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Artykuły w Czytelni Medycznej o SARS-CoV-2/Covid-19
© Borgis - New Medicine 1/2001, s. 2-4
Zofia Rajtar-Leontiew1, Zofia Konarska1, Teresa Wernik2
Bacterial meningitis in neonates
1Department of Neonatal Pathology, The Medical University of Warsaw
Head of the Department: Zofia Rajtar-Leontiew MD, PhD
2Bacteriological Laboratory, Clinical Hospital, The Medical University of Warsaw
Head of the Laboratory: Teresa Wernik
The authors discuss the aetiology, course and early complications of bacterial meningitis in the newborn. The paper presents a study of 50 neonates treated for purulent meningitis in the Department of Neonatal Pathology between 1988-1998.
Bacterial meningitis in neonates (BM) is always an acute, severe, life-threatening disease, frequently followed by immediate and/or long-term complications. It is usually an outcome of septicaemia from one or more locations. Bacteriaemia preceding the localisation of the disease, or developing in the course of septicaemia, is not always diagnosed on microbiological examination. This is due to many reasons: short-term presence of bacteria in the blood, difficulty in collecting sufficient material for examination, and, frequently in this group, administration of an antibiotic at the early stage of the disease. Early treatment of the neonate, prior to establishing the aetiology of the disease, is justified by the generally dramatic course of each infection and rapid consecutive stages of septicaemia which are difficult to reverse, or are irreversible. These include shock refractory to treatment, resistance to medication and administered fluids, and multi-organ damage (MODS) characterised by respiratory distress, anuria, acute liver failure, changes in consciousness and dissseminated intravascular coagulation (DIC). Therefore, neonates with presumed septicaemia in their first two weeks of life [hyper- or hypothermia, tachycardia, tachypnoea, leukocytosis or leukopaenia or a disturbed leukocyte ratio (immature cells to total granulocyte count] should undergo lumbar puncture, CFS examination, and blood culture, or possibly the collection of any other biological material available for examination.
Over a period of 11 years (1988-1998), bacterial meningitis was diagnosed in 50 neonates (2.56% of the total number of patients treated at the Department of Neonatal Pathology) (Table 1).
Table 1. Etiology of purulent bacterial meningitis in neonates.
C. albicans11 21      516.1
L. monocytogenes     1 22  412.9
S. agalactiae      1 11 39.7
P. aeruginosa    1 2    39.7
S. marcescens  1 11     39.7
K. pneumoniae      2   139.7
P. mirabilis   11      26.4
E. cloacae 1   1     26.4
N. meningitidis1         126.4
E. coli      1    13.2
S. aureus     1     13.2
C. freundi    1      13.2
Streptococcus sp.       1   13.2
Positive CSF culture was noted in 31 patients (62%), and in 17 of these (54.8%) blood culture grew the same bacteria, which confirmed the diagnosis of septicaemia. In 19 neonates (38%) the CSF culture was negative and the diagnosis was established from complete and chemical CSF examination. In 31 cases microbiological examination confirmed bacterial meningitis: G(-) bacteria were found in 17 patients (54.8%), G(+) organisms in 9 patients (29%), and Candida albicans was isolated in 5 patients (16.2%) (Table 2). In the G(+) group Listeria monocytogenes was isolated in 4 patients (12.9%).
Table 2. Purulent bacterial meningitis in neonates: Gram - negative vs. Gram - positive pathogens.
Gram - negativeGram - positiveCandida albicans
1.P. aeruginosa3L. monocytogenes4C. albicans5
2.S. marcescens3S. agalactiae3  
3.K. pneumoniae3S. spur.1  
4.P. mirabilis2S. aureus1  
5.E. cloacae2    
6.N. meningitidis2    
7.E. coli1    
8.C. freundi1    
The study group of 50 neonates included 22 pre-term infants (44%), haemorrhage into the CNS (II-IV) was diagnosed in 12 patients (24%), and 7 of them were premature infants. Eight infants (16%) had congenital defects, and 6 patients (12%) had hydrocephalus (congenital in 3 cases and dramatically progressing in the course of the CNS infection in 3 others). In 39 neonates (78%) bacterial meningitis was coexistent with other inflammatory foci (Table 3).
Table 3. Incidence of infections eoexistent with purulent bacterial meningitis in neonates.
NrDiagnosisNr of cases%
4.Otitis media48
5.Urinary tract infection36
7.Osteitis (multifocal)12
The above included: pneumonia (11 cases - 21%), infection of the body integument (omphalitis, pyodermia and conjunctivitis (9 cases - 18%), NEC (7 cases - 14%), otitis (4 cases - 8%), or urinary infections (3 cases - 6%). Multifocal, staphylococcal osteitis (the coxa and arm) was coexistent in 1 patient, and diarrhoea in 2 neonates.
In all 9 neonates with infection of the body, integument lesions had developed and were present prior to the diagnosis of meningitis, However, pneumonia, otitis, osteitis, and NEC were diagnosed simultaneously with CNS abnormalities or in the course of CNS infection.
Hyperbilirubinaemia was present in 6 neonates (12%) with bacterial meningitis. Bacterial meningitis was found in 30 boys and 20 girls (60% and 40% respectively). Most neonates developed bacterial meningitis within the first two weeks of life, this comprising 35 cases (70%) from the study group.
Twenty-two neonates (44%) developed the infection in the first week of life, 13 (26%) in the second week, 9 (18%) in the third week and 6 (12%) in the fourth week. The younger the neonate, the greater the risk of developing bacterial meningitis (Table 4). The most dangerous pathogens in the first week were mainly G() bacteria, in the second week G(-) bacteria, and Candida alb. in the third week - mainly Streptococcus agalactiae and Klebsiella pneumoniae. In the fourth week (at the end of the neonatal period) were 2 cases of infections due to Neisseria meningitidis. In none of the 50 neonates had meningitis been due to Haemophilus influenzae.
Table 4. Incidence of purulent bacterial meningitis in neonates according to weeks of age and aetiology.
 1st week of age2nd week of age3rd week of age3rd week of age4th week of ageTotal
No of neonates
1.C. albicans23--5
2.L. monocytogenes22--4
3.S. agalactiae1-2-3
4.P. aeruginosa12--3
5.S. marcescens1--23
6.K. pneumoniae-21-3
7.P. mirabilis2---2
8.E. cloacae1---1
9.N. meningitidis---22
10.E. coli1---1
11.S. aureus1---1
12.C. freundi1---1
13.S. species1---1
Brain abscess, as a severe, immediate complication of bacterial meningitis, was diagnosed in 3 (6%) neonates on USG examination. In one case it was due to Proteus mirabilis, and in 2 cases the cause was Listeria monocytogenes. In 3 patientcongenital hydrocephalus was treatea by neurosurgery. Three patients developed paresis of the limbs and trunk. Two severely affected children were transferred to a home for chronic disabled persons. We have no information about the children who were discharged home to go under the care of their district physicians. One child was adopted by a foreign family after an eighteen month hospitalisation and surgical treatment of NEC.
Our study of early complications in 50 neonates with bacterial meningitis allows us to conclude that in 14 patients (28%) the disease had a very poor outcome: 4 neonates (8%) died, 10 (20%) neonates had severe complications affecting their development - the quality of their own lives and that of their families, as well as increasing the financial burden on society.
Late complications have not been assessed. This should be done parallel to the rehabilitation and correction course and requires several (at least 5-7) years and should be carried out by many specialists: doctors, psychologists and teachers.
It is very difficult to make an objective assessment of numerous early and late complications following bacterial meningitis, particularly with regard to preterm infants with a low birth weight, children after cerebral haemorrhage, hypoxia, perinatal trauma, hyperbilirubinaemia or congenital defects.
All those factors may affect a child´s further development, impair movement, hearing, speech, sight, intellectual abilities, or emotions. Separation of what has been impaired or damaged by bacterial meningitis and what becomes impossible due to other harmful factors, is almost impossible, even with a long-term follow-up.
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New Medicine 1/2001
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