O’Connor et al. BMC Infectious Diseases
(2019) 19:863
https://doi.org/10.1186/s12879-019-4509-y

CASE REPORT

Open Access

A case report of multiple cerebral abscess
formation complicating serogroup B
Neisseria meningitidis meningitis
Ciara O’Connor1*, Aedin Collins2, Eilish Twomey3, Conor Hensey4, John Caird5 and Patrick J. Gavin2

Abstract
Background: Invasive meningococcal disease (IMD) presenting with meningitis causes significant mortality and
morbidity. Suppurative complications of serogroup B meningococcal sepsis are rare and necessitate urgent multidisciplinary
management to mitigate long-term morbidity or mortality.
Case presentation: We present a rare case of invasive meningococcal disease in a 28-month old boy complicated by
multiple abscess formation within a pre-existing antenatal left middle cerebral artery territory infarct. Past history
was also notable for cerebral palsy with right hemiplegia, global developmental delay and West syndrome (infantile spasms).
Two craniotomies were performed to achieve source control and prolonged antimicrobial therapy was necessary.
The patient was successfully discharged following extensive multidisciplinary rehabilitation.
Conclusions: Longstanding areas of encephalomalacia in the left MCA distribution may have facilitated the development
of multiple meningococcal serogroup B abscess cavities in the posterior left frontal, left parietal and left temporal
lobes following an initial period of cerebritis and meningitis. A combination of chronic cerebral hypoperfusion and some
degree of pre-existing necrosis in these areas, may also have facilitated growth of Neisseria meningitidis, leading
ultimately to extensive cerebral abscess formation following haematogenous seeding during meningococcemia.
In this case report we review similar cases of cerebral abscess or subdural empyema complicating serogroup B
meningococcal meningitis.
Keywords: Meningitis, Cerebral abscess, Neisseria meningitidis, Serogroup B, Meningococcus, Seizures

Background
Neisseria meningitidis is an opportunist Gram-negative
pathogen and commensal of the nasopharynx and upper
respiratory tract. Transmission is via aerosol, droplets or
direct contact with infected respiratory secretions. The
prevalence of asymptomatic carriage of all serotypes of
N. meningitidis increases with age, from 5% in childhood
to 20% in late teenage years [1]. There are 13 antigenically distinct serogroups of meningococci and most
disease-associated strains belong to serogroups A, B, C,
X, Y or W135. The incidence of meningococcal disease
varies worldwide but is estimated at 0.3–3 cases per 100,
000 in Europe and North America, with a predominance
of serogroups B and C. Overall, the incidence of
* Correspondence: ciaroconnor@rcsi.ie
1
Department of Clinical Microbiology, Temple Street Children’s University
Hospital, Dublin 1, Ireland
Full list of author information is available at the end of the article

meningococcal disease continues to decline in countries
where vaccines targeting serogroups C and more recently B, have been introduced [2].
Invasive meningococcal disease (IMD) presenting with
meningitis causes significant mortality, with a 10% case
fatality rate in the very young, and morbidity in up to
20% of survivors, predominantly neurological sequelae
(seizures, cognitive impairment), visual and/or auditory
impairment and amputation of necrotic digits and/or
limbs [3]. By contrast, acute suppurative complications
of N. meningitidis meningitis occur in less than 1% of
cases and are rarely reported [4, 5]. We report the successful treatment of multiple cerebral abscesses associated with serogroup B meningococcal meningitis in a
young infant with a prior cerebral infarct and complex
medical history. The overall aims of presenting this case
report are to increase awareness of the increased risk of
cerebral complications of meningococcal sepsis in patients

© The Author(s). 2019 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0
International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and
reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to
the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver
(http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

O’Connor et al. BMC Infectious Diseases

(2019) 19:863

with previous intracerebral neurovascular events and to
demonstrate the role of advances in molecular diagnostics,
permitting PCR detection of N. meningitidis DNA despite
preceding antimicrobial therapy.

Case presentation
A 28-month old boy presented with a 24-h history of
lethargy, pyrexia, mottled peripheries and decreased responsiveness. Past history was notable for antenatal left
middle cerebral artery (MCA) infarct, cerebral palsy with
right hemiplegia, global developmental delay and West
syndrome (infantile spasms). He was up-to-date with
vaccinations. Epilepsy was poorly controlled with up to
30 seizures per day despite maintenance clobazam, lacosamide, sodium valproate and levetiracetam treatment.
On examination he had neck stiffness and was haemodynamically unstable with persistent tachycardia and
hypotension. He was coagulopathic (platelets 94 × 10
[6]/L, INR 2.5, fibrinogen 4.03 g/L, prothrombin time
16.8 s), with elevated white cell count (WCC) 28.9 × 10
[6]/L, neutrophilia (25.8 × 10 [6]/L), normal lymphocyte
count (8.5 × 10 [6]/L) and c-reactive protein (CRP) 276
mg/L. He was transferred to the intensive care unit (day
0) where he required intubation, ventilation, fluid resuscitation and inotropic support. He was treated with
intravenous (IV) ceftriaxone, vancomycin and aciclovir.
Polymerase chain reaction (PCR) identified human
metapneumovirus, parainfluenza type-3 and adenovirus
in a nasal swab. Lumbar puncture demonstrated a
macroscopic yellow appearance: WCC 142 (predominantly polymorphonuclear); glucose, 1.6 mmol/L; and
protein, 5.46 g/L. No organisms were seen on Gram
stain. Blood and cerebrospinal fluid (CSF) were culture
negative (taken on antimicrobials) but PCR positive for
N. meningitidis serogroup B. Antimicrobial treatment

a

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was rationalised to cefotaxime monotherapy. He subsequently became more encephalopathic with persistent
pyrexia associated with rising blood WCC and CRP.
Brain computed tomogram (CT) and magnetic resonance imaging (MRI) demonstrated multiple abscesses in
the left MCA territory, cystic encephalomalacia of
posterior left frontal, left parietal and left temporal lobes,
and left hemispheric pial enhancement (Fig. 1a). Empiric
treatment for cerebral abscess with IV meropenem,
vancomycin and fluconazole was commenced.
A frameless stereotactic-guided endoscopic fenestration, drainage and washout of the cerebral abscesses was
performed and a left external ventricular drain was sited
(day 10). Further deterioration in neurological status
necessitated an extensive fronto-temporal-parietal craniotomy with evacuation and debridement of residual
collections and infected encephalomalacial tissue (day
16). Intraoperative fluid and parenchymal tissue was
culture negative but PCR positive for N. meningitidis
serogroup B and antimicrobial therapy was rationalised
to meropenem monotherapy. A second craniotomy was
performed for evacuation of a left frontal lobe abscess in
the context of persistent swinging pyrexia (day 18).
Intravenous linezolid was added for the treatment of a
surgical site infection in the left parietal region, associated with a toxic shock-like syndrome. Intra-operative
specimens were culture negative. The patient returned
to theatre for repeat burrhole drainage of an intracerebral collection (day 20; Fig. 1b demonstrates clinical status post-operatively day 21). Intraoperative specimens
were culture-negative again and were not sent for PCR
analysis. He was discharged from ICU for extensive
multidisciplinary rehabilitation (day 23). The patient was
discharged home on day 40 to complete a further 6weeks IV ceftriaxone. On outpatient follow-up, he is

b

Fig. 1 a: Axial contrast-enhanced CT day 10 of illness reveals an extensive area of cystic encephalomalacia in the left middle cerebral artery
territory with marginal enhancement. Pial enhancement is evident of the entire left cerebral hemisphere. There is longstanding ex vacuo
dilatation of the left lateral ventricle and new mass effect with shift of the anterior falx to the right. b: Axial contrast-enhanced T1 MRI on day 21
after two neurosurgical interventions. The extensive left craniotomy, evacuation and debridement of the infected encephalomalacic tissue is
evident with pronounced pial and leptomeningeal enhancement of the left cerebral hemisphere. There is discontinuity of the dura with overlying
extradural fluid and air. An extra-ventricular drain tip is located in the anterior left lateral ventricle

O’Connor et al. BMC Infectious Diseases

(2019) 19:863

back to his baseline functioning status with no evidence
of new neurological or auditory sequelae. Unfortunately,
his seizures, which had disappeared in the immediate
post-operative period, have since returned to their usual
frequency.

Discussion & Conclusions
The present case is an example of a rare meningococcal
complication with a positive outcome. Following the
introduction of N. meningitidis serogroup C conjugate
(MenC) vaccine in 2000, meningococcal B disease has
been the predominant cause of IMD in Ireland [7]. In
2015, the age specific incidence rate (ASIR) for meningococcal B disease in children aged between 1 and 4
years was 3.87/100,000 with a case fatality rate of less
than 5% [8]. Our patient was non-immune as vaccination against meningococcal serogroup B would not
have been offered to his age-cohort at the time of his
presentation.
His complex pre-admission intracerebral neuropathology likely increased the risk of meningococcal abscess
formation. We hypothesise that areas of encephalomalacia in the left MCA distribution (Fig. 1a, b) may have
facilitated the development of multiple meningococcal
serogroup B abscess cavities in the posterior left frontal,
left parietal and left temporal lobes following an initial
period of cerebritis and meningitis. A combination of
chronic cerebral hypoperfusion and some degree of preexisting necrosis in these areas, may also have facilitated
growth of N. meningitidis, leading ultimately to extensive
cerebral abscess formation following haematogenous
seeding during meningococcemia. West syndrome is not
known to confer an increased risk of meningitis [9].
Similar cases of cerebral abscess or subdural empyema
complicating serogroup B meningococcal meningitis are
rare (Additional file 1). Rothbaum et al. reported successful antimicrobial treatment and surgical drainage of
cerebral abscess in an area of left temporal lobe hypoperfusion in a previously healthy 5-month old with serogroup B meningococcal septic shock [5]. And more
recently, multiple cerebral abscesses were reported in association with serogroup B meningococcal meningitis in
a five-day old neonate in India [6].
With regard to learning outcomes from the present
case, we remain vigilant to the increased risk of cerebral
complications of meningococcal sepsis in all children,
but particularly those with previous intracerebral neurovascular events, and note again that diagnosis was facilitated by advances in molecular microbiology permitting
PCR detection of N. meningitidis DNA despite 16 days
of preceding antimicrobial therapy [8]. A previous study
from this centre, reviewing 266 cases of adult and paediatric IMD over 8 years (2001-2008), demonstrated that
63% of cases of meningococcal blood stream infection

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and 69% of cases of meningitis were diagnosed by PCR
alone, emphasising the necessity for clinicians to utilise
rapid PCR testing where IMD is suspected, to reduce
mortality and morbidity [10]. We also continue to promote meningococcal vaccination as a public health
initiative.

Additional file
Additional file 1: Table S1. Previous published papers describing
meningococcal abscess formation
Abbreviations
CRP: C-reactive protein; CSF: Cerebrospinal fluid; CT: Computed tomogram;
IMD: Invasive meningococcal disease; IV: Intravenous; MCA: Middle cerebral
artery; MRI: Magnetic resonance imaging; PCR: Polymerase chain reaction;
WCC: White cell count
Acknowledgements
The authors thank the staff of the Microbiology Laboratory at Temple Street
Children’s University Hospital, Dublin 1, Ireland and the Irish Meningitis and
Sepsis Reference Laboratory (IMSRL), Temple Street Children’s University
Hospital, Dublin 1, Ireland. Special thanks also to Deirdre Butler, secretary to
the Department of Infectious Diseases, Temple Street Children’s University
Hospital, Dublin 1, Ireland, for her invaluable administrative support.
Authors’ contributions
All authors contributed to this work, read and approved the manuscript.
COC, AC, JC, CH, and PJG wrote the manuscript; ET provided radiology
images and provided valuable feedback. COC, AC, ET, JC, CH, and PJG were
directly involved in the care of the patient.
Funding
No funding source received.
Availability of data and materials
No additional data are available.
Ethics approval and consent to participate
Not applicable.
Consent for publication
Yes, signed parental consent was obtained. Available on request.
Competing interests
The authors declare that they have no competing interests.
Author details
1
Department of Clinical Microbiology, Temple Street Children’s University
Hospital, Dublin 1, Ireland. 2Department of Infectious Diseases, Temple Street
Children’s University Hospital, Dublin 1, Ireland. 3Department of Radiology,
Temple Street Children’s University Hospital, Dublin 1, Ireland. 4Deparment of
General Paediatrics, Temple Street Children’s University Hospital, Dublin 1,
Ireland. 5Department of Neurosurgery, Temple Street Children’s University
Hospital, Dublin 1, Ireland.
Received: 9 August 2018 Accepted: 24 September 2019

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