Bacterial Meningitis

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Bacterial meningitis


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Bacterial Meningitis :

Bacterial Meningitis Dr.T.V.Rao MD Dr.T.V.Rao MD 1

What is meningitis?……:

What is meningitis? …… The brain and spinal cord are covered by connective tissue layers collectively called the meninges which form the blood-brain barrier. 1-the pia mater (closest to the CNS) 2-the arachnoid mater 3-the dura mater (farthest from the CNS). The meninges contain cerebrospinal fluid (CSF). Meningitis is an inflammation of the meninges, which, if severe, may become encephalitis, an inflammation of the brain . Dr.T.V.Rao MD 2

In Meningitis Meninges are infected and Inflamed:

In Meningitis Meninges are infected and Inflamed Dr.T.V.Rao MD 3

Causes of Meningitis:

Causes of Meningitis - Bacterial Infections -Viral Infections - Fungal Infections (Cryptococcus neoformans Coccidiodes immitus) -Inflammatory diseases (SLE) Cancer -Trauma to head or spine. Dr.T.V.Rao MD 4


Introduction Bacterial meningitis is an inflammation of the leptomeninges, usually causing by bacterial infection. Bacterial meningitis may present acutely (symptoms evolving rapidly over 1-24 hours), sub acutely (symptoms evolving over 1-7days), or chronically (symptoms evolving over more than 1 week). Dr.T.V.Rao MD 5


Epidemiology Annual incidence in the developed countries is approximately 5-10 per 100000 . 30000 infants and children develop bacterial meningitis in United States each year. Approximately 90 per cent of cases occur in children during the first 5 years of life. Dr.T.V.Rao MD 6


Epidemiology Cases under age 2 years account for almost 75% of all cases and incidence is the highest in early childhood at age 6-12 months than in any other period of life. There are significant difference in the incidence of bacterial meningitis by season. Dr.T.V.Rao MD 7

Bacterial meningitis….. Etiological Agents::

Bacterial meningitis … .. Etiological Agents: Pneumococcal, Streptococcus pneumoniae (38%) Meningococcal, Neisseria meningitides (14%) Haemophilus influenza (4%) Staphylococcal, Staphylococcus aureus (5%) Tuberculosis, Mycobacterium tuberculosis Dr.T.V.Rao MD 8

Etiology differs ….:

Etiology differs …. Causative organisms vary with patient age, with three bacteria accounting for over three-quarters of all cases: Neisseria meningitidis (meningococcus) Haemophilus influenza (if very young and unvaccinated) Streptococcus pneumoniae ( pneumococcus) Dr.T.V.Rao MD 9

Other Bacterial Etiologies :

Other Bacterial Etiologies Other organisms Neonates and infants at age 2-3 months Escherichia coli B-hemolytic streptococci Staphylococcus aureus Staphylococcus epidermidis Listeria Monocytogenes Dr.T.V.Rao MD 10

Etiology in ….:

Etiology in …. Elderly and immunocompromised Listeria Monocytogenes Gram negative bacteria Hospital-acquired infections Klebsiella Escherichia coli Pseudomonas Staphylococcus aureus Dr.T.V.Rao MD 11


Etiology The most common organisms Neonates and infants under the age of 2months Escherichia coli Pseudomonas Group B Streptococcus Staphylococcus aureus Dr.T.V.Rao MD 12


Etiology Children over 2 months Haemophilus influenza type b Neisseria meningitides Streptococcus pneumoniae Children over 12 years Neisseria meningitides Streptococcus pneumoniae Dr.T.V.Rao MD 13

Routes of Infection:

Routes of Infection Major routes of leptomeninges infection Bacteria are mainly from blood. Uncommonly, meningitis occurs by direct extension from nearly focus (mastoiditis, sinusitis) or by direct invasion (dermoid sinus tract, head trauma, meningo-myelocele). Dr.T.V.Rao MD 14


Pathogenesis Susceptibility of bacterial infection on CNS in the children Immaturity of immune systems Nonspecific immune Insufficient barrier ( Blood-brain barrier ) Insufficient complement activity Insufficient chemo taxis of neutrophils Insufficient function of monocyte-macrophage system Blood levels of diminished interferon (INF) -γand interleukin -8 ( IL-8 ) Dr.T.V.Rao MD 15


Pathogenesis Susceptibility of bacterial infection on CNS in the children Specific immune Immaturity of both the cellular and Humoral immune systems Insufficient antibody-mediated protection Diminished immunologic response Bacterial virulence Dr.T.V.Rao MD 16


Pathogenesis A offending bacterium from blood invades the leptomeninges. Bacterial toxics and Inflammatory mediators are released. Bacterial toxics Lipopolysaccharide, LPS Teichoic acid Peptidoglycan Inflammatory mediators Tumor necrosis factor, TNF Interleukin-1, IL-1 Prostaglandin E2, PGE2 Dr.T.V.Rao MD 17


Pathogenesis Bacterial toxics and inflammatory mediators cause Suppurative inflammation. Inflammatory infiltration Vascular permeability alter Tissue edema Blood-brain barrier destroy Thrombosis Dr.T.V.Rao MD 18


Pathology Diffuse bacterial infections involve the leptomeninges, arachnoid membrane and superficial cortical structures, and brain parenchyma is also inflamed. Meningeal exudate of varying thickness is found. There is purulent material around veins and venous sinuses, over the convexity of the brain, in the depths of the sulci, within the basal cisterns, and around the cerebellum, and spinal cord may be encased in pus. Ventriculitis (purulent material within the ventricles) has been observed repeatedly in children who have died of their disease. Dr.T.V.Rao MD 19


Pathology Invasion of the ventricular wall with perivascular collections of purulent material, loss of ependymal lining, and subependymal gliosis may be noted. Subdural empyema may occur. Hydrocephalus is an common complication of meningitis. Obstructive hydrocephalus Communicating hydrocephalus Dr.T.V.Rao MD 20


Pathology Blood vessel walls may infiltrated by inflammatory cells. Endothelial cell injury Vessel stenosis Secondary ischemia and infarction Ventricle dilatation which ensues may be associated with necrosis of cerebral tissue due to the inflammatory process itself or to occlusion of cerebral veins or arteries. Dr.T.V.Rao MD 21


Pathology Inflammatory process may result in cerebral edema and damage of the cerebral cortex. Conscious disturbance Convulsion Motor disturbance Sensory disturbance Meningeal irritation sign is found because the spinal nerve root is irritated. Cranial nerve may be damaged Dr.T.V.Rao MD 22

Symptoms of Meningitis and Septicemia :

Symptoms of Meningitis and Septicemia Meningitis and meningococcal septicemia may not always be easy to detect, in early stages the symptoms can be similar to flu.  They may develop over one or two days, but sometimes develop in a matter of hours It is important to remember that symptoms do not appear in any particular order and some may not appear at all. Dr.T.V.Rao MD 23

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Clinical manifestation:

Clinical manifestation Bacterial meningitis may present acutely (symptoms evolving rapidly over 1-24 hours) in most cases. Symptoms and signs of upper respiratory or gastrointestinal infection are found before several days when the clinical manifestations of bacterial meningitis happen. Some patients may access suddenly with shock and DIC. Dr.T.V.Rao MD 25

Clinical manifestation:

Clinical manifestation Toxic symptom all over the body Hyperpyrexia Headache Photophobia Painful eye movement Fatigued and weak Malaise, myalgia, anorexia, Vomiting, diarrhea and abdominal pain Cutaneous rash Petechiae, purpura Dr.T.V.Rao MD 26

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Clinical manifestation:

Clinical manifestation Clinical manifestation of CNS Increased intracranial pressure Headache Projectile vomiting Hypertension Bradycardia Bulging fontanel Cranial sutures diastasis Coma DE cerebrate rigidity Cerebral hernia Dr.T.V.Rao MD 28

Clinical manifestation:

Clinical manifestation Clinical manifestation of CNS Meningeal irritation sign Neck stiffness Positive Kernig ’ s sign Positive Brudzinski ’ s sign Dr.T.V.Rao MD 29

Kernig's sign.:

Kernig's sign. One of the physically demonstrable symptoms of meningitis is Kernig's sign. Severe stiffness of the hamstrings causes an inability to straighten the leg when the hip is flexed to 90 degrees. Dr.T.V.Rao MD 30

Brudzinski's sign:

Brudzinski's sign Another physically demonstrable symptoms of meningitis is Brudzinski's sign. Severe neck stiffness causes a patient's hips and knees to flex when the neck is flexed. Dr.T.V.Rao MD 31

Clinical manifestation:

Clinical manifestation Clinical manifestation of CNS Seizures Seizures occur in about 20%-30% of children with bacterial meningitis. Seizures is often found in Haemophilus influenza and pneumococcal infection. Seizures is correlative with the inflammation of brain parenchyma, cerebral infarction and electrolyte disturbances. Dr.T.V.Rao MD 32

Clinical manifestation:

Clinical manifestation Clinical manifestation of CNS Conscious disturbance Drowsiness Clouding of consciousness Coma Psychiatric symptom Irritation Dysphoria dullness Dr.T.V.Rao MD 33

Clinical manifestation:

Clinical manifestation Clinical manifestation of CNS Meningeal irritation sign Neck stiffness Positive Kernig ’ s sign Positive Brudzinski ’ s sign Dr.T.V.Rao MD 34

Clinical manifestation:

Clinical manifestation Clinical manifestation of CNS Transient or permanent paralysis of cranial nerves and limbs may be noted. Deafness or disturbances in vestibular function are relatively common. Involvement of the optic nerve, with blindness, is rare. Paralysis of the 6 th cranial nerve, usually transient, is noted frequently early in the course. Dr.T.V.Rao MD 35

Clinical manifestation:

Clinical manifestation Symptom and signs of the infant under the age of 3 months In some children, particularly young infants under the age of 3 months, symptom and signs of meningeal inflammation may be minimal. Fever is generally present, but its absence or hypothermia in a infant with meningeal inflammation is common. Only irritability, restlessness, dullness , vomiting, poor feeding, cyanosis, dyspnea, jaundice, seizures, shock and coma may be noted. Bulging fontanel may be found, but there is not meningeal irritation sign. Dr.T.V.Rao MD 36

Skin rashes:

Skin rashes Is due to small skin bleed All parts of the body are affected The rashes do not fade under pressure Pathogenesis: a. Septicemia b. wide spread endothelial damage c. activation of coagulation d. thrombosis and platelets aggregation e. reduction of platelets (consumption ) f. BLEEDING rashes 2.adrenal hemorrhage Adrenal hemorrhage is called Waterhouse-Friderichsen Syndrome.It cause acute adrenal insufficiency and is uaually fatal Dr.T.V.Rao MD 37

Skin rashes:

Skin rashes Dr.T.V.Rao MD 38

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‘Glass Test’ :

‘ Glass Test’ A rash that does not fade under pressure will still be visible when the side of a clear drinking glass is pressed firmly against the skin. If someone is ill or obviously getting worse, do not wait for a rash. It may appear late or not at all. A fever with a rash that does not fade under pressure is a medical emergency. Dr.T.V.Rao MD 40

Complications :

Complications Subdural effusion Subdural effusions occur in about 10%-30% of children with bacterial meningitis. Subdural effusions appear to be more frequent in the children under the age of 1 year and in Haemophilus influenza and pneumococcal infection. Clinical manifestations are enlargement in head circumference, bulging fontanel, cranial sutures diastasis and abnormal trans illumination of the skull. Subdural effusions may be diagnosed by the examination of CT or MRI and subdural pricking. Dr.T.V.Rao MD 41


Complication Ependymitis Neonate or infant with meningitis Gram-negative bacterial infection Clinical manifestation Persistent hyperpyrexia, Frequent convulsion Acute respiratory failure Bulging fontanel Ventriculomegaly (CT) Cerebrospinal fluid by ventricular puncture WBC>50×10 9 /L Glucose<1.6mmol/L Protein>o.4g/L Dr.T.V.Rao MD 42


Complications Cerebellar hyponatremia Syndrem of inappropriate secretion of antidiuretic hormone (SIADH) Hyponatremia Degrade of blood osmotic pressure Aggravated cerebral edema Frequent convulsion Aggravated c onscious disturbance Dr.T.V.Rao MD 43


Complication Hydrocephalus Increased intracranial pressure Bulging fontanel Augmentation of head circumference Brain function disorder Other complication Deafness or blindness Epilepsy Paralysis Mental retardation Behavior disorder Dr.T.V.Rao MD 44

Meningococcal Meningitis:

Meningococcal Meningitis Less common bacterial causes of Meningitis, such as Staphylococci, enteric bacteria, group B streptococci and Listeria, occur in sub-populations like the immunocompromised, neonates, or head trauma patients. Patients with Meningococcal Meningitis present with sudden onset of fever, intense headache, nausea, vomiting, stiff neck and, frequently, a petechial rash with pink macules or, very rarely, vesicles. Delirium and coma often appear. Case fatality rate is between 5% and 15%. Dr.T.V.Rao MD 45

Laboratory Findings:

Laboratory Findings Peripheral hemogram Total WBC count 20×10 9 /L ~ 40×10 9 /L WBC Decreased WBC count at severe infection Leukocyte differential count 80% ~ 90% Neutrophils Dr.T.V.Rao MD 46


Diagnosis Isolation of the organism from CSF or blood. Dr.T.V.Rao MD 47

Characteristics of CSF on common disease in CNS :

Characteristics of CSF on common disease in CNS PM TM VW FM TE Pressure ↑ ↑ - or↑ ↑↑ ↑ Cloudiness ++ or +++ + - ± - Pandy T ++ or +++ + or +++ ±or ++ + or +++ - WBC ↑↑↑ N ↑ L - or↑L ↑ M - Protein ↑ ↑ ↑ ↑ ↑ ↑ - or↑ ↑ ↑ - or ± Glucos ↓ ↓ ↓ ↓ ↓ - ↓ ↓ - Chloridate - or ↓ ↓ ↓ ↓ - ↓ ↓ - Cultivation Bacterium TB Viral Fungus - Dr.T.V.Rao MD 48

Laboratory Findings:

Laboratory Findings Rout e xamination of cerebrospinal fluid (CSF) Increased pressure of cerebrospinal fluid Cloudiness Evident Increased total WBC count (>1000×10 9 /L) Evident Increased neutrophils in leukocyte differential count Evident Decreased glucose (<1.1mmol/l) Evident Increased protein level Decreased or normal chlorinate CSF film preparation or cultivation : positive result Dr.T.V.Rao MD 49

Laboratory Findings:

Laboratory Findings Especial examination of CSF Specific bacterial antigen test Countercurrent immuno-electrophoresis Latex agglutination Immunoflorescent test Neisseria meningitides (meningococcus) Haemophilus influenza Streptococcus pneumoniae ( pneumococcus) Group B streptococcus Dr.T.V.Rao MD 50

Laboratory Findings:

Laboratory Findings Especial examination of CSF Other test of CSF LDH Lactic acid CRP TNF and Ig Neuron specific enolase (NSE) Dr.T.V.Rao MD 51

Laboratory Findings:

Laboratory Findings Other bacterial test Blood cultivation Film preparation of skin petechiae and purpura Secretion culture of local lesion Imageology examination Dr.T.V.Rao MD 52


Diagnosis Diagnostic methods A careful evaluation of history A careful evaluation of infant’s signs and symptoms A careful evaluation of information on longitudinal changes in vital signs and laboratory indicators Rout e xamination of cerebrospinal fluid (CSF) Dr.T.V.Rao MD 53

Differential diagnosis:

Differential diagnosis Clinical manifestation of bacterial meningitis is similar to clinical manifestation of viral, tuberculosis , fungal and aseptic meningitis. Differentiation of these disorders depends upon careful examination of cerebrospinal fluid obtained by lumbar puncture and additional immunologic, roentgenographic, and isotope studies. Dr.T.V.Rao MD 54

Treatment Antibiotic Therapy:

Treatment Antibiotic Therapy Therapeutic principle Good permeability for Blood-brain barrier Drug combination Intravenous drip Full dosage Full course of treatment Dr.T.V.Rao MD 55

Antibiotic Therapy:

Antibiotic Therapy Selection of antibiotic No Certainly Bacterium Community-acquired bacterial infection Nosocomial infection acquired in a hospital Broad-spectrum antibiotic coverage as noted below Children under age 3 months Cefotaxime and ampicillin Ceftriaxone and ampicillin (children over age 1months) Children over 3 months Cefotaxime or Ceftriaxone or ampicillin and chloramphenicol Dr.T.V.Rao MD 56

Antibiotic Therapy:

Antibiotic Therapy Certainly Bacterium Once the pathogen has been identified and the antibiotic sensitivities determined, the most appropriate drugs should selected. N meningitides : penicillin, - cephalosporin S pneumoniae: penicillin, - cephalosporin, Vancomycin H influenza: ampicillin, cephalosporin S aureus: penicillin, nefcillin , Vancomycin E coli: ampicillin, chloramphenicol , - cephalosporin Dr.T.V.Rao MD 57

Antibiotic Therapy:

Antibiotic Therapy Course of treatment 7 days for meningococcal infection 10 ~ 14 days for H influenza or S pneumoniae infection More than 21 days for S aureus or E coli infection 14 ~ 21 days for other organisms Dr.T.V.Rao MD 58

Treatment General and Supportive Measures:

Treatment General and Supportive Measures Monitor of vital sign Correcting metabolic imbalances Supplying sufficient heat quantity Correcting hypoglycemia Correcting metabolic academia Correcting fluids and electrolytes disorder Application of cortical hormone Lessening inflammatory reaction Lessening toxic symptom lessening cerebral edema Dr.T.V.Rao MD 59

General and Supportive Measures:

General and Supportive Measures Treatment of hyperpyrexia and seizures Pyretolysis by physiotherapy and/or drug Convulsive management Diazepam Phenobarbital Subhibernation therapy Treatment of increased intracranial pressure Dehydration therapy 20%Mannitol 5ml/kg vi q6h Lasix 1-2mg/kg vi Dr.T.V.Rao MD 60

General and Supportive Measures:

General and Supportive Measures Treatment of septic shock and DIC Volume expansion Dopamine Corticosteroids Heparin Fresh frozen plasma Platelet transfusions Dr.T.V.Rao MD 61

Treatment Complication Measures:

Treatment Complication Measures Subdural effusions Subdural pricking Draw-off effusions on one side is 20-30ml/time. Once daily or every other day is requested. Time cell of pricking may be prolonged after 2 weeks. Ependymitis Ventricular puncture — drainage Pressure in ventricle be depressed. Ventricular puncture may give ventricle an injection of antibiotic. Dr.T.V.Rao MD 62

Complication Measures:

Complication Measures Hydrocephalus Operative treatment Adhesiolysis By-pass operation of cerebrospinal fluid Dilatation of aqueduct SIADH (Cerebral hyponatremia) Restriction of fluid supplement of serum sodium diuretic Dr.T.V.Rao MD 63


Prognosis Appropriate antibiotic therapy reduces the mortality rate for bacterial meningitis in children, but mortality remain high. Overall mortality in the developed countries ranges between 5% and 30%. 50 percent of the survivors have some sequelae of the disease. Dr.T.V.Rao MD 64


Prognosis Prognosis depends upon many factors: Age Causative organism Number of organisms and bacterial virulence Duration of illness prior to effective antibiotic therapy Presence of disorders that may compromise host response to infection Dr.T.V.Rao MD 65

Aseptic Meningitis:

Aseptic Meningitis Definition: A syndrome characterized by acute onset of meningeal symptoms, fever, and cerebrospinal fluid pleocytosis, with bacteriologically sterile cultures. Laboratory criteria for diagnosis : CSF showing ≥ 5 WBC/cu mm No evidence of bacterial or fungal meningitis. Case classification Confirmed : a clinically compatible illness diagnosed by a physician as aseptic meningitis, with no laboratory evidence of bacterial or fungal meningitis Comment Aseptic meningitis is a syndrome of multiple etiologies, but most cases are caused by a viral agent Dr.T.V.Rao MD 66

Viral Meningitis:

Viral Meningitis Etiological Agents: Enteroviruses (Coxsackie's and echovirus): most common. -Adenovirus -Arbovirus -Measles virus -Herpes Simplex Virus -Varicella Reservoirs: -Humans for Enteroviruses, Adenovirus, Measles, Herpes Simplex, and Varicella -Natural reservoir for arbovirus birds, rodents etc. Modes of transmission : -Primarily person to person and arthopod vectors for Arboviruses Incubation Period: -Variable. For enteroviruses 3-6 days, for arboviruses 2-15 days Treatment : No specific treatment available . Most patients recover completely on their own . Dr.T.V.Rao MD 67

Non Polio Enteroviruses:

Non Polio Enteroviruses Types : 62 different types known: -23 Coxsackie A viruses, -6 Coxsackie B viruses, -28 echoviruses, and 5 other How common? -90% of all viral meningitis is caused by Enteroviruses -Second only to "common cold" viruses, the rhinoviruses. -Estimated 10-15 million/ more symptomatic infections/yr in US Who is at risk? Everyone. How does infection spread? Virus present in the respiratory secretions & stool of a patient. Direct contact with secretions from an infected person. Parents, teachers, and child care center workers may also become infected by contamination of the hands with stool. Dr.T.V.Rao MD 68

Public Health Importance:

Public Health Importance Challenges: -Educating public -Timely reporting and records keeping -Updating information daily. -Alleviating public anxiety and concerns -Collaborating with health partners Opportunities : -Educating public -Communication -Strengthening partnerships Dr.T.V.Rao MD 69

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Programme Created by Dr.T.V.Rao MD for Medical and Paramedical Students in the Developing World Email Dr.T.V.Rao MD 70

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