2007 meningococo

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Case Report

Meningoccocal meningitis complicated with subdural effusion:areport of two infant casesVictor Perez-Pico,

1

Eduardo Llausas-Magana,1

Angel Leon-Ramirez,1

Giordano Perez-Gaxiola,2

and Nidia Leon-Sicairos.3

1Department of Infectious Diseases,

2Department of Medical Education and

3Department of Research, Hospital Peditrico de

Sinaloa, Dr. Rigoberto Aguilar Pico, Constitucin y Donato Guerra S/N, Colonia Almada, C.P. 80200, Culiacn Sinaloa, Mxico.

AbstractNeisseria meningitidisis a major cause of invasive bacterial infection in children of all ages. Children less than 1 year of age areat greater risk of invasive disease than older children. In endemic countries, the invasive meningococcal infections are a leadingcause of bacterial meningitis in older children and adults but it is particularly rare in newborns and infants less than 1 year old.Besides meningitis, hemorrhagic skin findings have been described as part of the typical case scenario. In this report, wepresent two cases of meningococcal meningitis occurring in children under the age of 3 months in a non-endemic setting. Bothpatients did not manifest any skin lesions but had subdural effusion, an unusual complication for meningococcal meningitis.

Key Words: Neisseria meningitidis,meningococcal meningitis,subdural effusion.

J Infect DevelopingCountries2007; 1(1):74-77.

Received 23April 2007 -Accepted 16 May2007.

Copyright 2007 Victor Perez-Picoet al. This is an open access article distributed under the Creative Commons Attribution License, whichpermits unrestricted use, distribution, and reproduction in any medium, provided the original work isproperly cited.

IntroductionNeisseria meningitidis is a causative agent of

meningitis, and it is responsible for considerablemorbidity and mortality throughout the world [1, 2].

However, the aetiology of bacterial meningitis haschanged substantially in the last decade with theintroduction of conjugate vaccines againstHaemophilus influenzae type b, Streptococcuspneumoniae and N. meningitidis [1, 2]. Theincidence has decreased by more than 90% invarious countries where universal vaccinationagainst these bacteria has been established. In theUSA, invasive infection by Haemophilus hasdecreased by 99%, i.e. 1 case in 100,000 childrenless than 5 years old per year; and in England,with the introduction of the meningococcal vaccine,

the incidence of invasive infection secondary tothese bacteria has declined by 81% [3-5].Nevertheless, N. meningitidis remains a majorcause of serious bacterial infection in children of allages, particularly in endemic places, and infantsless than 1 year of age are especially at greaterrisk of invasive disease than older children [1]. It isknown that in most Latin American countries theincidence of N. meningitidis is rare and

furthermore, subdural effusion is an unusualcomplication of meningococcal meningitis;therefore, it is of interest to report the clinicaloutcome of two infant cases seen in our hospital.

Case ReportsCase 1

A previously healthy two-month-old male wasadmitted to the emergency room with five dayshistory of fever, irritability and feeding refusal. Thelaboratory tests revealed leucocytes of 8,200/mm3(neutrophils 69%), platelets 377,000/mm3;procalcitonin 0.89 ng/mL, and blood glucose 112mg%. Also urinary tests revealed 2-3 leucocytes;and cerebrospinal fluid (CSF) showed a clearappearance, proteins 434 mg/dl, chloride 108.9

mg/dl, glucose 1 mg/dl, cells 605/mm3(polymorphonuclear cells 98%) and Gram-stainnegative diplococci. Coagglutination was positiveforN. meningitidis (E. coli K1). CSF cultures werepositive for N. meningitidis group B. Cefotaxime200 mg/kg/d (IV) commenced with clinicalimprovement during the first 3 days, and animprovement in the CSF was seen as follows:lightly turbid, proteins 111 mg/dl, glucose 61 mg/dl,


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J Infect Developing Countries2007; 1(1): 74-77.

cells 200/mm3 (mononuclear cells 81%). Gramstain, coagglutination and cultures were negative.

On the 10th day of treatment, persistent fever,irritability, and bulging anterior fontanel appeared.A fresh CSF examination revealed clearappearance, proteins 104 mg/dl, glucose 40 mg/dl,

cells 217/mm3 (mononuclear cells 70%). A headCT scan showed, at the front and anterior sidesand evidence of fluid collection (Figure. 1). Adiagnosis of subdural effusion was then made. Theinfant was continued on the same treatment andthe fever disappeared after five days. The totalduration of antimicrobial therapy was 15 days. Thepatient had a good outcome and the CSF atdischarge (21st day) was of clear appearance,proteins 289 mg/dl, glucose 41 mg/dl, cells119/mm3 (mononuclear cells 94%). Prophylaxiswith Rifampin was administered to household

contacts. At follow-up the patient showed goodpsychomotor development and hearing tests werenormal.

Figure 1.Case 1. Subdural effusion. Contrastenhanced axial CT demonstrating fluid collection into

the subdural space.

Case 2A previously healthy 3-month-old female was

admitted to the emergency department,

hypoactive,with fever, easy crying, and a bulginganterior fontanel. The disease manifested abruptlythe day before presentation. Laboratory tests:leucocytes 6,600/mm3 (neutrophyls 66%);platelets 133,000/mm3; and procalcitonine 5.92ng/mL. CSF: turbid appearance, proteins 231mg/dl, glucose 27 mg/dl (blood glucose 72),countless cells (polymorphonuclear cells 84%),Gram-stain negative diplococci, coagglutination

positive to N. meningitidis, and culture positive toN. meningitidis group C (W135). Antimicrobialtreatment with Cefotaxime was commenced andthe patient showed good outcome during the firstweek. A repeat CSF analysis revealed lightly turbidCSF, proteins 56 mg/dl, glucose 34 mg/dl, cells

352/mm3 (polymorphonuclear cells 80%), andGram-stain negative.On the 12th day, fever and generalized-tonic

colonic seizures appeared. The CSF examinationrevealed turbid appearance, proteins 119 mg/dl,glucose 36 mg/dl, cells 2116/mm3(polymorphonuclear cells 90%), and a few Gram-negative diplococci. CSF culture was negative.The head CT scan showed right frontoparietalsubdural effusion (Figure 2).

Figure 2.Case 2. Subdural effusion. Contrastenhanced axial CT demonstrating fluid collection into

the subdural space.

The antimicrobial plan was changed toCiprofloxacine and Chloramphenicol. The patientwas on this new regimen for a total of 10 daysalthough the fever persisted for the first four daysof therapy. On the 16th day of admission, surgicaldrainage of the subdural effusion was performedand the patient began to show progressive

improvement. One week later, the CSF wasreported as showing xantochromic appearance,proteins 650 mg/dl, glucose 61 mg/dl, and cells83/mm3 (polymorphonuclear cells 80%). Gram-stain and culture were negative. Prophylaxis withRifampin was administered to household contactsas it has been shown that use of antibioticprophylaxis in asymptomatic contacts results indecreased carriage rates and thus prevents


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spread of the disease [6]. At follow-up, the patientshowed good developmental progress and hearingtests were normal.

DiscussionIt is known that the most common aetiology of

bacterial meningitis in newborns and infants areStreptococcus agalactiae and Gram-negativebacilli [7]. To the best of our knowledge, this is thefirst report on meningococcal meningitiscomplicated with subdural effusion in infants inMxico. In fact, reports of meningococcalmeningitis in those ages are extremely rare [8]. Ininfants and children younger than 5 years, incountries where universal vaccination against H.influenzae type b and pneumococcus is not done,these microorganisms are usually the mostfrequent cause of meningitis; in older children and

S. pneumoniae are even more frequently foundbacteria [6].N. meningitidis is endemic in the USA,

England, Spain, and Africa, where severalserogroups are predominant. For example, in theUSA there are reported incidences of serogroupsB, C, Y and W135 [9]. In Africa, group A is themost frequent [10], whereas in England it is groupC [1]. The cases observed in our hospital weregroups B and C, coincident with reports in theliterature from Latin America, where the greatestprevalence is group B [11]. It is important toemphasize that in the first case in our study, co-agglutination was likely positive to E. coli K1 as across-reaction, because the capsularpolysaccharides are immunologically similar oridentical in both microorganisms [12]. The sourceof infection was likely in the home because thismicroorganism is found in the nasopharynx of 5-10% of adults [12], and there have been reportswith outbreaks in families [13].

Also, it is known that the clinical pattern ofmeningococcemia includes bleedingmanifestations such as petechiae or purpura inaround one third of all cases [14,15]. Nevertheless,there are many reports where meningococcalmeningitis doesnot reveal vascular changes of theskin [6,14,16-19], as seen in our patients. The restof the clinical manifestations that are describedaccording to the age of our patients, like lethargy,irritability, refusal to take food, and bulgingfontanelle, occurred in both patients [8]. Seizuresare more common in children with meningitis

caused by H. influenzae compared with childrenwith meningococcal meningitis [20]; nevertheless,the seizures in the second case in this studyprobably were due to the mass effect of subduralfluid collection [21]. The CSF changes wereconsistent with those of bacterial meningitis, i.e.,

turbid appearance, high cellularity withpredominant polymorphonuclear cells, lowglucose, high levels of proteins, and correlationbetween Gram-stain, coagglutination and culture.

Both patients were treated with Cefotaxime, asit is considered the drug of choice for empirictherapy according to the literature [22]. They had atorpid outcome. However, it was only in the secondpatient that the treatment plan was changedbecause the subdural effusion had to be surgicallydrained (Fig. 2). It is important to consider that thisis an unusual complication [19,23], occurring more

commonly in meningitis caused by S. pneumoniaeand H. influenzae type b rather than N.meningitidis [7, 19]. The use of Chloramphenicol,Imipenem or Fluorquinolones has been thealternative to multi-resistant serotypes of N.meningitidis [18], as was suspected in the secondcase. Unfortunately, susceptibility testing was notperformed, but the clinical improvement and thenegative result of cultures after the change oftherapy strongly supported that possibility. Thethree weeks of antimicrobial therapy in both casescontrasts with the literature where duration oftreatment is shorter, 4 or 7 days [6, 24]. However,this is not surprising if we take into considerationthe complications of these patients, i.e., subduraleffusion and persistent fever despite the treatment[25].

Post meningitis subdural fluid collection is aclassical complication of bacterial meningitis ininfants. Its incidence has been estimated to be ashigh as one half of the cases of meningitis, with H.influenzae being the most common bacterialcause. N. meningitis has become more prevalentsince the introduction of vaccination against H.influenzae and S. pneumoniae, and many authorsnow estimate that 5% of N. meningitidis infection ininfants is complicated by a significant subduraleffusion. A temporarysurgical drain is advised forall cases in which a significant mass effect isapparent on imaging or there is a torpid evolution.

In conclusion, these reported cases occurringin a non endemic area are of relevance as theycould represent a change in the epidemiology of


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this disease. Secondly, subdural effusion shouldbe considered in patients with fever after 8 days oftherapy, in the absence of a sterile repeat CSFculture. Finally, the development and availability ofa safe and effective vaccine that can induceprotection against all encapsulated meningococci

in all age groups should be the ultimate goal[20,21].

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3. Martin M, Casellas JM, Madhi SA, Urquhart TJ, DelportSD, Ferrero F, Chamany S, Dayan GH, Rose CE, LevineOS et al (2004) Impact of haemophilus influenzae type b

conjugate vaccine in South Africa and Argentina. PediatrInfect Dis J 23: 842-847.4. Black S, Shinefield H, Baxter R, Austrian R, Bracken L,

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10. Robbins JB, Schneerson R, Gotschlich EC, Mohammed I,Nasidi A, Chippaux JP, Bernardino L, Maiga MA (2003)Meningococcal meningitis in sub-Saharan Africa: thecase for mass and routine vaccination with availablepolysaccharide vaccines. Bull World Health Organ 81:745-750.

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Infectious diseases of children 11th Ed. St. Louis, MO:Mosby Year book Inc 21: 373-390.

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16. Oostenbrink R, Moons KG, Theunissen CC, Derksen-Lubsen G, Grobbee DE, Moll HA (2001) Signs ofmeningeal irritation at the emergency department: howoften bacterial meningitis? Pediatr Emerg Care 17: 161-

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meningitis: case reports and review of literature. PediatrInfect Dis J 15: 1134-1136.

18. Ma JS (2005) Neisseria meningitidis subdural empyemain a young infant. Pediatr Infect Dis J 24: 750-751.

19. Topalovic R, Bauman S (2000) Acute meningococcemiain a 4-month-old infant. Med Pregl 53: 401-404.

20. Feigin R, Cherry J, Demmler G, Kaplan S, Ralph Feigin(2004) Textbook of pediatric infectious diseases 5th Ed.Philadelphia: Saunders 1: 1270-1277.

21. Chang CJ, Chang HW, Chang WN, Huang LT, HuangSC, Chang YC, Hung PL, Chang CS, Chuang YC, HuangCR (2004) Seizures complicating infantile and childhoodbacterial meningitis. Pediatr Neurol 31: 165-171.

22. Latorre C, Gene A, Juncosa T, Munoz C, Gonzalez-Cuevas A (2000) Neisseria meningitidis: evolution ofpenicillin resistance and phenotype in a children'shospital in Barcelona, Spain. Acta Paediatr 89: 661-665.

23. Snedeker JD, Kaplan SL, Dodge PR, Holmes SJ, FeiginRD (1990) Subdural effusion and its relationship withneurologic sequelae of bacterial meningitis in infancy: aprospective study. Pediatrics 86: 163-170.

24. Kaplan SL (1999) Clinical presentations, diagnosis, andprognostic factors of bacterial meningitis. Infect Dis ClinNorth Am 13: 579-594, vi-vii.

25. Nelson JD (1985) Management problems in bacterialmeningitis. Pediatr Infect Dis Suppl 4: 41-44.

Corresponding Author: Victor Perez-Pico,Departmentof Infectious Diseases. Hospital Peditrico de Sinaloa,Dr. Rigoberto Aguilar Pico, Constitucin y DonatoGuerra S/N, Colonia Almada, C.P. 80200, CuliacnSinaloa, Mxico, Telephone and Fax (52)-667-716-46-86, e-mail: [email protected].

Conflict of Interests: The authors declare that theyhave no conflict of interests.


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