PPN62303: Musculoskeletal & Nervous Systems SELF-LEARNING PACKAGE

KULLIYYAH OF MEDICINE & HEALTH SCIENCES

(Student’s copy)

Course Musculoskeletal & Nervous Systems

Semester/Year
4/ 2
Topic
Parasitic diseases of Central Nervous System
Date

Time

Student’s Name/ ID

Lecturer Name
Lee Ii Li

Overview

This is the Self-Learning Package (SLP) for Musculoskeletal & Nervous Systems (MNS).
The exercise will help students to understand the pathophysiology, clinical manifestation,
diagnosis and treatment and, prevention and control measures for parasitic diseases of central
nervous system.

Parasitic diseases of the central nervous system are associated with high mortality and
morbidity, especially in resource-limited settings. The burden of these diseases is amplified as
survivors are often left with neurologic sequelae affecting mobility, sensory organs, and
cognitive functions, as well as seizures/epilepsy. These diseases inflict suffering by causing
lifelong disabilities, reducing economic productivity, and causing social stigma. The
complexity of parasitic life cycles and geographic specificities, as well as overlapping clinical
manifestations in the host reflecting the diverse pathogenesis of parasites, can present
diagnostic challenges.
(Source: Carpio, A., Romo, M. L., Parkhouse, R. M., Short, B., & Dua, T. (2016).
Parasitic diseases of the central nervous system: lessons for clinicians and policy makers.
Expert review of neurotherapeutics, 16(4), 401–414.
https://doi.org/10.1586/14737175.2016.1155454)

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Topic Learning Outcomes (TLOs)

Students should be able to:

1. List the parasites that can cause diseases of the Central Nervous System
2. Describe the diseases caused by parasites of the Central Nervous System and their
treatment

References:
1. John, D.T. and Petri, W.A. (2006). Markell and Voge's Medical Parasitology. (9th ed).
India Saunders Elsevier.
2. Paniker, C.K. (2007). Textbook of Medical Parasitology. (6th ed). New Delhi Jaypee
Brothers Medical.

Using the references provided and other possible resources in the library, answer the
following questions.

1. Classify parasitic infections of the central nervous system.

Protozoa Helminths
Nematoda Trematoda Cestoda
malaria toxocariasis schistosomiasis cysticercosis

American angiostrongyliasis paragonimiasis coenurosis

trypanosomiasis
African strongyloidiasis hydatidosis
trypanosomiasis
toxoplasmosis filariasis sparganosis

amebiasis dracunculiasis

leishmaniasis dicronemiasis

microsporidia gnathostomiasis

Onchocerciasis lagochilascaris
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2. List the characteristics of main parasitic infections of the central nervous system.

Parasite Disease Causative Vector/ Mode of

Organism Intermediate Host Transmission

Taeniasis/ Taenia solium Pigs, humans Fecal–oral,

Cysticercosis ingestion of eggs
from human feces
(ingestion of larval
cyst from pig
muscle leads to
taeniasis)

Toxoplasmosis Toxoplasma gondii Cats, intermediate Ingestion of

hosts in nature oocysts (cat feces)
(including birds and or tissue cysts
rodents) (undercooked
meats), blood
transfusion,
transplacentally
from mother to
fetus

Echinococcosis Echinococcus EG: Sheep, goats, Ingestion of

(Hydatidosis) granulosus, cattle, pigs, yaks or
Echinococcus other farm animals
multilocularis contaminated soil,

EM: Small
mammals (rodents water or food,

and lagomorphs) contact with

infected animals

Schistosomiasis Schistosoma Freshwater snail Penetration of skin

japonicum, mansoni, by cercariae in
and haematobium freshwater
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Paragonimiasis Paragonimus Freshwater snails, Fecal–oral, raw,

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westermani crustacean-eating undercooked

mammals freshwater
crustaceans

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Malaria Plasmodium Vector borne, Insect bite

falciparum Anopheles mosquito

Toxocariasis Toxocara canis, Cats, humans Fecal–oral,

Toxocara cati contaminated soil

Onchocerciasis Onchocerca volvulus Blackfly (Similium) Insect bite

Chagas disease Trypanosoma cruzi Triatomine bug Insect bite

African Trypanosoma brucei Tsetse fly Insect bite

trypanosomiasis gambiense,
Trypanosoma brucei
rhodesiense

3. List parasitic diseases of central nervous system according to presentation.

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4. Describe the following diseases

Parasite Disease Description

Human taeniasis is a parasitic infection caused by three tapeworm
species, T. saginata (known as the beef tapeworm), T. solium (pork
tapeworm), and T. asiatica (the Asian tapeworm). Humans are the only
hosts for these Taenia tapeworms. Humans pass the tapeworm
Taeniasis/Cysticer segments and/or eggs in feces and contaminate the soil in areas where
cosis sanitation is poor. Taenia eggs can survive in a moist environment and
remain infective for days to months. Cows and pigs become infected
after feeding in areas that are contaminated with Taenia eggs from
human feces. Once inside the cow or pig, the Taenia eggs hatch in the
animal’s intestine and migrate to striated muscle to develop into
cysticerci, causing a disease known as cysticercosis. Cysticerci can
survive for several years in animal muscle. Humans become infected
with tapeworms when they eat raw or undercooked beef or pork
containing infective cysticerci. Once inside humans, Taenia cysticerci
migrate to the small intestine and mature to adult tapeworms, which
produce segments and eggs that are passed in feces.
Toxoplasmosis

Toxoplasmosis is considered to be a leading cause of death attributed

to foodborne illness in the United States. More than 40 million men,
women, and children in the U.S. carry the Toxoplasma parasite, but
very few have symptoms because the immune system usually keeps the
parasite from causing illness. However, women newly infected with
Toxoplasma during or shortly before pregnancy and anyone with a
compromised immune system should be aware that toxoplasmosis can
have severe consequences.

Echinococcosis
(Hydatidosis)
Echinococcosis is a parasitic disease caused by infection with tiny
tapeworms of the genus Echinocococcus. Echinococcosis is classified
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as either cystic echinococcosis or alveolar echinococcosis.

Cystic echinocccosis (CE), also known as hydatid disease, is caused by

infection with the larval stage of Echinococcus granulosus, a ~2–7
millimeter long tapeworm found in dogs (definitive host) and sheep,

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cattle, goats, and pigs (intermediate hosts). Although most infections in

humans are asymptomatic, CE causes harmful, slowly enlarging cysts
in the liver, lungs, and other organs that often grow unnoticed and
neglected for years.

Alveolar echinococcosis (AE) disease is caused by infection with the

larval stage of Echinococcus multilocularis, a ~1–4 millimeter long
tapeworm found in foxes, coyotes, and dogs (definitive hosts). Small
rodents are intermediate hosts for E. multilocularis. Although cases of
AE in animals in endemic areas are relatively common, human cases
are rare. AE poses a much greater health threat to people than CE,
causing parasitic tumors that can form in the liver, lungs, brain, and
other organs. If left untreated, AE can be fatal.

Schistosomiasis is an acute and chronic parasitic disease caused by

Schistosomiasis
blood flukes (trematode worms) of the genus Schistosoma. Estimates
show that at least 236.6 million people required preventive treatment in
2019. Preventive treatment, which should be repeated over a number of
years, will reduce and prevent morbidity. Schistosomiasis transmission
has been reported from 78 countries. However, preventive
chemotherapy for schistosomiasis, where people and communities are
targeted for large-scale treatment, is only required in 51 endemic
countries with moderate-to-high transmission

Paragonimiasis
Infection with Paragonimus spp. can result in an acute
syndrome with cough, abdominal pain, discomfort, and low-
grade fever that may occur 2 to 15 days after infection.
Persons with light infections may have no symptoms.
Symptoms of long-term infection may mimic bronchitis or
tuberculosis, with coughing up of blood-tinged sputum.
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Infection with malaria parasites may result in a wide variety

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Malaria
of symptoms, ranging from absent or very mild symptoms to
severe disease and even death. Malaria disease can be
categorized as uncomplicated or severe (complicated). In

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general, malaria is a curable disease if diagnosed and

treated promptly and correctly.
All the clinical symptoms associated with malaria are
caused by the asexual erythrocytic or blood stage
parasites. When the parasite develops in the erythrocyte,
numerous known and unknown waste substances such as
hemozoin pigment and other toxic factors accumulate in the
infected red blood cell. These are dumped into the
bloodstream when the infected cells lyse and release
invasive merozoites. The hemozoin and other toxic factors
such as glucose phosphate isomerase (GPI) stimulate
macrophages and other cells to produce cytokines and
other soluble factors which act to produce fever and rigors
and probably influence other severe pathophysiology
associated with malaria.

Toxocariasis is an infection caused by the ingestion of larvae of

Toxocariasis
the dog roundworm Toxocara canis or the cat roundworm
Toxocara cati. The soil of parks and playgrounds is commonly
contaminated with the eggs of T canis, and infection may cause
human disease that involves the liver, heart, lung, muscle, eye,
and brain. [1, 2]

Three syndromes of Toxocara infection are generally

recognized, as follows:

● In children, covert toxocariasis is a mild, subclinical,

febrile illness. Symptoms can include cough, difficulty
sleeping, abdominal pain, headaches, and behavioral
problems. Examination may reveal hepatomegaly,
lymphadenitis, and/or wheezing.

● Visceral larva migrans is caused by the migration of

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larvae through the internal organs of humans and the

resulting inflammatory reaction. A constellation of
symptoms develops, including fatigue, anorexia, weight
loss, pneumonia, fever, cough, bronchospasm, abdominal

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pain, headaches, rashes, and, occasionally, seizures.

Examination may reveal hepatomegaly, lymphadenitis,
and/or wheezing. Occasionally, pleural effusions develop.
Chronic urticaria has been described. Severe cases can
lead to myocarditis or respiratory failure.

● Ocular larva migrans, which is caused by migration of

larva into the posterior segment of the eye, tends to occur
in older children and young adults. Patients may present
with decreased vision, red eye, or leukokoria (white
appearance of the pupil). Granulomas and chorioretinitis
can be observed in the retina, especially at the macula.
Unilateral visual loss, retinal fibrosis, retinoblastoma, and
retinal detachment occur. Serum antibodies to Toxocara
are often absent or present in low titers.

The blackflies that transmit the parasite bite during the day.
Onchocerciasis Female blackflies need to ingest blood for ovulation, so
they feed on humans. Some species of blackflies may also
feed on certain animals as well. If a blackfly bites an
infected person, onchocerciasis larvae can be ingested by
the blackfly after which they migrate to the flight muscles.
The larvae develop inside the blackfly and become infective
for humans in about one week. They migrate to the biting
parts of the fly where they can be transmitted back to
humans when it bites again.
Humans become infected when blackflies deposit
Onchocerca infective larvae into the skin when biting to
extract blood. Once inside the human body, the larvae
mature into adults in approximately 12–18 months. Most
adult female worms live in fibrous nodules under the skin
and sometimes near muscles and joints. Adult male worms
are usually found near the female worms. Nodules form
around the worms as part of the interaction between the
parasite and its human host. Inside the nodules the worms
are relatively safe from the human immune response. As
adults, female worms produce thousands of new larvae
daily. The larvae become detectable in the skin 12–18
months after the initial infection. The adult worms can live
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approximately 10–15 years inside the human body, and

their larvae have a lifespan of approximately 12–15 months.

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Chagas disease has an acute and a chronic phase. If

Chagas disease untreated, infection is lifelong.
Acute Chagas disease occurs immediately after infection,
and can last up to a few weeks or months. During the acute
phase, parasites may be found in the circulating blood. This
phase of infection is usually mild or asymptomatic. There
may be fever or swelling around the site of inoculation
(where the parasite entered into the skin or mucous
membrane). Rarely, acute infection may result in severe
inflammation of the heart muscle or the brain and lining
around the brain.

Following the acute phase, most infected people enter into

a prolonged asymptomatic form of disease (called “chronic
indeterminate”) during which few or no parasites are found
in the blood. During this time, most people are unaware of
their infection. Many people may remain asymptomatic for
life and never develop Chagas-related symptoms.
However, an estimated 20–30% of infected people will
develop severe and sometimes life-threatening medical
problems over the course of their lives.

Infection occurs in two stages, an initial haemolymphatic

African stage followed by a meningoencephalitic stage after the
trypanosomiasis trypanosomes invade the central nervous system (CNS).
However, many of the signs and symptoms are common to
both stages, making it difficult to distinguish between the
two stages by clinical features alone. First-stage symptoms
may be preceded by the development of a trypanosomal
chancre at the site of inoculation within two days to two
weeks of being bitten by an infected fly (occurs most
commonly with T. b. rhodesiense, rarely with T. b.
gambiense although chancres are observed with T. b.
gambiense in travelers from non-endemic countries). The
first stage involves nonspecific, generalized symptoms
occurring 1–3 weeks after the tsetse fly bite with T. b.
rhodesiense; the incubation period for T. b. gambiense is
less well characterized but disease progresses more slowly
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than that caused by T. b. rhodesiense. First-stage

symptoms for both types of sleeping sickness include
headache, malaise, weakness, fatigue, pruritis, and
arthralgia. First-stage signs can include hepato-

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splenomegaly, weight loss and intermittent fevers lasting

one day to one week. The intervals between fevers can last
days or months. Lymphadenopathy, mainly posterior
cervical but in some cases axillary, inguinal or epitrochlear,
may also occur. Posterior triangle cervical
lymphadenopathy, or “Winterbottom’s sign” is commonly
seen in T. b. gambiense infections.
T. b. gambiense infection progresses to the second stage
after an average of 300–500 days, whereas T. b.
rhodesiense infection progresses to the second stage after
an estimated 21–60 days. For both types of disease, the
stage is determined by examining cerebrospinal fluid (CSF)
and observing trypomastigotes. In second-stage disease,
invasion of the central nervous system causes a variety of
neuropsychiatric manifestations to appear in addition to the
first-stage signs and symptoms, with fever occurring less
frequently over time. The sleep/wake cycle becomes
reversed, hence the common name “African sleeping
sickness”, with daytime somnolence, nocturnal insomnia,
and sudden urges to sleep. The patient also experiences
mental (hallucinations, delirium, anxiety, emotional lability,
attention deficit, apathy, aggression, mania, confusion),
motor (motor weakness, abnormal tone, gait disturbance,
ataxia, tremor, speech disturbances), sensory
(paraesthesia, hyperaesthesia, anaesthesia, pruritis, visual
problems), and neurologic (abnormal reflexes, seizures,
coma) signs and symptoms. Compared to T. b. gambiense,
T. b. rhodesiense is more likely to result in endocrine
abnormalities such as adrenal insufficiency, thyroid
dysfunction and hypogonadism; and cardiac involvement,
such as myocarditis, is more severe.
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5. List the currently available antiparasitic drug regimens for parasitic infections of the
CNS.

Parasite Disease Antiparasitic Drug Regimens

Taeniasis/ Praziquantel is the medication most often used to treat active
Cysticercosis taeniasis, given at 5-10 mg/kg orally once for adults and 5-10 mg/kg
orally once for children. Available evidence suggests that using
10mg/kg once orally may have a higher rate of cure than the 5mg/kg
dose. Niclosamide is an alternative, given at 2 g orally once for adults
and 50 mg/kg orally once for children. Albendazole, given as 400mg
daily for three days, may be used as another option for the treatment
of taeniasis
Toxoplasmosis Most healthy people recover from toxoplasmosis without treatment.
Persons who are ill can be treated with a combination of drugs such
as pyrimethamine and sulfadiazine, plus folinic acid
Echinococcosis surgery was the only treatment for cystic echinococcal cysts
(Hydatidosis)

Schistosomiasis Schistosoma mansoni, S. haematobium, S. intercalatum

- 40 mg/kg per day orally in two divided doses for one day

S. japonicum, S. mekongi
- 60 mg/kg per day orally in three divided doses for one day
Paragonimiasis Praziquantel is the drug of choice: adult or pediatric dosage, 25
mg/kg given orally three times per day for 2 consecutive days. For
cerebral disease, a short course of corticosteroids may be given with
the praziquantel to help reduce the inflammatory response around
dying flukes.

Alternative: Triclabendazole, 2 doses of 10 mg/kg given 12 hours

apart in patients 6 years of age and older.
Malaria

Toxocariasis

Onchocerciasis

Chagas disease
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African
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