Meningitis-0

Doc uCo m P DF Tria l ww w.pd fwiz ard. com 需无水印完整版请发邮件：wzxidian@gmail.com Doc uCo m P DF Tria l ww w.pd fwiz ard. com MENINGITIS Edited by George Wireko-Brobby 需无水印完整版请发邮件：wzxidian@gmail.com Doc uCo m P DF Tria l ww w.pd fwiz ard. com Meningitis Edited by George Wireko-Brobby Published by InTech Janeza Trdine 9, 51000 Rijeka, Croatia Copyright © 2012 InTech All chapters are Open Access distributed under the Creative Commons Attribution 3.0 license, which allows users to download, copy and build upon published articles even for commercial purposes, as long as the author and publisher are properly credited, which ensures maximum dissemination and a wider impact of our publications. After this work has been published by InTech, authors have the right to republish it, in whole or part, in any publication of which they are the author, and to make other personal use of the work. Any republication, referencing or personal use of the work must explicitly identify the original source. As for readers, this license allows users to download, copy and build upon published chapters even for commercial purposes, as long as the author and publisher are properly credited, which ensures maximum dissemination and a wider impact of our publications. Notice Statements and opinions expressed in the chapters are these of the individual contributors and not necessarily those of the editors or publisher. No responsibility is accepted for the accuracy of information contained in the published chapters. The publisher assumes no responsibility for any damage or injury to persons or property arising out of the use of any materials, instructions, methods or ideas contained in the book. Publishing Process Manager Tajana Jevtic Technical Editor Teodora Smiljanic Cover Designer InTech Design Team First published March, 2012 Printed in Croatia A free online edition of this book is available at www.intechopen.com Additional hard copies can be obtained from orders@intechopen.com Meningitis, Edited by George Wireko-Brobby p. cm. ISBN 978-953-51-0383-7 需无水印完整版请发邮件：wzxidian@gmail.com Doc uCo m P DF Tria l ww w.pd fwiz ard. com 需无水印完整版请发邮件：wzxidian@gmail.com Doc uCo m P DF Tria l ww w.pd fwiz ard. com 需无水印完整版请发邮件：wzxidian@gmail.com Doc uCo m P DF Tria l ww w.pd fwiz ard. com Contents Preface IX Chapter 1 Bacterial Meningitis and Deafness in Sub-Saharan Africa 1 George Wireko-Brobby Chapter 2 Emerging Pathogens in Neonatal Bacterial Meningitis 9 Marisa Rosso, Pilar Rojas, Gemma Calderón and Antonio Pavón Chapter 3 Perspectives of Neonatal-Perinatal Bacterial Meningitis 21 Kareem Airede Chapter 4 Neurologic Complications of Bacterial Meningitis 35 Emad uddin Siddiqui Chapter 5 Early Neurologic Outcome and EEG of Infants with Bacterial Meningitis 45 Adrián Poblano and Carmina Arteaga Chapter 6 Vaccines to Prevent Bacterial Meningitis in Children 51 Joseph Domachowske Chapter 7 Tuberculous Meningitis 65 Maria Kechagia, Stavroula Mamoucha, Dimitra Adamou, George Kanterakis, Aikaterini Velentza, Nicoletta Skarmoutsou, Konstantinos Stamoulos and Eleni-Maria Fakiri Chapter 8 Molecular Epidemiology and Drug Resistance of Tuberculous Meningitis 85 Kiatichai Faksri, Therdsak Prammananan, Manoon Leechawengwongs and Angkana Chaiprasert Chapter 9 Aseptic Meningitis Caused by Enteroviruses 113 Takeshi Hayashi, Takamasa Shirayoshi and Masahiro Ebitani Chapter 10 An Overview on Cryptococcal Meningitis 125 Marcia S. C. Melhem and Mara Cristina S. M. Pappalardo 需无水印完整版请发邮件：wzxidian@gmail.com Doc uCo m P DF Tria l ww w.pd fwiz ard. com VI Contents Chapter 11 Cryptococcal Meningitis 135 Claudia Fabrizio, Sergio Carbonara and Gioacchino Angarano Chapter 12 Human Parechoviruses, New Players in the Pathogenesis of Viral Meningitis 145 Kimberley Benschop, Joanne Wildenbeest, Dasja Pajkrt and Katja Wolthers Chapter 13 Strategies for the Prevention of Meningitis 163 J.J. Stoddard, L.M. DeTora, M.M. Yeh, M. Bröker and E.D.G. McIntosh Chapter 14 Laboratory Diagnosis of Meningitis 185 S. Nagarathna, H. B. Veenakumari and A. Chandramuki Chapter 15 Role of Dexamethasone in Meningitis 209 Emad uddin Siddiqui and Ghazala Irfan Qazi Chapter 16 Treatment of Adult Meningitis and Complications 217 Sónia Costa and Ana Valverde 需无水印完整版请发邮件：wzxidian@gmail.com Doc uCo m P DF Tria l ww w.pd fwiz ard. com 需无水印完整版请发邮件：wzxidian@gmail.com Doc uCo m P DF Tria l ww w.pd fwiz ard. com 需无水印完整版请发邮件：wzxidian@gmail.com Doc uCo m P DF Tria l ww w.pd fwiz ard. com Preface This book focuses on two primary objectives. It aims to provide general practitioners, paediatricians, and specialist physicians with an essential text written in an accessible language, and also to highlight the differences in pathogenesis and causative agents of meningitis in the developed and the developing world. Meningitis is a medical emergency requiring a rapid diagnosis and an immediate transfer to an institution supplied with appropriate antibiotic and supportive measures. Especially in the developing world, where malaria is rampant, one must maintain a high level of caution when confronted with a febrile child or one who has an altered mental status, as the first ten hours of care may make a crucial difference in the outcome. Bacterial or purulent meningitis is the most important form of infection in the United States in terms of incidence, sequela and ultimate loss of productive life. Aseptic meningitis, usually caused by a virus, is also common, however significant sequela are rare and the disease is self-limiting. In Sub-Saharan Africa, seasonal outbreaks and epidemics of meningitis and septicaemia numerically present the greatest public health impact on the continent. The three polysacharide encapsulated bacteria for which licensed vaccines are curable are Pneumococcus, Haemophilius influenza type b (Hib) and the Neisseia Meningococcus. They are also the most common causative agents of bacterial meningitis in Sub Saharan Africa. Especially in South Africa, granulomatous meningitis, caused either by M. tuberculosis or fungi is a major cause of neurologic injury and death. The necessary factors to consider for the epidemiology of the disease include age, ethnicity, season, host factors and regional pattern of the antibiotic resistance among likely pathogens. The first month after birth represents the period of highest attack rate for meningitis with likely pathogens including S. agalactiae(group B streptococcus), E. coli, other gram 需无水印完整版请发邮件：wzxidian@gmail.com Doc uCo m P DF Tria l ww w.pd fwiz ard. com X Preface negative enteric organisms, and L. monocytogenes. Beyond the neonatal period the most important pathogens are H. influenza type B, 1 up to 6 years of age, N. menigococcus and S. pneumoniae. In the US and Europe, the disease is reported with increased frequency among African Americans, Native Americans and individuals in rural areas. Even in Africa, patients with poor socio-economic factors suffer more from the devastating effects of meningitis. In West Africa, the meningitis belt passes through the Northern part of the countries where people live in overcrowded huts. It has been documented that especially in the dry season, meningococcal, pneumococcal and Haemoiphilus infection spread by the respiratory route, which is aided by overcrowding. It has also been documented that host factors predisposing the infection include congenital or Acquired Immune Deficiency status, Sickling Haemoglobinopathies, chronic liver or renal disease. The classic triad of symptoms in meningitis is fever, headache, and stiff neck. However in children under 2 years of age, stiff neck or other signs of meningial irritation may be absent. Alterations level of consumers is a common finding present in up to 90% of patients. In this book a detailed chapter on laboratory findings has also been provided. Once meningitis is suspected, an immediate examination of the CSF is indicated, except if a strong suspicion of an intracranial mass lesion is present, where lumbar puncture may be delayed until a CT scan or an MRL has been done. Effective treatment of meningitis depends on early aggressive supportive therapy and a selection of empiric antimicrobials appropriate for the likely pathogens. In Europe and the USA, 1 third generation cephalosporine has become the first-line therapy, but while these drugs remain relatively expensive, it is probably reasonable for most African hospitals to continue with the combination of a peniciline and chloramphenicol as initial therapy as long as clinicans are aware of the risk of recondescences, particularly if steroids are used. Common neurological complications in both adults and children are motor deficit, cognition deficit, hemiplegia epilepsy, developmental and learning disabilities, including blindness and deafness. A special chapter on the devastating effects of sensorineural hearing loss and the benefits of early rehabilitation is also included in this book. Prof. Dr. Dr. Sir George Wireko-Brobby President of the Ghana Postgraduate College of Physicians and Surgeons Professor of Otorhinolaryngology, Department of Eye, Ear, Nose and Throat, School of Medical Science, KNUST, Kumasi, Ghana 需无水印完整版请发邮件：wzxidian@gmail.com Doc uCo m P DF Tria l ww w.pd fwiz ard. com 需无水印完整版请发邮件：wzxidian@gmail.com Doc uCo m P DF Tria l ww w.pd fwiz ard. com 需无水印完整版请发邮件：wzxidian@gmail.com Doc uCo m P DF Tria l ww w.pd fwiz ard. com 1 Bacterial Meningitis and Deafness in Sub-Saharan Africa George Wireko-Brobby College of Health Science, School of Medical Sciences, KNUST, Kumasi Ghana 1. Introduction Bacterial Meningitis is a leading cause of childhood Deafness in Ghana and the sub- Saharan Africa. Children are predominantly at risk of bacterial meningitis mainly because of their immature immune system, and malnutrition especially in our part of the world. Lack of immunization practices also makes them more susceptible to significantly high morbidity and mortality. Even with the provision of highly effective antibiotic therapy, death and long-term disabilities are the common but still serious consequences of acute bacterial meningitis in developing countries. Common neurological complications in both adult and children are motor deficit, cognition deficit, hemiplegia, epilepsy, developmental and learning disabilities, blindness and Deafness. In this chapter, we shall focus more on the devastating effects of sensorineural Hearing loss or Deafness, after bacterial meningitis. Delay in the Diagnosis of Hearing loss occurs firstly because language development of Hearing impaired children, parallels that of normal infants till the age of nine months. Secondly, because children with profound hearing loss coo and bable until this age, the parents are likely to ignore any subtle evidence of hearing impairment such as lack of response to environmental sound. Damage to the Cochlea, occurs in the early stages of the illness and it is often permanent and irreversible. Woodrow & Brobby (1997); Daya et al. (1998). Prevention of deafness relies on early treatment with appropriate antibiotics, but adjunctive treatment with dexametnasore though controversial may be useful in preventing the sequel of sensorineural Hearing loss. In the long term vaccinations may be the most practicable means to reducing the burden of meningitis in the developing countries of Africa. Facilities for audiological assessment and management of children recovering from meningitis are crucial for the detection of significant hearing impairment and the implementation of rehabilitation programmes. 需无水印完整版请发邮件：wzxidian@gmail.com Doc uCo m P DF Tria l ww w.pd fwiz ard. com Meningitis 2 Our observation at our University Teaching Hospital (KATH) is that about 20% of patients who survive with neurological sequelae, permanent sensorineuraal Hearing loss, accounts for approximately 75% of these cases. In a study on causes of Deafness in Ghana, Brobby (1998) Meningitis was rated the 3rd amongst other childhood infections. Recent observations predict that meningitis has taken the 2nd position after measles. This is worrying because even a mild hearing loss of less than 40 Db may have long-term developmental consequences. Given the scale of this problem, there is the need to review critically our knowledge about the natural history of the hearing loss which may follow meningitis and to discuss the applicability of recent therapeutic interventions studied in industrial nations to the diseases in the African contest. 2. Microbiology In Africa, acute bacterial meningitis has an overall annual endemic rate in the region of 10- 50 per 105 populations, a figure at least 10 times that for Europe and the United States, and this disparity appears to be growing. Fortnum (1992). More than 70 per cent of cases are caused by either Streptococcus pneumonia (pneumococcal) or Neisseria meningitides (meningococcal). Haemophius influenza type b (Hib) is responsible for fewer cases in the population as a whole although it is a major problem in children less than 12 months of age, Airede (1993). Epidemics of meningococcal meningitis sweep through the sub-Saharan ‘meningitis belt’ every 8 to 12 years. Annual incidence may reach 1 per cent of the population in certain areas. Although this review concentrates on acute bacterial meningitis in Ghana, tuberculous meningitis is also relatively common in certain areas and is the leading cause of meningitis in the Western Cape Province of South Africa, where deafness. Deafness is a well- recognized complication. From our experience, viral meningitis has only rarely been associated with deafness. In Africa seasonal outbreaks and epidemics of meningecal meningitis and septicaemia, numerically represent their greatest public health impact on the continent. In Ghana, the three polysaccharide encapsulated bacteria for which licensed vaccines are curable are Pneumococcus, Haemophilus influenza type b (Hib) and the Neisseria Menigococcus. Our observation is that Haemophilus influenza type b is responsible for fewer cases of meningitis in our sub-region. 3. Epidemiology A number of factors appear to influence the frequency of post-meningitis hearing loss but it is not possible to predict hearing loss accurately in individual cases. Factors affecting this figure including the causative organism, the pneumococcus causing the highest rate of deafness (31.8 per cent) in comparison with the meningococcus (7.5 per cent) and Hib (11.4 per cent) All ages may develop deafness – the fact that most cases occur in infants may reflect their greater susceptibility to severe infection rather than a particular vulnerability to 需无水印完整版请发邮件：wzxidian@gmail.com Doc uCo m P DF Tria l ww w.pd fwiz ard. com Bacterial Meningitis and Deafness in Sub-Saharan Africa 3 hearing impairment. At a community level, meningitis is one of the most common causes of hearing loss. In Kumasi, Ghana, meningitis is responsible for 8.5 per cent of cases of sensorineural hearing impairment in children.Brobby (1998) 4. Natural history Sensorineural heating loss is typically bilateral, and occurs within 48 hours of the development of meningitis, with the majority of children who go on to suffer permanent damage having abnormal hearing tests on admission to hospital. There appears to be an initial phase of mild, reversible damage. Significant sensorineural hearing loss persisting after the acute phase of the illness is characteristically permanent although cases of partial recovery have been documented on certain occasions. Mild, temporary, conductive deficits are common in the recovery phase. Pathological correlates for these clinical findings are still lacking but potential pathophysiological mechanisms are discussed below.DAYA et al (1997) 5. Pathology The auditory lesion in post-meningitic hearing loss remains obscure. It is likely that more than one mechanism of auditory pathway damage occurs. A body of clinical and experimental evidence suggests that the cochlea is the most frequent site of sensorineural damage, bacteria gaining access to the labyrinth via the cochlear aqueduct. DAYA et al (1998) Cell wall components directly toxic to cochlear hair cells, setting up a serous labyrinthitis In addition, these components also stimulate the inflammatory response, leading to suppurative labyrinthitis and permanent damage; in severe cases the labyrinth may be completely obliterated and neo-ossification occurs. The vestibular apparatus is commonly damaged in conjunction with this process. Other potential mechanisms of deafness include septic thrombophlebitic or embolisation of blood vessels supplying the inner ear and damage to the VIIIth cranial never or central auditory pathways. 6. Diagnosis Screening for deafness during hospitalization is an accurate predictor of hearing impairments at follow-up, and ideally should be performed on all cases. It is also important to examine the middle ear with tympanometry in order to assess conductive impairments, which can be expected to improve with time. A follow-up assessment at approximately 6 weeks, when acute inflammation has subsided, confirms the degree of sensorineural damage and allows appropriate rehabilitation to be instituted. Assessment of hearing loss following meningitis is currently based on audiometric methods. Unfortunately the inaccuracy of age-appropriate tests in healthy children, the infants’ lack of consistent response to sound and the effect of associated motor disorders tend to impair the validity of audiometry. More objective methods such as Brainstem Audiometry Evoked Responses (BAERs) and Oto-Acoustic Emissions (OAEs) have yet to reach the clinic in most parts of the continent. More objective methods such as Brainstean Auditory Evoked responses (BAERs) and Oto- Acustic Emulsions (OAEs) are the latest state of the art equipments for this purpose. (DAYA et, al 1998) 需无水印完整版请发邮件：wzxidian@gmail.com Doc uCo m P DF Tria l ww w.pd fwiz ard. com Meningitis 4 Fortunately, the Kumasi Hearing Assessments Centre established through the magnificent generosity of the Commonwealth Society for the Deaf is the only centre, recognized by the WHO, in Africa, South of the Sahara which has all these facilities. 7. Acute management Prompt Empirical antibiotic treatment should include Agents active agent all main pathogens for the eradication of the infecting organism in order to ensure optimal outcome. The introduction of sulphonamides in the 1950s (primarily for meningococcal meningitis) and of penicillins in the 1960s had a striking effect on incidence of mortality and mobility. The spread of plasmid-borne betalactamases in Hib led to the addition of chloramphenicol to therapy. This combination is still standard in most African countries. The latest challenge to this regimen has been the relatively recent appearance of penicillin-resistant pneumococci and meningococci. Further, some pneumococci are also chloramphenicol-resistant. This will undoubtedly affect the choice of antibiotics although the number of studies documenting a worsening clinical outcome is still small. In Europe and the USA third-generation cephalosporins have become first-line therapy but while these drugs remain relatively expensive, it is probably reasonable for most African hospitals to continue with the combination of a penicillin and chloramphenic