Parasitology Department

z
PARASITE
INFECTION IN
CNS
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• NEUROCYSTICERCOSIS
CESTODE
INFECTION

• GRANULOMATOUS AMOEBIC
ENCEPHALITIS (GAE)
FREE LIVING • PRIMARY AMOEBIC
AMOEBA MENINGOENCEPHALITIS (PAM)
INFECTION

• CEREBRAL TOXOPLASMOSIS
SPOROZOA • CEREBRAL MALARIA
INFECTION
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Neurocysticercosis
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NEUROCYSTICERCOSIS
z
General

§ Caused by the infestation of Taenia solium

larvae
§ There is no pathognomonic clinical feature or
a typical neurocysticercosis syndrome
(Takayanagui et al., 2007)
§ The development of diagnostic resulted in
the increasing reported cases of
neurocysticercosis.
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z NEUROCYsTICERCOSIS
Epidemiology

§ World wide distribution

with high prevalence ,
such as: Mexico, North
America and South,
India, Africa and China.
§ In Indonesia, Bali and
Papua have many cases
reported.
§ Human is the definitive
host
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z
NEUROCYCTICERCOSIS
Pathogenesis
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NEUROCYSTICERCOSIS
z
Pathogenesis

§ Route of infection:
§ Raw meat consumption
(contamination by Taenia
solium larvae) à human as
DH
§ Auto infection: regurgitation
and swallowing the eggs
§ Fecal-oral route ova ingestion
from the tapeworm carriers
§ Larvae (cysticercus cellulose) in
brain can develop from eggs.
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z NEUROCYSTICERCOSIS
Pathogenesis

§ Neurologic symptom arises when the cysticercus

cellulose dies and the host (human) mounts an
associated inflammatory response.
§ Cyst produces paramiosin and taeniastatin (inhibitor
protease serin) enzymes that bind C1q and blocking
its classic pathway or alternative.
§ Cyst wall is covered by polysaccharide sulfa activating
complement to avoid the parasite interfering.
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 Primary Amoebic
z
Meningoencephalitis (PAM)
Free living amoebic
infection
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Primary Amebic Meningoencephalitis
z General

§ Etiology: Naegleria fowleri

§ Thermophilic, tolerating temp

40-45⁰C.
§ Sources:
§ Soil
§ Sewage sludge
§ Nasal & throat swabs
§ Water: tap water, lakes,
stream, ponds, swimming
pool, thermal spring.
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Primary Amebic Meningoencephalitis
z Transmission

§ Transmission via inhalation

§ Contaminated dust
§ Nasal instillation

§ Organism enters host’s nasal cavity & infects the

mucous membranes and the paranasal sinuses.
§ Then the trophozoites penetrate the cribriform plate
and follow the olfactory nerve to the brain where
they multiply and may be isolated from the CSF
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Primary Amebic Meningoencephalitis
z Diagnosis

§ Usually patient dies before diagnosis is made

§ High index of suspicion is vital
§ Motile trophozoites seen in CSF

§ Large lobopodia, single nucleus which contains

a prominent central karyosome, surrounded by
a halo
§ CSF culture on NNA overlay with E. coli

§ At autopsy, brain biopsy shows trophozoites

only and no cysts
§ Amoeba does not encyst in tissue
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Primary Amebic Meningoencephalitis
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Prevention

§ No easy control of Naegleria

as they are ubiquitous in
nature
§ Guidelines from the Australian
health commission: “keep
head above water.”
 Granulomatous Amoebic
z
Encephalitis (GAE)
Free living amoebic
infection
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Granulomatous Amoebic Encephalitis
z General

§ Etiology: Acanthamoeba sp.

§ CNS infection is acquired hematogenously by

inhalation, aspiration of trophozoites and cysts,
resulting in pneumonitis, or through skin and
mucosal ulceration with direct vascular invasion.

§ This usually happens in immunosuppressant

patient.
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https://courses.lumenlearning.com/microbiology/chapter/protozoan-and-helminthic-infections-of-the-skin-and-eyes/
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z Granulomatous Amoebic
Encephalitis

§ In brain invasion moves from deeper areas to

the surface
§ Trophozoites and cysts can be found in CNS
lessions
§ Slow progression of disease (weeks to months)
§ Clinical picture is that of space occupying
lesions
§ Headache, nausea, vomitting related to
formation of granuloma
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Cerebral malaria
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Cerebral Malaria
z General

§ Etiology: Plasmodium falciparum.

§ Mortality rate is high for malaria cases due to cerebral

malaria (15% adult & 20% children).
§ Early stage: schizont in liver will rupture in 4 days after
infection.
§ Microscopic examination: only ring and gametocyte
stages.
§ Trophozoite and schizont will disappear in peripheral
blood (24 hours) and stay in internal organ capillary.
§ Incubation periode : 9-14 days.
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Cerebral Malaria
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Pathogenesis

§ Complex, at times confusing &

conflicting hypothesis
§ Lack of satisfactory model hampered
understanding
§ Several hypothesis:
§ Permeability
§ Mechanical
§ Immunological

Congestion & pigmentation

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z
Cerebral Malaria
Pathogeneses

§ Permeability hypothesis:
Infected red blood cells (IRBC) –
cytoadherence è è Blood barrier brain
impairment/ damage (cerebral oedema)
§ Increase permeability of capillaries is caused by
vasoactive kinin
§ Passage of toxic compounds to CNS
§ Neurological dysfunction
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Rosetting

Sequestration
Sludging
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Cerebral Malaria
z
Pathogenesis

§ Mechanical:
IRBC- cytoadherence è reduced IRBC
deformability
§ Anemia
§ Rossette formation
§ Microvascular obstruction
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Cerebral Malaria
Pathogeneses
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§ Immunological hypothesis:
Immune complex vasculitis release
ROS(Reactive Oxygen Spesies) : Nitric Oxide
(NO)
§ Inflammation: IL-1, IL-6, TNF-a

§ Fever
§ Coma
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 Cerebral
toxoplasmosis
z
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z Cerebral Toxoplasmosis
General

§ Etiology : Toxoplasma
gondii
§ Cerebral toxoplasmosis is
one of the most common
opportunistic neurological
infections in AIDS patients.
§ It is also directly related to
the prevalence of anti-T
gondii antibodies in the
general population
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z
Cerebral Toxoplasmosis
Pathogenesis

§ Cerebral toxoplasmosis usually represents

reactivation of chronic infection.
§ Reactivation possibly results from the rupture
of a cyst.
§ Normally the bradyzoites destroyed by the
host’s immune responses.
§ In immunosuppressive patient, rupture of cyst
may result in renewed multiplication.
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