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Central Nervous System Infections Infectious Agents leading to CNS Infections BacterialAcute Pyogenic (Bacterial) Infection Neonates Eschericia coli Group B Streptococci Streptococcus pyogene Streptococcus agalactiae Infant Hemophilus influenza (before vaccination)Streptococcus pneumoniae Adolescent and young adults Nisseria meningitidis Elderly Streptococcus pneumoniae Listeria monocytogene Chronic Granulomatous Infection Mycobacterium sppSpirochete Treponema pallidum Fungal Chronic Meningitis Cryptococcus spp. Vasculitis Mucor Aspergillus spp. Parenchymal Infection Granulomatous Cryptococcus spp. Abcess Candida spp.Unclassified Mucor (in Diabetic Ketoacidocis)Viral (Asceptic)Echovirus Coxsackievirus Nonparalytic poliomyelitis Herpes simplexRabies Protozoal Malaria Toxoplasma spp. Entameoba histolytica Trypanosome spp. Types of CNS Infections Bacterial InfectionsAcute Pyogenic Meningitis Chronic Granulomatous Meningitis Tuberculous meningitis Neurosyphilis Neurborelliosis Tabes dorsalis Abscess Epidural abscess Subdural abscess Brain abscess Fungal Infections Chronic fungal meningitis Viral InfectionsAcute asceptic meningitis Viral encephalitis Herpes simplex encephalitis Protozoal InfectionToxoplasmosis Prions DiseasesCreutzfeldt-Jakob Disease (CJD)Gerstman-straussler Syndrome (GSS)Fatal familial insomnia Kuru Bacterial InfectionsDiseasePathogenesisMorphologyClinical ManifestationLaboratory FindingsMacroscopicMicroscopicAcute Pyogenic Meningitis Bacterial infection of the Arachnoid membraneSubarachnoid space CSF Heamatogenous spread (the most common)The etiological agents spread from distant area of the body and lodged at the CNS Direct implantation of organisms TraumaCongenital malformation – ventricular septal defect Iatrogenic Lumbar puncture Local extension Sinusitis Mastoid sinus Frontal sinus Infected tooth Osteomyelitis of the Cranium Spine Pathophysiology Vasculitis of the leptomeningeal arteries lead to an ischemic attack of the brain Hypoxic-Ischemic Encephalopathy (HIE) will then develop Infection hs led to disturbance in vascular permeability of the brain This has led the to brain edema and leakage of protein into the CSF Ultimately, increased in ICPYellow-tan exudate This purulent exudate covers the cerebral hemispheres It usually settles at Along the base of the brain Around cranial nerves Openings to the 4th ventricle Meningeal arteries appeared engorged Neutrophilic exudate is seen involving the meninges Prominent dilated blood vessels especially the Leptomeningeal vessels Edema and focal inflammation extending into the superficial brain parenchyma (Virchow-Robin space)Initial symptoms Fever Severe headache Stiff neck Progression of disease Confusion Coma SeizureDue to ↑ICP HIE Toxic Metabolic Encephalopathy Later complicationsCranial nerve deficits Ischemic infarction Hydrocephalus Lumbar puncture Increased in ICP Abundant neutrophils Elevated proteins Reduced glucose Lumbar puncture is only indicated in pts without sign of PapiloedemaComplicationsCranial Nerves deficits and ischemic infarction During infection, veins may inflamed and lead to Phlebitis Phlebitis may disrupt blood flow, turbulance may lead to formation of blood clot Blood clot may ultimately occlude smaller vessels and lead to liquefactive necrosis of the brain Hydrocephalus Purulent fibrinous exudate of infection may organize into fibrous tissueThis fibrous tissue may block the exit of CSF at the 4th ventricle and lead to communicating hydrocephalus Complications take times to develop, sometimes it develops long after the disease subsides Bacterial InfectionsDiseasePathogenesisMorphologyClinical ManifestationMacroscopicMicroscopicBrain AbscessLocal extension Sinusitis Mastoid sinus Frontal sinus Infected tooth Osteomyelitis of the Cranium Spine Heamatogenous spread (the most common)The etiological agents spread from distant area of the body and lodged at the CNS Direct implantation of organisms TraumaPost meningitis Evolution of the Abscess The brain undergoes acute inflammatory response after come into contact with foreign agents, characterized with Neutrophilic infiltration Cerebritis When the brain tries to heal the lesion, granulation tissue forms at the peripheral of the lesion; middle zone undergoes liquefactive necrosis Sattellite abscess has a very poor capsulation at the medial side; therefore it is easily rupture and the pus may enter the ventricle Descrete lesion with liquefactive necrosis Edema Presented with expanded white matter adjacent to the abscess Dense aggregates of neutrophils Necrotic area surrounded with granulation tissue Neovascularization Outside the capsule of abscess is the zone of gliosis With numerous Gemistocytic Astrocytes Most commonly affected area Frontal lobeParietal lobeCerebellum Features Progressive focal deficit Loss of neurological function due to destruction of the brain tissue Subsequent increased in ICPProgrssive herniation If the abscess ruptures, it will lead to Ventriculitis Meningitis Venous sinous thrombosis DiseasePathogenesisEtiological agentsClinical ManifestationEpidural AbscessUssually occurs due to complication of vertebral osteomyelitis Sometimes due to complications of Spinal surgery Trauma Spinal anesthesia Staphylococcus aureus (most cases)Gram negative rods Bacteroides Streptococci spp. Mycobacterium tuberculosis Initially presented with Fever Back pain Progression Weakness of the lower extremities Impaired Bowel function Bladder function Ends up with paralysis Subdural AbscessExtension of bacterial or fungal infection of the Cranium Sinuses Middle ear Headache Fever Neck stiffness Signs and symptoms of origin infection Ultimately will lead to mass effect if the pus is massive Bacterial InfectionsDiseasePathogenesisMorphologyClinical ManifestationLaboratory FindingsMicroscopicMacroscopicTuberculous Infection of CNS Spreaded through heamatogenous route and usually comes about from disseminated pulmonary tuberculosis Mixture of Lymphocytes Plasma cells Macrophages Florid cases show well-formed granulomas Often presented with caseating necrosis and giant cells Mimicking the morphology of pulmonary tuberculosis Obliterative endarteritis of artery running through subarachnoid space Same appearance for Tuberculoma Subarachnoid space contains Gelatinous Fibrinous exudate This exudate most often finds at the base of brain, obliterating Cisterns Encasing cranial nerves May present with descrete white granules scattered over the LeptomeningesTuberculoma may have a bigger lesion Generalized Headache Malaise Mental confusion Vomiting Lumbar puncture Elevated protein Glucose may be Moderately reduced Normal ComplicationsHydrocephalus Exudate may organize and form arachnoid fibrosis which may occlude the arachnoid granulation leading to communicating hydrocephalus Obliterative Endarteritis Artery may become occluded during healing and subsequently leads to cerebral infarction Bacterial Infections DiseasePathogenesisMorphologyClinical ManifestationMicroscopicMacroscopicNeurosyphilis Types Meningovascular neurosyphilis Paretic neurosyphilis Tabes dorsalis Happens during the tertiary syphilis This occurs in about 10% of syphilitic patients who didn’t have proper treatment It is caused by spirochete Treponema pallidum Meningovascular Neurosyphilis (Meninges)Meningovascular Neurosyphilis Apathy Seizures General paresis with dementia Paretic Neurosyphilis Insidious loss of mental and physical function Mood alteration Delusion of grandeurTerminating with severe dementia Tabes Dorsalis Impaired joint position sense Locomotor ataxia Loss of pain sensation Charcot’s joint Skin and joint damage Lightning pains Loss of deep tendon reflex Lymphocytes and plasma cells appeared at the peripheral to blood vessels Heubner Arteritis Marked endothelial thickening, thickened Tunica media Tunica adventitia Primarily involved the meninges of the Base of the brain Subarachnoid space Blood vessels Paretic Neurosyphilis (Brain Parenchyma)Loss of neurons with microglial (rod cells) proliferation Gliosis Loss of Ependymal lining with subependymal gliosis Granular ependymitis Brain appeared Shrunken Firm Frontal lobe is atrophic Leptomeninges is thickened With or wihout hydrocephalus Tabes Dorsalis (Spinal Cord)Loss of axons and myelin sheath at the Dorsal ColumnPallor and atrophy of the Dorsal Column Fungal Infections Primarily happens in Immunocompromised patients HIV patients Debilitated patients Patients undergoing chemoCharacterized by 3 patterns Chronic fungal meningitis Cryptococcus spp.Vasculitis Mucor Aspergillus spp. Invasion of the blood vessel leading to HeamorrhageThrombosis Branching of hyphae can be seen invading the cerebral vessels Parenchymal Invasion Abscess forming lesion Candida sppGranulomatous lesion CryptococcusDiseasePathogenesisMorphologyClinical ManifestationLaboratory FindingsMicroscopicMacroscopicChronic Fungal MeningitisUsually caused by Cryptococcus spp. Brain usually one of the latest organs to infected after disseminated fungal infection Spreaded through heamatogenous route Usually well-formed granuloma is hardly seen Infiltration of chronic inflammatory cells including Fibroblasts Mononuclear giant cells With presence of Cryptococci spp.Tubercle like nodule on the Leptomeninges at the base of the brain The infections can be Fulminant and fatal within 2 weeks Indolent and evolving up to months or years CSF findings High protein concentration Few cells Presence of mucoid encapsulated yeast in Indian Ink Viral InfectionsDiseasePathogenesisMorphologyClinical ManifestationLaboratory Findings MicroscopicMacroscopicAcute Aseptic MeningitisGenerally viral in origin Echovirus Coxsackievirus Nonparalytic poliomyelitis Sometimes can be non-viral in origin (drug-induced) NSAIDsAntibiotics Usually no abnormalities can be found Sometimes mild to moderate lymphocytic infiltration of the LeptomeningesNo distinctive changes can be seen on the brain Sometimes, brain appears edematous Less fulminant, and usually self-limiting CSF findings Increased in pressure Clear color Increased numbers of Lymphocytes Slightly increased protein Normal glucose level Smear and culture appear negative for bacteria Viral EncephalitisNervous system tropism Certain virus affects certain cells Others have preference towards particular area of the brain Temporal lobe/ limbic system Herpes simplex Capacity of latency Varicella-zoster may remain dormant at the dorsal root gangliaIt may also follow an immune mediated disease pathway This has no evidence of direct viral invasion For example Acute Disseminated Encephalitis Intrauterine infection May lead to congenital malformation May follow a slowly degenerating disease Postencephalitic Parkinsonism General characteristics Perivascular and parenchymal mononuclear cells infiltration Lymphocytes Plasma cells Macrophages Gliosis with/out nodules Neurophagia Nuclear/cytoplasmic inclusion bodies can be found Herpex Simplex Encephalitis Large eosinophilic intranuclear inclusion Rabies Negri bodies Round to oval in shape Eosinophilic cytoplasmic inclusion Found in Neurons in Hippocampus Pyramidal cells of the Cerebellum CMV Owl eyes Intranuclear and cytoplasmic inclusion Measles Warthin Finkeldey Bodies in Subacute Sclerosing Panencephalitis (SSPE)JC VirusProgressive Multifocal Leucoencephalopathy (PML)General characteristicsAlmost invariably with meningeal inflammation Meningoencephalitis Sometimes with the involvement of the spinal cord Encephalomyelitis Herpex Simplex Encephalitis Petechiae are seen on the Temporal lobe Rabies Intense edematous brain Vascular congestion Protozoal InfectionsDiseasePathogenesisMorphologyClinical ManifestationMicroscopicMacroscopicToxoplasmic EncephalitisCerebral Toxoplasmosis can be either Acquired Toxoplasmosis Congenital ToxoplasmosisIngestion of the cysts will lead to infection The initial infection takes place at the intestion and regional lymph nodes The cysts formation occurs at the CNS EyesCardiac muscle Skeletal muscleToxoplasma pseudocyst with bradyzoites With/out granuloma Abscess formation Often present with multiple foci of calcification During an acute infection, patients usually appear assymptomatic But when the cysts forms in the CNS, patients will develop Fever Headache Lethargy Altered mental status Focal neurological deficits ConvulsionsMay end with fatality Single or multiple lesions can be seen at the Basal Ganglia Junction between the white and gray matter Prions DiseasesDiseasePathogenesisMorphologyClinical ManifestationMicroscopicMacroscopicPrions Diseases Creutzfeldt-Jakob Disease (CJD)Gerstman-straussler Syndrome (GSS)Fatal familial insomnia Kuru Groups of diseases with abnormal form of a specific protein, Prion Protein (PrP)It is itself transmissable particles Can be directly inoculated PrP undergoes conformational change from Normal α-helix-containing isoform (PrPc) Abnormal β-helix-pleated sheet isoform (PrPsc)PrPsc is located at the Chromosome 20 Accumulation of PrPsc in the neurons appear to be the cause of pathology Largely how does this happens, remains unknown Spongiform cerebral cortex Small vacoules in dendritic cytoplasm Grape-like cluster Astrocytocis Neuronal lossBrain atrophy The progression of disease can be either Very slow Rapid Most patients develop Dementia CauseAppearancePolymorphonuclear cellLymphocyteProteinGlucosePyogenic?bacterial meningitisYellowish, turbidMarkedly increasedSlightly increased or NormalMarkedly increasedDecreasedViral meningitisClear fluidSlightly increased or NormalMarkedly increasedSlightly increased or NormalNormalTuberculous meningitisYellowish and viscousSlightly increased or NormalMarkedly increasedIncreasedDecreasedFungal meningitisYellowish and viscousSlightly increased or NormalMarkedly increasedSlightly increased or NormalNormal or decreased ................
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