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bacterial meningitis references to bacterial infection r e f e r e n c e s n a v i g a t o r < Adams, J.H., Duchen, L.W. (Eds) Greenfield’s Neuropathology, fifth edition 1992, London : Edward Arnold.Ahmed A, Hickey SM, Ehrett S, Trujillo M, Brito F, Goto C, Olsen K, Krisher K, McCracken GH Jr. Cerebrospinal fluid values in the term neonate. Pediatr Infect Dis J. 1996 Apr;15(4):298-303. Alviedo JN, Sood BG, Aranda JV, Becker C. Diffuse pneumocephalus in neonatal Citrobacter meningitis. Pediatrics. 2006 Nov;118(5):e1576-9. Berman PH, Banker BQ. Neonatal meningitis. A clinical and pathological study of 29 cases. Pediatrics 1966;38:6–24. Bockova J, Rigamoti D.Intracranial empyema. Pediatr Infect Dis J.2000;19(8):735-737. Bonfield CM, Sharma J, Dobson S. Pediatric intracranial abscesses. J Infect 2015;71 Suppl 1:S42-S46. Bucci S, Coltella L, Martini L, Santisi A, De Rose DU, Piccioni L, Campi F, Ronchetti MP, Longo D, Lucignani G,De Vries LS. Viral infections and the neonatal brain. 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Gallagher PG, Ball WS (1991) Cerebral infarctions due to CNS infection with Enterobacter sakazakii. Pediatr Radiol 21:135–136.Govaert P, de Vries LS (2010) Chapter 63; Bacterial meningitis, ventriculitis, 384. In: An Atlas of Neonatal Brain Sonography. Clinics in Developmental Medicine No.182-183. Mc Keith Press 2nd Ed. Gupta N, Grover H, Bansal I, Hooda K, Sapire JM, Anand R, Kumar Y (2017) Neonatal cranial sonography: Ultrasound findings in neonatal meningitis - A pictorial review. Quantitative Imaging in Medicine and Surgery 7(1), 123–131.  Han BK, Babcock DS, McAdams L (1985) Bacterial meningitis in infants: sonographic findings. Radiology 154:645–650. Harik N, DeBiasi RL (2018) Neonatal nonpolio enterovirus and parechovirus infections. 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Arch Dis Child Fetal Neonatal Ed 84(2):F85-9.  Huo L, Fan Y, Jiang C, Gao J, Yin M, Wang H, Yang F, Cao Q (2019) Clinical Features of and Risk Factors for Hydrocephalus in Childhood Bacterial Meningitis. Journal of Child Neurology, 34(1), 11–16. Jaremko JL, Moon AS, Kumbla S (2011) Patterns of complications of neonatal and infant meningitis on MRI by organism: A 10 year review. European Journal of Radiology 80(3), 821–827. Jéquier S, Jéquier J-C (1999) Sonographic Nomogram of the Leptomeninges (Pia-Glial Plate) and Its Usefulness for Evaluating Bacterial Meningitis in Infants. AJNR Am J Neuroradiol 20(7), 1359-64 Kadambari S, Braccio S, Ribeiro S, Allen DJ, Pebody R, Brown D, Cunney R, Sharland M,  Ladhani S (2019) Enterovirus and parechovirus meningitis in infants younger than 90 days old in the UK and Republic of Ireland: a British Paediatric Surveillance Unit study. Archives of Disease in Childhood 104(6), 552–557.  Kim KS (2010) Acute bacterial meningitis in infants and children. The Lancet Infectious Diseases 10(1), 32–42. Kumar R, Singhi P, Dekate P, Singh M, Singhi S (2015) Meningitis Related Ventriculitis - Experience from a Tertiary Care Centre in Northern India. Indian Journal of Pediatrics 82(4), 315–320.  Larroche JC (1977) Developmental pathology of the neonate. Elsevier, Amsterdam. Chapter 23: bacterial meningo-encephalitis, p 462.Lequin MH, Vermeulen JR, van Elburg RM, Barkhof F, Kornelisse RF, Swarte R, Govaert PP (2005) Bacillus cereus meningoencephalitis in preterm infants: neuroimaging characteristics. Am J Neuroradiol 26;8:2137-43.Li ST, Chiu NC, Hsu CH, Chiang MF. Empyema of the cavum septum pellucidum. Pediatr Neurol. 2002 May;26(5):391-3. Licht-van der Stap RG, de Vries LS, Alarcon A, Govaert P, Steggerda SJ; EurUS.Brain group. Cranial ultrasound in neonatal brain infections. Dev Med Child Neurol. 2025 Aug;67(8):986-1003. doi: 10.1111/dmcn.16279. Epub 2025 Feb 25. PMID: 39996578; PMCID: PMC12237230. Li ST, Chiu NC, Hsu CH, Chiang MF (2002) Empyema of the cavum septum pellucidum. Pediatr Neurol 26(5):391-3 Littwin B, Pomiećko A, Stępień-Roman M, Spârchez Z, Kosiak W (2018) Bacterial meningitis in neonates and infants – the sonographic picture. Journal of Ultrasonography 18(72), 63–70.  Lorber J, Pickering D (1966) Incidence and treatment of post-meningitic hydrocephalus in the newborn. Arch Dis Child 41:44–50.Mactier H, Galea P, McWilliam R (1998) Acute obstructive hydrocephalus complicating bacterial meningitis in childhood. BMJ 316:1887-9 Mahajan R, Lodha A, Anand R, Patwari AK, Anand VK, Garg DP (1995) Cranial sonography in bacterial meningitis. Indian Pediatrics 32(9), 989–993 Masand R.Ali A, Purohit A. Neonatal brain abscess: An atypical presentation. Journal of pediatric neurosciences. 2015;10(3):282. Meijler GSJS, Steggerda SJ. Neonatal cranial ultrasonography. 3th edition ed. Springer Cham. 2019. Miyairi I, Causey KT, DeVincenzo, JP, Buckingham SC (2006) Group B Streptococcal Ventriculitis: A Report of Three Cases and Literature Review. Pediatric Neurology 34(5), 395–399. Nickerson JP, Richner B, Santy K, Lequin MH, Poretti A, Filippi CG, et al. Neuroimaging of pediatric intracranial infection--part 1: Techniques and bacterial infections. Journal of neuroimaging. 2012;22(2):e42-e51. Peros T, van Schuppen J, Bohte A, Hodiamont C, Aronica E, de Haan T (2020) Neonatal bacterial meningitis versus ventriculitis: a cohort-based overview of clinical characteristics, microbiology and imaging. European Journal of Pediatrics 179(12), 1969–1977. Polin RA, Harris MC. Neonatal bacterial meningitis. Semin Neonatol 2001;6: 157–172. Pooboni SK, Mathur SK, Dux A, Hewertson J, Nichani S (2004) Pneumocephalus in neonatal meningitis: diffuse, necrotizing meningo-encephalitis in Citrobacter meningitis presenting with pneumatosis oculi and pneumocephalus. Pediatr Crit Care Med 5(4):393-5 Raghav B, Goulatia R, Gupta AK, Misra NK, Sing M. Giant subdural empyema in an infant. sonographic observations. Neuroradiology. 1990;32(2):154-155. Reeder JD, Sanders RC (1983) Ventriculitis in the neonate: recognition by sonography. Am J Neuroradiol 4:37–41. Rennie JM, Hagmann CF, Robertson N (2008) The baby with a suspected infection. Chapter 13; 270. In: Neonatal Cerebral Investigation. Ed: Cambridge. ISBN-13 978-0-511-41368-1 Ries M, Deeg K-H, Heininger U, Stehr K (1993) Brain abscesses in neonates—report of three cases. Eur J Pediatr 152:745–746.Schellinger D, Grant EG, Manz HJ, Patronas NJ, Uscinski RH (1986) Ventricular septa in the neonatal age group: diagnosis and considerations of etiology. Am J Neuroradiol 7:1065–1071. Stevens JP, Eames M, Kent A, Halket S, Holt D, Harvey D (2003) Long term outcome of neonatal meningitis. Arch Dis Child Fetal Neonatal Ed 88:F179-F184  Tibussek D, Sinclair A, Yau I, Teatero S, Fittipaldi N, Richardson SE, Mayatepek E, Jahn P,  Askalan R (2015) Late-onset group b streptococcal meningitis has cerebrovascular complications. Journal of Pediatrics 166(5), 1187-1192.e1.  Valverde E, Ybarra M, Bravo MC, Dudink J, Govaert P, Horsch S, Steggerda S, Pellicer A; EurUS.Brain Group. State-of-the-art cranial ultrasound in clinical scenarios for infants born at term and near-term. Dev Med Child Neurol. 2025 Mar;67(3):322-347. doi: 10.1111/dmcn.16133. Epub 2024 Oct 21. PMID: 39432744. Van Hinsberg TMT, Elbers RG, Hans Ket JCF, Van Furth AM, Obihara CC (2020) Neurological and neurodevelopmental outcomes after human parechovirus CNS infection in neonates and young children: a systematic review and meta-analysis. Lancet Child Adolesc Health 4:592-605. Verboon-Maciolek MA, Truttmann AC, Groenendaal F, Skranes J, Døllner H, Hunt RW, Hayman M, Dippersloot RJ, Van Loon AM, De Vries LS (2012) Development of cystic periventricular leukomalacia in newborn infants after rotavirus infection. Journal of Pediatrics 160(1). Veyrac C, Couture A, Baud C (1994) ‘La pathologie infectieuse.’ In: Couture, A., Veyrac, C., Baud, C. (Eds.) Echographie Cérébrale du Foetus au Nouveau-né. Montpellier: Sauramps Médical, pp. 371–382. Wolthers KC, Kornelisse RF, Platenkamp GJ, Schuurman-Van Der Lem MI, van der Schee C, Hartwig NG, Verduin CM (2003) A case of Mycoplasma hominis meningo-encephalitis in a full-term infant: rapid recovery after start of treatment with ciprofloxacin. Eur J Pediatr 162(7-8):514-6. Yikilmaz A, Taylor GA (2008) Sonographic findings in bacterial meningitis in neonates and young infants. Pediatric Radiology Vol. 38, Issue 2, pp. 129–137. > During bacteraemia the newborn infant may develop brain complications from systemic effects. For example, an accompanying haemorrhagic diathesis may provoke a subarachnoid haematoma which is often fatal. Hypotension, hypoxia and metabolic acidosis may lead to arterial infarction and/or leukomalacia. Severely ill neonates are prone to venous thrombosis, which may involve the superior sagittal sinus.  Bacterial and viral meningitis affect 0.21 and 0.05 per 1000 live births, respectively (Holt et al. 2001). The organism responsible may not always be isolated from CSF, therefore the diagnosis is often established on cerebrospinal fluid chemical findings and blood culture (Kim et al. 2010, Jaremko et al. 2011).  The spectrum of CUS findings and complications in neonatal CNS infection has been reported in clinical series and reviews (Tatsuno et al. 1993, Mahajan et al. 1994, Rudas G et al. 1998, Jéquier et al 1999, Couture et al. 2001, de Vries et al. 2006, Miyairi et al. 2006, Yikilmaz et al. 2008, Rennie et al. 2008, Govaert et al.  2010, Verboon-Maciolek et al. 2012, Kumar et al 2014, Tibussek et al. 2015, Gupta et al. 2017, Littwin et al. 2018, Peros et al. 2020, de Vries et al. 2020, Bucci et al. 2022, Licht-van der Stap et al. 2025, Valverde et al. 2025). algorithm clinical context bacterial meningitis ultrasound findings liquefaction typical examples Somewhat different patterns are ascribed to various bacteria (Jaremko et al. 2011, Licht-van der Stap et al. 2025, Valverde et al. 2025). If meningitis or ventriculitis are added, there may appear arteritis with focal ischaemia, presenting as brain abscess or haemorrhagic brain necrosis. During a period of bacteraemia, germs can enter the brain along a GMH/IVH started on a haemodynamic basis. About 10 % each of neonatal meningitis cases lead to severe or moderate impairment. The mean intelligence quotient is significantly less than normal. About 4 % have sensorineural hearing loss, 3 % persisting hydrocephalus. At least 5 % receive treatment for seizures. Gram-negative infections (except E Coli) and GBS meningitis carry the worst prognoses as a group.  infection sequence pneumocephalus examples of bacterial infection haemorrhagic stroke Ventriculitis/plexitis (Gupta N et al. 2017, Mactier et al. 1998) is a determinant of type and duration of treatment, be it based on subjective criteria (Miyairi et al. 2006, Kumar et al 2014, Peros et al. 2020): increased ependymal echogenicity, intraventricular debris or septae, intraventricular hyperechoic content and increased echogenicity or irregularity of the plexus. The detection of CSF flow on colour Doppler imaging at the level of the aqueduct may add to the diagnosis (Tatsuno et al. 1993, Couture et al. 2001), although this is non-specific and can be confused with intraventricular bleeding. As near the pial surface, purulent inflammation near the ventricle lining may lead to local thrombophlebitis with periventricular infarction. Alviedo et al. 2006:  intracranial gas collection in a neonate with Citrobacter koseri meningitis. The clinical presentation was acute with pneumocephalus demonstrated by cranial sonography and computed tomography. The clinical course was fatal despite prompt administration of antibiotics. Meningeal thickening (hyperechoic widening of the sulcus), reported prevalence between 23 to 83% of the infants) (Yikilmaz et al. 2008). Measurements can be taken in the coronal plane, at the level of the foramina of Monro outside the gyrus frontalis superior. Depending on the point where the measurement is made, meningeal thickness can be defined as 1.3 mm or higher, when measured from the gyral surface, or 2 mm or higher when measured within a groove (Mahajan et al. 1994, Littwin et al. 2018). This is often transient and no correlation with outcome has been substantiated (Jéquier et al 1999, Kim et al. 2010). GBS arachnoiditis gram-negatives The prevalence of ventricular dilatation after bacterial meningitis is highly variable (16-60% of infected infants) (Yikilmaz et al. 2008). Ventriculomegaly can develop during the acute phase due to increased CSF production, hindered circulation and decreased absorption. Hydrocephalus can develop later as a result of adhesions, aqueduct stenois, progressive fourth ventricle trapping or multiloculated cyst formation (de Vries et al. 2006).  Several risk factors have been related to the development of hydrocephalus after bacterial meningitis, such as CSF parameters (glucose < 2 mmol/l, proteins > 2 g/L), increased serum C-reactive protein, positive blood culture and the presence of echogenic debris at the subdural space of the lumbosacral spine (Rudas G et al. 1998, Littwin et al. 2018, Huo et al. 2019, Chen et al. 2021). Ventricular dilation may also be present in chronic stages due to parenchymal atrophy (ex-vacuo) (de Vries et al. 2006, Littwin et al. 2018). empyema of the cavum septi pellucidi, reversed after regression of ventriculomegaly (Li et al. 2002) ventriculitis leukomalacia Abscess formation is associated with gram negative as well as positive organisms and yeasts (Jaremko et al. 2011). A brain abscess is seen at first as a round echogenicity, followed by central dissolution sometimes with a level between fluid and necrotic debris, surrounded by a hyperechoic rim (de Vries et al. 2006, Govaert and de Vries 2010). Micro-abscesses in the subcortical-periventricular white matter and basal ganglia have been described in fungal meningitis as scattered, small, round hyperechoic lesions (Rennie et al. 2008). Some of these abscesses may well follow focal infarction of either venous or arterial ischaemic origin. abscedation hydrocephalus empyema cavum SP Bacterial meningitis is complicated by arterial ischaemic stroke in up to 5-10% (Hernandez et al. 2011, de Veber et al. 2006, Chang et al. 2003). Neonatologists should be aware of this possibility, in particular in Streptococcus group B meningitis, especially if seizures are present. The stroke pattern is variable with cortical multifocal ischaemia, basal ganglia involvement or a large territorial arterial infarct. Inflammation of pial arteries and superficial veins, subarachnoid inflammation at the base of the brain and secondary vasospasm at the level of the circle of Willis and/or perforator arteries may explain the different patterns observed (Tibussek et al. 2015).  Sinovenous thrombosis is diagnosed in up to 7-16% of cases with meningitis in different population-based studies (Fitzgerald et al. 2007). However, the diagnosis is challenging even in expert hands, except when the venous thrombotic changes are near a fontanelle. stroke Direct parenchymal destruction. White matter is especially vulnerable to infection (Govaert et al. 2010), appearing as areas of increased echogenicity in the periventricular or subcortical white matter. Non-vascular necrosis of the brain parenchyma has been described in gram-negative encephalitis, involving a destructive process named liquefaction necrosis (Yikilmaz et al. 2008, Govaert et al. 2010, Gupta et al. 2017, Littwin et al. 2018).  meningeal thickening The initial finding during meningitis is brain swelling with slitlike ventricular cavities and limited extracerebral spaces. The sulci may widen and become hyperechoic due to exudation, but also due to increased reflections from the inflamed surrounding (sub)cortex. The latter may indicate the onset of gyral venous infarction (Berman and Banker 1966). During the first few days fine intraluminal linear and nodular reflections may appear, commonly called ‘debris’, usually in the occipital or frontal horns. Such debris is also associated with IVH and consequently not diagnostic of ventriculitis, whereas septation tends to be. After some hours the ventricles widen due to exudation and, later, due to obstruction of CSF flow by inflammatory tissue (Hill et al. 1981, Reeder and Sanders 1983, Schellinger et al. 1986, Yikilmaz 2008, Gupta 2017). This may occur at the level of the aqueduct, near the exit foramina of the fourth ventricle or during pericerebellar or pericerebral ascent of CSF. Thick exudate has been reported with many organisms including mycoplasma meningitis (Wolthers et al. 2003). Hydrocephalus, both internal and external, is a potential complication. ‘Isolated fourth ventricle’ is possible through proximal and distal occlusion. Ventricular dilatation can occur even weeks after discontinuation of antibiotics, due to adhesions.  Common findings are ventriculitis and choroid plexitis, represented by an echoic and thickened lining of the ventricular ependyma, intraventricular strands and debris, and an irregular choroid plexus (Hill et al. 1981). Septation may lead to compartmentalization with multiloculated cavities (Hill et al. 1981, Reeder and Sanders 1983, Schellinger et al. 1986). Extracerebral effusion (subarachnoid) with debris in the acute stage and empyema later on can (rarely in ~1 %)) appear as either hypoechoic collections or areas of heterogeneous echogenicity (Yikilmaz et al. 2008, Gupta 2017). A round or biconvex hyperechoic collection is found between bone and cortex. Compression and not dilatation of the underlying sulci allows differentiation from a subarachnoid collection due to CSF retention. The echoreflections in the subdural collection are fine and may show strand formation. Interhemispheric location may occur. Based on CUS alone it can be difficult to differentiate between sterile and purulent effusions although a heterogeneous echogenicity and debris are suggestive of the latter (Raghav et al. 1990, Bockova et al. 2000, Nickerson et al. 2012). While effusion resolves spontaneously, empyema needs aspiration or drainage. Analysis of the fluid confirms the diagnosis. bacterial meningitis and complications: ultrasound findings CUS is usually the first imaging tool in the neonate with suspected meningitis. Acute bacterial meningitis leads to characteristic CUS changes in up to 65% of patients, figures that rise to 100% in the infected newborn with abnormal neurological signs (Mahajan et al. 1994, Yikilmaz et al. 2008). A baseline CUS on admission is recommended in neonates with clinical suspicion of CNS infection. If meningitis is confirmed or the condition deteriorates, serial studies rule out complications that need additional monitoring or treatment. Optimized settings should include a high frequency linear probe for a proper assessment of the meninges and extra-axial space (also via the mastoid fontanel, Meijler et al. 2019), as well as a complete Doppler assessment to discard sinovenous thrombosis. CUS informs about the optimal timing to determine the extent of injury with MRI. Foci of hyperechogenicity in white matter may occur in the acute stage around the ventricle and close to the cortex. Such parenchymal abnormalities are caused by vasculitis, haemorrhagic-ischaemic infarction, and abscess formation (Volpe et al. 2018). The lesions are focal or diffuse, often changing in appearance over time. Ischaemic stroke, common in GBS meningitis, is initially difficult to detect but becomes apparent when a scan is repeated beyond 48-72 hours of admission (Hernandez 2011). Typical are infarcts in deep grey matter (perforator stroke) and focal cortical infarctions. In contrast, liquefaction necrosis is often detected early as a very irregular area of increased echogenicity.  Brain abscesses are uncommon in neonates but when they do occur, they are mostly located in the frontal lobes (Enzmann et al. 1982, Gallagher and Ball 1991, Ries et al. 1993, de Vries et al. 2006, Masand et al. 2015). Usually they start with infarction, then parenchymal necrosis becomes infected and forms an abscess (Volpe et al. 2018). Haematogenous seeding is the alternative. Abscesses can become large, and often multiple. Larger lesions cause mass effect. Their appearance changes as they become demarcated over time, with a hyperechoic rim and central echolucency due to liquefaction and cavitation. The combination of infection and venous infarction (thrombophlebitis) eventually gives rise to periventricular cysts, sometimes of a porencephalic nature. The distinction between the loculated part of a ventricle and a periventricular postnecrotic cavity, infected or not, is not always easy. Later periventricular calcification may be expected. bacterial encephalitis: liquefaction necrosis Haemorrhagic necrosis of the brain may occur in fulminating gram-negative brain infection. The echographic changes e.g. in the parenchyma of a preterm infant with fatal pseudomonas bacteraemia with meningitis, are impressive. After a few days the brain substance becomes granularly hyperechoic everywhere, as if crowded by small haemorrhages or areas of infarction. Within five days there can be rapid progression toward scattered generalized microcystic necrosis with, in the ventricle, septation on top of blood clot. Even without postmortem confirmation such evolution is compatible with meningo-encephalitis and ventriculitis. Serratia marcescens or Citrobacter are also often implicated in published cases of haemorrhagic meningo-encephalitis.  If the culture of blood or liquor shows a Gram-positive agent, Listeria monocytogenes is the presumed causative agent.  Bacillus cereus, although rare, is also a candidate. In most cases cereus infection is fatal, due to extensive damage and necrosis of infected tissue caused by the toxins produced by Bacillus cereus. The organism itself is swarming out from veins into tissue. The enterotoxin, phospholipases, proteases and haemolysins induce a widespread liquefactive necrosis.  bacteria swarming through white matter (Larroche 1977) Prior normal scans make PVL a less likely cause of destruction of the white matter. PVL can be an ongoing process, starting with symmetrical flaring in the periventricular white matter from day one and this can evolve into massive cystic destruction of the white matter. Hyperechoic changes are however not abutting on cortex as in bacterial encephalitis.  Thrombosis of the deep cerebral veins can also lead to haemorrhagic destruction of white matter, in many cases in both hemispheres.  Another differential diagnosis is the acute stage of multicystic encephalopathy in the context of monozygous twinning and birth asphyxia: such histories show transition from abnormal hyperechogenicity to slow (over a few weeks) destruction. This is in contrast with the presentation of bacterial encephalitis, where a very rapid destruction is observed in an initially normal brain.  Viral encephalitis is also a differential diagnostic entity. Especially Herpes simplex and enteroviral agents can destroy white matter in the neonatal period. It may be important to identify rapid and extensive brain destruction with CUS in a neonate with signs of sepsis and altered consciousness or convulsions: the supratentorial periventricular and subcortical white matter seem to be the first target. This preference may be explained by the easy spread of infection along white matter tracks. Further in the process the cortex is affected (Larroche 1977, Lequin et al. 2005). MRI can better delineate the extent of the brain destruction than US or CT. DWI can even show cytotoxic edema in areas where the conventional T1 and T2 weighted MR images and CUS do not show clear abnormalities.  Bacillus cereus encephalitis in a preterm infant bacterial brain infection patterns lumbar punctures in newborn infants -------------------------------------------------------- - indications       symptomatic infant with suspected sepsis      positive blood culture      age >7 days - contraindications       haemodynamic instability      thrombocytopenia - controversies       asymptomatic, high risk infant bacterial meningitis: clinical context predictors of adverse outcome  ----------------------------------------- seizure duration of >72 hours coma  notably abnormal EEG use of inotropes  leukopenia Stevens et al. 2003: total of 111 neonatal meningitis instances versus 113 matched controls;  5.4% of cases and 1.7% of hospital controls had treatment for seizures - mean intelligence quotient (IQ) of the cases (88.8) was significantly less than that of the hospital controls (99.4) - the mABC score was significantly worse for the cases ( - 3.6% sensorineural hearing loss, 2.7% hydrocephalus treatment summary ----------------------------------------------------------------------------------------------------- - empirical therapy for meningitis in the first week of life: ampicillin + gentamicin + cefotaxime - empirical therapy for meningitis after the first week of life: ampicillin + cefotaxime + an aminoglycoside - repeat lumbar puncture at 24-48 hours - if CSF culture positive at 48-72 hours and/or suspicion of brain complications perform US and/or MRI - reassess therapy based on culture and antibiotic susceptibility results: if group B streptococcus, use high dose penicillin; discontinue aminoglycoside when clinically stable and CSF sterilised - if Gram negative, use cefotaxime and an aminoglycoside; discontinue aminoglycoside after two weeks and complete course with cefotaxime - continue antibiotic therapy (intravenously) for at least two (GBS and Listeria) or three weeks (Gram negative bacteria) after sterilisation of CSF cultures - consider longer duration of therapy if focal neurological signs persist at two weeks, if >72 hours required to sterilise CSF, or if obstructive ventriculitis, infarcts, encephalomalacia or brain abscesses are found by imaging studies; a late repeat lumbar puncture may guide duration of therapy in these circumstances  clinical alarm signs (Polin and Harris 2001) -------------------------------------------------------------- less well temperature instability, fever relapse of jaundice apnoea, grunting, tachypnoea tachycardia, poor skin circulation, slow refill, cold acra ileus irritability, dislike of handling, high pitched cry,       tense fontanelle, seizures, lethargy, blank and staring expression neck retraction, painful on handling, diaper-pain pale and mottled skin petechiae/omphalitis/paronychia/phlebitis pneumonia disseminated intravascular coagulation sclerema pseudoparalysis 2 bacterial brain infection algorithm 1 Mac OS X  2°âATTRâ¼&¼com.apple.TextEncodingËcom.apple.quarantineutf-8;134217984q/0082;69f201a5;Hype4;