How is neonatal meningitis transmitted




















Gram-positive bacteria usually clear rapidly within 24—48 hours from the CSF, whereas Gram-negative bacteria may persist for several days in severe cases [ 18 , 97 ]. A delayed clearance of a Gram-negative organism may be an indication for antimicrobial resistance and prompts a change in therapy or diagnostic neuroimaging showing a purulent focus of the disease such as an emphysema, obstructive ventriculitis, or brain abscess requiring additional intervention or increased duration of antimicrobial therapy [ 18 , 97 , ].

Additionally, performing repeating LP is also reasonable for discontinuing combination therapy. Delayed sterilization of the CSF is associated with an increased risk of poor outcome [ 17 , 87 , ]. So, a repeat LP may have therapeutic and prognostic significance. Conversely, some experts recommend a repeat LP only if the patient does not exhibit a satisfactory clinical response by 24—72 hours after initiation of antimicrobial therapy or show a complicated clinical course, including seizures, abnormal neuroimaging, or prolonged positive CSF cultures [ 4 , ].

The decision of whether to perform an LP before completion of therapy in the neonates with meningitis caused by GBS, L. Neuroimaging is recommended to assist in defining the potential complications of neonatal meningitis [ 50 , 87 ]. Ultrasonography, which is a safe, convenient, and noninvasive method, can be done at bedside early in the course of the disease.

It provides rapid and reliable information regarding ventricular size, the presence of hemorrhage, and development of hydrocephalus [ , ]. It is also useful to detect periventricular white matter injury which may initially be manifested by increased periventricular echogenicity and later by cystic periventricular leukomalacia, ventriculitis, echogenic sulci, and extracerebral fluid collections [ , ]. Computed tomography is rapid and easy imaging modality, but carries the risk of neonatal brain to radiation.

It is useful to provide information on whether the course of meningitis has been complicated by hydrocephalus, brain abscess, or subdural collection. These findings may have a role in decision-making for potential neurosurgical interventions or duration of antimicrobial therapy [ 28 , 87 ].

Magnetic resonance imaging MRI is the best currently available modality for evaluation of the neonatal brain [ ].

It provides information on the status of white matter, cortex, subdural and epidural spaces, and even the posterior fossa, when performed either early or late in the course of the disease. It is useful to document the distribution pattern, severity, and complications of the disease [ , ]. It has also been used in providing the best prognostic information [ 28 ]. For these reasons, it is recommended that at least one brain MRI should be performed on every case of neonatal meningitis, especially those caused by organisms that have a propensity for formation of intracranial abscesses [ 17 , 28 , 87 ].

Ideally in all cases, MRI scans must include pre-contrast and post-contrast-enhanced T1-weighted and T2-weighted images in at least two perpendicular planes. Fluid attenuated inversion recovery FLAIR sequence and diffusion weighted imaging DWI are preferred whenever purulent collections are suspected because of their high sensitivity in showing pus accumulation [ ]. Bacterial meningitis in the newborn infant is characterized by high risk of mortality and serious neurological sequelae among most survivors.

It is believed that most sequelae occur as a result of neural injury during the acute inflammatory process that characterizes bacterial meningitis. Given that corticosteroids may help attenuate the acute inflammatory process, adjuvant corticosteroid treatment in children with bacterial meningitis may reduce mortality in S pneumoniae meningitis but not in H.

Additionally, these beneficial effects of corticosteroids have been reported in the reports from high-income countries, but not in those from low-income countries, probably due to the types of pathogens prevalent in the developing world, delay in the initiation of appropriate antibiotic treatment, partial treatment involving indiscriminate antibiotic use outside of hospitals, or lack of facilities [ 7 ]. A few studies suggest that some reduction in death and hearing loss is evident when adjunctive steroids are used in the treatment of neonatal meningitis, but experimental animal studies reported that adjunctive treatment with corticosteroid is associated with an increase in hippocampal neuronal apoptosis [ ].

In conclusion, it should not be used routinely in the treatment of neonatal meningitis due to limited data [ ]. Similarly, the limited studies showed that glycerol, when used as osmotic therapy, may reduce neurological deficiency and deafness in adults and children with acute bacterial meningitis [ ], but it is not currently recommended in neonates with bacterial meningitis [ 4 ]. Short-term neurological complication of neonatal bacterial meningitis includes cerebral edema, increased intracranial pressure, ventriculitis, cerebritis, hydrocephalus, brain abscess, cerebrovascular disease including ischemic arterial stroke and cerebral venous thrombosis, and subdural effusion or empyema [ 18 , ].

Cerebral edema results from vasogenic changes, cytotoxic cell injury, and occasionally inappropriate antidiuretic hormone secretion [ 28 ]. Inflammatory exudate covers the epidermal lining and the choroid plexus, disrupts ependymal lining, and causes subependymal venous thrombosis and eventually necrosis [ 28 ].

It is usually associated with obstruction of CSF outflow [ ]. Cerebritis results from extension of exudate along perivascular space [ 18 , 28 ].

Hydrocephalus, which occurs in approximately one-quarter of neonates with meningitis, develops as a result of fibrous inflammatory exudate obstructing CSF flow through the ventricular system or dysfunction of arachnoid villi [ 18 , 28 , , ]. The mechanisms leading to cerebrovascular complications in bacterial meningitis are not completely understood and likely are multifactorial [ 15 , 62 ].

Brain abscesses, which occur in approximately 10 percent of patients with neonatal meningitis, may result from a hematogenous spread of microorganism into infarcted brain, or by local spread [ 28 , ]. Neonates with bacterial meningitis should be monitored for signs of these complications throughout their treatment.

It must be suspected when there is a failure to respond clinically and microbiologically to appropriate antimicrobial therapy, or a focal neurologic deficit, or new-onset seizures, especially focal seizures, or when there are signs of increased intracranial pressure such as bulging fontanelle, accelerated head growth, bradycardia, hypertension, and separation of the cranial sutures [ 18 , ].

Acute deterioration in an otherwise stable neonate with meningitis can occur if the abscess ruptures into ventricular system or subarachnoid space [ 28 , ]. In case of suspicion regarding these complications, additional evaluation including neuroimaging studies, neurosurgical consultation, and prolonged duration of antimicrobial treatment may be required.

Mortality is higher among preterm infants, in cases with meningitis caused by microorganism that causes vasculitis and brain abscess and in late-onset cases [ 26 , 27 , 28 , 29 ]. Long-term complications in survivors are mental and motor disabilities including mental retardation, learning disabilities, cerebral palsy, and behavioral problems, seizures, hydrocephalus, language disorders, hearing loss, and impaired visual acuity [ 4 , 5 , 14 , 27 ].

Neonatal meningitis caused by S. All infants experienced with bacterial meningitis should be followed long-term for development of neurological sequelae. Intrapartum antibiotic prophylaxis for GBS colonized women or based on the presence of clinical risk factors is efficacious against early onset GBS disease but has no impact on late-onset disease, when most GBS meningitis occurs [ 5 , ].

Vaccines against GBS can reduce the number of missed opportunities due to various reasons. So, maternal immunity to the most common serotypes of GBS serotypes Ia, Ib, and III can be transferred passively to the fetus and protect against invasive infection in infancy due to covered serotypes [ ]. Clinical trials of a trivalent GBS vaccine are encouraging in this regard. The prevention of the spread of the pathogens responsible for neonatal sepsis and meningitis also has an impact on disease burden [ 6 ].

Several interventions, which can be introduced at the community level, with prevention strategies applied during the antenatal, intrapartum, and early neonatal period, will reduce the number of early-onset diseases [ 16 , ].

Prevention of nosocomial infections is based on strategies that aim to limit susceptibility to infections by enhancing host defenses, interrupting transmission of organisms by healthcare workers, and by promoting the judicious use of antimicrobials [ ]. Bacterial meningitis is associated with significant morbidity and mortality in the neonatal population.

Although overall incidence and mortality have declined over the last several decades, morbidity associated with neonatal meningitis remains unchanged. Prompt diagnosis and treatment are mandatory to improve both short- and long-term outcomes. CSF culture obtained via LP is the gold-standard method for the diagnosis of meningitis, which is the key to rapid institution of effective antimicrobial therapy.

Prevention strategies, adjunctive therapies, improved diagnostic strategies, and development of vaccines may further reduce the burden of this devastating disease. Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution 3. Help us write another book on this subject and reach those readers. Login to your personal dashboard for more detailed statistics on your publications.

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Downloaded: Keywords neonate meningitis diagnosis treatment outcome. Table 1. Bacteria causing neonatal meningitis in developed countries. For more, see Ref. Age [Ref. Table 2. Differential diagnosis Besides sepsis and other specific infections, symptoms and signs may be due to noninfectious conditions such as cardiac, pulmonary, gastrointestinal, and metabolic disorders [ 11 , 18 ].

Alternatives to ampicillin in nursery-acquired infections: vancomycin or nafcillin. Alternatives to cefotaxime: ceftazidime, cefepime, or meropenem limit use to multidrug-resistant organisms in nursery e. Bacteroides fragilis spp. Metronidazole IV Alternative: meropenem. Coliform bacteria E coli , Klebsiella sp.

Cefotaxime IV, IM, and gentamicin Discontinue gentamicin when clinical and microbiologic response is documented. Alternative: ampicillin if organism is susceptible; meropenem or cefepime for multiresistant organisms. Lumbar intrathecal or intraventricular gentamicin usually not beneficial. Table 3. Enterobacter sp.

Pseudomonas sp. Citrobacter sp. Detection of growth in urine culture could be a reflection of metastatic dissemination of the organism to the bladder, thus cannot be relied upon as a locator of infection in young infants [ 1 ]. Lumbar puncture LP is an irreplaceable diagnostic tool in neonatal meningitis. Cerebrospinal fluid CSF obtained through LP should be examined directly and as Gram- and Giemsa-stained smears under microscope, cultured, and, if needed, sent for polymerase chain reaction.

Direct microscopy should be performed as soon as possible, because the later it is performed, the more likely the erythrocytes and leukocytes undergo cellular lysis and escape detection. LP should ideally precede the initiation of antimicrobial therapy, but if, delayed for any reason, such as deteriorating clinical status of the patient, empirical antibiotic therapy should be started immediately.

Interpretation of CSF findings is more difficult in neonates than in older children, since the glucose, protein concentrations, and cell count of CSF are higher due to the high permeability of the blood-brain barrier Table 2. Means and normal ranges of cerebrospinal parameters in neonates [ 12 ].

If only one of these parameters is in the normal range, this cannot be accepted as an evidence against the presence of meningitis. If all three parameters are normal, then it can be presumed that meningitis is not present; nevertheless, keeping in mind that completely normal CSF findings may be observed during the very early course of neonatal meningitis, the most prudent approach would be to repeat LP after 24—72 h in such borderline cases.

If the infant had meningitis, pleocytosis and other abnormalities consistent with meningitis would be detected in CSF obtained in this second LP [ 3 ]. Pleocytosis is more marked in bacterial and Gram-negative meningitides than in viral and Gram-positive meningitides [ 1 ]. CSF protein may also be found to be high in parameningeal infections like brain abscess, congenital infections, and intracranial hemorrhage [ 3 ].

CSF glucose to serum glucose ratio is not a reliable indicator of meningitis in the first 28 days of life, because newborns often receive intravenous glucose infusions and serum glucose concentrations can rise abruptly with stress [ 3 ].

In case of a bloody tap, assessing the CSF leucocyte count by correcting it with respect to that of the peripheral blood is not recommended in that it decreases the sensitivity and provides only a slight increase in specificity.

Although, as noted above, signs of sepsis and meningitis intertwine in the newborn period, some neonatologists consider that it is unnecessary to perform LP on neonates evaluated for sepsis, especially those with early neonatal sepsis [ 19 , 20 ].

Blood cultures are negative in one-third of neonates with meningitis who are very low birth weight and born over 34 weeks of gestation [ 1 ]. Thus, in case LP is not performed, a significant portion of neonates with meningitis would not get a correct diagnosis and would not be observed for the likely complications of meningitis; for that reason, the author is in favor of the opinion that LP should always be performed as soon as the infant becomes clinically stable and can tolerate the procedure if it has not been possible to be performed at the first suspicion of meningitis.

It should be kept in mind that findings of CSF inflammation last for a considerably long duration days, sometimes weeks , which allows the clinician diagnose or exclude the diagnosis of meningitis.

Ultrasonography is valuable in the follow-up, especially for the cases, in which hydrocephalus has developed as a complication of meningitis. If the disadvantage of radiation exposure is left aside, computed tomography can accelerate the decision making of ventriculostomy in cases of hydrocephalus and surgical drainage in patients with cranial abscesses.

Magnetic resonance MR is the imaging modality of choice in conditions, such as focal neurologic abnormalities, resistant infection, and clinical deterioration.

MR is the most precise tool for the diagnosis of complications, like sinus vein thrombosis, ventriculitis, and subdural deposits. Electroencephalography has no diagnostic value in neonatal meningitis [ 12 ]. History of premature or prolonged labor, intrauterine scalp monitorization, traumatic birth, and maternal peripartum infection should be noted. Physical signs may be subtle in neonatal meningitis, in which either fever or hypothermia may be the only clue to diagnosis.

Pleocytosis under direct microscopy or the presence of bacteria in Gram smear suggests meningitis. Definitive diagnosis is made with the isolation of causative organism in CSF. The differential diagnosis includes other causes of neonatal seizures, partially treated meningitis, intracranial abscess, intracranial hemorrhage, intracranial aneurysm, cerebral vein thrombosis, head trauma, and congenital metabolic diseases.

Hospitalized neonates who previously received antibiotics eg, for early-onset sepsis may have resistant organisms; fungal disease may also be considered in a septic-appearing neonate after prolonged hospitalization.

Ill neonates with hospital-acquired infection should initially receive vancomycin see table Vancomycin Dosage for Neonates plus an aminoglycoside with or without a 3rd-generation cephalosporin or a carbapenem with activity against Pseudomonas aeruginosa , such as cefepime or meropenem , depending on the concern for meningitis. Antibiotics are adjusted when results of CSF culture and sensitivities are known.

The results of the Gram stain should not be used to narrow coverage before culture results are available. If clinical improvement occurs or sterilization of CSF is documented, gentamicin can be stopped. For enterococci or L. In gram-negative bacillary meningitis, treatment is difficult. Instead, a 3rd-generation cephalosporin eg, cefotaxime should be used in neonates with proven gram-negative meningitis.

If antibiotic resistance is a concern, both an aminoglycoside and a 3rd-generation cephalosporin or extended-spectrum beta-lactam eg, meropenem may be used until sensitivities are known. Parenteral therapy for gram-positive meningitis is given for a minimum of 14 days, and for complicated gram-positive or gram-negative meningitis, a minimum of 21 days.

Intraventricular instillation of antibiotics is not recommended. Because meningitis may be considered part of the continuum of neonatal sepsis, the adjunctive measures used in treating neonatal sepsis Other treatment Neonatal sepsis is invasive infection, usually bacterial, occurring during the neonatal period. Corticosteroids are not used in treatment of neonatal meningitis. Patients should be closely monitored for neurologic complications during early childhood, including for sensorineural hearing loss.

The most common causes of neonatal bacterial meningitis are group B streptococcus, E. Manifestations are often nonspecific eg, temperature instability, respiratory distress, jaundice, apnea. Although central nervous system signs eg, lethargy, seizures, vomiting, irritability may be present, classic findings such as a bulging or full fontanelle and nuchal rigidity are not common.

Cerebrospinal fluid CSF culture is critical because some neonates with meningitis have normal CSF indices eg, white blood cell count, protein and glucose levels. Begin empiric treatment with ampicillin , gentamicin , and cefotaxime followed by specific drugs based on the results of cultures and susceptibility testing.

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Empiric antibiotic therapy Organism-specific antibiotic therapy Adjunctive measures. Group B strep cannot be prevented by the mother taking antibiotics before going into labor. Neonatal meningitis is a serious condition. Take steps to educate yourself about the condition before you have a baby so that you can be familiar with the warning signs and minimize your child's risk of infection.

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