B.2.

PARASITES
CAUSING
NEUROMUSCULOSKELETAL PROBLEMS

PARASITOLOGY DEPT, 2014

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 Learning Objectives

1. Understanding parasite diseases causing

neuromuscular (including CNS) complaints

2. Understanding the epidemiology of parasites

causing neuromuscular complaints

3. Understanding diagnosis of parasitic infection

causing neuromuscular complaints

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 1. PROTOZOA:
Malaria cerebral
Toxoplasmosis
Trypanosomiasis
Free living Amoeba

2. HELMINTHS:
Neurocysticercosis
Hydatidosis
Sparganosis
Angiostrongyliasis
Strongyloidiasis

3. VENOMOUS ARTHROPODS

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 Malaria

1. Epidemiology of malaria, particularly malaria

in Indonesia
2. What kind of malaria can cause neurosensory
complaints?
3. Pathogenesis ?

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 Gething PW et al, 2011

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 CEREBRAL MALARIA
• Most severe neurological complication
• Infection with P.falciparum malaria
• Endemic in developing countries
• A few patients may experience a neurological syndrome
after a complete recovery (post malaria neurological
syndrome/PMNS)

Clinical Features & Diagnosis

WHO Definition :
• Seizure
• Coma
• Parasite on peripheral blood smears

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 Diagnosis Criteria
• Patient come from endemic area
• Fever
• Confusion with/without symptom
• Parasite on peripheral blood smears

Treatment
• Antimalarial drugs iv

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 Toxoplasmosis

1. Epidemiology of toxoplasmosis, particularly

in Indonesia
2. How toxoplasmosis can cause neurosensory
complaint?
3. Pathogenesis

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 General information

• Cosmopolitan distribution
• Infection in the immunocompetent hosts asymptomatic
common sign: generalized lymphadenopathy (20%)
Symptomatic CNS toxoplasmosis rarely develops during primary
infection in normal hosts,
Seropositive prevalence varies: 20-75%
• Incidence of Toxoplasma encephalitis correlates with the prevalence
of anti T.gondii antibodies

• Unusual cases of CNS involvement in immunocompetent patients

can be associated with drowsiness, confusion, seizures, and even
coma.

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 Pathophysiology, signs & symptoms

• Congenital infection (Block 2.1)

• Infection in the immunocompromised host
responsible :> 1/3 of neurologic symptoms in AIDS patients
Enchepalitis: reactivation of chronic latent infection
CD4+ falls bellow 100
Clinical manifestation: varies, seizure up to 30%
• 25-50% T. gondii seropositive AIDS patients 
toxoplasma encephalitis

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 Cerebral Toxoplasmosis
In AIDS patients T.gondii is the most common opportunitis
infection that causes focal brain lesions.

Clinical Manifestation:
• Headache
• Altered mental state
• Seizures
• Focal neurologic deficit
• Hemiparesis
• Ataxia
• Facial Weakness

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• DIFFERENTIAL DIAGNOSIS
• DIAGNOSIS

Serology
Immunocompetent ?
Immunocompromised ?
transplant patients
patients with HIV/AIDS
Neuroimaging
CT
MRI

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 Trypanosomiasis
1. Epidemiology of trypanosomiasis
2. How trypanosomiasis causes neurosensory
complaints?
3. Does all type of trypanosoma sp parasites
cause neurosensory complaints?
4. Parasitology

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 Sleeping Sickness

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 Life cycle

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 Parasites
Trypanosoma brucei:
• T. brucei brucei
• T. brucei gambiense
• T. brucei rhodesiense

Vectors: Glossina

Geographical distribution

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 DISEASE
LOCAL EFFECTS SYSTEMIC EFFECTS
• Trypanosomal chancre • Parasitemia 12-15%
• 2-3cm after bite, after bite (early stage)
increases in 2-3 weeks • Parasitemia ~ fever
• T. b. rhodesiense> t.b. • CNS via choroid plexus
gambiense Or by transcytosis
• Local lymphadenopathy across endothelial cells
to cause a lymphocyte
meningoencephalitis
(late stage)

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 PATHOGENESIS & CLINICAL PICTURE
BRAIN & Other Organs:
• Perivascular infiltration with lymphocytes,
plasma cells, macrophages, morular cells
• Microglial dan Astrocyte proliferation may be
associated with neuronal destruction &
demyelination in the brain

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 T. b. gambiense
Early Stage
• Fever, headache, join pains,
or asymptomatic
• Winterbottom’s sign
• Odd skin rashes, pruritus,
thickening of facial tissue
• Enlarged spleen (moderate)
• Last many months- 2 years
• CNS involvement
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Late Stage
• Disturbed cerebral function
predominate
• Behavioural changes
• Sleeping disorders
• Disturbed speech & motor
function
• CNS, extrapyramidal &
cerebral function
• Kerandel’s sign
• Death after few month/a year
of CNS involvement
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 T. b. rhodesiense
• More acute & virulen infection than T.
gambiense, fever & siystemic symptoms
prominent
• Serous effusions (pleural & pericardial spaces) are
common, myocarditis
• Early stage: hepatocellular jaundice, anemia
• Liver & spleen enlarged slightly
• Lymph gland enlargement (seldom)
• Fatal within few weeks of the onset, more likely
because of myocarditis rather than CNS

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 DIAGNOSIS
Early stage disease
• Demonstration of parasites:
1. Blood film
2. Concentration methods
3. Gland puncture
4. Bone marrow aspiration
5. The chancre
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Late stage disease (CNS)
• Neurological signs
• Cerebrospinal fluid (CSF)
• Raised CSF cell count
(5/mm3)
• Immunological dx methods
CATT
• Routine lab. Findings;serum
& CSF IgM level are high
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 Treatment & Control

T. gambiense & rhodesiense Sleeping sickness control

Early: 1. Detection & treatment of
• Suramin cases
• Pentamidine 2. Vector control

Late:
Melarsoprol
Eflornithine

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 Primary Amoebic Meningoencephalitis (PAM)
Granulomatous Amebic Encephalitis (GAE)

1. What are PAM and GAE

2. Signs and symptoms
3. Parasitology

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 PRIMARY AMOEBIC
MENINGOENCEPHALITIS

CAUSED BY
PARASITE

Naegleria fowleri
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 LIFE CYCLE OFNaegleria fowleri
Naegleria fowleri produces an acute, and
usually lethal, central nervous system (CNS)
disease called primary amebic
meningoencephalitis (PAM).
Clinical Features:
Acute primary amebic meningoencephalitis
(PAM) is caused by Naegleria fowleri.
It presents with severe headache and other
meningeal signs, fever, vomiting, and focal
neurologic deficits, and progresses rapidly (<10
days) and frequently to coma and death.

N. fowleri commonly found in lakes, swimming

pools, tap water, and heating and air
conditioning units
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 DIAGNOSIS & TX

In Naegleria infections, the diagnosis can be

made by microscopic examination of
cerebrospinal fluid (CSF). A wet mount may
detect motile trophozoites, and a Giemsa-
stained smear will show trophozoites with
typical morphology.

Tx: Amphotericin iv

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 Neurosensory complaints caused by
helminth parasites

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 Taenia solium cysticercosis
& Neurocysticercosis

• =pork tapeworm
• Endemic in developing countries
• Infection of human CNS by its larvae
(cysticerci)
• Important causes of seizures & epilepsy (most
common)
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 Life cycle, route of infection

• Definitive host
• Intermediate hosts
• Accidental Ingestion
of eggs
• Embryos cross
intestinal mucosa
circulatory system 
establish &encyst
larva
vesicles/cysticerci 
definitive size in 2-3
months

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 Clinical Features & Diagnosis
• Outside CNS
• In the CNS or eye
(Neurocysticercosis/NCC)
• In brain parenchyma: viable
cyst, rounded small vesicles
with transluscent
membranes
•  degeneration, vesicular
fluid opaque & dense,
cyst’ edges become
irregular & shrink
•  round, calcareous nodule
with residual calcification
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• Outside the brain
parenchyma, cyst tends to
grow & infiltrate
• Associated with
hydrocephalus &
intracranial hypertension
(rare cases)
Dx:
CT/MRI
Western blot & ELISA : ab in
serum/CNS
Patient with calcified NCC: ?
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 Hydatidosis
• Causal agents:
• larval stages of cestodes (tapeworms)
of the genus Echinococcus.
• E. granulosus causes cystic
echinococcosis, the form most
frequently encountered;
• E. multilocularis causes alveolar
echinococcosis;
• E. vogeli causes polycystic
echinococcosis;
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• Geographic Distribution:
E. granulosus occurs practically
worldwide, and more frequently in
rural, grazing areas where dogs ingest
organs from infected
animals. Sheeps/cattle by
swallowing Taenia-like egg in a dog
faeces
• E. multilocularis occurs in the
northern hemisphere, including
central Europe and the northern
parts of Europe, Asia, and North
America. Associated with wild
canine, rodents.
• E. vogeli and E. oligarthrus occur in
Central and South America.
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 Hydatid cyst & alveolar hydatid cyst
the differences:

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 Clinical Features & Dx
• Clinical Features:
Echinococcus granulosus
infections remain silent for years
before the enlarging cysts cause
symptoms in the affected organs.
• Hepatic, Pulmonary involvement
• Rupture of the cysts can produce
fever, urticaria, eosinophilia, and
anaphylactic shock, as well as cyst
dissemination.
• Other organs (brain, bone, heart)
can also be involved, with
resulting symptoms. Brain:
convulsion/mass effect; Eye:
protopsis & chemosis
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• Laboratory Diagnosis:
ultrasonography and/or other
imaging techniques supported by
positive serologic tests.
• In seronegative patients with
hepatic image findings
compatible with echinococcosis,
ultrasound guided fine needle
biopsy may be useful for
confirmation of diagnosis
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SPARGANOSIS
Sprirometra ,
Spargana tapeworm

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 Clinical Features:
Migrating spargana:
various symptoms depending on the
final location e.g.
subcutaneous tissue, breast, orbit,
urinary tract, pleural cavity, lungs,
abdominal viscera and the central
nervous system.

When spargana settle in the brain or

spine, a variety of neurological
symptoms may occur, including
weakness, headache, seizure, and
abnormal skin sensations, such as
numbness or tingling.

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 Angiostrongyliasis
• Angiostrongylus Learn:
cantonensis
• life cycle ?
• Parasitic nematode
• rat lungworm
• Pathogenesis ?
• South East Asia, Pacific • Involvement of
islands, Africa neurosensory organ ?
• Snail as primary • Diagnosis ?
intermediate host (larvae
develops here till infective)
• Human as incidental host
• Eosinophilic meningitis

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 Other helminths?
• Strongyloides stercoralis
Learn:
• life cycle ?
• Pathogenesis ?
• Involvement of neurosensory organ ?
• Diagnosis ?

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 Neurosensory complaints caused
by venomous arthropods

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 VENOMOUS ARTHROPODS
Arthropods that produce toxins:
1. Ordo Araneida (spider)
2. Ordo acarina (ticks and mites)
3. Ordo Scorpionida (scorpion)
4. Ordo Chilopoda (centipedes)
5. Class Insecta (ordo Coleoptera, Lepidoptera,
Hymenoptera)

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 Types of Toxins:
1. Hemolytic toxin
2. Hemorragic toxin
3. Neurotoksik toxin
4. Vesicating toxin

Toxin enters the victims via: arthropods bites

(spiders, centipedes), stings (scorpion, bee),
direct contact ( caterpillar), spray (whip
scorpion)

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 Araneida (spider)
• Cheliceras contains toxin
• Lactrodectus mactans (black widow spider):
toxalbumin (neurotoxin)
5%  fatal

• Tarantula
(lycosa tarantula) : long-haired and bushy
bite cause pain but no systemic manifestation (low toxicity)

• Laxosceles: necrotic arachnidism

gangren at the bite site

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 SPIDERS

Cutaneous anesthesia after

spider bite
Eg: Loxosceles reclusa (brown
recluse spider),
Commonly known to cause
cutaneous necrosis,
ulceration and others:
fever, macular rash,
pyoderma
gangrenosum,
hemolysis, renal failure,
Gross et al, 1990. Southern Medical Journal,
death Vol 83, No 11

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 Acarina (ticks)

• Ticks: ixovotoxin
(neurotoxin affects CNS, act
at neuromuscular-
junction).
• Causing tick-paralyse
• Hard ticks (Ixodidae), soft
ticks (Argasidae)
• Example of hard tick:
Dermacentor andersoni

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 OTHERS
SCORPION
Centruroides vittatus
Sculptured scorpion:
C. exilacauda (can be fatal in
children)
Hymenoptera
• Apitoxin ( formiat acid,
saponin, histamin, melittin 
hemolitik, dehydrogenase
inhibitor, hyaluronidase)
• Hemolitic, neurotoxin,
hemorragic , histaminik
• Clinical manifestations:
bronchial ashmatic, urticaria,
angioedema, cyanosis, syock,
failure to breath)
• Management

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