Biological Sciences
Bacterial Meningitis
Bacterial meningitis is a serious infection of the protective membranes covering the brain and spinal cord. It is caused by various bacteria, with symptoms including severe headache, fever, and stiffness in the neck. Prompt diagnosis and treatment with antibiotics are crucial to prevent potential complications such as brain damage or even death.
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12 Key excerpts on "Bacterial Meningitis"
eBook - PDF- George Wireko-Brobby(Author)
- 2012(Publication Date)
- IntechOpen(Publisher)
14 Laboratory Diagnosis of Meningitis S. Nagarathna, H. B. Veenakumari and A. Chandramuki Department of Neuromicrobiology, National Institute of Mental Health and Neurosciences (NIMHANS), Bengaluru Karnataka, India 1. Introduction Meningitis is an infection of the membranes (meninges) surrounding the brain and spinal cord. Meningitis is usually of multiple etiology-bacterial, fungal or viral yet bacteria remain the common etiological agent (Reid & Fallon, 1992). Meningitis can be acute, with a quick onset of symptoms, or chronic, lasting a month or more, or can be mild or aseptic, but the emphasis should be on identification of cause so that appropriate interventions can be applied. Bacterial Meningitis continues to be a potentially life threatening emergency with significant morbidity and mortality throughout the world and is an even more significant problem in many other areas of the world, especially in developing countries (Carbonnelle, 2009, Brouwer et al., 2010). Types of bacteria that cause Bacterial Meningitis vary by age group. Currently, the average age of contracting meningitis is above 25 years with Streptococcus pneumoniae, Neisseria meningitidis and Haemophilus influenzae being the most common pathogens (Ogunlesi et al., 2005, Brain, 2004 as cited in Maleeha Aslam et al., 2006). Trauma to the skull gives bacteria the potential to enter the meningeal space. Similarly, individuals with a cerebral shunt or related device are at increased risk of infection through those devices. In these cases, infections with Staphylococci, Pseudomonas aeruginosa and other gram-negative bacilli are more likely. Recurrent Bacterial Meningitis may be caused by persisting anatomical defects, either congenital or acquired, or by disorders of the immune system. (Brouwer et al., 2010) Tuberculous meningitis (TBM), is common in those from countries where tuberculosis is common, and is also encountered in those with immune problems, such as AIDS.
- Karen L. Roos, Allan R. Tunkel(Authors)
- 2010(Publication Date)
- Elsevier(Publisher)
Chapter 4 Bacterial Meningitis KAREN L. ROOS 1 * AND DIEDERIK VAN DE BEEK 2 1 Departments of Neurology and Neurosurgery, Indiana University School of Medicine, Indiana University Hospital, Indianapolis, IN, USA 2 Center of Infection and Immunity, Academic Medical Center, Amsterdam, The Netherlands INTRODUCTION Bacterial Meningitis is initially an acute purulent infec-tion of the meninges and subarachnoid space. It is a complex disorder in which injury is caused, in part, by the causative organism, and in part, by the host’s own inflammatory response. The inflammatory reac-tion involves the meninges, the subarachnoid space, the brain parenchyma, and the cerebral arteries and veins. The incidence of Bacterial Meningitis is esti-mated at 5–10 cases per 100, 000 persons per year (van de Beek et al., 2004, 2006a). There are approxi-mately 25, 000 cases of Bacterial Meningitis annually in the USA. This disease is more common in developing countries. In the meningitis belt of Africa, a region that extends from Ethiopia in the east to Senegal in the west, there are outbreaks of Bacterial Meningitis every 8–12 years with attack rates of 500–1000 cases per 100, 000 persons. In 1996, 152, 813 cases were reported to the World Health Organization with 15, 783 deaths (Rosenstein et al., 2001). Bacterial Meningitis is a neurological emergency that requires prompt recognition and initiation of therapy. ETIOLOGY The most common organisms that cause meningitis are bacteria with a polysaccharide capsule. The host’s initial response to a bacterial infection is to mount an antibody response. The inability to develop sufficient concentrations of antibody to the capsular polysaccha-ride results in invasive disease. Patients with defective humoral immunity are unable to mount an antibody response to a bacterial infection, and they are therefore unable to control infection caused by encapsulated bac-teria.
eBook - ePubInfections of the Central Nervous System
Pathology and Genetics
- Fabrice Chretien, Kum Thong Wong, Leroy R. Sharer, Fabrice Chretien, Kum Thong Wong, Leroy R. Sharer, Katy Keohane, Francoise Gray(Authors)
- 2020(Publication Date)
- Wiley-Blackwell(Publisher)
30 Pyogenic Infections of the CNS 1 : Acute Bacterial Meningitis Loic Le Guennec1,2 and Sandrine Bourdoulous11 Inserm, U1016, Institut Cochin, CNRS, UMR8104, Paris University, Paris, France2 La Pitie‐Salpetriere Hospital, APHP, Paris, FranceAbbreviations
BBBblood‐brain barrierBMBacterial MeningitisCNScentral nervous systemCSFcerebrospinal fluidDICdisseminated intravascular coagulationE. coliEscherichia coliEEGelectroencephalographyEoDearly‐onset diseaseGBSgroup B StreptococcusHibHaemophilus influenzae type b:L. monocytogenesListeria monocytogenesLoDlate‐onset diseaseLPLumbar punctureMRImagnetic resonance imagingM. tuberculosisMycobacterium tuberculosisNCAMneural cell adhesion moleculeN. meningitidisNeisseria meningitidisPCRpolymerase chain reactionPCV1313‐valent pneumococcal conjugate vaccinePMNLpolymorphonuclear leukocytesPPV2323‐valent pneumococcal polysaccharide vaccineIntroduction, definition, and historical perspective
Bacterial Meningitis (BM ) is an acute purulent infection of the meninges. It is the most common bacterial infection of the CNS and is a medical emergency that still has a high mortality and morbidity despite the overall improvements in its diagnosis and management. BM is one of the top 10 causes of infection‐related deaths worldwide, and about 40% of the survivors suffer neurological sequelae [1 ]. Hippocrates described meningitis 25 centuries ago [2 ], but the first described meningitis outbreak was in Geneva in 1805. An African outbreak was reported in 1840. One of the main causative bacteria, Neisseria meningitidis, was described by Anton Weichselbaum, an Austrian pathologist in 1887 (which he named “Diplococcus intracellularis meningitidis”) [3 ]. The clinical features were described by Kernig, a Russian neurologist in 1884, and later by Brudinski, a Polish physician. Both their names are associated with the classical signs of testing resistance to stretching of the inflamed meninges [4 ]. Meningococcal vaccine was developed in the 1970s and since then, vaccines have been introduced for several serotypes of meningococcus, pneumococcus, and other causes of BM (e.g.Haemophilus influenzae b[Hib
eBook - PDFThe Blood-Brain Barrier in Health and Disease, Volume Two
Pathophysiology and Pathology
- Katerina Dorovini-Zis(Author)
- 2015(Publication Date)
- CRC Press(Publisher)
5 The Blood-Brain Barrier in Bacterial Infections of the Central Nervous System Kwang Sik Kim Introduction Bacterial Meningitis, an in fl ammation of the meninges affecting the pia, arachnoid, and subarachnoid space that occurs in response to bacteria and bacterial products in the brain, continues to be an important cause of mortality and morbidity in infants, children and adults (Kim 2010). A major contributing factor to such mortality and morbidity is the incomplete understanding of the pathogenesis of Bacterial Meningitis. Almost all bacteria that are pathogenic to human beings have the potential to cause meningitis, but a relatively small number of bacteria account for most cases of acute Bacterial Meningitis in infants, children and adults, which include group B Streptococcus (GBS), Escherichia coli ( E. coli ), Listeria monocytogenes ( L. monocytogenes ), Streptococcus pneumoniae ( S. pneumoniae ), Neisseria meningitidis ( N. meningitidis ) and Haemophilus in fl uenzae type b (Hib), and the reasons for their predominance in causing Bacterial Meningitis remain incompletely understood. Several lines of evidence from human cases and experimental animal models of meningitis indicate that Bacterial Meningitis usually follows a high-level of bacteremia for GBS, E. coli , S. pneumoniae and Hib, and cerebral capillaries are the portal of entry into the brain. The blood-brain barrier protects the brain from any microbes Division of Pediatric Infectious Diseases, Johns Hopkins University School of Medicine, 200 North Wolfe St., Room 3157, Baltimore, MD 21287. Email: [email protected] The Blood-Brain Barrier in Bacterial Infections of the Central Nervous System 119 circulating in the blood. Recent studies, however, have demonstrated that meningitis-causing bacteria exhibit the ability to penetrate the blood-brain barrier and cause central nervous system (CNS) in fl ammation, resulting in meningitis (Kim 2001, 2002, 2003, 2008, 2010, 2012) .
eBook - PDFAM:STARs Infectious Diseases and Immunizations
Adolescent Medicine: State of the Art Reviews, Vol. 21, No. 2
- Paula K. AAP Section on Adolescent Health, Robert W. Frenck, Cynthia Holland Hall, Paula K. AAP Section on Adolescent Health, Robert W. Frenck, Cynthia Holland Hall(Authors)
- 2010(Publication Date)
- American Academy of Pediatrics(Publisher)
Meningitis and Encephalitis in Adolescents W. Garrett Hunt, MD, FAAP* Section of Infectious Diseases, Department of Pediatrics, College of Medicine, The Ohio State University, Nationwide Children’s Hospital, 700 Children’s Drive, Columbus, OH 43205 Meningitis is inflammation of the protective membranes that cover the brain and spinal cord, known collectively as the meninges, and encephalitis is inflammation of the brain. 1,2 Because central nervous system (CNS) infections occur within the confined space of the cranium or spinal column, they may be associated with increased intracranial and intraspinal pressure, altered blood flow, and, ultimately, neuronal injury. 3 These changes may lead to serious long-term consequences, in-cluding deafness, epilepsy, hydrocephalus, cognitive deficits, or even death, if not prevented or treated by certain emergency measures. 4,5 The objective of this review is to summarize the current epidemiology, diagnostic, and therapeutic algorithms, as well as prevention of meningitis and encephalitis in immunocompetent adolescents. Meningitis is signaled by the clinical symptoms of fever, meningismus (neck stiffness), and headache. 6,7 When altered mental status accompanies one or more of these symptoms, encephalitis or meningoencephalitis is present. 6,8,9 Patients with encephalitis should be distinguished from those with encephalopathy, de-fined as cerebral dysfunction without associated inflammation. Fever, cerebro-spinal fluid (CSF) pleocytosis, focal neurologic signs, and abnormalities on magnetic resonance imaging (MRI) of the brain are uncommon in patients with encephalopathy, whereas they are common in patients with encephalitis. In general, causes of meningitis are classified as bacterial or nonbacterial, equivalent to the terms septic and aseptic, respectively (see Fig. 1). The classic definition of bacterial (septic) meningitis requires identification of pyogenic bacteria on Gram stain or growth of bacteria on a culture medium.
- Pratibha Singhi, Diane E Griffin, Charles R Newton(Authors)
- 2014(Publication Date)
- Mac Keith Press(Publisher)
12 ACUTE Bacterial Meningitis Pratibha Singhi and Sunit Singhi Bacterial Meningitis is a devastating infection of the central nervous system (CNS) that has a high mortality and morbidity in spite of the availability of several new potent anti-microbials. CNS damage in meningitis is caused not only by the bacterial invasion, but also largely by the severe inflammatory response and its consequences. Early diagnosis, prompt antimicrobial therapy and supportive management are the keys to improving outcome. Aetiology Bacterial Meningitis beyond the neonatal period is caused in more than 90% of cases by the three major meningeal pathogens, Haemophilus influenzae , Neisseria meningitidis and Streptococcus pneumoniae . The incidence of H. influenzae type b (Hib) and S. pneumoniae meningitis decreased after the introduction of vaccines, and S. pneumoniae predominates in many parts of the world. Neonatal meningitis is caused mainly by group B streptococci, gram-negative bacilli and Listeria monocytogenes , and occasionally by other organisms. Group B streptococci are the main causative organisms in resource-rich countries, gram-negative bacilli in resource-poor ones (Zaidi et al. 2009). Listeria is rarely reported from resource-poor countries (Furyk et al. 2011). The aetiological organisms vary mainly with the age, the nutritional and immune status of the child, and the coexistence of other clinical conditions. The common pathogens that cause meningitis in various age groups and with specific predisposing conditions are shown in Tables 12.1 and 12.2. Epidemiology Bacterial Meningitis is essentially a disease of infants and children, although it can occur at any age. According to the World Health Organization (WHO), about 170 000 deaths per year are due to meningitis; the fatality rate is as high as 50% in untreated cases (WHO 2011).
eBook - PDF- Rachel L. Chin, Bradley W. Frazee, Zlatan Coralic(Authors)
- 2018(Publication Date)
- Cambridge University Press(Publisher)
50 Chapter 50 Introduction Although there is a broad differential in a patient presenting with fever and headache, a few infectious diagnoses need to be ruled in or out immediately. Acute Bacterial Meningitis is a critical diagnosis because delay of appropriate antimicrobial therapy increases morbidity and mortality. Distinguishing between bacterial, viral, and more chronic meningitides requires careful interpretation of multiple clinical and laboratory findings. The microbiology of meningitis is discussed below. Epidemiology The most recent US data studying hospitalizations for menin- gitis estimates that more than 800,000 people were hospital- ized for meningitis from 1988 to 1999. The majority of these hospitalizations were for viral (50%) and Bacterial Meningitis (23%). Fungal meningitis accounted for 9% of the hospitalizations and unspecified for 18%. As these numbers describe only hospi- talized patients, they underrepresent the actual incidence, espe- cially of viral meningitis. Although recent data on meningitis as a whole is lacking, the incidence of acute Bacterial Meningitis fell 31% between 1998 and 2011, primarily because of increased vac- cination in the United States during these years. However, there are still estimated to be over 4,000 reported cases of Bacterial Meningitis annually in the United States. The case-fatality rate has remained relatively stable over 1998 to 2007, though limited data suggests that widespread use of adjuvant corticosteroid therapy may be reducing the mortality rate of pneumococcal meningitis. Microbiology Acute Bacterial Meningitis Causes of acute Bacterial Meningitis vary by age. Neonates acquire organisms such as group B Streptococcus, Escherichia coli, or less commonly, Listeria monocytogenes, from passage through the mother’s birth canal.
eBook - PDF- Dawn Collins, John Goodfellow, Dulanka Silva, Ronan Dardis, Sanjoy Nagaraja(Authors)
- 2016(Publication Date)
- Scion Publishing(Publisher)
Epidemiology The annual incidence of bacterial menin-gitis is 4 per 100,000 in the UK, with peaks in infants and adolescents. Vaccinations against the common causes, Haemophilus influenzae type B and N. meningitidis type C, have significantly reduced the rate of new cases. Aetiology The pathogens responsible for bacte-rial meningitis vary depending on patient age, immune status and clinical setting ( Table 8.3 ). These associations predict the most effective initial broad spectrum antibi-otic therapy if meningitis is suspected. Pathogenesis Common bacteria in community-acquired meningitis, i.e. H. influenzae , Streptococcus pneumoniae and N. meningitidis , all normally colonise nasal cavities and skull sinuses. Invasion of intracranial compartments is more likely in the context of immunodefi-ciency or a breach in structural defences, for example after trauma or surgery. Bacterial invasion precipitates an acute inflammatory response with aggregation of polymorphonuclear cells. Spread through the subarachnoid space causes local and systemic complications ( Table 8.4 ). Clinical features Meningitis classically presents with fever and meningism (the triad of headache, pho-tophobia and neck stiffness or rigidity). The condition is usually be preceded by a pro-drome, such as respiratory tract or ear infec-tion. It is also associated with risk factors depending on the cause, for example trau-matic skull fracture with cerebrospinal fluid leak. The presence of a purpuric non-blanching rash strongly suggests meningococcal sep-ticaemia. The pathogenesis is a systemic in-flammatory response with likely disseminated intravascular coagulopathy, causing a combi-nation of severe vasodilation, capillary leak-age, haemorrhaging into skin and microvas-cular thromboses.
eBook - PDFFundamentals of Neurology
An Illustrated Guide
- Marco Mumenthaler, Heinrich Mattle(Authors)
- 2011(Publication Date)
- Thieme(Publisher)
e., the Lasègue, Brudzinski, and Kernig signs (p. 16). The clinical aspects of individual types of meningitis de-pend on the inciting organism and the immune state of the host. Acute Meningitis Acute Bacterial Meningitis Acute Bacterial Meningitis is caused by bacteria that can reach the meninges by any of three routes: hematogenous spread (e. g., from a focus of infec-tion in the nasopharynx), continuous extension (e. g., from the middle ear or paranasal sinuses), or direct contamination (through an open wound or CSF fistula). The clinical onset of purulent mening-itis is usually acute or subacute and patients very quickly become severely ill. The initiation of antibi-otic therapy as rapidly as possible is essential for a good outcome. Etiology. The organisms that most commonly cause acute, purulent meningitis are: in neonates , Escherichia coli , group B streptococci, and Listeria monocytogenes ; in children , Hemophilus influenzae , pneumococci, and meningococci ( Neisseria meningitidis ); in adults , pneumococci, meningococci, and, less commonly, staphylococci and gram-negative entero-bacteria. Clinical manifestations. The course of purulent meningitis is characterized by the meningitic signs and symptoms listed above, as well as by: myalgia, back pain; photophobia; if the infection is mainly located over the cerebral convexity, with irritation of the underlying brain parenchyma, epileptic seizures (40 %); cranial nerve deficits (10 to 20 %, sometimes per-manent deafness, particularly after pneumococcal infection); variably severe impairment of consciousness; in infection with Neisseria meningitidis , there may be petechial cutaneous hemorrhages and hemorrhagic necrosis of the adrenal cortex due to endotoxic shock (Waterhouse−Friderichsen syndrome). Diagnostic evaluation. The most important and most urgent component of the diagnostic evaluation is lumbar puncture.
eBook - ePub- Randall T. Hayden, Karen C. Carroll, Yi-Wei Tang, Donna M. Wolk, Randall T. Hayden, Karen C. Carroll, Yi-Wei Tang, Donna M. Wolk(Authors)
- 2016(Publication Date)
- ASM Press(Publisher)
References
1. Radetsky M . 2014. Fulminant Bacterial Meningitis. Pediatr Infect Dis J 33 : 204–207.[PubMed] [CrossRef]2. Mook-Kanamori BB , Geldhoff M , van der Poll T , van de Beek D . 2011. Pathogenesis and pathophysiology of pneumococcal meningitis. Clin Microbiol Rev 24 : 557–591.[PubMed] [CrossRef]3. Le EM , Loghin ME . 2014. Posterior reversible encephalopathy syndrome: a neurologic phenomenon in cancer patients. Curr Oncol Rep 16 : 383. [PubMed] [CrossRef]4. Pruitt AA , Graus F , Rosenfeld MR . 2013. Neurological complications of solid organ transplantation. Neurohospitalist 3 : 152–166.[PubMed] [CrossRef]5. Bruner KE , Coop CA , White KM . 2014. Trimethoprim-sulfamethoxazole-induced aseptic meningitis–not just another sulfa allergy. Ann Allergy Asthma Immunol 113 : 520–526.[PubMed] [CrossRef]6. Capone PM , Cohen ME . 1991. Seizures and cerebritis associated with administration of OKT3. Pediatr Neurol 7 : 299–301.[PubMed] [CrossRef]7. Heckenberg SG , Brouwer MC , van de Beek D . 2014. Bacterial Meningitis. Handb Clin Neurol 121 : 1361–1375.[PubMed] [CrossRef]8. Pruitt AA . 2012. CNS infections in patients with cancer. Continuum 18 : 384–405.[PubMed] [CrossRef]9. Safdieh JE , Mead PA , Sepkowitz KA , Kiehn TE , Abrey LE . 2008. Bacterial and fungal meningitis in patients with cancer. Neurology 70 : 943–947.[PubMed] [CrossRef]10. Tunkel AR , Hartman BJ , Kaplan SL , Kaufman BA , Roos KL , Scheld WM , Whitley RJ . 2004. Practice guidelines for the management of Bacterial Meningitis. Clin Infect Dis 39 : 1267–1284.[PubMed] [CrossRef]11. Swanson PA 2nd , McGavern DB . 2015. Viral diseases of the central nervous system. Curr Opin Virol 11C : 44–54.[PubMed] [CrossRef]12. Zunt JR , Baldwin KJ . 2012. Chronic and subacute meningitis. Continuum
eBook - PDF- Stanley Finger, Francois Boller, Kenneth L. Tyler(Authors)
- 2009(Publication Date)
- Elsevier(Publisher)
These characteristics are the sudden invasion, the violence of the headache, the vomiting, and especially the rapidity of the termination. It forms then, a distinct species, and the name of cerebral malignant, non-contagious (sic) fever is that which appears the best. The brain is the only Fig. 28.2. Gaspard Vieusseux (1746–1814). (From E.-R. Mullener, Six Geneva physicians on meningitis, J Hist Med Allied Health Sci 20: 1–26, 1965, with permission of Oxford University Press, publisher.) A HISTORY OF Bacterial Meningitis 421 organ in which post-mortem inspection has shown any alteration; the affection of the other parts appears to come only from the brain, and all the symptoms of it are nervous. (Vieusseux, 1806; translated by Major, 1945, pp. 188–189) Vieusseux’s colleague Andre ´ Matthey (1778–1842) reported on the same epidemic the following year, including a clear description of the cardinal pathologi-cal features including basilar accumulation of pus and congestion of the meningeal vessels. The vessels of the meninges were notably con-gested. A gelatinous humour covering the brain was markedly tinged with blood. There was fluid in the ventricles . . . The base of the brain was covered by a yellow puriform matter, with no obvious change in the underlying cerebral tis-sue. This exudation covered the optic chiasma and extended backwards towards the cerebel-lum, reaching for the space of an inch down the vertebral canal. (Matthey, 1806; quoted in Foster and Gaskell, 1916, pp. 2–3) Virtually identical outbreaks to the one in Geneva occurred in America in Massachusetts in 1806 and in Connecticut in 1807. Credit for the first American description of meningococcal meningitis is often given to Elisha North (1771–1843; Fig. 28.3) for his description of the Connecticut outbreak in his Treatise on a Malignant Epidemic Commonly Called Spotted Fever (North, 1811; Pleadwell, 1924).
eBook - PDF- Luca Saba(Author)
- 2016(Publication Date)
- CRC Press(Publisher)
650 22.8 Conclusion .................................................................................................................................................................. 652 References ................................................................................................................................................................................ 652 TABLE 22.1 Preconditions for Infection 1—Breach of barrier: surgical, medical, or traumatic 2—Immune dysfunction: AIDS, steroids, chemotherapy, and genetic 3—Change in micro- or macroenvironment 4—Loss of natural competitive regulatory factors 5—Evolution or mutation in the organism resulting in increased propensity for pathogenicity: HIV, other viruses, and bacterial resistance 6—Weaponization TABLE 22.3 Patterns of Brain Infection: From Peripheral to Central Neuritis—peripheral nerve Meningitis—coverings of the brain Empyema—surface collection Ventriculitis—inner surface of the brain Cerebritis—infection within brain parenchyma Abscess—infected collection within brain parenchyma TABLE 22.4 Patterns of Infection: Spine Discitis/osteomyelitis—infection of disc/endplate Epidural abscess—within the canal Paraspinal abscess, phlegmon, or cellulitis Meningitis Myelitis—infection of cord parenchyma Radiculitis/neuritis—infection of nerve roots TABLE 22.2 Vectors of CNS Infection I—Bacterial II—Viral III—Fungal IV—Parasitic V—Transmissible protein or prion 613 Infectious Diseases of the Brain and hang upside down and die spreading fungal spores all over the ground. This last example was observed by A. R. Wallace, a contemporary of Darwin, in the late 1800s, but not till 2009 did D. Hughes prove the connection [8] (Figure 22.1). Other examples of pathogen host behavioral influence are being actively studied. In sum, CNS infections involve many different infec-tious agents, some working solo and some working together, which display nonspecific but occasionally typical behaviors.
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