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Fungal infections of the brain
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Increasing incidence because of growing numberpatients who have compromise of the immunesystem
The widespread use of immunosuppressiveagents for inflammatory conditions, organtransplantation, malignancies, and AIDS is
responsible for the increasing number ofimmunocompromisde hosts
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Aspergillus Species Infections
Commonly found in soil, water and decaying
vegetation
Large organism with Y-shaped branching hyhae
Most infections in humans are caused byAspergillus fumigatus andAspergillus flavus,which act as opportunistic pathogens
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Aspergillus Species Infections
The lungs are the primary site of infection: after
inhalation of spores or mycelial framents
followed by the GI tract
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Aspergillus Species Infections
Predisposing conditions
- immunosuppressive therapy
- diabetes mellitus
- neutropenia
- Cushings syndrome
- cancer- mulnutrition
- hepatic failure- chronic pulmonary disease
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Aspergillus Species Infections
Pathogenesis:
Cerebral aspergillosis-Hematogenous spreading
-when multiple systemic sites are involved
-rarely cause maningitis because of their
large size (prevents them from reaching themicrovasculature)
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Aspergillus Species InfectionsPathogenesis:
Aspergillus sp. Selectively infiltrates and destroys the
internal elastic layer ofmedium-sized and largeblood vessels
Leading thrombosis, occlusion, cerebral infarction
Region ofbrain necrosis develop fungal abscess
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Aspergillus Species Infections
Pathogenesis:
Other modes of CNS invasion:-head trauma
-neurosurgery
-direct extension from orbit, mastoid air cells
or paranasal sinuses
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Aspergillus Species Infections
Diagnosis:
Cerebral aspergillosis can be difficult to detectand diagnosis is often made at autopsy
Pt. have significant mass effect fromhemorrhagic lesions or abscess LP
Aspergillus sp. abscess can appear on CT/ MRIring enhancing lesions with surrounding
cerebral edema
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Aspergillus Species InfectionsTreatment:
Brain lesion suggestive of an abscess on
neuroimaging tissue sampling is necessary toDx
If Definitive Dx isAspergillus sp. Abscess
-surgical debridement / resection
-antifungal therapy: systemic AmphotericinB
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Mucor Species Infections
Found in soil and decaying organic material
Nonseptated fungi with branch at right angles Spores can inhaled as infected dust and can
frequently be culture from nose&throat ofhealthy individuals
Immunocompetent hosts are rarely affected
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Mucor Species Infections
Predisposing factor:
-poorly controlled DM: ketoacidosis-chronic renal failure
-leukemia
-neutropenia
-iron overload-immunosuppressive agents
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Mucor Species Infections
Riskfor isolateted intracerebral mucormycosis
:IVDU direct inoculation of fungal elementsinto bloodstream
Intracerebral site of infection : Basal ganglia
gait difficulties, ataxia or hemiparesis
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Mucor Species InfectionsPathogenesis:
Cerebral mucormycosis:
-direct extension from nasophrynx or face(by inhalation of the fungus)
-skin can become infected following trauma orburns
-infitration ofmedium sized and large arteriesthrombosis andwidespread necrosis of
nasal mucosa & orbitofacial skull base
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Mucor Species Infections
Pathogenesis:
Spread along skull base may involve sphenoidsinus, sella turcica and cribiform plate withintracranial extension though optic canal andsuperior orbital fissure
Advanced stage : blindness carotid arteryocclusion, carvernous sinus thrombosis and
bifrontal brian abscesses
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Mucor Species Infections
Signs&symptoms:
-facial edema
-necrotic nares
-chemosis(edema of mucous membrane of
eyeball&eyelid lining)-ophthalmoplegia
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Mucor Species InfectionsDiagnosis:
Radiographic apperance - nonspecific
CT with contrast : the lesions are hypodensewith significant surrounding cerebral edema,usuallybasal ganglia or brainstem (with orwithout hemorrhage)
The pattern of enhancement is either diffuse orring enhancing, depending on the stage of theabscess
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Mucor Species InfectionsDiagnosis: Rhino-orbito-cerebral mucormycosis
-bony destruction eg. Facial bone-air-fluid level in paranasal sinuses
Diagnosis can be confirmed by culture or
histopathological from debrided necrotic material
Diagnosis of intracerebral Mucor sp.-stereotacticbrain biopsy(CSF analysis is non specific)
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Mucor Species InfectionsTreatment:
Correction of metabolic abnormalities eg.
Ketoacidosis Initiation of high-dose systemic AmphotetricinB
Aggressive local debridement of necrotic materialin the sinuses: prevent extension of the infection
intracranially The disease extends into the brain: craniotomywith abscess resection (for prolong survival )
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Candida Species Infections
Normal flora ofGI & reproductive tract
Oval shaped and reproduce inyeast forms,connected to form pseudohyphae
True hyphae are found onlyactive infection
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Candida Species Infections
Risk factors:
-antimicrobial therapy-corticosteroid therapy
-bone marrow transplantation
-burn
-chemotherapy-low birth weigth
-prematurity
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Candida Species InfectionsPathogenesis:
MC clinical manifestations of systemic candidiasis
are oral & esophageal thrush & vulvovaginitis
Systemic infection
- fungal element reach the submucosal bloodvessels and hematoganous spread
-direct inoculation of the blood stream eg.IVDU, surgery, indwelling vavscular catheter
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Candida Species Infections
C.Albicans is the organism responsible for most
CNS infections and can involve the meninges,brain parenchyma
Noncaseating granulomas and multiple micro
abscesses, usually at gray-white junction,represent the parenchymal manifestations ofCNS candidiasis
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Candida Species Infections
Other uncommon manifestations of CNS
candidiasis :-mycotic aneurysm
-intraventriicular fungal balls
-vasculitis thrombosis stroke
Focal neurological deficit uncommon Clinical picture is more reflective of a
progressive encephalopathy
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Candida Species Infections
Candida meningitis symptom(bbacterial
meningitis)-fever
-photophobia
-headache
-nuchal rigidity
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Candida Species Infections
Treatment:
Systemic AmphotericinBs
flucytocine
Candida shunt infections should by treated byremoval of the shunt and IV AmphotericinB s
intrathecal AmphotericinB
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Cryptococcus Species Infections
Cryptococcus neoformans is the onlyencapsulated yeast species known to bepathogenic to human
The polysaccharide capsules : virulence of the
organism impairs Ag presentation & inhibitsphagocytosis
Found in soil contaminated bybird excreta
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Cryptococcus Species Infections
Pathogenesis:
Enter the body byinhalation of infected dust Disseminated Cryptococcus can infect all organsystem
90% of pt. with systemic infection have CNS
involvement usually in the form ofmeningoencephalitis
Hematogenous spreading
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Cryptococcus Species Infections
The main predisposing factor for disseminatedcryptococcus is defective T-lymphocyte function
Conditions associated with cryptococcosis;-hematologic malignancy-collagen vascular diseasee-corticosteroid therapy
-immunosuppression after organ transplantation-AIDS
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Cryptococcus Species Infections
Symptoms associated with cryptococcalmeningitis:
-can develop hydrocephalus
-symptom ICP eg. Headache, nausea,vomiting
-confusion & psychosis-decrease VA due to papilledeme
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Cryptococcus Species Infections
Diagnosis:
Pt. with immune defects who present withsymptom ofmeningitis or hydrocephalus
blood ,urine, CSF : india-ink preparation &culture for definitive DX
Enzyme immunnoassays & rapid latexagglutination tests can detect the cryptococcalcapsular polysaccharide Ag in serum & CSF
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Cryptococcus Species Infections
Treatment:
Cryptococcus meningoencephalitis:AmphotericinB+ flucytocine 6 weeks
Cryptococcus meningitis:AmphotericinB+ flucytocine 2 weeks followed
by long-term oral Fluconazole
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Cryptococcus Species InfectionsTreatment:
Cryptococcus meningitis develop ICP
-without hydrocephalus: Acetazolamide &daily LP forCSF pressure >180 mm
-with hydrocephalus: ventriculoperitoneal shunt
Neurosurgical intervention:brain biopsy or CSFdiversion
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Parasitic Infections of the CNS
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Neurocysticercosis
Common cause ofseizures and hydrocephalus indeveloping country
May effect cerebral parenchyma, subarachnoidspace or ventricular system
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NeurocysticercosisPathogenesis:
Caused by the pork tapeworm Taenia solium
Human are only definitive host, acquire wheningests the undercooked pork(cysticercus)
Larva matures in human gut
Penetrate the gut wall into bloodstream,may seedmultiple organs
Lodging in the microvasculature of the gray-whitejunction, creating intraparenchymal lesion
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Neurocysticercosis Clinical manifestation(Depend on: cyst
morphology, anatomical location, No. of lesions):
-neurological symptom: seizure,symptom ofhydrocephalus eg. Headache, vomiting,ataxia
-focal deicits result from cerebral edema
(induced by drying cysticercus)
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Neurocysticercosis Clinical manifestation:
-numerous small parenchymal lesions:
cognitive dysfunction, but meningitis is rare
-cerebral infarction
-inflammation of blood vessels in basilarsubarachnoid space
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Neurocysticercosis
Diagnosis:
Prolong exposure ,living in endemic area
Positive stool assays for ova and parasites(T.solium proglottids) as well as eosiniphilia in
PBS
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Neurocysticercosis
Treatment:
Medical:
-Antihelminthics: praziquantel & albendazole
-Dexamethazole
Surgical: goal prevention & alleviation
hydrocephalus-CSF diversion, CSF shunting
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Toxoplasmosis
Pathogenesis:
Toxoplasma gondiioligate intracellular parasite
Obtained byingestion improperly cooked meatharboring the organisms cysts
Rapidly proliferating & migrates throughout thebody in cell ofthe lymphoid-macrophage system
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Toxoplasmosis
Pathogenesis:
Develop cyst in any organ: brain, lung, muscle,liver
In the brain, the microscopic cyst elicits aninflammatory infiltrate with PMN, leucocytes,
lymphocytes, macrophage and plasma cell
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Toxoplasmosis
Clinical manifestation:
Reactivation of parasite: focal deficits in thesetting of global encephalopathy period 1-2 week
Nonspecific finding(50%): lethargy, confusion,headache
MC focal finding is hemiparesis Seizure and brain stem finding less common
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Toxoplasmosis
Diagnosis:
HIV positive pt. present with mass lesion &neurological deficit
Ring-enhancing mass lesion
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ToxoplasmosisTreatment:
Medical:
-pyrimethamine (200 mg loading dose followedby 50-70 mg PO qd)
-folinic acid (10 mg PO qd)
-clindamycin (600mg PO/ IV q 6 hr)orsulfadiazine (4-8 g PO/ IV qd)
Surgical:
-setereotactic biopsy
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Cerebral malaria
P.Falciparum is MC parasitic infection in CNS
CNS symptom rersult from engorgement of thecerebral microvasculature secondry tosequestration of erythrocytes containing PF
Cerebral malaria as coma lasting greater than 6
hr in pt. with parasitemia Coma may develop slowly or suddenlyafter a
seizure 48-72 hr
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Cerebral malaria
Pt. may show signs ofsymmetric UMN lesions
Imaging finding: increase brain volumesecondry to vascular engorgement withoutsignificant cerebral edema
Treatment:
-antimalarial therapy-suppoortive chemotherapy
-anticonvulsants
-blood replacement for anemia
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Cerebral malaria
Mortality rate 5-50%
Long-term sequalae 5-18% :
-cognitive deficits
-hemiplegia
-cortical blindness-cerebellar ataxia
Children- highest rate of sequalae