1 fungus parasite

8/9/2019 1 Fungus Parasite

1/50

Fungal infections of the brain


2/50

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


3/50

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


4/50


The lungs are the primary site of infection: after

inhalation of spores or mycelial framents

followed by the GI tract


5/50


Predisposing conditions

- immunosuppressive therapy

- diabetes mellitus

- neutropenia

- Cushings syndrome

- cancer- mulnutrition

- hepatic failure- chronic pulmonary disease


6/50


Pathogenesis:

Cerebral aspergillosis-Hematogenous spreading

-when multiple systemic sites are involved

-rarely cause maningitis because of their

large size (prevents them from reaching themicrovasculature)


7/50

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


8/50


Pathogenesis:

Other modes of CNS invasion:-head trauma

-neurosurgery

-direct extension from orbit, mastoid air cells

or paranasal sinuses


9/50


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


10/50

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


11/50

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


12/50


Predisposing factor:

-poorly controlled DM: ketoacidosis-chronic renal failure

-leukemia

-neutropenia

-iron overload-immunosuppressive agents


13/50


Riskfor isolateted intracerebral mucormycosis

:IVDU direct inoculation of fungal elementsinto bloodstream

Intracerebral site of infection : Basal ganglia

gait difficulties, ataxia or hemiparesis


14/50

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


15/50


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


16/50


Signs&symptoms:

-facial edema

-necrotic nares

-chemosis(edema of mucous membrane of

eyeball&eyelid lining)-ophthalmoplegia


17/50

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


18/50

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)


19/50

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 )


20/50

Candida Species Infections

Normal flora ofGI & reproductive tract

Oval shaped and reproduce inyeast forms,connected to form pseudohyphae

True hyphae are found onlyactive infection


21/50


Risk factors:

-antimicrobial therapy-corticosteroid therapy

-bone marrow transplantation

-burn

-chemotherapy-low birth weigth

-prematurity


22/50

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


23/50


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


24/50


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


25/50


Candida meningitis symptom(bbacterial

meningitis)-fever

-photophobia

-headache

-nuchal rigidity


26/50


27/50


Treatment:

Systemic AmphotericinBs

flucytocine

Candida shunt infections should by treated byremoval of the shunt and IV AmphotericinB s

intrathecal AmphotericinB


28/50

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


29/50


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


30/50


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


31/50


Symptoms associated with cryptococcalmeningitis:

-can develop hydrocephalus

-symptom ICP eg. Headache, nausea,vomiting

-confusion & psychosis-decrease VA due to papilledeme


32/50


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


33/50


Treatment:

Cryptococcus meningoencephalitis:AmphotericinB+ flucytocine 6 weeks

Cryptococcus meningitis:AmphotericinB+ flucytocine 2 weeks followed

by long-term oral Fluconazole


34/50

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


35/50

Parasitic Infections of the CNS


36/50

Neurocysticercosis

Common cause ofseizures and hydrocephalus indeveloping country

May effect cerebral parenchyma, subarachnoidspace or ventricular system


37/50

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


38/50


39/50

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)


40/50

Neurocysticercosis Clinical manifestation:

-numerous small parenchymal lesions:

cognitive dysfunction, but meningitis is rare

-cerebral infarction

-inflammation of blood vessels in basilarsubarachnoid space


41/50

Neurocysticercosis

Diagnosis:

Prolong exposure ,living in endemic area

Positive stool assays for ova and parasites(T.solium proglottids) as well as eosiniphilia in

PBS


42/50

Neurocysticercosis

Treatment:

Medical:

-Antihelminthics: praziquantel & albendazole

-Dexamethazole

Surgical: goal prevention & alleviation

hydrocephalus-CSF diversion, CSF shunting


43/50

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


44/50

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


45/50

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


46/50

Toxoplasmosis

Diagnosis:

HIV positive pt. present with mass lesion &neurological deficit

Ring-enhancing mass lesion


47/50

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


48/50

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


49/50

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


50/50

Cerebral malaria

Mortality rate 5-50%

Long-term sequalae 5-18% :

-cognitive deficits

-hemiplegia

-cortical blindness-cerebellar ataxia

Children- highest rate of sequalae

1 fungus parasite

Documents