neuropathology iii infections of the cns dept. of pathology dept. of pathology ams07 ams07

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NEUROPATHOLOGY III INFECTIONS OF THE CNS INFECTIONS OF THE CNS DEPT. OF PATHOLOGY DEPT. OF PATHOLOGY AMS07 AMS07

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Page 1: NEUROPATHOLOGY III INFECTIONS OF THE CNS DEPT. OF PATHOLOGY DEPT. OF PATHOLOGY AMS07 AMS07

NEUROPATHOLOGY III

INFECTIONS OF THE CNSINFECTIONS OF THE CNS

DEPT. OF PATHOLOGYDEPT. OF PATHOLOGY

AMS07 AMS07

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NEUROPATHOLOGY III INFECTIONS OF THE CNS. INFECTIONS OF THE CNS.

*Viral*Viral-acute-acute-latent-latent-slow virus infections-slow virus infections

*Bacterial*Bacterial-acute(pyogenic)-acute(pyogenic)-chronic(granulomatous):AIDS(atypical myco -chronic(granulomatous):AIDS(atypical myco

bacteria), non-AIDS(mycobacterium TB, sy bacteria), non-AIDS(mycobacterium TB, sy philis)philis)

*Fungal *Parasitic*Fungal *Parasitic

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NEUROPATHOLOGY III INFECTIONS OF THE CNS...INFECTIONS OF THE CNS...

*Portal of entry.*Portal of entry.

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NEUROPATHOLOGY III INFECTIONS OF THE CNS..INFECTIONS OF THE CNS.. Acute viral infections.Acute viral infections.

*Aseptic meningitis*Aseptic meningitis*Poliomyelitis/Polioencephalomyelitis*Poliomyelitis/Polioencephalomyelitis*Encephalitis:*Encephalitis:

-Herpes simplex encephalitis-Herpes simplex encephalitis-Neonatal HSV encephalitis-Neonatal HSV encephalitis-Varicella-zoster virus infections-Varicella-zoster virus infections-CMV infection-CMV infection-Rubella encephalitis -Rabies infection-Rubella encephalitis -Rabies infection-Arbovirus infection-Arbovirus infection

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NEUROPATHOLOGY III INFECTIONS...INFECTIONS... ASEPTIC MENINGITIS.ASEPTIC MENINGITIS. *It is a benign, short-lived meningeal infla- *It is a benign, short-lived meningeal infla-

mmation *Viral mmation *Viral causes include:causes include:

-Enteroviruses(MOST common)-Echovi -Enteroviruses(MOST common)-Echovi ruses/Coxsackie A and Bruses/Coxsackie A and B

-Herpes simplex type 2-Herpes simplex type 2-Mumps, Measles and Adenovirus-Mumps, Measles and Adenovirus

*Scanty meningeal infiltrate*Scanty meningeal infiltrate*Death may be due to secondary systemic disease vgr.: viral *Death may be due to secondary systemic disease vgr.: viral myocarditismyocarditis

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NEUROPATHOLOGY III

ASEPTIC MENINGITIS...ASEPTIC MENINGITIS...

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NEUROPATHOLOGY III

ASEPTIC MENINGITIS...ASEPTIC MENINGITIS...

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NEUROPATHOLOGY III

ASEPTIC MENINGITIS...ASEPTIC MENINGITIS...

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NEUROPATHOLOGY III VIRAL ENCEPHALITIS....VIRAL ENCEPHALITIS....

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NEUROPATHOLOGY III POLYOMYELITIS.POLYOMYELITIS. *Enteroviruses:*Enteroviruses:

-Poliovirus-small RNA viruses-Poliovirus-small RNA viruses-Infrequent since Salk vaccine(inactiva- -Infrequent since Salk vaccine(inactiva-

ted) or Sabin(attenuated)development ted) or Sabin(attenuated)development-Rare reversion to virulence in attenua- -Rare reversion to virulence in attenua- ted ted

virusvirus-Echovirus or Coxsackie A/B are rare causes -Echovirus or Coxsackie A/B are rare causes

in populations immunizated against poliovir. in populations immunizated against poliovir. --Fecal-oral transmissionFecal-oral transmission

-Lytic inf. of motor neurons in spinal -Lytic inf. of motor neurons in spinal cord/braincord/brainneuronophagia+microglia nodls.neuronophagia+microglia nodls.

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NEUROPATHOLOGY III POLYOMYELITIS...POLYOMYELITIS...

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NEUROPATHOLOGY III POLYOMYELITIS....POLYOMYELITIS....

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NEUROPATHOLOGY III POLYOMYELITIS...POLYOMYELITIS...

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NEUROPATHOLOGY III

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NEUROPATHOLOGY III

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NEUROPATHOLOGY III

POLYOMYELITIS...POLYOMYELITIS...

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NEUROPATHOLOGY III HERPES VIRUSES – routes of infectionHERPES VIRUSES – routes of infection

*HSV type 1.*HSV type 1.-Direct contact w/infect.secretions from -Direct contact w/infect.secretions from mouth vesicles(“cold sore”) mouth vesicles(“cold sore”) --Involvement of olphactory tract after na Involvement of olphactory tract after na sopharyngeal infection sopharyngeal infection --Reactivation of latent infection(trigem. Reactivation of latent infection(trigem. ganglia, temporal lobe or other areas of ganglia, temporal lobe or other areas of CNS.CNS. *HSV type 2.*HSV type 2.-General mucocutaneous infection -General mucocutaneous infection --React. of latent infect. in sacral dorsal root React. of latent infect. in sacral dorsal root ganglion ganglion

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NEUROPATHOLOGY III

HERPES VIRUS....HERPES VIRUS....

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NEUROPATHOLOGY III HERPES VIRUS...HERPES VIRUS...

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NEUROPATHOLOGY III HERPES ENCEPHALITIS.HERPES ENCEPHALITIS.

*Hemorrhagic ncrosis of temporal lobes, *Hemorrhagic ncrosis of temporal lobes, insula, cingulate gyri and posterior orbital insula, cingulate gyri and posterior orbital frontal lobefrontal lobe

*Intense perivascular inflammation, micro- *Intense perivascular inflammation, micro- glial nodules, glial nodules, eosinophilic inclusions and necrosiseosinophilic inclusions and necrosis

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NEUROPATHOLOGY III HERPES ENCEPHALITISHERPES ENCEPHALITIS

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NEUROPATHOLOGY III HERPES ENCEPHALITIS...HERPES ENCEPHALITIS...

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NEUROPATHOLOGY III HERPES ENCEPHALITIS...HERPES ENCEPHALITIS...

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NEUROPATHOLOGY III

NEONATAL HSV ENCEPHALITIS.NEONATAL HSV ENCEPHALITIS.*Etiologic agent is commonly HSV – 2*Etiologic agent is commonly HSV – 2*Acquired during delivery or by feto-mater *Acquired during delivery or by feto-mater nal transmission nal transmission in uteroin utero during early during early preg nancypreg nancy

-15-20% of cases caused by HSV-1infec -15-20% of cases caused by HSV-1infec tion tion*Diffuse necrotizing encephalitis*Diffuse necrotizing encephalitis

-May occur as part of a systemic HSV-2 -May occur as part of a systemic HSV-2 infection infection

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NEUROPATHOLOGY III

VARICELLA-ZOSTER INFECTION.VARICELLA-ZOSTER INFECTION.

*Due to reactivation of latent infection in dorsal *Due to reactivation of latent infection in dorsal root or trigeminal gangliaroot or trigeminal gangliashinglesshingles

*Risk factors for reactivation:*Risk factors for reactivation:

-Cancer-Cancer

-Lymphoma-Lymphoma

-Ionizing radiation-Ionizing radiation

-Immunosuppresion-Immunosuppresion

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NEUROPATHOLOGY III VARICELLA – ZOSTER INFECTION....VARICELLA – ZOSTER INFECTION....

*Adult infections include:*Adult infections include:-Zoster encephalitis/myeloradiculitis-Zoster encephalitis/myeloradiculitis-Zoster intracranial vasculopathy/vasculi -Zoster intracranial vasculopathy/vasculi

tis(autoimmune process) tis(autoimmune process) * Childhood infections include:* Childhood infections include:

-Varicella cerebellitis-Varicella cerebellitis-Varicella meningoencephalitis-Varicella meningoencephalitis-Intrauterine VZ infection-Intrauterine VZ infection-Neonantal VZ infection-Neonantal VZ infection

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NEUROPATHOLOGY III VARICELLA – ZOSTER INFECTION...VARICELLA – ZOSTER INFECTION...

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NEUROPATHOLOGY III VARICELLA-ZOSTER....VARICELLA-ZOSTER....

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NEUROPATHOLOGY III VARICELLA.ZOSTER....VARICELLA.ZOSTER....

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NEUROPATHOLOGY III VARICELLA – ZOSTER...VARICELLA – ZOSTER...

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NEUROPATHOLOGY III CYTOMEGALOVIRUS INFECTION.CYTOMEGALOVIRUS INFECTION.

*Congenital CMV infection.*Congenital CMV infection. -Is the commonest intrauterine viral infect. (0.2 – -Is the commonest intrauterine viral infect. (0.2 – 2% of live births)2% of live births) -Fetomaternal transplacental transmission-Fetomaternal transplacental transmission -About 20% risk of transmission during pri -About 20% risk of transmission during pri mary maternal infection(2% during recrudes cence)mary maternal infection(2% during recrudes cence) -Necrotizing encephalitis-Necrotizing encephalitis -Ventriculoencephalitis-Ventriculoencephalitis -Complications: microcephaly, microgyria,poren cephaly, -Complications: microcephaly, microgyria,poren cephaly, hydrocephaly, periventricular calcific.hydrocephaly, periventricular calcific.

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NEUROPATHOLOGY III CMV INFECTION...CMV INFECTION...

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NEUROPATHOLOGY III CMV INFECTION...CMV INFECTION...

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NEUROPATHOLOGY III

CMV INFECTION...CMV INFECTION...*CMV encephalitis and myeloradiculitis is *CMV encephalitis and myeloradiculitis is common in AIDS patientscommon in AIDS patients*Patterns of CNS infection:*Patterns of CNS infection:

-Low grade encephalitis-Low grade encephalitis-Necrotizing encephalitis w/large cysts -Necrotizing encephalitis w/large cysts -Ventriculoencephalitis w/hemorrhagic -Ventriculoencephalitis w/hemorrhagic

necrosis necrosis-Lumbosacral myeloradiculitis-Lumbosacral myeloradiculitis

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NEUROPATHOLOGY III CMV INFECTION...CMV INFECTION...

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NEUROPATHOLOGY III ARBOVIRUS INFECTIONS.ARBOVIRUS INFECTIONS.

*Small enveloped RNA v iruses transmitted by arthropod vectors *Small enveloped RNA v iruses transmitted by arthropod vectors from birds/rodents to man/horses, often in summer and fallfrom birds/rodents to man/horses, often in summer and fall*Mosquito borne encephalitis: *Mosquito borne encephalitis: TOGAVIRIDAE.TOGAVIRIDAE.

-Eastern equine encephalitis-Eastern equine encephalitis-Western equine encephalitis-Western equine encephalitis-Venezuelan equine encephalitis-Venezuelan equine encephalitisFLAVIVIRIDAE. -St.Louis encephalitisFLAVIVIRIDAE. -St.Louis encephalitisBUNYAVIRIDAE. La crosse(California sero BUNYAVIRIDAE. La crosse(California sero

group)group)|| *Tick-borne encephalitis: Colorado tick fever *Tick-borne encephalitis: Colorado tick fever

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NEUROPATHOLOGY III ARBOVIRUS INFECTION...ARBOVIRUS INFECTION...

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NEUROPATHOLOGY III ARBOVIRUS....ARBOVIRUS....

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NEUROPATHOLOGY III ARBOVIRUS...ARBOVIRUS...

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NEUROPATHOLOGY III ARBOVIRUS...ARBOVIRUS...

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NEUROPATHOLGOY III PROGRESS.MULTIF.LEUKOENCEPHALOP.PROGRESS.MULTIF.LEUKOENCEPHALOP.

*JC virus detectable in tonsilar tissue of 1/3 of children and adults*JC virus detectable in tonsilar tissue of 1/3 of children and adults*50% of adolescents and 75% of adults have serological evidence of *50% of adolescents and 75% of adults have serological evidence of JC virus infect. (JC virus infect. (The The JC virusJC virus (JCV) is a type of human (JCV) is a type of human polyomaviruspolyomavirus (formerly known as (formerly known as papovaviruspapovavirus) and is ) and is genetically similar to genetically similar to BK virusBK virus and and SV40SV40. It was . It was discovered in 1971 and named after the two initials of a discovered in 1971 and named after the two initials of a patient with patient with progressive multifocal progressive multifocal leukoencephalopathyleukoencephalopathy (PML).(PML).[1][1] The virus causes PML and other diseases only The virus causes PML and other diseases only in cases of in cases of immunodeficiencyimmunodeficiency, as in , as in AIDSAIDS or during or during treatment with drugs intended to induce a state of treatment with drugs intended to induce a state of immunosuppressionimmunosuppression (e.g. (e.g. organ transplantorgan transplant patients). patients). *Oligodendroglia support productive infect.*Oligodendroglia support productive infect. cell cell lysislysisdemyelinationdemyelination*Astrocytes produce infect.*Astrocytes produce infect.morphological transformation and morphological transformation and bizarre appearancebizarre appearance

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NEUROPATHOLOGY III PROGRESSIVE MULTIFOCAL.....PROGRESSIVE MULTIFOCAL.....

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NEUROPATHOLOGY III PROGRESSIVE MULTIFOCAL..PROGRESSIVE MULTIFOCAL..

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NEUROPATHOLOGY III PROGRESSIVE MULTIFOCAL... PROGRESSIVE MULTIFOCAL...

*Result from reactivation of latent JC virus *Result from reactivation of latent JC virus infection due to impaired cell-mediated immunity:infection due to impaired cell-mediated immunity:

-Post-renal transplants-Post-renal transplants-Lymphoma/leukemia patients-Lymphoma/leukemia patients-Acquired immune deficiency syndrome -Acquired immune deficiency syndrome

(accounts for 89% of PML cases) (accounts for 89% of PML cases)*Clinical:*Clinical:

-Focal neurologic deficits – dysartria,paresis, -Focal neurologic deficits – dysartria,paresis, ataxia, visual deficits, personality changes ataxia, visual deficits, personality changes and and occasionally seizures.occasionally seizures.

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NEUROPATHOLOGY III PROGRESSIVE MULTIFOCAL...PROGRESSIVE MULTIFOCAL...

*Pathology:*Pathology:-Multifocal white matter demyelination-Multifocal white matter demyelination-Scanty perivascular lymphocytic infiltr.-Scanty perivascular lymphocytic infiltr.-Bizarre pleomorphic,hyperchromatic -Bizarre pleomorphic,hyperchromatic astrocytesastrocytes-Enlarged oligodendroglia w/intranucl. -Enlarged oligodendroglia w/intranucl. inclusionsinclusions-CSF + for JC viral nucleic acid-CSF + for JC viral nucleic acid*Progression of relentless w/increasing neurologic *Progression of relentless w/increasing neurologic deficits, dementia and death.deficits, dementia and death.

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NEUROPATHOLOGY III PROGRESSIVE MULTIFOCAL...PROGRESSIVE MULTIFOCAL...

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NEUROPATHOLOGY III PROGRESSIVE MULTIFOCAL...PROGRESSIVE MULTIFOCAL...

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NEUROPATHOLOGY III PROGRESSIVE MULTIFOCAL...PROGRESSIVE MULTIFOCAL...

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NEUROPATHOLOGY III PROGRESSIVE MULTIFOCAL....PROGRESSIVE MULTIFOCAL....

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NEUROPATHOLOGY III CHRONIC/SUBACUTE VIRAL INFECT.CHRONIC/SUBACUTE VIRAL INFECT.

*Subacute Measles encephalitis.*Subacute Measles encephalitis.-Measles inclusion encephalitis:-Measles inclusion encephalitis: Develops several months after infect.Develops several months after infect. Most are immunosuppressedMost are immunosuppressed*Subacute sclerosing panencephalitis:*Subacute sclerosing panencephalitis: Chronic progressive encephalitis that Chronic progressive encephalitis that follows exposure to measles virus by follows exposure to measles virus by several yrs. several yrs.*Progressive Rubella panencephalitis*Progressive Rubella panencephalitis Delayed complication of intrauterine or Delayed complication of intrauterine or chilhood infection chilhood infection

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NEUROPATHOLOGY III

SUBACUTE SCLEROSING PANENCEPHSUBACUTE SCLEROSING PANENCEPH

*Refers to viral persistence related to hyper- *Refers to viral persistence related to hyper- mutation of susceptible regions of mutation of susceptible regions of virus encoding M,H and F proteinsvirus encoding M,H and F proteins

*Non-production of altered proteins*Non-production of altered proteinseffective effective evasion of immune responseevasion of immune response

*Persistent cell fusion ability results in persistent in-*Persistent cell fusion ability results in persistent in-

fectionfection

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NEUROPATHOLOGY III

SUBACUTE SCLEROSING PANENCEPHSUBACUTE SCLEROSING PANENCEPH (SSPE)...(SSPE)...*Is an uncommon clinical syndrome characte *Is an uncommon clinical syndrome characte

rized by: cognitive rized by: cognitive decline, spasticity of limbs and seizuresdecline, spasticity of limbs and seizures

*It occurs in children or young adults, months *It occurs in children or young adults, months or years after an initial, early age or years after an initial, early age acute infec tion w/measles acute infec tion w/measles

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NEUROPATHOLOGY III

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NEUROPATHOLOGY III SSPE....SSPE....

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NEUROPATHOLOGY III

PROGRESSIVE RUBELLA PANENCEPHALITIS.PROGRESSIVE RUBELLA PANENCEPHALITIS.

*Clinical presentation is between ages of 8 tand 20 yrs. *Clinical presentation is between ages of 8 tand 20 yrs. with insidious onset of dementia and ataxia with insidious onset of dementia and ataxia

*Other features:*Other features:

-Seizures, spasticity, choreoathetosis and myo--Seizures, spasticity, choreoathetosis and myo-

clonus clonus

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NEUROPATHOLOGY III RETROVIRAL INFECTIONS OF CNS.RETROVIRAL INFECTIONS OF CNS.

*Human T cell leukemia/lymphotropic virus – *Human T cell leukemia/lymphotropic virus – 1(HTLV –1).1(HTLV –1).

Tropical spastic paraparesisTropical spastic paraparesis -progressive spastic paraparesis-progressive spastic paraparesis -demyelination+gliosis of lateral columns-demyelination+gliosis of lateral columns

and less often anterior and posterior cols. and less often anterior and posterior cols. -HTLV-1 is endemic in Caribbean, South-HTLV-1 is endemic in Caribbean, South America, Japan, Seychelles, etc.America, Japan, Seychelles, etc.

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NEUROPATHOLOGY III

RETROVIRAL INFECTIONS...RETROVIRAL INFECTIONS...

*Human Immunodeficiency Virus(HIV)*Human Immunodeficiency Virus(HIV)

-Direct HIV infection of CNS+AIDS -Direct HIV infection of CNS+AIDS de- de- mentia mentia complexcomplex

-Vacuolar myelopathy-Vacuolar myelopathy

-Opportunistic infections of -Opportunistic infections of CNS(CMV)CNS(CMV)

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NEUROPATHOLOGY III RETROVIRAL INFECTIONS....RETROVIRAL INFECTIONS....

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NEUROPATHOLOGY III

RETROVIRAL INFECTIONS...RETROVIRAL INFECTIONS...

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NEUROPATHOLOGY III HIV INFECTION...HIV INFECTION...

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NEUROPATHOLOGY III HIV INFECTION...HIV INFECTION...

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NEUROPATHOLOGY III

BACTERIAL INFECTIONS .BACTERIAL INFECTIONS .

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NEUROPATHOLOGY III MENINGITIS, SUBDURAL EMPYEMA, MENINGITIS, SUBDURAL EMPYEMA,

ABSCESS, VENTRICULITIS.ABSCESS, VENTRICULITIS.*Etiology:*Etiology:

-Neonate –Group B Streptococci, E.coli -Neonate –Group B Streptococci, E.coli -1-10 yrs – H.influenza(most common), -1-10 yrs – H.influenza(most common), N.meningitides,Streptococcus pneumon. N.meningitides,Streptococcus pneumon. -11-20 yrs – N.meningitides(most common), -11-20 yrs – N.meningitides(most common), S. pneumoniae S. pneumoniae

->30 yrs – S. pneumoniae, N. Meningitides, ->30 yrs – S. pneumoniae, N. Meningitides, gram negative bacilli gram negative bacilli -Mycobacteria-Mycobacteriameningitis, tuberculomameningitis, tuberculoma

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NEUROPATHOLOGY III

BACTERIAL MENIGITIS.BACTERIAL MENIGITIS.*Sporadic – aprox.15,000 children/year, *Sporadic – aprox.15,000 children/year, 6-9 months old 6-9 months old -Epidemic -Epidemic

*Mode of entry to CNS *Mode of entry to CNS -Hematogenous -Hematogenous -Compound Fx -Compound Fx -Otitis media -Otitis media -Sinusitis -Sinusitis -Bacterial endocarditis -Bacterial endocarditis

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NEUROPATHOLOGY III

BACTERIAL MENINGITIS....BACTERIAL MENINGITIS....

*Factors influencing outcome: *Factors influencing outcome: -Age, immune status(AIDS),sickle-cell -Age, immune status(AIDS),sickle-cell ane- mia ane- mia -Virulence of agent, vgr. -Virulence of agent, vgr. meningococcus - skin meningococcus - skin rash,septicemia,adrenal hemorrhagerash,septicemia,adrenal hemorrhageshock(W-F shock(W-F syndrome) -Duration of syndrome) -Duration of infection before Tx.infection before Tx.

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NEUROPATHOLOGY III

BACTERIAL MENINGITIS... BACTERIAL MENINGITIS... *Complications: *Complications: -Cerebral edema -Cerebral edemaraised raised intracranial press. intracranial press. herniation herniation - -Angiitis/obliterative endarteritisAngiitis/obliterative endarteritisbrain in- brain in- farction(TB) farction(TB) -Inappropiate ADH -Inappropiate ADH secretion secretion -Cranial nerve palsy(e.g.sensori-neural deafness)-Cranial nerve palsy(e.g.sensori-neural deafness)

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NEUROPATHOLOGY III

BACTERIAL MENINGITIS.... BACTERIAL MENINGITIS.... *Complications... *Complications... -Subdural -Subdural effusion(empyema) effusion(empyema) -Hydrocephalus -Hydrocephalus -Motor deficits -Motor deficits -Seizures -Seizures -Mental -Mental retardationretardation

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NEUROPATHOLOGY III

BACTERIAL MENINGITIS.... BACTERIAL MENINGITIS.... *Dx.: *Dx.: -Headache, malaise, mental confusion, -Headache, malaise, mental confusion, fever, vomiting,convulsions or seizures(TB) fever, vomiting,convulsions or seizures(TB) -Physical examination showing neck stiff- -Physical examination showing neck stiff- ness, Kernig´s sign ness, Kernig´s sign -Lab.: CSF examination -Lab.: CSF examination w/Gram stain, w/Gram stain, culture. culture. PCR for HSVPCR for HSV

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NEUROPATHOLOGY III CSF . CSF .

-Normal. Meningitis -Normal. Meningitis pressurepressure pyogenicpyogenic TBTB 60- 60-120mm >200 mm >200mmH2O 120mm >200 mm >200mmH2O appearance appearance crystal clear turbid crystal clear turbid opalescent opalescent cell contentcell content 0-4mononucl. >1000PMN´s lymphos. 0-4mononucl. >1000PMN´s lymphos. proteins proteins 0.2-0.4g/l 1-10 g/l 1-3g/l 0.2-0.4g/l 1-10 g/l 1-3g/l glucose glucose 50-80 mg/100ml 50-80 mg/100ml decreaseddecreased low low

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NEUROPATHOLOGY III SYPHILIS.SYPHILIS.

*Asymptomatic.*Asymptomatic.-CSF pleocytosis,increased Igs+serology -CSF pleocytosis,increased Igs+serology *Meningitis. -1-2 yrs after *Meningitis. -1-2 yrs after initial infection *Meningovascular initial infection *Meningovascular syphilis -Arteritis syphilis -Arteritis *General paresis *General paresis -Chronic meningoencephalitis -Chronic meningoencephalitis -10-20 yrs after initial infection -10-20 yrs after initial infection -Psychiatric disord.,seizures,intellectual -Psychiatric disord.,seizures,intellectual decline, loss of motor control, incontinence decline, loss of motor control, incontinence *Tabes dorsalis-chronic inflamm. of *Tabes dorsalis-chronic inflamm. of dorsal roots+ gangliadorsal roots+ gangliacolumn degenerationcolumn degeneration

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NEUROPATHOLOGY III

FUNGAL INFECTIONS.FUNGAL INFECTIONS.

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NEUROPATHOLOGY III

FUNGAL INFECTIONS.FUNGAL INFECTIONS.*Most fungal infections occur as opportunistic *Most fungal infections occur as opportunistic infectionsinfections*Predisposing factors for opportunistic infections:*Predisposing factors for opportunistic infections: -Immunosuppresive therapy, HIV infect., -Immunosuppresive therapy, HIV infect., diabetes mellitus,neutropenia,alcoholism, diabetes mellitus,neutropenia,alcoholism, IV drug abuser,malnutrition,etc. IV drug abuser,malnutrition,etc. *Most common: Candidosis, *Most common: Candidosis, Cryptococcosis,As- pergillosis, Cryptococcosis,As- pergillosis, Mucormycosis.Mucormycosis.

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NEUROPATHOLOGY III FUNGAL....FUNGAL....

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NEUROPATHOLOGY III FUNGAL...FUNGAL...

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NEUROPATHOLOGY III

BRAIN ABSCESS.BRAIN ABSCESS. Etiology. Etiology.

*Streptococci milleri(most common) gram- *Streptococci milleri(most common) gram- bacilli, Staph.aureus,bacteriodes bacilli, Staph.aureus,bacteriodes -Direct spread from paranasal sinuses(50%) -Direct spread from paranasal sinuses(50%) -Hematogenous(25%)from lung -Hematogenous(25%)from lung abscess,sub acute abscess,sub acute endocarditis, bronchiectasis,etc. -endocarditis, bronchiectasis,etc. -Mortality – 20% Mortality – 20% -Morbidity w/focal neurologic deficits or epilepsy -Morbidity w/focal neurologic deficits or epilepsy (50%) (50%)

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NEUROPATHOLOGY III

PARASITIC INFECTIONSPARASITIC INFECTIONS

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NEUROPATHOLOGY III

AMEBIASIS.AMEBIASIS.

*Primary – Naegleria fowleri- acute hemorrhagic *Primary – Naegleria fowleri- acute hemorrhagic necrotizing encephalitis in healthy necrotizing encephalitis in healthy individuals w/recent past individuals w/recent past history of swimming on fresh waters history of swimming on fresh waters

*Granulomatous-Acanthameba sp.-immune com *Granulomatous-Acanthameba sp.-immune com promised patients promised patients

*Cerebral amebic abscess-disseminated E.hystoly- *Cerebral amebic abscess-disseminated E.hystoly- tica infectiontica infection

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NEUROPATHOLOGY III

TOXOPLASMOSIS.TOXOPLASMOSIS.

*CNS infections seen in:*CNS infections seen in:

-Defective cell immunity such as in AIDS -Defective cell immunity such as in AIDS and is secondary to reactivation of dormant and is secondary to reactivation of dormant infection. infection.

-Congenital infection following transplacen -Congenital infection following transplacen tal spread tal spread

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NEUROPATHOLOGY III

CYSTICERCOSIS.CYSTICERCOSIS.*Epidemiology. *Epidemiology.

-Endemic in all countries except in -Endemic in all countries except in Australia Australia-Very common in L.A.-1.4-3.6% in auto -Very common in L.A.-1.4-3.6% in auto

psies(México)psies(México)-Caused by Tenia solium(pig tapeworm) -Caused by Tenia solium(pig tapeworm)

-Man is definitive host-adult parasite -Man is definitive host-adult parasite in in small intestinesmall intestine

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NEUROPATHOLOGY III

CYSTICERCOSIS...CYSTICERCOSIS...

-Acquired after ingestion of larval stage in -Acquired after ingestion of larval stage in unhygienic pork meat unhygienic pork meat

-Pig is intermediate host-Pig is intermediate host

-Infection after ingestion of eggs(fecal cont) -Infection after ingestion of eggs(fecal cont) -Human cysticercosis when -Human cysticercosis when man is interme- diate host man is interme- diate host w/ingestion of eggs.w/ingestion of eggs.

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NEUROPATHOLOGY III

CYSTICERCOSIS... CYSTICERCOSIS... *Clinical: *Clinical: -Parenchymal cysts-seizures, focal signs -Parenchymal cysts-seizures, focal signs without increased ICPwithout increased ICP

-Meningeal cysts(often basal)-hydrocephal., -Meningeal cysts(often basal)-hydrocephal., vascular occlusion vascular occlusion

-Ventricular cysts-most commonly in 4th ventricle-Ventricular cysts-most commonly in 4th ventricle

-Spinal cord cysts-uncommon-Spinal cord cysts-uncommon

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NEUROPATHOLOGY III

CYSTICERCOSIS...CYSTICERCOSIS...

*Dx.:*Dx.:

-CT and MRI scans-cystic lesions+calcifica -CT and MRI scans-cystic lesions+calcifica tions in chronic tions in chronic casescases

-CSF serology-ELISA-CSF serology-ELISA90% sensitivity90% sensitivity

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NEUROPATHOLOGY III PRION DISEASES.PRION DISEASES.

*Creutzfeldt-Jakob disease(CJD)*Creutzfeldt-Jakob disease(CJD)*Gerstmann-Strausler-Scheinker dis.(GSS)*Gerstmann-Strausler-Scheinker dis.(GSS)*Fatal familial insomnia(FFI)*Fatal familial insomnia(FFI)*Kuru*KuruCOMMON FEATURES.COMMON FEATURES.-Accumulation of abnormal cellular protein-Accumulation of abnormal cellular protein-Transmission: sporadic(85%),familial(15%),iatrogenic CJD(ino- -Transmission: sporadic(85%),familial(15%),iatrogenic CJD(ino- culation, tissue transplant),endocannibalism(kuru) culation, tissue transplant),endocannibalism(kuru) -Epidemiology: CJD incidence 1-2/million -Epidemiology: CJD incidence 1-2/million

age of onset 55-75 M=Fage of onset 55-75 M=F

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NEUROPATHOLOGY III PRION DISEASES....PRION DISEASES....

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NEUROPATHOLOGY III PRION DISEASES...PRION DISEASES...

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