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Part One--Bacteria
Neuropathology: Non-viral Infections
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Mechanisms of CNS injury by infections
A. direct destruction of CNS tissue
1. necrosis2. abscess
B. inflammation and edema compromise neural function
C. edema and mass effect from abscess cause herniationD. effects on vasculature lead to infarction
E. effects on CSF flow lead to hydrocephalus
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Routes of Injury of the Nervous System
Hematogenousarteriesemissary veins from face or scalp
Direct implantationtrauma, iatrogenic
Local extensiondental abscess
cranial air sinus (mastoid or frontal sinuses most common)Effects at a distance mediated by neurotoxinsdiphtheriaClostridium tetani (muscle rigidity and spasms)
Clostridium botulinum (paralysis at neuromuscular junction, blocksneurotransmitter release)shigellosis (encephalopathy with convulsions, lethargy, confusion,
severe headache)
legionellosis (encephalopathy,acute ataxia, dysarthria)
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Acute Bacterial Meningitis
Meningitis is an inflammation of meninges,especially the leptomeninges.
Meningoencephalitis is an inflammation of boththe meninges and brain parenchyma.
Cerebritis is an inflammation of the brainparenchyma and may accompany bacterial
meningitis.
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CNS Drugs. 2001;15(12):909-19
Organisms causing bacterial meningitis
Vaccinations againstH. influenzae type B in infants have dramaticallyreduced this organism as a cause of meningitis. Similar reductions areoccurring with S. pneumoniae andN. meningitidis.
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Effect ofH. influenzaevaccine on causes of
bacterial meningitis
1986, beforeH. inf. vaccine
1995, afterH. inf. vaccine
Postgrad.
Med.11
4:43(2003)
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http://www.cdc.gov/nip/recs/child-schedule.htm
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Meningococcal Polysaccharide Vaccine
Recommendations
Not recommended for rout ine vaccination ofcivilians
Recommended for certain high-riskpersons:
Terminal complement deficiency
Functional or anatomic aspleniaCertain laboratory workers
Travelers to and U.S. citizens residing incountr ies in which N. meningiditis ishyperendemic or epidemic (e.g., Africanmeningitis belt)
Meningococcal Polysaccharide Vaccine
Recommendations
Control of outbreaks
Outbreak definition:
3 or more confirmed or probablecases
Period 10 cases per
100,000 population*
*Population-based rates should be used rather
than age-specific attack rates
Meningococcal Endemic Areas 2000
Equator
http://www.cdc.gov/nip/ed/slides/mening8p.ppt
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Signs and symptoms of meningitisHeadachePhotophobia
IrritabilityImpaired consciousness
Neck stiffness
CSF characteristicsInflammatory cells
Increased pressure
Increased protein
Reduced glucose
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Gross appearanceInflammatory exudate within the arachnoid andperivascular spaces (Virchow-Robin spaces),extending to ventricles
Congestion of blood vesselsLocalization of exudate varies with organisms
Microscopic appearanceMultitudes of neutrophils in the subarachnoid space,particularly around leptomeningeal blood vessels
Cerebritis from local extension into brainThrombosis of involved vessels with cerebralinfarction
Gram stain should always be performed
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Pneumococcal meningitis
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Meningitis at base of brain
exudate with H. influenzae is more pronounced at base of brain
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N. meningitides (Gram neg diplococci) in CSF
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Route of entryinto CSF by
N. meningitidis
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(A) Meningitis from S. pneumoniae begins with
invasion of mucosal epithelium. (B)
Neutralization of IgA protease facilitates this
step. The organisms then enter the bloodstream
and evade destruction by the alternativecomplement pathway because its polysaccharid
capsule resists binding of factor B to C3b,
preventing activation of C5-C9. (C) It is
hypothesized that at the blood-brain barrier
during infection, activated endothelial cells
release cytokines that stimulate increased
surface expression of platelet activating factor
(PAF) receptors. The organisms bind to PAF
receptors via their cell-wall phosphorylcholine.
(D) PAF receptor cycling brings the pathogen
across the endothelium and into the
extracellular matrix, where it binds to
fibronectin, proliferates and spreads to the CSF.
Route of entry
into CSF by
N. meningitidis
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Lancet Infect Dis. 2002 Dec;2(12):721-36
Pathogenic steps leading topneumococcal meningitis
IgR=immunoglobulinreceptor
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Cerebral infarcts with pneumococcal meningitis
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Neonatal meningiti
(group B
streptococcus)
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Ventriculitis from shunt infection with S. aureus
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Inflammatory exudate of meningitis
inflammation around perivascular spaces (Virchow-Robin spaces)
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Inflammatory exudate of meningitis
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Meningitis is often preceded by a prodromal respiratoryinfection, the neurologic signs and symptoms come on quickly
leading to changes in consciousness and coma. Dehydration iscommon and vascular collapse may lead to shock (Waterhouse-Friderichsen syndrome).
http://aci.mta.ca/Courses/Biology/Images/bacterial%20folder/Meningitis43.jpeg
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http://aci.mta.ca/Courses/Biology/Images/bacterial%20folder/Meningitis44.jpeg
Rash of meningococcemia
(sepsis caused byNeisseria meningitidis)
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Suppurative Infections
Brain abscessOrganisms: Streptococci and staphylococci
Context: Local extension of neighboringinfection, hematogenous spread frominfections in heart (especially valves), lungs,
or bonesRisk factors: cyanotic congenital heart disease
(right-to-left shunt) and chronic pulmonarysepsis.
Gross and microscopic pathology: Liquefactivenecrosis with fibrous reaction at gray whitejunction or white matter
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Brain abscesses
Chronic frontal sinus infectionRight-to-left shunt
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Subdural empyemaPus in the dural space but not involving the
underlying leptomeninges
Risk of thrombosis and infarction
Extradural (epidural) abscessAssociated with neighboring bone or sinus
infectionDangerous because of mass effect (herniation)
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Subdural empyema from S. aureus
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Subdural empyema
Loculated collections of pus in the subdural space with mass effec
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Epidural abscess
CT scan with contrast
enhancement.
meninges surrounding the
abscess enhances
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Acute cerebritis adjacent to petrous temporal bone infection
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Chronic Bacterial Infections
TuberculosisClinical picture: Chronic meningitisCSF with moderately increased number of cells
and increased protein
Gross and microscopic pathology:Base of brainTuberculomas
Chronic inflammatory cells with granulomas andacid-fast bacilli
Arachnoid fibrosis leads to hydrocephalus
Obliterative endarteritis leads to infarction
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Tuberculousmeningitis atbase of brain
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Tuberculousmeningitis
Acid-fast staining
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Neurosyphilis
1. Meningeal-meningovascular neurosyphilis:
rich in perivascular plasma cells and iscommonly at the base of the brain, cerebralconvexities, and spinal meninges
2. Paretic neurosyphilis: invasion of thebrain by Treponema pallidum with loss of
brain function (general paresis of the insane(GPI))
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Neurosyphilis
3. Tabes dorsalis (spinal cord)
Loss of axons and myelin in the dorsal columns
because of damage by T. pallidum to dorsal
roots. Impaired sense of joint position and ataxia
Loss of pain sensation leading to joint damage
(Charcot joints) Sensory disturbances (lightning pains)
Absence of deep tendon reflexes
Hi t f hili i t
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History of syphilis in stages
JAMA. 2003 Sep 17;290(11):1510-4
S hiliti t iti f iddl b l t
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Syphilitic arteritis of middle cerebral artery
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Gumma of tertiary syphilis
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Gumma of tertiary syphilissoft, gummy mass with tissue resembling granulation tissue and
central necrosis
Paretic neurosyphilis
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Paretic neurosyphilisatrophy of the frontal gyri
P ti hili
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perivascular inflammationwith plasma cells proliferation of microglia
Paretic neurosyphilis
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Lyme diseaseSymptoms:
aseptic meningitis
7th nerve palsy
encephalopathy
polyneuropathy
Microscopic pathologymicroglial proliferation
vasculitis
L di i l i i h l
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Lyme disease involving peripheral nerve
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Neuropathology: Non-viral Infections
Part TwoFungi, Protozoa, Helminths, andRickettsiae
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Rhinocerebralmucormycosis
often in diabeticswith ketoacidosis
Rhinocerebral m corm cosis
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Rhinocerebral mucormycosis
A i i
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Aspergillosis
V l i i b A ill
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Vascular invasion byAspergillus
Candida abscess in patient with AIDS
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Candida abscess in patient with AIDS
C t i i b l li
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Cryptococcosis in basal ganglia
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Histoplasmosis
yellow-gray exudate over
base of brain at optic
chiasm and left temporal
pole
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Histoplasma yeastsin meningeal
exudate
Coccidioidomycosis spherules with endospore
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Coccidioidomycosis spherules with endospore
Trophozoite ofEntamoeba histolytica in cerebral abscess (PAS)
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p y ( )
Primary amebic meningoencephalitis (Naegleria fowleri)
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Granulomatousamebic encephalitis
(Acanthamoeba)
Slate gray brain in cerebral malaria
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g yPlasmodium falciparum
Red blood cells with malaria parasites
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p
Toxoplasma gondii cyst with bradyzoites
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Microglial nodule in African trypanosomiasisSl i i k d b T b i h d i
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Sleeping sickness caused by Trypanosoma brucei rhodesiense or
T. b. gambiense
Morular cells of African trypanosomiasisplasma cells with globules of immunoglobulin characteristic but not specific
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plasma cells with globules of immunoglobulin--characteristic but not specific
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Trypanosoma cruziChagas disease in heart
Parasites in amastigote stage
in cardiac myofiber
Trypanosoma cruzi
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yp
Chagas disease in brain
abundant amastigoteparasites mostly in astrocytes
and macrophages
necrotizing lesion of T.
cruzi in patient with AIDS
Cysticerosis (larval form of Taenia solium
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Cysticerosis (larval form of Taenia solium
Intraventricular cysticerci of Taenia solium
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Intraventricular cysticerci of Taenia solium
Scolex of Taenia solium
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Visceral larva migrans in brain(Toxocara canis = dog ascarid)
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( g )
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Schistosomiasis
granuloma from
Schistosoma japonicum
Red structures indicate immunohistological staining of Rickettsia rickettsiiin endothelial cells of a blood vessel from a patient with fatal RockyMountain spotted fever
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Mountain spotted fever
http://www.cdc.gov/ncidod/dvrd/rmsf/Laboratory.htm
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