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Indian Pediatr 2013;50: 601-603 |
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Meningitis due to Neisseria meningitidis
Serogroup B in India
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Meenakshi Aggarwal, Vikas Manchanda and *B Talukdar
From the Departments of Clinical Microbiology and
Infectious Diseases Division, *Pediatric Medicine, Chacha Nehru Bal
Chikitsalaya, Raja Ram Kohli Marg, Geeta Colony, Delhi, India.
Correspondence to: Dr Vikas Manchanda, Room # 101,
Clinical Microbiology and Infectious Diseases Division, Chacha Nehru Bal
Chikitsalaya, Raja Ram Kohli Marg, Geeta Colony, Delhi 110 031, India.
Email: [email protected]
Received: September 29, 2012
Initial review: October 22, 2012;
Accepted: January 24, 2013.
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Invasive meningococcal disease has a
fulminant course and high mortality. Neisseria meningitidis
serogroup A is predominantly responsible for meningococcal disease in
India and the developing countries. Group B meningococcus, which is
prevalent in the developing world is uncommon in India. We herein report
the second case of group B meningococcal infection from the country, two
decades after the reporting of the first case. Ineffective vaccines
against serogroup B warrant the need for close surveillance of this
disease.
Key words: Child, India, N. meningitides
serogroup, Surveillance.
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Invasive meningococcal disease
commonly follows a fulminant course and has high mortality
[1]. Thirteen serogroups of Neisseria meningitidis
have been identified, but six of these serogroups (A, B, C,
W135, X and Y) are responsible for majority of the
infections worldwide [1]. Serogroup A strains are
predominantly responsible for meningococcal disease in
developing countries, including India [2]. Serogroup B
strains are responsible for outbreaks of meningitis in the
developed world where vaccines against serotypes A,C,Y and
W135 are extensively used [3]. Group B meningococcus is not
prevalent in India, with only one previous report [4]. We
herein report the second case of group B N. meningitidis
infection from the country.
Case Report
The patient was a one-year-old, boy
weighing 7kg who presented to the pediatric emergency with
seizures, history of high-grade fever, vomiting, lethargy
and decreased oral acceptance since three days. He had
multiple episodes of generalized tonic clonic seizures in
last 24 hours. He was delivered at full term through an
uneventful vaginal delivery. Immunization history was
appropriate for age. No history of similar illness was
present in the family and immediate contacts. On
examination, child was conscious, had no cyanosis and had
bilaterally constricted pupils with sluggish reaction to
light. He was febrile (101 0F)
with heart rate of 172 beats per minute and respiratory rate
42 per min. Capillary filling time was less than 3 sec.
Anterior fontanelle was full and pulsatile. Neck rigidity
was present. There was increased tone in all four limbs,
deep tendon reflexes were brisk with bilateral extensor
plantars. He had no skin rash. Initial clinical diagnosis of
meningitis was made and therapy with intravenous ceftriaxone
and anticonvulsants was started, in addition to supportive
management.
Laboratory reports revealed that the
child had hemoglobin of 8.1 g/dL with total white blood cell
count of 10,610/mm 3
(56% neutrophils, 38% lymphocytes, 3.9% monocytes and 1.2 %
eosinophils), and platelet count of 5.9 lakh/mm3;
C-reactive proteins was raised (178.97 mg/L). The blood pro-calcitonin
levels were 118.23 ng/mL (≥10
ng/mL and plasma lactate levels were also raised (30.5 mg/dL).
Renal function tests and serum electrolytes were within the
normal range. The cerebrospinal fluid showed raised protein
levels (113 mg/dL), and low levels of glucose (26 mg/dL).
CSF cytology could not be reported because of hemmorhagic
nature of tap. CSF lactate levels were increased at 83.93mg/dL
and CSF chloride levels were 123 nmol/L. Latex agglutination
was performed on the CSF sample and was reactive for N.
meningitidis group B (Pastorex Meningitis, BIO-RAD).
Blood and CSF culture grew N. meningitidis as
identified by Vitek 2 Compact system (BioMerieux, France).
Serogrouping was done by N.meningitidis antisera (Remel
Europe Ltd. UK) and was confirmed was as N.meningitidis
serogroup B. The strain was found resistant to
penicillin (MIC, 0.5 mg/mL)
and ciprofloxacin (MIC, 0.5
mg/mL),
and sensitive to ceftriaxone (MIC, 0.094
mg/mL),
chloramphenicol (MIC, 0.19
mg/mL),
azithromycin (MIC, 0.5 mg/mL),
rifampicin ((MIC, 0.032
mg/mL), and meropenem (MIC, 0.032
mg/mL)
as determined using E test and interpreted in accordance
with CLSI guidelines. Blood and CSF samples tested positive
for ctrA gene for N.meningitidis by Real time
PCR assay. DNA extraction from blood and CSF samples was
performed using the Magnapure Compact automated nucleic acid
extraction system. (Roche Diagnostics, Basel, Switzerland)
as per manufacturer’s protocol. A 111 bp region of ctrA
gene was amplified using ctrA specific primers, with slight
modification [6]. N. meningitidis ATCC 13090 was used
as the positive control.
The cranial ultrasonography showed slight
ventricular prominence with normal cerebral parenchyma. The
patient was placed under isolation and chemoprophylaxis with
ciprofloxacin given to the close contacts of the patient.
The patient was continued on intravenous ceftriaxone and
phenytoin. He was put on mechanical ventilation because of
repeated seizures and declining oxygen saturation. High
grade fever and seizures were persisting till the 5 th
day of admission despite midazolam infusion (2mg/kg/min).
Intravenous dexamethasone 1 mg 8 hourly was initiated along
with other therapy on day 5. The patient started showing
clinical improvement from the 7th
day onwards with no fresh seizures, repeat blood culture
showing no growth, and improved blood counts. Midazolam was
discontinued on 9th
day of admission. After 16 days of antibiotic therapy,
repeat CSF examination was within normal limits and culture
did not yield any growth. Despite the clinical and
laboratory improvement, the antibiotic therapy was
maintained for a total of 21 days. Dexamethasone was
discontinued after 10 days of therapy. By day 29, the child
had recoverd and was discharged on oral anticonvulsants from
the hospital. Meningococcal carriage screening of the
patient and the parents did not yield any positive results.
Discussion
Meningococcal meningitis is a serious
infection and if untreated, may be fatal with case fatality
rates reaching 5-10% in developed countries and upto 20% in
developing countries [7]. The neonate in the previous study
had died within 6 hours of admission. However, in our study,
the child survived and recovered after a prolonged hospital
stay. The source of Group B meningococcus could not be
ascertained in this case. The reason for very low prevalence
of serogroup B in India is not known. It may be postulated
that predominance of serogroup A might lead to suppression
of serogroup B in the Indian population similar to the
phenomenon observed in pre-vaccine era in developed
countries. In addition to the varying geographical
distribution, the proportion of cases caused by each
serogroup may also vary by age. US studies describe
serogroup B to be causing 30-50% of cases in infants younger
than 1 year of age, while serogroups C, Y, and W135 causing
75% of meningococcal disease in those 11 years and older
[7,8]. Both the cases from India (including the present
case) were below one year of age.
Effective vaccines are available for
meningococcal serogroups A, C ,Y and W135. Consequently,
serogroup B, N. meningitis has become the major cause
of bacterial meningitis especially in countries where
vaccine for other serotypes has been introduced [4]. Vaccine
against serogroup B strains for global use has been
challenge. This is due to frequent antigenic variations
among this serogroup. Antigenic mimicry of serogroup B
polysaccharide with human neurologic tissues is also a
problem [9]. Vaccines based on other bacterial cell
components have shown poor protective immune response in
children under 24 months of age [10]. Thus, the occurrence
of even a single case Group B meningococcal meningitis in
India has important public health implications.
Indian data on meningococcal disease is
sparse and is limited to the studies undertaken during or
immediately after suspected outbreaks. Studies during
inter-epidemic period and constant surveillance of the
invasive meningococcal disease can help understanding the
epidemiology of this highly fatal disease. Though there is a
gap of two decades between the first and the second case
report, there is a strong need for close surveillance and
documentation for further group B meningococcal
infections in India. With recent licensing of conjugated
quadrivalent vaccines in the country, it will be interesting
to observe changing epidemiology of invasive meningococcal
disease in India.
Contributors: All the authors have
prepared, designed and approved the study.
Funding: None; Competing interests:
None stated.
References
1. Manchanda V, Gupta S, Bhalla P.
Meningococcal disease: History, epidemiology, pathogenesis,
clinical manifestations, diagnosis, antimicrobial
susceptibility and prevention. Indian J Med Microbiol.
2006;24:7-19.
2. Sinclair D, Preziosi MP, John TJ,
Greenwood B. The epidemiology of meningococcal disease in
India. Trop Med Int Health. 2010;15:1421–35.
3. Khatami A, Pollard AJ. The
epidemiology of meningococcal disease and the impact of
vaccines. Expert Rev Vaccines. 2010;9:285–98.
4. Suri M, Kabra M, Singh S, Rattan
A, Verma IC. Group B meningococcal meningitis in India.
Scand J Infect Dis. 1994;26:771-3.
5. Corless CE, Guiver M, Borrow R,
Edwards-Jones V, Fox AJ, Kaczmarski EB. Simultaneous
detection of Neisseria meningitidis, Haemophilus
influenzae, and Streptococcus pneumoniae in
suspected cases of meningitis and septicemia using real-time
PCR. J Clin Microbiol. 2001;39:1553–8.
6. Initiative for Vaccine Research.
Bacterial Infections. Meningococcal Disease. Available from:
URL:
http://www.who.int/vaccine_research/diseases/soa_bacterial/en/index1.html.
Accessed on September 1, 2012.
7. Rosenstein NE, Perkins BA, Stephens
DS, Lefkowitz L, Cartter ML, Danila R, et al. The
changing epidemiology of meningococcal disease in the United
States, 1992–1996. J Infect Dis. 1999;180:1894-901.
8. CDC. Prevention and Control of
Meningococcal Disease: Recommendations of the Advisory
Committee on Immunization Practices (ACIP). MMWR 2005;54
(No. RR-7).
9. Granoff DM. Review of meningococcal
group B vaccines. Clin Infect Dis. 2010;50:S54–65.
10. Tappero JW, Lagos R, Ballesteros AM, Plikaytis B,
Williams D, Dykes J, et al. Immunogenicity of two
serogroup B outer-membrane protein meningococcal vaccines: a
randomized controlled trial in Chile. JAMA. 1999;281:1520-7.
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