assoc prof dr meral sonmezoglu yeditepe university hospital

Assoc Prof Dr Meral SonmezogluYeditepe University Hospital

Acute and chronic meningitis, encephalitis III

Acute and chronic meningitis, encephalitis III

The two major divisions in the nervous system

are the central nervous system (CNS), composed

of the brain and the spinal cord, and the

peripheral nervous system (PNS), composed of

afferent (input to CNS) and efferent (output to

periphery) neurons.

Within the PNS, major divisions are the somatic

nervous system (controls skeletal muscle) and

in the autonomic nervous system, which has

two branches: the parasympathetic (rest and

digest) and the sympathetic (emergency)

branches.

Protection of the BrainProtection of the Brain

The brain is protected by bone, meninges, and cerebrospinal fluid (CSF)

The CSF circulates through the ventricular system

• CSF is produced by the choroid plexus inside the ventricles.

• It circulates through the ventricles.

• From the fourth ventricle, CSF enters the subarachnoid space, between the arachnoid mater and pia mater.

• Reabsorbed from subarachnoid space into venous blood via the arachnoid villi

Meninges (s. meninx)Meninges (s. meninx)

Three connective tissue membranes external to the CNS – dura mater, arachnoid mater, and pia mater

Functions:

Cover and protect the CNS

Protect blood vessels and enclose venous sinuses

Contain cerebrospinal fluid (CSF)

Form partitions within the skull

MeningesMeninges

Dura MaterDura Mater

Tough meninx composed of two fibrous CT layers. Layers separate in certain areas and form dural sinuses. Dural sinuses collect venous blood from the brain.

3 dural septa limit excessive movement of the brain

Falx cerebri – dural fold that dips into the longitudinal fissure

Falx cerebelli – runs along the vermis of the cerebellum

Tentorium cerebelli – horizontal fold extending into the transverse fissure

Dura MaterDura Mater

Arachnoid MaterArachnoid Mater

Separated from the dura mater by the subdural space (a narrow serous cavity)

Beneath the arachnoid is a wide subarachnoid space filled with CSF and large blood vessels

Arachnoid villi protrude superiorly and permit CSF to be absorbed into venous blood

Pia MaterPia Mater

Deepest meninx – delicate CT that clings tightly to the brain and follows convolutions

Cerebrospinal Fluid (CSF)Cerebrospinal Fluid (CSF)

Watery, similar in composition to blood plasma, but contains less protein and different ion concentrations than plasma

Forms a liquid cushion that gives buoyancy to the CNS organs, prevents the brain from crushing under its own weight

Protects the CNS from blows and other trauma

Nourishes the brain and may carry chemical signals from one part of the brain to another

Choroid PlexusesChoroid Plexuses

Clusters of interwoven capillaries in each ventricle between the pia mater and a layer of ependymal cells.

Ion pumps allow them to alter the ion concentrations of the CSF

Help cleanse CSF by removing wastes

Circulation of CSFCirculation of CSF

Blood-Brain BarrierBlood-Brain Barrier

Protective mechanism that helps maintain a stable environment for the brain

Bloodborne substances in brain capillaries are separated from neurons by:

Continuous endothelium of capillary walls

Relatively thick basal lamina

Bulbous feet of astrocytes

Least permeable capillaries in the body due the nature of the tight junctions between endothelial cells

Blood-Brain Barrier: FunctionsBlood-Brain Barrier: Functions

Selective barrier that allows nutrients to pass freely

Is ineffective against substances that can diffuse through plasma membranes (fats, gasses, alcohol)

Absent in some areas (vomiting center and the hypothalamus), allowing these areas to monitor the chemical composition of the blood

MeningitisMeningitis

Meningitis is a clinical syndrome characterized by inflammation of the meninges

ClassificationClassification

• Depending on the duration of symptoms, meningitis may be classified as acute or chronic.

• Acute meningitis denotes the evolution of symptoms within hours to several days, while chronic meningitis has an onset and duration of weeks to months.

• The duration of symptoms of chronic meningitis is characteristically at least 4 weeks.

ClassificationClassification

• Meningitis can also be classified according to its etiology.


• Bacterial

• Viral ( aseptic)

• TB

• Fungal

• Chemical

• Parasitic

• ? Carcinomatous

Classification of MeningitisClassification of Meningitis

• Infectious• Bacterial

• Viral

• Fungal

• Non-infectious• Drug-Induced

• Neoplastic

• Autoimmune

22%

54%

24%

Bacterial Viral Non-Infectious

Bacterial Meningitis in AdultsBacterial Meningitis in Adults

•Deeks SL. Bacterial meningitis in Canada (1994-2001). Canadian Communicable Disease Report. Dec 2005. 31:23.

Viral MeningitisViral Meningitis

Enteroviruses85%

HSV3%

Arborviruses10%

Other2%


• Aseptic meningitis is a broad term that denotes a non-pyogenic cellular response, which may be caused by many different etiologic agents

• Many of these cases are found to have a viral etiology and can then be reclassified as acute viral meningitis (eg, enterovirus meningitis, herpes simplex virus [HSV] meningitis).

Bacterial Bacterial MeningitisMeningitis

• Definition

• Bacterial meningitis is an inflammatory response to bacterial infection of the pia-arachnoid and CSF of the subarachnoid space

• Epidemiology

• Incidence is between 3-5 per 100,000

• More than 2,000 deaths annually in the U.S.

• Relative frequency of bacterial species varies with age.


• Epidemiology

• Neonates (< 1 Month)

• Gm (-) bacilli 50-60%

• Grp B Strep 20-40%

• Listeria sp. 2-10%

• H. influenza 0-3%

• S. pneumo 0-5%


• Epidemiology

• Children (1 month to 15 years)

• H. influenzae 40-60%– Declining dramatically in many geographic regions

• N. meningitidis 25-40%

• S. pneumo 10-20%


• Epidemiology

• Adults (> 15 years)

• S. pneumo 30-50%

• N. Meningitidis 10-35%

– Major cause in epidemics

• Gm (-) Bacilli 1-10%

– Elderly

• S. aureus 5-15%

• H. influenzae 1-3%

• >60 include Listeria, E. coli, Pseudomonas


• Pathogenesis

• Majority of cases are hematogenous in origin

• Organisms have virulence factors that allow bypassing of normal defenses

• Proteases

• Polysaccharidases


• Pathology and Pathogenesis

• Sequential steps allow the pathogen into the CSF

• Nasopharyngeal colonization

• Nasopharyngeal epithelial cell invasion

• Bloodstream invasion

• Bacteremia with intravascular survival

• Crossing of the BBB and entry into the CSF

• Survival and replication in the subarachnoid space

Nasopharynx -> blood -> subarachnoid space

Pathophysiology of Bacterial MeningitisPathophysiology of Bacterial Meningitis

• Bacterial colonization within the subarachnoid space

• Initiation of inflammatory response which leads to:• Endothelial damage

• Disruption of the blood-brain barrier

• On a larger scale, this results in:• Cerebral edema

• Cytotoxic

• Vasogenic

• Interstitial

• Increased ICP


• Pathology and Pathogenesis

• Key advances in the pathophysiology of meningitis include the pivotal role of cytokines (eg, tumor necrosis factor-alpha [TNF-alpha], interleukin [IL]–1), chemokines (IL-8), and other proinflammatory molecules in the pathogenesis of pleocytosis and neuronal damage during bacterial meningitis.

• Increased CSF concentrations of TNF-alpha, IL-1, IL-6, and IL-8 are characteristic findings in patients with bacterial meningitis


• Pathology

• Hallmark

• Exudate in the subarachnoid space

• Accumulation of exudate in the dependent areas of the brain

• Large numbers of PMN’s

• Within 2-3 days inflammation in the walls of the small and medium-sized blood vessels

• Blockage of normal CSF pathways and blockage of the normal absorption may lead to obstructive hydrocephalus


• Overall, the net result is vascular endothelial injury and increased BBB permeability leading to the entry of many blood components into the subarachnoid space.

• This contributes to vasogenic edema and elevated CSF protein levels.

• In response to the cytokines and chemotactic molecules, neutrophils migrate from the bloodstream and penetrate the damaged BBB, producing the profound neutrophilic pleocytosis characteristic of bacterial meningitis.

Pathophysiology of Bacterial MeningitisPathophysiology of Bacterial Meningitis

Complications:

• Seizures

• Hydrocephalus

• Infarction

• Herniation •From van de Beek D Community-acquired bacterial meningitis in adults. 354:1. 44.

Clinical Presentation of Clinical Presentation of MeningitisMeningitis

• Classic signs ;

• fever, headache, neck stiffness, photophobia, nausea, vomiting, and signs of cerebral dysfunction (eg, lethargy, confusion, decreased level of consciousness coma).

• The triad of fever, nuchal rigidity, and change in mental status is found in only two thirds of patients

• Atypical presentation may be observed in certain groups (elderly, diabetic, neutropenic, immunocompromised hosts..).

Clinical Presentation of Clinical Presentation of MeningitisMeningitis

• Signs of cerebral dysfunction are common, including confusion, irritability, delirium, and coma. These are usually accompanied by fever and photophobia.

• Signs of meningeal irritation are observed in only approximately 50% of patients with bacterial meningitis, and their absence certainly does not rule out meningitis

MeningitisMeningitis• Clinical Manifestations – Nuchal rigidity

• Kernig’s

• Pt supine with flexed knee has increased pain with passive extension of the same leg

• Brudzinski’s

• Supine pt with neck flexed will raise knees to take pressure off of the meninges

• Present in 50% of acute bacterial meningitis cases

• Cranial Nerve Palsies

• IV, VI, VII

• Seizures

Brudzinski’s SignBrudzinski’s Sign

Kernig’s SignKernig’s Sign

Amos’s SignAmos’s Sign

Hips & knees flexed

Back arched

Neck in extension

Trunk supported by arms


• Focal neurologic signs may develop as a result of ischemia from vascular inflammation and thrombosis

• Papilledema and other signs of increased ICP may be present.

• Coma, increased blood pressure with bradycardia, and cranial nerve III palsy may be present.

• The presence of papilledema also suggests a possible alternate diagnosis (eg, brain abscess).


•Papilledema


• Clinical Manifestations - Meningococcemia

• Prominent rash

• Diffuse purpuric lesions principally involving the extremities

• Fever, hypotension, DIC

• History of terminal complement deficiency

• Classic findings often absent

• Neonates

• Elderly

Diagnosis of Diagnosis of MeningitisMeningitis

• Diagnosis

• Assess for increased ICP

• Papilledema

• Focal neurologic findings

• Defer LP until CT scan or MRI obtained if any of above present

• If suspect meningitis and awaiting neuroimaging

• Obtain BC’s and start empiric Abx


Obtain CT scan before lumbar puncture in patients with:

• Immunucompromised state

• History of CNS disease

• New onset seizures

• Papilledema

• Altered level of consciousness

• Focal neurologic signs


• Obtain blood cultures and give empiric antibiotics if LP is delayed

• Spinal tap is performed

• needle is inserted into an area in the lower back

• Identification of the type of bacteria

• is important for selection of correct antibiotics.

Diagnosing MeningitisDiagnosing Meningitis

Lumbar punctureLumbar puncture

LP-CSFLP-CSF

• Tube # 1 Protein & Glucose

• Tube # 2 Gram stain & Culture

• Tube # 3 Cell count & differential

• Tube # 4 Store ( PCR, viral studies etc)


• Diagnosis• CSF Findings :

Opening pressure

Appearance

Cell count & differential

Glucose

Protein

Gram stain & culture

Bacterial MeningitisBacterial Meningitis

• Opening pressure: high, > 200 mmH20

• Cloudy

• 1000-5000 cells/mm3 with a neutrophil predominance of about 80-95%

• <40mg/dl and less than 2/3 of the serum glucose

• Protein elevated

Agent Opening Pressure

WBC count per µL

Glucose (mg/dL)

Protein (mg/dL)

Microbiology

Bacterial meningitis

200-300 100-5000; >80% PMNs*

<40 >100 Specific pathogen demonstrated in 60% of Gram stains and 80% of cultures

Viral meningitis

90-200 10-300; lymphocytes

Normal, reduced in LCM and mumps

Normal but may be slightly elevated

Viral isolation, PCR† assays

Tuberculous meningitis

180-300 100-500; lymphocytes

Reduced, <40 Elevated, >100 Acid-fast bacillus stain, culture, PCR

Cryptococcal meningitis


Reduced 50-200 India ink, cryptococcal antigen, culture

Aseptic meningitis


Normal Normal but may be slightly elevated

Negative findings on workup

Normal values 80-200 0-5; lymphocytes 50-75 15-40 Negative findings on workup

•


• Diagnosis

• Rapid Tests

• CIE (Counter immunoelectrophoresis/ latex agglut.)

• PCR

• CT/MRI

• Little role in DIAGNOSIS of meningitis

• Obtain if suspect increased ICP


• Diagnosis

• Additional Tests

• CBC w/ diff

• Blood cultures

• CXR

• Electrolytes and renal function

Bacterial CulturesBacterial Cultures

• “Gold standard”

• Positive in 75-85% who have not been treated with antibiotics


• Differential Diagnosis

• CNS infections (abscess, encephalitis)

• Viral/ Tb/ Lyme meningitis

• Ricketsial infections

• Cerebral vasculitis

• Subarachnoid hemorrhage

• Neurosyphilis

Risk and/or Predisposing Factor Bacterial Pathogen

Age 0-4 weeks S agalactiae (group B streptococci)E coli K1L monocytogenes

Age 4-12 weeks S agalactiae E coli H influenzae S pneumoniae N meningitidis

Age 3 months to 18 years N meningitidis S pneumoniae H influenzae

Age 18-50 years S pneumoniae N meningitidis H influenzae

Age older than 50 years S pneumoniae N meningitidis L monocytogenes Aerobic gram-negative bacilli

Immunocompromised state S pneumoniae N meningitidis L monocytogenes Aerobic gram-negative bacilli

Intracranial manipulation, including neurosurgery

Staphylococcus aureus Coagulase-negative staphylococciAerobic gram-negative bacilli, includingPseudomonas aeruginosa

Basilar skull fracture S pneumoniae H influenzae Group A streptococci

CSF shunts Coagulase-negative staphylococciS aureus Aerobic gram-negative bacilliPropionibacterium acnes

Fungi Cryptococcus neoformans C immitis B dermatitidis H capsulatum Candida speciesAspergillus species

Viruses Enterovirus PoliovirusEchovirusCoxsackievirus ACoxsackievirus BEnterovirus 68-71

Herpesvirus HSV-1 and HSV-2Varicella-zoster virusEBVCMVHHV*-6HHV-7

Paramyxovirus Mumps virusMeasles virus

Togavirus Rubella virus

Flavivirus Japanese encephalitis virusSt. Louis encephalitis virus

Bunyavirus California encephalitis virusLa Crosse encephalitis virus

Alphavirus Eastern equine encephalitis virusWestern equine encephalitis virusVenezuelan encephalitis virus

Reovirus Colorado tick fever virus

Arenavirus LCM virus

Rhabdovirus Rabies virus

Retrovirus HIV

MeningitisMeningitis• Treatment

• Emergent empirical antimicrobial therapy• Based on age and underlying disease status

• Empiric antibiotic regimines

• Neonates (<3 months)

– Ampicillin plus a third generation cephalosporin

• Children

– Third generation cephalosporin ( alternative -ampicillin and chloramphenicol)

• Young adults

– Third generation cephalosporin (Ceftriaxone) + Vancomycin


• Treatment

• Empiric Antibiotic Regimines

• Older adults– Ampicillin in combination with third generation ceph.

• Postneurosurgical Pt’s– Vancomycin plus ceftazidime until cultures are

available


• Treatment

• N. Meningitidis

• High dose Pen G

• S. pneumoniae

• Ceftriaxone

• For areas with high level resistance – Vancomycin plus third generation cephalosporin or

rifampin


• Treatment

• Gm (-) Enterics

• Third generation cephalosporins

• L. monocytogenes

• Ampicillin

• S. aureus

• Vancomycin or Nafcillin

• S. epidermidis

• Vancomycin

TreatmentTreatment

Predisposing Feature Antibiotic(s)

Age 0-4 weeks Ampicillin plus cefotaxime or an aminoglycoside

Age 1-3 months Ampicillin plus cefotaxime plus vancomycin*

Age 3 months to 50 years Ceftriaxone or cefotaxime plus vancomycin*

Older than 50 years Ampicillin plus ceftriaxone or cefotaxime plus vancomycin*

Impaired cellular immunity Ampicillin plus ceftazidime plus vancomycin*

Neurosurgery, head trauma, or CSF shunt

Vancomycin plus ceftazidime

Bacteria Susceptibility Antibiotic(s)Duration(Days)

S pneumoniae Penicillin MIC <0.1 mg/L Penicillin G 10-14

MIC 0.1-1 mg/L Ceftriaxone or cefotaxime

MIC >2 mg/L Ceftriaxone or cefotaxime

Ceftriaxone MIC >0.5 mg/L Ceftriaxone or cefotaxime plus vancomycin or rifampin

H influenzae Beta-lactamase-negative Ampicillin 7

Beta-lactamase-positive Ceftriaxone or cefotaxime

N meningitidis ... Penicillin G or ampicillin 7

L monocytogenes ... Ampicillin or penicillin G plus an aminoglycoside

14-21

S agalactiae ... Penicillin G plus an aminoglycoside, if warranted

14-21

Enterobacteriaceae

... Ceftriaxone or cefotaxime plus an aminoglycoside

21

P aeruginosa ... Ceftazidime plus an aminoglycoside

21

•


• Treatment

• Duration of Treatment

• Dependent on infecting organism

– Average of 10-14 days

– Gm (-) bacilli for 3 weeks


• Treatment

• Steroids– Shortly before or along with antibiotics. Do not

give steroids after antibiotic treatment.

– de Gans J, van de Beek D. Dexamethasone in adults with bacterial meningitis. N Engl J Med. 2002;347:1549-56.

Corticosteroids in ChildrenCorticosteroids in Children

• Despite the conclusion of the Cochrane review, use is still controversial

• CPS statement:• No recommendations for routine use

• If used, should only be given to children > 6 wks and before or within 1 hr of antibiotics

• Current Capital Health practice is to limit the use of steroids to children presenting with severe sepsis

•Canadian Paediatric Society Statement. Therapy of suspected bacterial meningitis in Canadian children six weeks of age and older. Ped & Child Health. 6:3. March 2001. 147-52. Reaffirmed February 2006.

ComplicationsComplications

• The long-term neurologic sequelae can be grouped into 3 categories as follows:

• Hearing impairment

• Obstructive hydrocephalus

• Brain parenchymal damage: Most important feared complication of bacterial meningitis. It could lead to sensory and motor deficits, cerebral palsy, learning disabilities, mental retardation, cortical blindness, and seizures.

MMortality of mortality of meningitiseningitis

• Overall mortality rate from bacterial meningitis has decreased but remains alarmingly high. It is reported to be approximately 25%.

• Among the common causes of acute bacterial meningitis, the highest mortality rate is observed with pneumococcus.

• 19-26% for S pneumoniae meningitis,

• 3-6% for H influenzae meningitis,

• 3-13% for N meningitidis meningitis,

• 15-29% for L monocytogenes meningitis.


• Prognosis

• Pneumococcal Meningitis

• Associated with the highest mortality rate– 19-26%

• Permanent neurologic sequelae– 1/3 of pts

– Hearing loss

– Mental retardation

– Seizures

– Cerebral Palsy

Vaccination Vaccination

• The use of the HIB vaccination is strongly recommended in susceptible individuals.

• Vaccination against S pneumoniae is strongly encouraged in susceptible individuals, (older than 65 years and with chronic cardiopulmonary illnesses).

• Vaccinations against encapsulated bacterial organisms (eg, S pneumoniae, N meningitidis) are encouraged for those with functional or structural asplenia.

• Offer vaccination with quadrivalent meningococcal polysaccharide vaccine to all high-risk populations, including those with underlying immune deficiencies, those who travel to hyperendemic areas and epidemic areas, and those involved with laboratory work that deals with routine exposure to N meningitidis. College students who live in dormitories or residence halls are at modest risk; inform them about the risk and offer vaccination.

• Vaccination against N meningitidis is recommended for all adolescents aged 11-18 years.

• Vaccination against measles and mumps effectively eliminates aseptic meningitis syndrome caused by these pathogens.


• Vaccinations

• Asplenic pts should have had a pneumoccocal vaccine prior to their splenectomy

• Vaccines available for H. influenza

• Prophylaxis for N. meningitidis contacts

• Rifampin

PreventionPrevention

• The widespread use of viral vaccines for polio, measles, mumps, rubella and varicella has almost eliminated CNS complications from these in the US.

• Domestic rabies vaccinations have reduced the frequency of rabies encephalitis.

Prevention IIPrevention II

• Control of encephalitis from arboviruses has been less successful without specific vaccines.

• Control of insect vectors by spraying methods and eradication of insect breeding sites hasreduced incidence of these infections.

Meningococcal vaccineMeningococcal vaccine

ChemoprophylaxisChemoprophylaxis


• Conclusion

• Meningitis is an infectious disease emergency

• Mortality is often high but can be prevented with appropriate medical therapy

• If you consider meningitis in your differential, you are committed to an LP and empiric antibiotics

Three types ofThree types ofBacterial Bacterial MeningitisMeningitis

Hemophilus Influenzae

Streptococcus Pneumoniae

Neisseria Meninditidis (meningococcus)

Neisseria Neisseria MeningitidisMeningitidis

Gram – diplocci

Transmission

Treatment

Vaccination

Neisseria meningitidis: The meningococcus

http://www.nfid.org/

http://www.nfid.org/ncai

Incubation Period:

• The incubation period is variable,

• 2-10 days, but usually 3-4 days

Infectious Period:

• An infected person is infectious as long as meningococci are present in nasal and oral secretions or until 24 hours after initiation of effective antibiotic treatment.

Meningococcal DiseaseMeningococcal Disease

Two presentations:

1. meningococcemia, characterized by skin lesions (with or without meningitis)

2. acute bacterial meningitis, initially characterized by chills, fever, headache, nausea and vomiting

A transient bacteremic illness characterized by a fever and malaise may occur; symptoms resolve spontaneously in 1 to 2 days

PathogenesisPathogenesis

Clinical manifestations of meningitis

Infants : Irritability and refusal to take food; Fever (>2months), vomiting may lead to dehydration. Disturbances in motor tone, and coma.

Older children and adults: fever, headache and altered mental status. Nausea, vomiting, and photophobia are common.

Neurologic signs: convulsions or coma, signs of meningeal irritation such as spinal rigidity, hamstring spasms and exaggerated reflexes.

Petechiae (minute hemorrhagic spots in the skin) or purpura

Fulminant meningococcemia (occurs in 5 to 15% of patients with meningococcal disease), begins abruptly with sudden high fever, chills, myalgias, weakness, nausea, vomiting, and headache. Pulmonary insufficiency develops.

The characteristic skin rash (purpura) of meningococcal septicemia, caused by Neisseria meningitidis

http://www.nfid.org/

2 Primary Virulence Factors of Neisseria meningitidis

1. major toxin is lipooligosaccharide, LOS -mechanism is endotoxic

2. antiphagocytic polysaccharide capsule

Host Defenses

N. mengingitidis establishes systemic infections only in individuals who:1. lack serum antibodies against the capsular antigen or2. lack serum antibodies against noncapsular (cell wall) antigens or3. are deficient in the late-acting complement components

Factors in prevention of invasive disease1. integrity of the pharyngeal and respiratory epithelium2. presence of serum bactericidal IgG and IgM3. importance of complement

Epidemiology

N. meningitidis is a component of the normal flora

Carrier rate of pathogen = 5-30%

Attack rates highest in infants 3 months to 1 year old

Highest incidence during late winter and early spring

Epidemic virulence of Group A strains

Treatment and Control

Penicillin is the drug of choice to treat meningococcemia and meningitis.

Rifampin is the chemoprophylactic agent of choice.

Group A, C, AC, and ACYW135 capsular polysaccharide vaccines are available.

Hemophilus InfluenzaeHemophilus Influenzae

Gram – coccobacilli

Six Serological types

Transmission

Treatment

Vaccination

http://www.brisbio.ac.uk/ROADS/cgi-bin/tempbyhand.pl?database=BRISBIO+IMAGES&query=BRISBIO-9326

•Small, pleomorphic gram-negative bacteria; "coccobacilli".

•• Erythrocytes supply two factors, X (= hemin) and V (NAD), which are required for growth.

•• Rich medium, usually containing heated blood ("chocolate agar”).

•Satellite-ing of H. influenzae around Staph. aureus streak on agar.

•• Prevalence: nonencapsulated 50-80% and encapulated ~5%.

•• Encapsulated strains causes most severe disease.

•• Nonencapsulated strains causes most illnesses

•• 95% systemic H. influenzae infections of children caused by type b organisms (= “Hib”).

•• Highest risk of severe disease from type b organisms: children 6 months to 4 years.

•Epidemiology of Hemophilus influenzae

•• Commensal and pathogen.

•• Aerosol and direct contact with saliva and respiratory secretions (like N. meningitidis)

•• Upper respiratory tract carriage begins soon after birth.

•• Epidemics of H. influenzae do not occur, but increased risk of meningitis among young household members of a case.

•Haemophilus influenzae epidemiology

Streptococcus Streptococcus PneumoniaePneumoniae

Gram +, lancet-shaped cocci

Serotypes

Transmission

Treatment

Vaccination

•Pneumococcal meningitis in a patient with alcoholism. Courtesy of the CDC/Dr. Edwin P. Ewing, Jr.

Follow-upFollow-up

• Close follow-up needed after hospital discharge:• Hearing should be assessed 1-2 mo. after d/c using

BEARS testing

• Neuromuscular assessment at the time of d/c should be documented and periodically assessed outpatient to detect any deficiencies

• Learning disabilities, behavior disorders and speech delay require close monitoring after d/c

•Shock: Sepsis

•Protocol

An Approach to the

Adult Patient with

Suspected Bacterial

Meningitis

Summary:

•From supplement to:

•Van de Beek D. Community-acquired bacterial meningitis in adults. N Engl J Med. 2006; 354:44-53

•Shock: Sepsis

•Protocol

Indications

Age > 60

Recent seizures

Immunocompromised

Prev CNS disease or hardware

Focal neurological deficits

Papilledema

Altered LOC*

•Summary:

•An Approach to the

•Adult Patient with

•Suspected Bacterial

•Meningitis



•Shock: Sepsis

•Protocol

•Summary:




•Meningitis•Corticosteroids

•Give dexamethasone IV before or with 1st dose of

antibiotics

•Contraindications

•Antibiotics w/in 48 hrs

•Shunt

•Head trauma



•Shock: Sepsis

•Protocol

•Summary:




•Meningitis



•Contraindications to LP

•Recent seizure

•Signs of herniation at any time

•GCS < 11 or rapidly declining LOC

•Focal neurologic deficits

•Papilledema *

•SOL or brain shift on CT

•Coagulopathy

•Shock: Sepsis

•Protocol



•Summary:




•Meningitis

•Empiric Antibiotic Therapy

•Cefotaxime 2g IV or Ceftriaxone 2g IV

•+/- Ampicillin 3g IV

•+/- Vancomycin 1g IV

Chronic meningitisChronic meningitisCategory Agent

Bacteria M tuberculosis B burgdorferi T pallidum Brucella speciesFrancisella tularensis Nocardia speciesActinomyces species

Fungi C neoformans C immitis B dermatitidis H capsulatum Candida albicans Aspergillus speciesSporothrix schenckii

Parasites Acanthamoeba speciesN fowleri Angiostrongylus cantonensis G spinigerum B procyonis Schistosoma speciesS stercoralis Echinococcus granulosus

EncephalitisEncephalitis

• Encephalitis, an inflammation of the brain parenchyma, presents as diffuse and/or focal neuropsychological dysfunction.

• Encephalitis is distinct from meningitis, though on clinical evaluation the 2 often coexist with signs and symptoms of meningeal inflammation, such as photophobia, headache, or a stiff neck.


• Acute encephalitis is most commonly a viral infection with parenchymal damage varying from mild to profound

• Subacute and chronic encephalopathies, most likely toxoplasmosis in immunocompromised patients


• Individuals at the extremes of age are at highest risk, particularly for HSE

EncephalitisEncephalitis• The classic presentation is encephalopathy with

diffuse or focal neurologic symptoms, including the following:

• Behavioral and personality changes, decreased level of consciousness

• Stiff neck, photophobia, and lethargy

• Generalized or localized seizures (60% of children with California encephalitis [CE])

• Acute confusion or amnestic states

• Flaccid paralysis (10% with WNE)

Infectious etiologies of EncephalitisInfectious etiologies of Encephalitis• Viral agents, such as HSV type 1 and 2 (almost

exclusively in neonates),

• VZV, EBV,

• Measles virus (PIE and SSPE), mumps, and rubella are spread through person-to-person contact.

• Human herpesvirus 6 may also be a causative agent.

• Bacterial pathogens, such as Mycoplasma species, rickettsial or catscratch disease,

• Toxoplasma gondii

• West Nile virus can be transmitted by means of an organ transplant and via blood transfusions.

EncephalitisEncephalitis• Laboratory tests (biochemical).

• Viral serology

• CT scan

• EEE

• CSF analysis

EncephalitisEncephalitis• The goal of treatment for acutely ill patients is

administration of the first dose or doses acyclovir with or without antibiotics or steroids as quickly as possible

• Look for and treat systemic complications, particularly in HSE, EEE, JE, such as hypotension or shock, hypoxemia, hyponatremia (SIADH), and exacerbation of chronic diseases

assoc prof dr meral sonmezoglu yeditepe university hospital

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