial meningitis, sepsis and generalized disease,
especially in the pediatric population [8]. Attack rates

CONTACT Despoina Gkentzi gkentzid@hotmail.com Department of Pediatrics, Patras Medical School, Rio, Patras, Greece

Joint first coauthors.
ß 2020 Informa UK Limited, trading as Taylor & Francis Group

are highest amongst children less than 1 year old and
there is also a second peak of the disease amongst
adolescents [1,8]. It rarely occurs in the neonatal
period, as there are very few published case reports
and cases series worldwide [2,6–34]. In that age group
it is associated with a high rate of mortality [7]. Of
note, the first case of neonatal meningococcal menin-
gitis was reported in 1916 in a 3-day-old infant born
after a prolonged labor who eventually survived, but
later developed hydrocephalus [33].
The aim of the present review is to summarize the
published data on meningococcal disease in the neo-
natal period.
Neonatal meningococcal disease incidence,
rarity and means of transmission
The leading causes of neonatal meningitis and septi-
cemia are group B streptococci, E. Coli and Listeria
monocytogenes [31]. All of these pathogens frequently
colonize the maternal genitourinary tract and anorec-
tal area, while N. meningitidis does so rarely [31]. The
latter could potentially change in the future due to
the increased frequency of oral-genital sexual practices
which has been shown to facilitate transfer of oral
flora to the genital area [21]. The true incidence of
neonatal meningococcal disease has not been accur-
ately determined, and based on data from the Center
for Diseases Control and Prevention during the 1980s,
it was assumed that only 0.54% of neonatal meningitis
cases were caused by meningococci [7,30]. Data col-
lected in the Unite States through the “Bacterial Core
Surveillance Program” during the 1990s showed an
annual incidence of 9/100.000 newborns, putting the
incidence much closer to that of the 6–23 month old
age group than was previously thought [8]. A more
recent report came from Korea which reported that
only 2/125 cases of neonatal meningitis were caused
by meningococcus (1.6%) between 1996 and 2005
[16]. It was also reported that during New Zealand’s
meningococcal epidemic during the years 2001–2008,
only 10 cases out of 2706 involved neonates [10]. Two
other major reports came from France and while the
first by Gaschignard et al. [23] showed similarly low
incidence rates, the second by Bilal et al. [14] showed
higher rates. The latter was a retrospective review of
831 cases of neonatal meningitis between 2001 and
2013 which demonstrated that N. meningitidis was the
third most frequent cause of meningitis, following
group B streptococci and E. coli, but more frequent
than Listeria monocytogenes [14]. Serogroup B
accounted for the majority of cases (78%) and all
THE JOURNAL OF MATERNAL-FETAL & NEONATAL MEDICINE 4191
patients were term infants, although prematurity is
considered a risk factor [7,14].
The rarity of the disease is believed to be due to
protective antibodies passed passively from the
mother to the fetus in utero through transplacental
transfer [7,8,10,20]. This belief is grounded in research
during the 1960s when it was found that more than
50% of newborns had protective bactericidal antibod-
ies at birth against most serogroups, which gradually
decline and they are only present in fewer than
25% of infants at 6–23 months of age [8,35,36].
Transplacental transfer of antibodies against
serogroups A and C has been proven by Carvalho
et al. [37] but they stated in their report that passive
transfer is irregular. Maternal antibodies are due to
previous meningococcal disease or colonization
[11,36]. Prematurity and other factors are thought to
hinder their transfer [8]. In cases when the patients
are not born prematurely and should normally have
had acquired the antibodies, other predisposing fac-
tors such as immunological immaturity, complement
deficiencies or other immune deficiencies are thought
to accommodate the development of the dis-
ease [1,7,8].
A case of neonatal meningococcal disease was pub-
lished in 2007 by Falc~ao et al. [20] where the mother
had Systemic Lupus Erythematosus and it was specu-
lated that the immunosuppressive therapy she was
receiving could have impeded the transplacental
transfer of antibodies. There was, however, another
risk factor present as the neonate required intubation
which could have damaged its nasopharynx providing
a point of entry for N. meningitidis [20].
Although they are often difficult to accurately
ascertain, there are three theories regarding possible
modes of transmission: intrauterine acquisition, intra-
partum acquisition and post-partum acquisition in a
manner similar to that of older age groups [2,8,25]. In
1976 Jones et al. [24] reported a case of fetal menin-
gococcemia where the cervicovaginal colonization of
the mother was culture proven at 36 weeks of gesta-
tion. The conjunctiva has been linked to intrapartum
acquisition as a possible entry point, although N.
meningitidis is a rare cause of acute neonatal conjunc-
tivitis [13,15,19,21]. Most cases of primary neonatal
conjunctivitis at delivery are caused by Neisseria gonor-
rhoeae and Chlamydia trachomatis [15,21]. In a review
of 21 cases of primary meningococcal conjunctivitis 9
were neonates and the general percentage of evolu-
tion into invasive meningococcal disease was 17.8%
[38]. In 1992 Ellis et al. [19] reported two cases of neo-
natal conjunctivitis that evolved into meningitis and in
4192 D. FILIPPAKIS ET AL.
one case the pathogen was also detected in vaginal
swabs from the mother. Fiorito et al. [21] described a
case of neonatal conjunctivitis acquired at delivery
from the mother, and they also demonstrated the
cross transmission between the mother’s genitourinary
tract, both parents’ nasopharynx and the infant. A
more recent case of purulent meningococcal conjunc-
tivitis which evolved into septicemia, while both
parents were asymptomatic carriers of the pathogen,
was published in 2017 [15]. Molecular evidence sup-
porting intrauterine transmission of serogroup A men-
ingococcus was published in 2006 by Arya et al. [12] A
case of intrauterine transmission of serogroup B N.
meningitidis was published in 2010 by Kurlenda et al.
[25] where the mother was admitted to the hospital at
31 weeks of gestation with fever and ruptured mem-
branes revealing stained amniotic fluid. In 24 h, N.
meningitidis was isolated from vaginal swabs and a
cesarean delivery was performed to minimize the neo-
nate’s risk of infection, but the infant was infected
nonetheless [25]. It is of note that there are no official
recommendations of how to deal with carrier mothers
or infection monitoring during pregnancy [25].
Characteristics of published cases
The most comprehensive published literature review of
the disease was published in 2017 by Basani et al. [2]
in which 127 case reports were included from 1916 to
2017 and the authors stated that the true incidence of
the disease may be underestimated. Of the 127 cases,
the first 11 were published before 1951 and are consid-
ered to be in the pre-antibiotic era while the rest 116
are considered to be in the post-antibiotic era [2,26].
Only 23 cases are confirmed to be early onset (approxi-
mately 18%) and they had a high mortality rate of
approximately 35% [2]. Overall, serogroup B was the
most frequent pathogen with 19 out of 127 cases
(14.9%) although in over 90 cases out of 127 the
serogroup was not specified [2]. The overall mortality
also cannot be specified as the outcome is not
reported in the vast majority of cases, however, at least
49 out of 127 (38.5%) survived [2]. Another review on
early onset cases reported a mortality rate close to 50%
[26]. Data from the “Bacterial Core Surveillance
Program” showed a mortality rate of 14% [8].
The initial clinical presentation of neonatal menin-
gococcal disease is often atypical and can even be
asymptomatic until the late stages [22,26]. Common
symptoms include fever, a history of poor feeding and
irritability [11,20,28,31]. Other reported symptoms are
jaundice, seizures, respiratory distress, a bulging
anterior fontanel and hypotonia [2,7,18,20,31]. The
classical hemorrhagic rash is present in neonates only
rarely, even though it is considered characteristic of
meningococcal infections [31]. Despite its atypical and
unclear initial presentation, the disease can rapidly
become fulminant in less than 12 h with septic shock,
hypotension, purpura fulminans with skin necrosis, dis-
seminated intravascular coagulation (DIC) and multiple
organ dysfunction syndrome (MODS) [7,20,31]. It is
believed that purpura is only present rarely and in the
late stages of disease because its mechanism involves
vascular inflammation and antibody-antigen reactions
that the neonate’s immature immune system is not
capable of producing [7,20]. Bleeding reported in the
late stages of disease is possibly a secondary effect of
septic shock and DIC [20]. The absence of typical fea-
tures of meningococcemia can lead to treatment
delays, although, even if there is immediate clinical
suspicion, antibiotic treatment and advanced intensive
care support, mortality remains high [7]. Generally,
patients with purpura fulminans, shock, acidosis, DIC
and positive blood cultures have poorer prognosis
[31]. It is worth mentioning at this point that atypical
meningococcal disease (caused predominantly by
serogroup W meningococci) may occur in all ages and
may present with atypical signs and symptoms of the
disease, such as acute gastrointestinal symptoms, sep-
tic arthritis, bacteremic pneumonia and severe upper
respiratory tract infection (notably epiglottitis) [39].
Diagnosis of meningococcal disease is established
by isolation of the pathogen from a normally sterile
bodily fluid such as blood or cerebrospinal fluid (CSF)
[1]. In the majority of cases the diagnosis was estab-
lished by positive blood cultures, positive CSF cultures
or both [7]. In some cases, CSF cultures were positive
for N. meningitidis without pleocytosis or other bio-
chemical parameters suggesting meningitis [18,31], a
fact historically reported in textbooks about meningo-
coccus in general [1]. This highlights the importance
of CSF culture to avoid missing the diagnosis in the
neonatal age group, when the procedure is not con-
traindicated [18]. Other, infrequently used, types of
laboratory examinations of the CSF include PCR
screening for meningococcus and latex particle agglu-
tination [11,13].
The empirical antibiotic regimen for early onset
neonatal sepsis, which includes ampicillin in combin-
ation with an aminoglycoside, can also cover menin-
gococcus before culture results are obtained, as the
pathogen remains sensitive to penicillin [10]. Once the
diagnosis is made, treatment can consist of penicillin
G, ampicillin, cefotaxime of ceftriaxone [1]. It is
 THE JOURNAL OF MATERNAL-FETAL & NEONATAL MEDICINE 4193

important to note that ceftriaxone should not be used

reported
reported

reported
reported

None reported
None reported
Complications
in neonates receiving intravenous calcium and neo-
nates with jaundice [10]. Based on a previous literature

None
None

None
None
review, penicillin G and cefotaxime were the most fre-

–
–
quently used antibiotics in neonatal cases, followed by
ampicillin and gentamicin [7]. Rifampicin or a third

Both survived
Outcome generation cephalosporine can be used for chemo-
Survived
Survived

Survived

Survived
Survived
prophylaxis and nasopharyngeal clearance [10].
Died
Died
Besides having a high mortality rate, neonatal men-
ingococcal disease also has a high probability of
neurological complications [20]. Based on published
data in the literature, neurosurgical complications
include hydrocephalus, subarachnoid hemorrhage,
Penicillin G in both cases

cerebral abscess, spinal dysfunction and subdural

Cefotaxime þ Gentamicin
Cefotaxime þ Gentamicin

Penicillin G þ Cefotaxime
Ampicillin þ Gentamicin
Antibiotic

empyema [2]. A case report by Basani et al. [2] is not-

able as it is the first case of neonatal meningococcal
Benzylepinicillin

disease complicated by multiple cerebral abscesses.

Ceftriaxone

Neonatal meningitis by any pathogen frequently leads

to complications, including but not limited to deafness
–

(most common), blindness, learning disabilities, speech

disabilities, motor disorders and chronic seizures
B in both cases

[1,31]. Long term monitoring and neuroimaging of

Serogroup

survivors for any neurodevelopmental sequelae is

important [31].
C
B
B

B
B
–
Y

New cases and cases not included in previous

Blood culture in both cases þ PCR in
Blood culture þ conjunctival exudate

literature reviews
Table 1. Comparative table of new cases and cases not included in previous reviews.

During our research we found nine published cases of

Blood culture þ CSF culture

Blood culture þ CSF culture

Blood culture þ CSF exam

neonatal meningococcal disease not included in previ-

Diagnosis

ous literature reviews [6,9,10,13,15,22,29,34]. A com-

CSF (2nd case)

parative table based on these case reports is

Blood culture

presented below (Table 1). The case by Banerjee et al.

CSF culture
PCR in CSF

[13] is worth commenting because during hospitaliza-

tion and the administration of antibiotics, the patient
was diagnosed with coarctation of the aorta and
underwent cardiac surgery. In the two cases where
Patient age (days)

the neonates died, the patients’ condition deteriorated

rapidly [22,29]. In the case published by Onyejiaka
et al. [29] the patient displayed disseminated intravas-
7 and 2

cular coagulation, metabolic acidosis, petechiae, pur-

12

16
6

8
5
3

pura and died within 12 h of the initial presentation to

the emergency department. In the case published by
Fox et al. [22] the patient was asymptomatic until only
one hour before death, when a diffuse petechial rash
was discovered. Upon arrival at the hospital the
Aldabbagh et al. 2018 [10]

Mubashar et al. 2020 [34]

Onyejiaka et al. 2010 [29]
Ahmareen et al. 2008 [9]
Banerjee et al. 2001 [13]

patient was in cardiopulmonary arrest and, despite

Cruz et al. 2017 [15]
Fox et al. 2015 [22]

intubation, was pronounced dead at the emergency

Kim et al. 2018 [6]

department [22]. The case published by Cruz et al.

[15] was previously mentioned in the “means of trans-
Author

mission” part of our review. In this case, N. meningitidis

was isolated from both parents’ nasopharynx and the
4194 D. FILIPPAKIS ET AL.
mother’s vagina [15]. It is assumed to have been trans-
mitted intrapartum, causing conjunctivitis which pro-
gressed to septicemia [15]. In the case published by
Aldabbagh et al. [10] the patient’s condition also
deteriorated rapidly, and necrotic lesions were devel-
oped on the skin, scrotum and heels but the
patient survived.
Conclusion
Neonatal meningococcal disease remains a rare but
potentially fatal disease, whose true incidence is not
known. Genitourinary colonization of the mother and
nasopharyngeal carriage of both parents should be
assessed, especially in early onset cases. N. meningitidis
should be suspected in cases of neonatal sepsis and
seizures, even in the absence of typical symptoms
associated with meningococcemia, as progression is
often rapid. A high level of clinical suspicion and quick
initiation of therapy are needed to improve the clinical
outcome, and patients who survive require long term
follow-up to detect possible neurodevelopmen-
tal sequelae.
Disclosure statement
No potential conflict of interest was reported
the author(s).
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