untan neurosains parasit 2008

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Untan-neurosains sem 4-2008 1

Parasitic Infections in

Central Nervous System

Agnes Kurniawan

Dept of Parasitologi FKUI



BASIC PARASITOLOGY

•The science that deals with

organisms that take up their abodes• Temporarily or permanently

• On or within other living organisms

• Procuring food with the relationshipof these organisms to their hosts

2Untan-neurosains sem 4-2008



CLASSIFICATION

• Ecto-parasite :

Parasite that lives outside the body of the

host (infestation)

• Endo-parasite :

Parasite which lives within the body of thehost (infection)




• Obligate-parasite :

Parasites are completely dependent upon the

host

e.g : Ascaris lumbricoides

• Facultative-parasite :

Parasites are capable of leading both a free anda parasitic existence upon the host

e.g : - Strongyloides stercoralis, Tick

CLASSIFICATION




Parasite

Phytoparasite Zooparasite Spirochaeta

Virus

Protozoa Metazoa

Helminths Arthropods

Nematode Trematode Cestode5Untan-neurosains sem 4-2008



HOST

• Harboring parasite species

• Usually a larger organism that providesphysical protection and nourishment




DEFINITIVE HOST

• The host that harbors the adult or sexual stageof the parasite

e.g : - Ascaris lumbricoides man

- Plasmodium mosquito

• Intermediate host :

Another animals that take place part or all of thelarval or asexual stage

e.g : - Plamodium mosquito man

- Filaria man mosquito




RESERVOIR HOST

• Animals that harbor the same species of

parasites as man and act as additional

sources of human infection

E.g : - Trichinella spiralis Rh : pig, rat,

bear

- Brugia malayi Rh : monkey,

cat, dog




VECTORS

• Hosts that transmit parasites to man

e.g. : mosquitos in malaria / filariasis

glossina in sleeping sickness Africa

ZOONOSIS• Animal diseases which can be transmitted

to human




NEMATHELMINTHES

• Roundworm , unsegmented

• Posses a body cavity

• Have a complete digestive system

• The sexes are separate




PLATYHELMINTHES

• Flatworms

• Bilaterally symmetrical

•

Leaf –

shaped or band –

shaped• Without a body cavity

• Have no digestive tract

• Hermaphrodite




Protozoa

• an unicellular animal cell

• living either in colonies or solitaire which is

able to perform all physiological function of

its own




Classification :

E Rhizopoda

E Mastigophora/Flagellata

E Cilliophora/Ciliata

E Sporozoa




Reproduction

asexual : binary fission, schizogony,

cyst formation sexual : Gametogony, sporogony,

conjugation

alternating asexual and sexual




Pathology

Tissue damage by :

• invasion

• enzyme• toxin

• immune response




Infection

• Acute fatal

•

Sub clinical• Chronic/latent

• Relapse/ acute exacerbation




Entomology

deals with insects, arachnids, and other arthropods which cause pathology / rolein transmission infective agents

The arthropods involved may be as :1. the causal agents

2. intermediate hosts

3. vectors.




Intermediate hosts

• Transmission in a passive capacity.

• Part or all of the larval or asexual stage maytake place in another animal such as the snail ,

Cyclops or Diaptomus.




Role Of Vector In

Disease Transmission

Depends on :

• Infection intensity

• Anthropophylic• High density of vector species

• Mosquito life span / longevity

• Supported by Experimental evidence





DISEASE CAUSE STAGE DEFINITIVE

HOST

Cerebral malaria P. falciparum Schizont Mosquito

Neurocysticercosis Taenia solium Larva Human

Cerebral toxoplasmosis Toxoplasma gondii Tachyzoite Cat

Brain abscess E.histolyt ica Trophozoites Human

Sleeping sickness African Trypanosoma Trypomastigote Human

Granulomatous Ensefalitis Acanthamoeba sp Trophozoite Free living

Meningoensefalitis (PAM) Naegleria fowleri Trophozoite Free living




Malaria

• Trias: fever, anemia and splenomegaly

• Caused by 4 species of human

plasmodial:- P. falciparum

- P. vivax

- P. malariae

- P. ovale




Plasmodium falc iparum

- Main cause of severe / complicated malaria

- Specific behaviour: sequestration in deep capillary

for schizogony and gametogony process.- Sequestration in : capillary of brain, lung, heart,liver, kidney, gastrointestinal, etc.

- Sequestration forms sludgeinhibits micro-

circulation temporary organ dysfunction/ failure.

If patients are cured in this stage no sequel




Parasite` sequestration




Severe malaria




Pathogenesis

of Cerebral Malaria

• Capillary obstruction mechanism: – Rosetting (erythrocyte segregation )

– Cytoadherence (erythrocyte adherence to

endothel)• Impaired delivery substrate: hypoglycaemia,

hypoxia, anemia

• Impaired perfusion: shock, acidosis,hypovolemia




Pathogenesis

of Cerebral Malaria

• Endotoxin mechanism: NO, cytokines, etc

• Clotting

• Increased intracranial pressure:pediatric cases only




Malaria diagnosis

1. Microscopic (Giemsa, QBC) : to findparasite or parasite product in blood

make thick and thin blood smear ,

stain Diagnosis stage and species2. Serology (rapid test) : P. falciparum

Antigen (HRPII)

3. Detection DNA or RNA parasite (PCR)




Neurocysticercosis




Important Taenia species

in Indonesia

• Taenia saginata; intermediate host: cow

• Taenia solium; intermediate host: pig, dog




Taeniasis/cysticercosis

in Indonesia




Cysticercosis

• aetiology:cysticercuscellulosae (larvae

of the tapeworm T.solium)

• Larvae areacquired byingestion of

T. solium ova

Microscopically, T.saginata &T. solium

eggs are similar




Cysticercus :

a white opalescent vescicle, ovoid to round,

measuring 8-15 mm x 5-8 mm

containing only one protoscolex

May infect many organs

(subcutaneous tissue, brain, eye, muscles).




Cysticercosis

• the onchospheres

migrate to the

tissues and develop

into cysticerci• the cysticercus dies

and becomes

calcified

• calcified cysticerci

in muscle




Cysticercosis

Location of Cysticercus :

• subcutaneous tumor (subcutaneous

cysticercosis)

• eye

• muscle

• cerebral tumor




Pathogenesis of

Neurocysticercosis

• mechanical compression & damage

of tissue e.g. granuloma

• immunopathological eg cellular infiltration

• late secondary sequelae of

cysticercosis e.g. fibrotic scar




Clinical Manifestions

• epilepsy

• cerebellar ataxia

• sensory defect• acute onset of focal seizures

• less common: hemiparesis, visual

changes and sensory disturbances

• no fever




Risk Factors

• Immigrant from endemic area

• poor sanitation, use of sewage for

fertilizer and lack of controlled pens

for pigs

• Contact with other householdmember who often travel to endemic

area (carrier)




Diagnosis

• Microscopic: to find Taenia egg examine stools

for ova and parasites (3 consecutive days)

• Serology: antibody detection by enzyme-linked

immunotransfer blot (EITB) and ELISA• Radiology:

1. CT scan shows the cyst (solitary or multiple and

usually 5-20 mm in diameter) and granuloma

stages of neurocysticercosis. Most often in the

cortex / gray-white junction.

2. MRI




Cysticercus in the brain (CT Scan)




Cerebral Toxoplasmosis




Toxop lasma gond ii

• Host: man, animal

• Mode of infection:

- ingestion of cyst in

raw meats- ingestion of oocyst (in

cat faeces)

- transplacental

- transfusion- organ transplantation

- laboratory accident




Organ damage

• depends on host age, virulence and organinfected (CNS and eye: more severe)

• CNS:

- meningoencephalitis

- brain abscess (multiple)

- aquaductus sylvii congestion

hydrocephalus- intracranial calcification

- mental and motoric retardation




Acquired Toxoplasmosis in

Immunocompetent Host• Rarely detected (asymptomatic)

• Lymphadenopathy (self limiting)

• Fever, headache, myalgia, sore throat,

hepatosplenomegaly

• Retinochoroiditis

• Myocarditis

• Encephalitis




Toxoplasmosis In

Immunocompromised Host

• Can be fatal

• Reactivation of congenital and required

infection

• CNS: toxoplasmic encephalitis

• Pulmonary involvement




Congenital Toxoplasmosis

Disease in Infants

• Normal at birth

• Hepatosplenomegaly

• Icterus

• Lymphadenopathy

• Erythroblastosis

• Hydrops foetalis• Death: 5% - 15%




Congenital Toxoplasmosis

Disease in Infants

Classic triad:

1. Hydrocephalus

2. Intracranial calcification

3. Retinochoroiditis: atrophy of retina &

choroid pigmentation

4. + Psychomotoric retardation Tetrade Sabin




Toxoplasmosis Serology

Acute toxoplasmosis:

• Serial blood exam: IgG increase

significantly after 3 weeks or more (4fold)

• Conversion: negative to positive

• IgG and IgM in neonatal blood

• Polymerase chain reaction




E. h isto lyt ica

• cause brain abscess usually occurs in theframework of systemic amebiasis

• < 10% of patients with a hepatic amebicabscess have cerebral amebiasis

• the cerebral abscesses are usuallymultiple with accompanying cerebraledema.

• abscesses are most commonly located inthe cerebral hemisphere, although acerebellar location is not infrequent




Pathogenesis

• habitat: colon,particularly rectum,sigmoid

• trophozoitesadhere to colonicepithelial cellsthrough the

galactose/N-acetyl

galactosaminespecific lectin

Pathogenesis




Pathogenesis

Amebapores →

human cells

become immobile

within minutes andlose their

cytoplasmic

granules,structures and

their nucleus




Amebic colitis

E.histolytica cysteineproteinases digestextracellular matrix

proteins →trophozoite invasioninto and within thesubmucosal tissues

→ amebic colitis

chronic amoebiasis colitis




chronic amoebiasis colitis

↓

portal vein↓

amebic lever abscess

↓ hematogenous spread

↓

pulmonary amoebiasis abscess↓

brain abscess




Clinical manifestations

• usually preceded by gastrointestinal or hepatic or respiratory symptoms.

• an abrupt onset of mental status changeand/or focal neurologic deficits, headache,nausea, vomiting, delirum, coma, sensorialalteration

• meningitis can occur

• cranial nerve involvement is frequent• death occurs over 12-72 hours without

adequate therapy




Diagnosis

• Serologic tests, such as IFA, ELISA, for

specific antibodies to E. histolytica are

very helpful in diagnosis of invasive

amebiasis• Computed tomograph (CT) and nuclear

magnetic resonance (NMR) for the brain

abscess




Free living amoeba




Trofozoit Acanthamoeba sp




Brain Biopsy




Naeg leria fow leri

• Infect immunocompetent host

• Infective stage : the trophozoites

• Mode of infection :

1. through the olfactory neuroepithelium

2. nasal passages when water is forced into the

nose via diving or jumping or submergedunderwater

• Trophozoites are found in cerebrospinal fluid

and tissue

Primary Amebic




Primary Amebic

Meningoencephalitis (PAM)

• an acute, a deadly disease of the braincharacterized by necrotizing andhaemorrhagic meningoencephalitis,

symptoms usually occurs 3-7 days after infection

• Aetiology: Naegleria fowleri

• Epidemiology: individuals with warmwater related activities, diving in the river,summer time




Clinical features

• Fever

• Sore throat

• Swelling in nose

• Severe headache

• Stiff neck and back

• Nausea, vomiting• Confusion, seizures




Diagnosis

• Microscopic examination

• Culture

• Immunofluorescent antibody

• Polymerase chain reaction

Granulomatous Amebic




Granulomatous Amebic

Encephalitis

• Aetiology: Acanthamoeba sp- Acanthamoeba castellani

- Acanthamoeba polyphaga

- Acanthamoeba culbertsoni

- Balamuthia mandrillaris (non free living)

free living amoeba capable of causing subacuteor chronic in individuals with imunocompetentand compromised and also in animals

• The trophozoites and cysts are the infectiveforms entry into the body through the lower respiratory tract, ulcerated or broken skin and

invade the central nervous system byhemato enous dissemination




Clinical features

• Subfebris

• Headache

• Altered mental status

• Stiff neck

• Nausea and vomit

• Focal neurologic deficit which progressesover several weeks to death




Trypanosomiasis

1. T. rhodesiense

2. T. gambiense

African trypanosomiasis/




African trypanosomiasis/

sleeping sickness

• Chancre trypanosoma on port d’ entrée

• Fever

• Hepatosplenomegaly

• Lymphadenopathy (winter bottom sign)

• Meningoencephalitis: apathy, letharghy,

coma and death (T. rhodesiense morevirulent)




Winter bottom sign

American trypanosomiasis/





Chagas disease

• .• caused by T.cruzi

• amastigot forms in

macrophages on

port d’ entrée • granuloma formation

• unilateral orbital

edema andconjunctivitis

(romana sign)






Chagas disease

• Hepatosplenomegaly, generalized

lymphadenopathy

• Myocarditis

• Meningoencephalitis, ganglion cell

disruption and autonomic function loss

resulting in megaesophagus and

megacolon




Diagnosis

1. Finding the parasite (biopsy, blood

examination,etc)

2. Culture

3. Inoculation / xenodiagnosis

4. Immunological reactions

5. PCR



Thank You

untan neurosains parasit 2008

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