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CNS INFECTIONS Prof.Dr. Reha Cengizlier 1 April 2014

CNS INFECTIONS Prof.Dr. Reha Cengizlier 1 April 2014

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Targets and behavior After this lesson, a student could be able to; Diagnose a CNS infection Make differential diagnose Treat the infection Informed the family about these illnesses

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Page 1: CNS INFECTIONS Prof.Dr. Reha Cengizlier 1 April 2014

CNS INFECTIONS

Prof.Dr. Reha Cengizlier1 April 2014

Page 2: CNS INFECTIONS Prof.Dr. Reha Cengizlier 1 April 2014

Aim;

Students must learn; what are the CNS infectionsWhat are the symptoms and signs of each How to make differential diagnoseHow to treat these infectonsWhat are the prognosis

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Targets and behavior

After this lesson, a student could be able to;

Diagnose a CNS infectionMake differential diagnoseTreat the infectionInformed the family about these illnesses

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LOCALISATIONS

Meningitis:Inflammation of the meninges of the brain and spinal cord, superficial cortical structures,and blood vesselsEncephalitis: Brain involvedEncephalomyelitis: Spinal cord also involvedBrain abscess

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MENINGITISACUTE BACTERIAL MENINGITIS

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Predisposition

Immun deficiencies HemoglobinopathiesAspleniaChronic liver and kidney diseaseRinore, otoreVentriculo-peritoneal shuntAnatomic defects (dermal sinus,encephalocel)

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Etiology

More than 95 % three microorganism; S. pneumoniae N. meningitidisH. influenzae type B

Newborns; Group B streptococcus, Gram-negative enteric bacilli Listeria monocytogenes

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PathogenesisNeonatal period: Acquired during birth by contact and aspiration of intestinal and genital tract secretions

Infants and children:After hematogeneous dissemination with bacteria that have colonized in the nasopharynxDirect extension from a paranasal sinus or from the middle ear to the mastoid and to the meningesSevere head traumaDirect inoculation of bacteria into the CSF with congenital dural defects

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PathophysiologyOnce meningeal pathogens have entered the CNS they replicate rapidly and liberate active cell wall or membrane associated components (lipoteichoic acid,peptidoglycan,endotoxin)Stimulate cytokines(TNF,IL 1-6-8, PAF, NO, arachidonic acid metabolites)Attract neutrophiles to these siteLeukocytes release proteolytic products and toxic oxygen radicalsInjury of the vascular endothelium and alteration of blood-brain barrier permeabilityAlteration of CSF dynamics-brain edema, intracranial hypertension

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PathologyThe entire surface and base of the brain can be covered by a layer of a thick purulent fibrinous exudateGeneralized vasculitis-thrombosis of vessel walls –cerebral edemaInflamatory exudate=PNL+fibrin+bacterial clumps+RBC (impaired CSF flow through and out of the ventricular system=hydrocephalus)

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Physical examinationNeck stiffnessFontanel bulging (infant)Positive Brudzinski’s sign: Rapid flexion of the neck is followed involuntarily brisk flexion of the kneesPositive Kernig’s sign: Marked resistance to extension of the leg when the patient is in the supine position with the thigh flexed at the hip and the leg flexed at the knee

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Brudzinski

Kernig

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Clinical manifestations:

Petechial and purpuric eruptions in meningococcemiaJoint involvement-in meningococcal and H.influenzae meningitisDraining ear (history of head trauma; associated with pneumococcal meningitis)

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Clinical manifestations:

INFANTS:3 months-1 year of ageFever, vomiting, irritability, convulsions, somnolance, abnormal cry, tense bulging fontanel

NEONATESDifficult to recognize; Clinical manifestations are nonspesificRefusal of feedings,vomiting, excessive irritability, irregular respirations

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Diagnosis

Lumbar puncture(LP) is useful in the differential diagnosis of meningitisExamination of CSF reveals:

Cloudy appereanceIncreased WBC count with a

polymorphonuclear leukocyte predominance

Low glucose concentrationElevated protein concentration Smear and culture positive for the causative microorganismHigh pressure

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Lumbar punctionApplied in L3-L4 or L4-L5 levels

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ContraindicationEvery patient suspected menengitis is LP endicatedContra-indications;

Intracranial pressure increased (brain edema, abscess, tumor etc.)

Pupil unresponsiveness to lightDecerebre / decortice postureAbnormal breathing patternPapil edemaHypertansion and bradicardiaCardiopulmonary insufficienyConvulsion within last 30 min.Skin infection of LP areaThrombocytopenia (<20,000) (relative)

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Treatment

Appropriate antimicrobial therapyFluid and electrolyte adjustmentsControl of cardiovascular stability and

intracranial pressureAnticonvulsant therapy

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Complications

Acute:ShockDehydrationBrain edemaDICAsidosisHypoglisemia

Subacute:I-ADH secretionConvulsionSubdural effusion/ampiyemBrain abscessPersistent fever

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Complications

Late periodHearing loss (most frequent late compl.)Speech disordersVision anomaliesLearning difficultiesMotor development disordersConvulsive diseasesHydrocephalusDiabetes insipidus

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VIRAL MENINGITIS

A benign syndrome of multiple etiology Characterized by headache, fever, vomiting and meningeal signsCSF shows an increase in mononuclear cells and yields no bacterial or fungal growth on cultureRecovery occurs in about 3-10 days and is nearly always complete

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EtiologyMumpsEchovirusPoliovirusCoxachieAdenovirusHerpes 1,2,6Herpes zosterEBVHIVParainfluenzae type 3

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GRANULOMATOUS MENINGITISCaused by tuberculosis and certain fungiOccur predominantly at the base of the brain

TUBERCULOUS MENINGITISSpread of the tubercule bacilli to the CNS Occurs hematogenously and is associated with the miliary or disseminated form of tbcThe resultant inflammatory response-marked fibrotic thickening of the involved meningesMicroscopically tbc meningitis produces the characteristic GRANULOMA

Page 30: CNS INFECTIONS Prof.Dr. Reha Cengizlier 1 April 2014

In the early stages of formation a granuloma is typified by a core of histiocytes and giant cells surrounded by lymphocytes

Another typical finding is VASCULITIS –an intense inflamatory reaction concentrated primarily in the adventitia of the blood vessel with some extension into the tunica media

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FUNGAL MENINGITIS

The most common cause is CRYPTOCOCCUSThe gross findings are typified by a creamy gelatinous exudate concentrated over the base of the brainMay also extend into the ventricles and cause choroid plexitisMicroscopically the cryptococcal organisms may be found in giant cells and histiocytes

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ENCEPHALITISInflammation of the cerebral parenchyma-brainInflammation caused by a virus may also be called acute viral encephalitisThey are characterized 1.mild abortive infection

2.like aseptic meningitis 3.severe involvement of CNS

Sudden onset, high fever,meningeal signs, stupor, disorientation, tremors, convulsions, spasticity, coma, deathMany different kinds of viruses can cause encephalitisThe most dangerous and rare one is;

HERPES SIMPLEX VIRUS (may be fatal in almost half of the patients)

Page 36: CNS INFECTIONS Prof.Dr. Reha Cengizlier 1 April 2014

Milder forms of encephalitis can follow or accompany common childhood ilnesses, including mumps, measles, chickenpox and infectious mononucleosisEncephalitis is divided into two categories 1.Direct viral invasion of CNS 2.Postinfectious-after a common acute non CNS infection followed by an immune reactive demyelinating process

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How can virus reach CNS

Extension of virus into neuronal and glial cells adjacent infected endothelial cells and small capillaries

Directly into CSF from the vessels of the choroid plexus via ependyma

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Healing

FOR MOST FORMS-the acute phase lasts from a few days to one weekUnless the illness is severe, recovery usually takes 2-3 weeksIn a small percentage of cases encephalitis can be a life threatening-recovery may take longer and cause neurological problems

Page 39: CNS INFECTIONS Prof.Dr. Reha Cengizlier 1 April 2014

DiagnosisCSF is clearPressure-normal to markedly elevated Pleocytosis- 10 to 1000 cells chiefly mononuclearThe protein and glucose values may be slightly elevated or normalEEG-General diffuse bilateral slowing background activityCTMRIThe specific type can be determined by;

isolation or identification of the virus demonstration the rise of antibody level in convalescence

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Treatment

Antibiotics are not used Antiviral drugs like acyclovir can be used to treat some forms of encephalitis especially the type caused by the HSVCS may also be used to reduce brain edema

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BRAIN ABSCESS and CEREBRITIS

At least 75% of cerebral abcesses are associated with infections elsewhere in the bodyIn the preantibiotic era most of them were secondary to direct extension of mastoid, middle ear or the paranasal sinuse infectionsSince the advent of antibiotics; most infections associated with cerebral abcesses are migrated to the lungs and endocardiumThe mortality rate varies from 33-50%They begin as focal bacterial encephalitis or cerebritis Characterized by neutrophilic infiltration and edema

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Treatment

AntibioticSurgery is indicated when the abscess is ;

larger than 2.5 cm in diameter, gas is present in the abscess, the lesion is multiloculated, the lesion is located in the posterior fossa, a fungus is identified

Associated infectious processes, such as mastoiditis, sinusitis, or a periorbital abscess, may require surgical drainage

The duration of antibiotic therapy depends on the organism and response to treatment, but it is usually is 4–6 wk.

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