MCB 409: MEDICAL PARASITOLOGY

2024

Definition of Parasite
Parasite is a living organism, which lives in or upon another organism
(host) and derives nutrients directly from it, without giving any benefit to
the host. Protozoa and helminths (animal parasites) are studied in Medical
Parasitology.
Parasites may be classified as:
Ectoparasite: They inhabit the surface of the body of the host without
penetrating into the tissues. They are important vectors transmitting the
pathogenic microbes. The infection by these parasites is called as
infestation, e.g ., fleas or ticks
Endoparasite: They live within the body of the host (e.g., Leishmania).
Invasion by the endoparasite is called as infection. The endoparasites are of
following types:
 Obligate parasite: They cannot exist without a parasitic life in the
host (e.g., Plasmodium species).
 Facultative parasite: They can live a parasitic life or free-living life,
when the opportunity arises (e.g., Acanthamoeba).
 Accidental parasite: They infect an unusual host (e.g., Echinococcus
granulosus infect humans accidentally).
 Aberrant parasite or wandering parasite: They infect a host
where they cannot live or develop further (e.g., Toxocara in humans).

HOST OF PARASITES
Host is defined as an organism, which harbors the parasite and provides
nourishment and shelter. Hosts may be of the following types;
Definitive host: The host in which the adult parasites replicate sexually
(e.g., anopheles species), is called as definitive host. The definitive hosts
may be human or nonhuman living things.
Intermediate host: The host in which the parasite undergoes asexual
multiplication is called as intermediate host. (e.g., in malaria parasite life
cycle, humans are the intermediate hosts) Intermediate hosts are essential
for the completion of the life cycle for some parasites. Some parasites
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require two intermediate hosts to complete their different larval stages.

These are known as the first and second intermediate hosts respectively
(e.g., Amphibian snails are the first intermediate host and aquatic plants
are the second inter mediate host for Fasciola hepatica).
Hosts can also be;
Reservoir host: It is a host, which harbours the parasites and serves as an
important source of infection to other susceptible hosts. (e.g., dog is the
reservoir host for cystic echinococcosis).
Paratenic host: It is the host, in which the parasite lives but it cannot
develop further and not essential for its life cycle is known as paratenic
host (e.g., fresh water prawn for Angiostrongylus cantonensis, big suitable
fish for plerocercoid larva of Diphyllobothrium latum and freshwater fishes
for Gnathostoma spinigerum). It functions as a transport or carrier host.
Amplifier host: It is the host, in which the parasite lives and multiplies
exponentially.

HELMINTHS
General Characteristics of Helminths
 Helminths are elongated flat or round worm-like parasites measuring
few milimeters to meters.
 They are eukaryotic, multicellular and bilaterally symmetrical.
 They belongs to two phyla;
i. Phylum Platyhelminths (flat worms)—it includes three
classes:

Class: Cestoidea (tapeworms)

Class: Trematodea (flukes or digeneans)
Class: Monogenea (ectoparasite of fishes, don’t infect man)
ii. Phylum Nemathelminths

The classification of all the medically important helminths according to

their habitat is shown below;
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 Morphology of the Helminths

Helminths exist in three morphological forms:

(1) adult form (or the worm)
(2) larval form and
(3) eggs.
1. Adult Form

Phylum Platyhelminths
-Shape is tape like (in cestodes) or leaf like (in trematodes).
-They have a definite head end called as suckers.
-They lack body cavity.
-Alimentary canal is absent in cestodes but incomplete (rudimentary) in
trematodes
-They are monoecious or hermaphrodite (i.e. both the sexes are present in
the same
worm), except in Schistosoma (diecious).
Phylum Nematoda
-They are evolutionary more developed than Platyhelminths
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-They possess a definite body cavity (space between body wall and
alimentary canal)
-Alimentary canal is completed starting from mouth leading to esophagus,
intestine and ending at anus
-They are dioecious, i.e. male and female worms are separate
-The nervous system and excretory system are rudimentary and there is no
circulatory system.
2. Larval form

There are various larval forms of helminthes found in man and other hosts.
-In cestodes: Cysticercus, hydatid cyst, coenurus, cysticercoid,
coracidium, procercoid and plerocercoid forms.
-In trematodes: Cercaria, metacercaria, redia, miracidium and sporocyst
-In nematodes: Rhabditiform larva, filariform larva and microfi laria.
3. Eggs

Various helminths have distinct morphology of eggs which can be used to

differentiate the helminthes.
Reproduction in Helminthes
Based on their reproduction, helminths can be classified into the following:
i. Oviparous: Most of the helminths (cestodes, trematodes and
many nematodes) are oviparous, i.e. after fertilization, the adult
worm lay eggs
ii. Viviparous: Only few nematodes directly discharge the larval
forms after fertilization (e.g. filarial worm, Dracunculus and
Trichinella)
iii. Ovoviviparous: They lay egg containing larva that immediately
hatches out (e.g. Strongyloides).
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The word ‘helminth’ is a general term meaning ‘worm’, but there are many
different types of worms. Prefixes are therefore used to designate types:
platy-helminths for flat-worms and nemat-helminths for round-worms. All
helminths are multicellular eukaryotic invertebrates with tube-like or
flattened bodies exhibiting bilateral symmetry. They are triploblastic (with
endo-, meso- and ecto-dermal tissues) but the flatworms are acoelomate
(do not have body cavities) while the roundworms are pseudocoelomate
(with body cavities not enclosed by mesoderm). In contrast, segmented
annelids (such as earthworms) are coelomate (with body cavities enclosed
by mesoderm).
Many helminths are free-living organisms in aquatic and terrestrial
environments whereas others occur as parasites in most animals and some
plants. Parasitic helminths are an almost universal feature of vertebrate
animals; most species have worms in them somewhere.

Biodiversity
Three major assemblages of parasitic helminths are recognized: the
Nemathelminthes (nematodes) and the Platyhelminthes (flatworms), the
latter being subdivided into the Cestoda (tapeworms) and the Trematoda
(flukes):

Nematode Cestode Trematode

> Nematodes (roundworms) have long thin unsegmented tube-like

bodies with anterior mouths and longitudinal digestive tracts. They
have a fluid-filled internal body cavity (pseudocoelum) which acts as a
hydrostatic skeleton providing rigidity (so-called ‘tubes under
pressure’). Worms use longitudinal muscles to produce a sideways
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thrashing motion. Adult worms form separate sexes with well-

developed reproductive systems.
> Cestodes (tapeworms) have long flat ribbon-like bodies with a single
anterior holdfast organ (scolex) and numerous segments. They do not
have a gut and all nutrients are taken up through the tegument. They
do not have a body cavity (acoelomate) and are flattened to facilitate
perfusion to all tissues. Segments exhibit slow body flexion produced
by longitudinal and transverse muscles. All tapeworms are
hermaphroditic and each segment contains both male and female
organs.
> Trematodes (flukes) have small flat leaf-like bodies with oral and
ventral suckers and a blind sac-like gut. They do not have a body
cavity (acoelomate) and are dorsoventrally flattened with bilateral
symmetry. They exhibit elaborate gliding or creeping motion over
substrates using compact 3-D arrays of muscles. Most species are
hermaphroditic (individuals with male and female reproductive
systems) although some blood flukes form separate male and female
adults.

Unlike other pathogens (viruses, bacteria, protozoa and fungi), helminths

do not proliferate within their hosts. Worms grow, moult, mature and then
produce offspring which are released from the host to infect new hosts.
Worm burdens in individual hosts (and often the severity of infection) are
therefore dependent on intake (number of infective stages taken up).
Worms develop slowly compared to other infectious pathogens so any
resultant diseases are slow in onset and chronic in nature. Although most
helminth infections are well tolerated by their hosts and are often
asymptomatic, subclinical infections have been associated with significant
loss of condition in infected hosts. Other helminths cause serious clinical
diseases characterized by high morbidity and mortality. Clinical signs of
infection vary considerably depending on the site and duration of infection.
Larval and adult nematodes lodge, migrate or encyst within tissues
resulting in obstruction, inflammation, oedema, anaemia, lesions and
granuloma formation. Infections by adult cestodes are generally benign as
they are not invasive, but the larval stages penetrate and encyst within
tissues leading to inflammation, space-occupying lesions and organ
malfunction. Adult flukes usually cause obstruction, inflammation and
fibrosis in tubular organs, but the eggs of blood flukes can lodge in tissues
causing extensive granulomatous reactions and hypertension.
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General Life-cycles in Helminths

Helminths form three main life-cycle stages: eggs, larvae and adults. Adult
worms infect definitive hosts (those in which sexual development occurs)
whereas larval stages may be free-living or parasitize invertebrate vectors,
intermediate or paratenic hosts.
General Life Cycle in Nematodes
Nematodes produce eggs that embryonate in utero or outside the host. The
emergent larvae undergo 4 metamorphoses (moults) before they mature as
adult male or female worms.

General Life Cycle in Cestodes

Cestode eggs released from gravid segments embryonate to produce 6-
hooked embryos (hexacanth oncospheres) which are ingested by
intermediate hosts. The oncospheres penetrate host tissues and become
metacestodes (encysted larvae). When eaten by definitive hosts, they
excyst and form adult tapeworms.
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General Life Cycle in Trematodes

Trematodes have more complex life-cycles where ‘larval’ stages undergo
asexual amplification in snail intermediate hosts. Eggs hatch to release
free-swimming miracidia which actively infect snails and multiply in sac-
like sporocysts to produce numerous rediae. These stages mature to
cercariae which are released from the snails and either actively infect new
definitive hosts or form encysted metacercariae on aquatic vegetation
which is eaten by definitive hosts.

Modes of Transmission
The four main modes of transmission by which the larvae infect new hosts
are faecal-oral, transdermal, vector-borne and predator-prey transmission:

> faecal-oral transmission of eggs or larvae passed in the faeces of one

host and ingested with food/water by another (e.g. ingestion
of Trichuris eggs leads directly to gut infections in humans, while the
ingestion of Ascaris eggs and Strongyloides larvae leads to a pulmonary
migration phase before gut infection in humans).
> transdermal transmission of infective larvae in the soil (geo-helminths)
actively penetrating the skin and migrating through the tissues to the
gut where adults develop and produce eggs that are voided in host
faeces (e.g. larval hookworms penetrating the skin, undergoing
pulmonary migration and infecting the gut where they feed on blood
causing iron-deficient anaemia in humans).
> vector-borne transmission of larval stages taken up by blood-sucking
arthropods or undergoing amplification in aquatic molluscs
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(e.g. Onchocerca microfilariae ingested by blackflies and injected into

new human hosts, Schistosoma eggs release miracidia to infect snails
where they multiply and form cercariae which are released to infect new
hosts).
> predator-prey transmission of encysted larvae within prey animals
(vertebrate or invertebrate) being eaten by predators where adult
worms develop and produce eggs (e.g. Dracunculus larvae in copepods
ingested by humans leading to guinea worm infection, Taenia cysticerci
in beef and pork being eaten by humans, Echinococcus hydatid cysts in
offal being eaten by dogs).

NEMATODES (ROUND WORMS)

 All the important human parasites of the Phylum Nemathelminthes

(Aschelminthes) belong to the Class Nematoda.

GENERAL CHARACTERISTICS OF NEMATODES

They are un-segmented, elongated and cylindrical. They have

separate sexes with separate appearances. They have a tough
protective covering or cuticle. They have a complete digestive tract
with both oral and anal openings. The nematodes are free living
(Majority) or parasites of humans, plants or animals.

The parasitic nematodes:

The nematodes are generally light cream-white colored. Their life

cycle includes: egg, larvae and adult.

The parasitic nematodes are divided into:

1. Intestinal nematodes

1.1. Intestinal nematodes with tissue stage

A. Ascaris lumbricoides
B. Hookworms
C. Strongyloides stercoralis
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1.2. Intestinal nematodes without tissue stage

A. Enterobius vermicularis
B. Trichuris trichuira.
2. Tissue and blood dwelling nematodes

2.1.Filarial worms

2.2.Dracunculus medinensis
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2.3.Trichinella

2.4.Larva migrans.

2.1. INTESTINAL NEMATODES WITH TISSUE STAGE

2.1.1. ASCARIS LUMBRICOIDES

These are common roundworms infecting more than 700 million

people worldwide.

Morphology:

Male adult worm measures 15-20 cm in length. The posterior end is

curved ventrally. The female worm measures 20-40 cm in length. Its
posterior end is straight.

Infective stage and modes of infection:

The egg containing larva when ingested with contaminated raw

vegetables causes ascariasis.

Life cycle:

Ingested eggs hatch in the duodenum. The larvae penetrate the

intestinal wall and circulate in the blood. From the heart they
migrate to the lungs, ascend to the trachea, descend to the
esophagus and finally reach the small intestine to become adult. The
female pass immature eggs which pass to the soil and mature in 2
weeks.
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Figure 1.3. Life cycle of Ascaris lumbricoides

Pathogenecity and clinical features

Adult worms in the intestine cause abdominal pain and may cause
intestinal obstruction especially in children. Larvae in the lungs may
cause inflammation of the lungs (Loeffler’s syndrome) – pneumonia-
like symptoms.

Diagnosis
1. Examination of stool for eggs by direct saline smear method.
The egg is ovoidal, 75x60 microns, covered by albuminous
mamillatins.
2. Demonstration of adult worms
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Figure1.4. Egg of Ascaris lumbricoides

Treatment
Mebendazole, Albendazole and Piperazine

2.1.2. HOOK WORMS

There are two species of hookworm:
1. Ancylostoma duodenale
2. Necator americanus
The adults are found in the small intestines of man. Mixed infection is
common. Ancylostoma duodenale:

Grayish-white in color. The body is slightly ventrally curved. The

anterior end follows the body curvature. The buccal cavity is provided
ventrally with pairs of teeth and dorsally with a notched dental plate.
Distribution: This species is found in the northern part of the world
including China, Japan, Europe and North Africa.

Morphology
Male: The male measures 10 cm in length. The posterior end is
broadened into a membraneous copulatory bursa that is provided with
two long spicules.
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Female: The female measures 12 cm in length. The posterior end is

straight.

2.1.2.1. Necator americanus

This species, so called American hookworm, is found in predominantly

the tropics. The anterior end is hooked against the body curvature.
The mouth is provided ventrally and dorsally with cutting plate.

Morphology
Male: The male measures 8 cm in length. The posterior end is
broadened into a membraneous copulatory bursa, which is provided
with two long spicules fused distally.

Female: The female measures 10 cm in length. The posterior end is

straight
Infective stage and methods of infection:
The filariform larva infects by skin penetration.

Life cycle

Adult male and female worms live in the small intestine. The female
lays eggs (oval, 60x40 microns), which contain immature embryo in
the 4 cell stage. When the eggs pass in the stool to the soil and under
favorable conditions of temperature, moisture and oxygen, they hatch
into larvae, which molt twice and become infective. When the
filariform larvae penetrate the skin, they circulate in the blood, reach
the lungs, ascend to the trachea, descend to esophagus to reach
the small intestine and become adults.
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Figure1.5. Life cycle of hookworms

Pathogenecity

Adult worms in the intestine feed on blood causing iron deficiency

anemia. The larvae may cause inflammation of the lungs.

Diagnosis: Examination of stool by direct saline smear to detect the eggs.

Figure1.6. Egg of hookworm

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Treatment
Mebendazole: 1 tab 2x daily for 3 days.

2.1.3. LARVA MIGRANS

There are three types of larva migrans:

a. Cutaneous larva migrans (Creeping eruption)

Various animals harbor hookworms. Two species of dogs and cats
are important.
1. Ancylostoma braziliens: infects both dogs and cats.
2. Ancylostoma caninum: infects only dogs.
Both of these are common in the tropics and subtropical regions
where human hookworms can best complete their life cycles. If
man comes in contact with infective larvae, penetration of the
skin may take place; but the larvae are then unable to complete
their migratory cycle. Trapped larvae may survive for weeks or
even months, migrating through the subcutaneous tissues. They
may evoke a fairly severe reaction - pruritus and dermatitis. The
dermatitis leads to scratching and then bacterial superinfection.

Treatment
Thiabendazole: Applied topically.

b. Visceral larva migrans

A syndrome caused by the migration of parasitic larvae in the

viscera of a host for months or years. It may be caused by
transient larval migration in the life cycles of several parasites
such as hookworm, Ascaris lumbricoides, T. spiralis, S. strecoralis
and other filarial worms.

Toxocariasis

This is a kind of visceral larva migrans caused by

 Toxocara canis (Dog ascarid) and
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 Toxocara catis (Cat ascarid).

These cause persistent larval migration and thus the visceral larva
migrans is called toxocariasis.

Morphology

 The larvae of Toxocara canis and Toxocara catis measure about

400 m in length.
 The life cycle of these parasites in their respective hosts is similar
to that of A. lumbricoides in humans.

Epidemiology

Visceral larva migrans is cosmopolitan in distribution.

Transmission:

Ingestion of eggs of Toxocara species in contaminated food or soil

or direct contact with infected patients. Children are more at risk.

Clinical features:
 Majority are asymptomatic.
 Eosinophilia
 Cerebral, myocardial and pulmonary involvement may cause death.
Diagnosis - Identification of larvae in tissue.
Treatment - Thiabendazole: 25 mg/kg twice daily for 5 days.

C. Intestinal larva migrans

This is an extremely rare kind of larva migrans
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2.1.4. STRONGYLOIDES STERCORALIS

The worms may be present as parasitic in the host or free living in the soil.

Morphology:
Male: The male measures1 mm in length with curved posterior end
and carries two spicules
Female: The female measures 2.5 mm in length with straight posterior
end.

Infection: follows skin penetration by filariform larvae.

Life cycle

Adult male and female worms live in the small intestine. After
fertilization, the female penetrates the mucosa of the small intestine
and lay eggs in the submucosa. The eggs hatch and the larvae
penetrate the mucosa back to the lumen. If the environmental
conditions are favorable, the larvae will come out with the stool to
the soil. They transform into adults, which lay eggs, and hatching
larvae get transformed to adults and so on. If the environmental
conditions are not favorable, the larvae in the stool will moult and
transform into infective filariform larvae, which pierce the intestine
(auto-infection). Larvae penetrating the skin from the soil or by
autoinfection are carried by the blood to the lungs, ascend to the
trachea, descend to the esophagus and mature in the small intestine.
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Figure 1.7. Life cycle of Strongyloides stercoralis

Clinical presentation

The patient complains of mucoid diarrhea. Larvae in the lungs may

cause pneumonia.

Disseminated strongyloidiasis:

Multiplicity of symptoms are present due to the injury of other organs

by the migrating larvae. Organs such as liver, heart adrenals,
pancreas, kidneys, and CNS, etc. may be affected. This is usually seen
in immunocompromized individuals.

Diagnosis - Detection of rhabditiform larvae of strongyloides in stool.

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Figure 1.8. Larva of S. stercoralis

Treatment:
Thiabendazole: 25 mg/kg twice daily for 3 days.

2.2. INTESTINAL NEMATODES WITHOUT TISSUE STAGE

2.2.1. ENTEROBIUS VERMICULARIS (PIN WORM OR

THREAD WORM) Enterobius vermicularis is a small white worm
with thread-like appearance. The worm causes enterobiasis. Infection
is common in children.

Morphology
Male: The male measures 5 cm in length. The posterior end is
curved and carries a single copulatory spicule.
Female: The female measures 13 cm in length. The posterior end is
straight.

Infective stage
Infection is by ingestion of eggs containing larvae with
contaminated raw vegetables.

Mode of infection
 By direct infection from a patient (Fecal-oral route).
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 Autoinfection: the eggs are infective as soon as they are

passed by the female worm. If the hands of the patient get
contaminated with these eggs, he/she will infect
him/herself again and again.
 Aerosol inhalation from contaminated sheets and dust.

Life cycle

Adult worm lives in the large intestine. After fertilization, the male
dies and the female moves out through the anus to glue its eggs on
the peri-anal skin. This takes place by night. The egg is 50x25
microns, plano-convex and contains larva. When the eggs are
swallowed, they hatch in the small intestine and the larvae migrate to
the large intestine to become adult.

Figure 1.9. Life cycle of E. vermicularis

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Clinical presentation

The migration of the worms causes allergic reactions around the anus
and during night it causes nocturnal itching (pruritus ani) and
enuresis. The worms may obstruct the appendix causing appendicitis.

Diagnosis

 Eggs in stool: Examination of the stool by direct saline smear to

detect the egg: this is positive in about 5% of cases because the
eggs are glued to the peri-anal skin.

 Peri-anal swab: The peri-anal region is swabbed with a piece of

adhesive tape (cellotape) hold over a tongue depressor. The
adhesive tape is placed on a glass slide and examined for eggs.
The swab should be done in the early morning before bathing and
defecation.

Figure 1.10. Egg of E. vermicularis

Treatment
Mebendazole; Piperazine.
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2.2.2. TRICHURIS TRICHIURA (WHIP WORM)

The worm is divided into a thin whip-like anterior part measuring 3/5
of the worm and a thick fleshy posterior part of 2/5 the length.
Male: The male measures 3-4.5 cm in length. Its posterior end is
coiled and possesses a single cubicle.
Female: The female measures 4-5 cm in length. Its posterior end is
straight

Infective stage and mode of infection

Infection is by ingestion of eggs containing larvae with

contaminated raw vegetables.

Life cycle:

Ingested eggs hatch in the small intestine and the larvae migrate to
the large intestine to become adult. After mating, the female lays
immature eggs, which pass with the stool to the soil and mature in 2
weeks.

Figure 1.11. Life cycle of Trichuris trichiura

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Symptoms

The patient complains of dysentery (blood and mucus in stool together

with tenesmus). Rectal prolapse is also possible.

Diagnosis

Finding of characteristic eggs. The egg of trichuris is barrel-shaped,

50x25 microns. The shell is thick with a one mucoid plug at each pole.

Figure 1.12. Egg of Trichuris trichiura

Treatment
Mebendazole: 1 tablet twice daily for 2 days.

2.3. TISSUE NEMATODES

This group includes the filarial worms, the guinea worm

(Dranculuculus medinensis) and Trichinella spiralis.

2.3.1. FILARIAL WORMS

The filarial worms have complex life cycles involving a developmental

stage in an insect vector. They require an arthropod vector for their
transmission. The worms inhabit either the lymphatic system or the
subcutaneous tissues of man. The
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female worm gives rise to a young worm called microfilaria. The

microfilariae, when taken by the arthropod intermediate host during
biting, develop into filariform larvae, which are the infective stages.
Humans get infected when bitten by the infected arthropod
intermediate host.

2.3.1.1. Wuchereria bancrofti

This is a parasite of lymph nodes and lymphatic vessels- causing

lymphatic filariasis. This filarial worm is transmitted by the bite of
various species of mosquitoes. It is believed that over 100 million
people are infected. The microfilariae are nocturnal – seen in greatest
numbers in peripheral blood in the night between 10 PM -2 AM. The
physiological basis of this nocturnal periodicity is not understood.

Figure1.13. Life cycle of W. bancrofti

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Mode of transmission and pathogenesis

The filariform larvae are introduced through the skin by the bite of
the arthropod intermediate host. The larvae invade the lymphatics,
usually the lower limb, where they develop into adult worms. The
microfilariae are librated into the blood stream. They remain in the
pulmonary circulation during day, emerging into the peripheral
circulation only during night, to coincide with the biting habit of the
vector. Presence of the adult worms causes lymphatic blockage and
gross lymphedema, which sometimes lead to elephantiasis.

Pathogenecity and clinical features:

 The adult worm obstructs the flow of lymph in the lymph

nodes and the lymphatic vessels draining the lower limbs and the
external genitalia.
 The lower limbs and external genitalia become swollen. The skin
becomes thick and fissured. The disease is called bancroftian
elephantiasis.
 The major symptoms and findings include: lymphangitis,
lymphedema, fever, headache, myalgia, hydrocele and chyluria.

Diagnosis

 Blood film examination after staining by Giemsa or Leishman

stain to detect microfilaria. The film should be taken by night.
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Figure 1.14. Microfilaria of W. bancrofti in blood smear

Treatment - Diethyl carbamazine (DEC): 2 mg/kg 3x daily for 2 weeks.

Endemic non-filarial elephantiasis (Podoconiosis)

Non-filarial elephantiasis of the lower limbs is common. Silicon,

aluminium and iron particles in the red clay soil are absorbed through
skin abrasions in bare footed persons. The mineral particles cause
obstruction of the lymphatics.

2.3.1.2. Onchocerca volvulus

Morphology:

Male: Similar to that of Wuchereria bancrofti.

Female: The female measures 30-50 cm in length. It is present
inside of a fibrous nodule (onchocercomata or onchocerca tumor).
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Intermediate Host and vector

Female Simulium, (Simulium damnosum), Black fly, found around

plantations following rivers or river basins.

Microfilaria

Measures 300 microns in length. It is non-sheathed microfilaria. It is

present in the subcutaneous tissue fluids and not in blood.

Figure 1.15. Life cycle of O. volvulus

Infective stage and mode of infection is similar to that of Wuchereria

bancrofti.

Pathogenecity and clinical manifestations:

The disease, onchocerciasis or river blindness includes:
 Skin fibrous nodules (onchocercomata) enclosing female worms.
The nodules are common in neck, iliac crest and the coccyx.
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 Skin hypo- or hyper- pigmentation. Dermatitis is present. In

advanced cases, the skin becomes thickened and wrinkled, showing
lizard or leopard skin appearance.
 Elephantiasis of the external genitalia and corneal opacity and optic
atrophy may finally cause blindness.

Diagnosis

Superficial biopsy (skin snip) is taken from the skin using sharp razor
blade. The specimen is allowed to stand for 30 minutes in saline
before it is examined microscopically for microfilariae.

Figure 1.16. Microfilaria of O. volvulus

Treatment

Ivermectin: 50 mg/kg bodyweight, given every 6 or 12 months.

Because it kills microfilariae but not adult worms, retreatment is
necessary over a period of years.

Prevention
 Vector control
 Mass treatment
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 Establishment of villages away from Simulium breeding places.

 Use of repellents
 Protective clothing

2.3.1.3. Loa loa

The eye worm, Loa loa, causes Loiasis. The insect vectors include
mango flies of Chrysops - Chrysops silacea, Chrysops dimidiata.
Loiasis is endemic in Central and West Equatorial Africa. The
abundant rubber plantations provide a favorable environment for the
vector to transmit the disease.

Morphology
Adult male worms: 30-34 mm in
length Adult female worms: 40-70
mm in length

Pathogenesis

The microfilaria have a sheath. Their diurnal periodicity corresponds

to the feeding pattern of the insect vector, which bites humans from
10:00 AM to 4:00 PM.

Clinical Features

Incubation period is about one year. It causes calabar swelling

beneath the skin due to parasites. There is fever, pain, pruritus,
urticaria, allergic reactions, retinopathy, glomerulonephritis,
meningo-encephalitis etc.

Laboratory diagnosis

 Detection of microfilaria in peripheral blood, urine, sputum, CSF -

stained with Giemsa or unstained
 Eosinophilia
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Treatment

DEC, 6 to 10 mg per kilogram per day for 2 to 3 weeks: but has side
effects - allergic reactions

2.3.2. DRACUNCULUS MEDINENSIS (Guinea worm or Medina

worm)

Dracunculus medinensis causes dracunculiasis. The infection is

endemic to Asia and Africa: India, Nile Valley, central, western and
equatorial Africa.

Morphology

Gravid female worms measure 70-120 cm in length. Their body cavity

is almost fully occupied by a uterus greatly distended with
rhabditiform larvae (250-750 m in length). A digestive tube and
cuticular annulations distinguish the larvae from microfilariae.

Figure1.17 Larvae of D. medinensis

Pathogenecity and life cycle

Infection is acquired by drinking unfiltered or not boiled water that

contains Cyclops species. The larvae are released in the stomach,
penetrate the intestinal wall and find their way to the subcutaneous
tissue. Mating takes place in the axillary or inguinal regions 3 months
after infection. The male worms then die in the tissue and the female
worms move down to the limbs within 10 months. In
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about 1 year, female worms in the subcutaneous tissue provoke the

formation of a burning blister in the skin of the legs. When in water,
the blister bursts, and about 5 cm of the worm is extruded from the
resulting ulcer - thus releasing many thousands of first stage larvae.
The larvae swim in water and are ingested by the intermediate host -
Cyclops species- within about 4 days. Inside the Cyclops, the larvae
molt twice and become infective in 2 weeks

Figure 1.18. Life cycle of Drancunculus medinesis

Clinical feature

The female parasites in the subcutaneous tissue release toxic

byproducts of histamine-like nature, which cause systemic allergic
reactions, like erythema, urticaria, pruritus, fainting, asthma,
dyspnea, etc. This is followed by the appearance of a blister on the
legs, which ruptures on contact with water releasing larvae into the
water by the female worm. The wound may ulcerate. The worms
migrate into other tissues and may cause arthritis, pericarditis,
abscesses etc. It occasionally penetrates the eyeball and causes loss of
the eye.
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Diagnosis

1. Clinical: Observation of blister, worm or larvae

2. Histologic features of subcutaneous sinus tract
3. Eosinophilia and radiographic evidence

Treatment

Surgical excision when the worm is in

the leg Niridazole (Ambilhar) or DEC

Prevention

Health education on:

 Boiling or filtering of drinking water
 Treating of patients and educating them not to enter water bodies
 Using insect larvicides to kill Cyclops in water.

2.3.3. TRICHINOSIS

Etiologic agent - Trichinella spiralis

This is the only important species in this group. It causes trichinosis -
a cosmopolitan infection. More than 100 different animal species can
be infected with Trichinella species, but the major reservoir host for
human infections is swine.

Morphology

Adult female worm measures 3-4 mm in length and the adult male
worm measures 1.4-2.6 mm in length. The encysted larvae measure
800-1300 m in length.
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Pathogenecity and life cycle

After ingesting infected meat, the capsule of the encysted larvae is

digested by gastric juice, and the larvae are released in the duodenum
or jejunum where they molt four times to become adult worm. After
mating, the male worm dies and the female worm begins to deliver
the embryos 4-7 days after the infection. The larvae penetrate the
intestinal wall and migrate through the lymphatic vessels to the blood
stream, which carries them to various organs. Skeletal muscles and
diaphragm are most frequently parasitized. Others include the
tongue, masseter and ocular muscles.

Figure 1.19 Life cycle of Trichinella spiralis

Clinical features

There are two clinical phases.

1. The intestinal phase: lasting 1-7 days - asymptomatic; sometimes
cause nausea, vomiting, diarrhea, constipation, pain, etc, and
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2. The muscle phase: which causes myalgia, palpabral edema,

eosinophilia, fever, myocarditis, meningitis, bronchopneumonia etc.

Diagnosis:

 Muscle Biopsy
 Detection of larvae in blood or CSF
 Detection of larvae and adult worms in stool (rare).
 ELISA

Treatment - Thiabendazol

Prevention
 Cooking of all meat before consumption
 Inspection of pigs
 Pork must be stored at -150C for 20 days.
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CESTODES (TAPEWORMS)

INTRODUCTION

The tapeworms are hermaphroditic and require an intermediate host.

The adult tapeworms found in humans have flat body, white or grayish
in color. They consist of an anterior attachment organ or scolex and a
chain of segments (proglottids) also called strobilla. The strobilla is
the entire body except the scolex. The scolex has suckers or grooves.
It has rosetellum, which has 1 or 2 rows of hooks situated on the
center of the scolex.

Adult tapeworms inhabit the small intestine, where they live attached
to the mucosa. Tapeworms do not have a digestive system. Their
food is absorbed from the host’s intestine.

3.1. HYMENOLEPIS NANA (DWARF TAPEWORM)

Morphology

Adult worm measures 1-3 cm in length. It is made up of head (scolex),

neck and segmented body. The head carries four suckers and a
rostellum armed with one row of hooks. The segments of the body are
divided into mature and gravid segments. In the mature segment,
there are three testes in the middle.

Infective stage and mode of infection

The egg, which is immediately infective when passed by the patient, is

rounded, about 40 microns in diameter. It contains a six- hooked
oncosphere within a rigid membrane (the embryosphere). This
embryosphere has two polar thickening or knobs from which project
4-8 long, thin filaments called polar filaments.
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Infection takes place by:

1. Ingestion of egg with contaminated raw vegetables.
2. Direct infection from a patient
3. Auto infection: the eggs of H. nana are infective as soon as they
are passed with feces by the patient. If the hands of the patient
are contaminated by these eggs, she/he infects herself/himself
again and again.

Pathogenecity

Light infections produce no symptoms. In fairly heavy infections,

children may show lack of appetite, abdominal pain and diarrhea.

Treatment - Niclosamide: 4 tablets chewed in a single dose daily for 5

days.

3.2. HYMENOLEPIS DIMINUTA (RAT TAPEWORM)

Hymenolepis diminuta differs from Hymenolepis nana in that:

 The adult worm measures about 10-60 cm
 The rosetellum on the head has no hooks
 In the mature segment, there are two testes at one side and
another testis on the other side.

Life cycle

The adult worms are present in the small intestine of man and rats.
Eggs passed in stool are similar to the eggs of H. nana but are brown
in color with no polar filaments arising from the polar thickening. The
eggs are ingested by the rat flea where they develop to cysticercoid
stage. Infection to man takes place accidentally by food or
contaminated hands by cysticercoid stage.
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Pathogenecity

Most infections are asymptomatic, but occasionally, patients may

present with nausea, anorexia and diarrhea.

Treatment

same as Hymenolepis nana.

3.3. ECHINOCOCCUS

There are two different species. These are: Echinococcus granulosus

and
Echinococcus multilocularis

3.3.1. Echinococcus granulosus (dog tape worm)

Responsible for most cases of echinococcosis. Echinococcosis is

caused by larval tapeworms. The disease is common in East Africa
(the highest prevalence is seen in Kenya: 10-15%).

Morphology

The adult worm measures 3-6 mm in length (up to 1 cm). It has scolex,
neck and strobilla. Adult worms live in small intestine of definitive
host (dog). Man is an intermediate host - carrying the hydatid cyst
(larva). Man contracts infection by swallowing eggs in excreta of
definitive host.

Life cycle and Pathogenecity

Oncosphere hatch in duodenum or small intestine into embryos

(oncosphere) which:
 Penetrate wall
 Enter portal veins
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 Migrate via portal blood supply to organs: eg: lungs, liver, brain
etc., thus, causing extra intestinal infections. In these organs,
larvae develop into hydatid cysts. The cysts may be large, filled
with clear fluid and contain characteristic protoscolices
(immature forms of the head of the parasite). These mature into
developed scolices, which are infective for dogs.

Figure 1.20. Life cycle of Echinococcus granulosus

Mode of human infection

Ingestion of eggs by the following ways:

i) Ingestion of water or vegetables polluted by infected dog feces.
ii) Handling or caressing infected dogs where the hairs are
usually contaminated with eggs.

Clinical features
Asymptomatic infection is common, but in symptomatic patients
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 It may cause cough - with hemoptysis in lung hydatid disease.

 Hepatomegaly - with abdominal pain and discomfort
 Pressure -from expanding cyst
 Rupture of cyst - severe allergic reaction - anaphylaxis.

Diagnosis:
 X-ray or other body scans
 Demonstration of protoscolices in cyst after operation
 Serology

Treatment
 Surgery
 Albendazole 400 mg twice a day for one to eight periods of 28
days each, separated by drug-free rest intervals of 14 to 28 days.

3.3.2. Echinococcus multilocularis

Foxes are the definitive hosts, while various rodents such as mice
serve as intermediate hosts.

3.4. TAENIA SAGINATA (BEEF TAPEWORM)

In adult stage, T. saginata inhabits the upper jejunum where it may

survive for as long as 25 years. It causes intestinal infection,
Taeniasis. It has worldwide distribution.
These are one of the true and segmented tapeworms. Their body is
divided into three regions;
1. Scolex: the hold fast organ
2. Neck: posterior to the scolex
3. Stobilla: the main bulk, made up of proglottids.
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Morphology:

Adult worm measures 5-10 meters in length. The pyriform scolex has
4 suckers but no rostellum. The mature segments have irregularly
alternate lateral genital pores. Each of the terminal segments
contains only a uterus made up of a median stem with 15-30
lateral branches.

Life cycle

The adult worm lives in the small intestine of man. Gravid segments
pass out in the stool and become disintegrated and eggs come out to
the soil. The gravid proglottid uterus contains about 100,000 eggs.
The egg of T. saginata is round, about 40 microns in diameter. The 6-
hooked embryo is enclosed in a radially striated embryophore. Eggs
are ingested by an intermediate host, cattle. The 6- hooked embryo
escapes from its shell, penetrates through the intestinal wall into the
blood vessels and is carried to the muscles where it develops into a
larval stage, cysticercus bovis (made up of an invaginated /inverted
head and spherical body). Infection to man takes place by the
ingestion of raw or insufficiently cooked beef. In the small intestine of
man, the head of the cysticercus gets invaginated and the body
becomes segmented.
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Fig 1.21. Life cycle of Taenia saginata

Pathogenecity

Infected persons may complain of epigastric pain, abdominal

discomfort, diarrhea, weight loss, hunger sensation, vomiting, etc.

Diagnosis

Recovery of the gravid segments or the eggs from the stool

Figure1.22. Egg of Taenia Spp

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Treatment:
Niclosamide: Four tablets chewed in a
single dose. Mebendazole 100mg twice
daily for three days

Prevention:
 Thorough cooking of meat (above 570C).
 Proper disposal of human excret

3.5. TAENIA SOLIUM (PORK TAPEWORM)

The adult worms of T. solium reside or inhabit the upper jejunum.

Infection has worldwide distribution.

Morphology:

Adult worm measures about 3 meters in length. The globular scolex

has rostellum with 2 rows of hooklets. There are <1000 proglottids.
Gravid proglottid liberates about 30,000-50,000 eggs.

Life cycle

Embryonated eggs passed with stool are ingested by pig and the
embryo is released. It penetrates the intestinal wall and is carried by
vascular channels to all parts of the body. After a period of 2-3
months of development the encysted larval stage called cysticerci or
bladder worm occurs in the striated muscles of the tongue, neck,
trunk brain, eye, and the nervous system. The cysticercus survives for
5 years. Humans become infected by eating pork containing larvae,
cysticercus cellulosae. When improperly cooked cysticercus infected
meat is eaten by man, the scolex remains undigested and attaches
itself to the intestinal wall and chain of proglottids begin to grow to
adult worm.
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Clinical manifestations
Resembles that of T. saginata infection

Diagnosis
Demonstration of eggs in stool specimen

Treatment
Niclosamide: 2 gm PO stat

Prevention:
 Treatment of infected persons.
 Thorough cooking of pork and proper processing
 Proper disposal of human excreta (good hygiene/sanitation).

Table 1: Comparison between Taenia saginata and Taenia solium species

Taenia saginata Taenia solium

Length (m) 5-10 2-3
Proglottid 1000-2000 800-900
number
Hooklets Absent Present
Suckers Pigmented Non- Pigmented
Uterus branch 15-30 5-10

3.6. DIPHYLOBOTRIUM LATUM (FISH TAPEWORM OR BROAD

TAPEWORM

The broad tapeworm infecting man has worldwide distribution,

occurring in areas where improperly cooked or raw fresh water fish is
prominent in diet.

Morphology

Diphylobotrium latum is the broadest and longest tapeworm. The

adult worm measures up to 30 feet with 3000-4000 proglottids, which
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are wider than they are long. The tapeworm has no rostellum hooks or
suckers.
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Life cycle

Unlike Taenia, the gravid segments are retained by the worm.

Operculated eggs passed in feces hatch into small ciliated coracidium
larvae which swim about freely. These are eaten by crustaceans -
Cyclops or Diaptomus - in which the larvae develop into second stage
larvae- the procercoid. When the crustaceans are swallowed by fresh
water fish, the larvae migrate into the flesh of the muscle fish and
develop to pleurocercoid or sparganum larvae. Humans are infected
by ingesting raw or improperly cooked fish. The tapeworm matures in
the intestine and after 3 weeks, the adult worm discharges eggs. The
life cycle requires two intermediate hosts.

Clinical manifestation

Most infections are asymptomatic. Rarely, it causes severe cramping,

abdominal pain, vomiting, weakness and weight loss. Pernicious
anemia can also result, due to interference of vitamin B12 absorption
in jejunum.

Diagnosis
Eggs in stool: Single shell with operculum at one end and a knob on the
other.

Treatment
Niclosamide: 2 gm PO stat after light breakfast.

Prevention:
Prohibiting the disposal of untreated sewage into fresh
water /lakes. Personal protection: cooking of all fresh
water fish.

TREMATODES (FLUKES)

INTRODUCTION

Trematodes belong to the phylum platyhelminthes. They are found in

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a wide range of habitats. The great majority inhabit the alimentary

canal, liver, bile duct, ureter and bladder of vertebrate animals.
According to the sites they inhabit, there are four groups of flukes.
These are: Blood flukes, Intestinal flukes, Liver flukes, and Lung
flukes

1.1. BLOOD FLUKES

These are flukes that reside mainly in the blood vessels of various
organs and the schistosomes are the prototype and the commonest
flukes in our country.

1.1.1. SCHISTOSOMIASIS (BILHARZIASIS)

It is estimated that about 600 million people in 79 countries suffer
from schistosomiasis (Bilharziasis). The schistosomes cause intestinal,
hepato- splenic, pulmonary, urogenital, cerebral and other forms of
schistosomiasis. Schistosome is the only fluke with separate sexes.
The female worm lies in the gynecophoral canal of the male. This
condition is important for transportation.
There are five medically important species:
1. Schistosoma mansoni: causes intestinal schistosomiasis.
2. Schistosoma haematobium: causes vesical (urinary)
schistosomiasis.
3. Schistosoma japonicum: causes intestinal schistosomiasis.
4. Schistosoma intercalatum: causes intestinal schistosomiasis.
5.Schistosoma mekongi: causes intestinal schistosomiasis. This
seems to cause milder disease in man. It causes disease in
other vertebrate hosts.
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The first two schistosomes (S. mansoni and S. haematobium) are

prevalent.

SCHISTOSOMA MANSONI
Habitat - This species lives in the veins of the intestine.

Geographical distribution: It is found in Africa, South America,

Middle East (some Arab countries) etc. Stream and lake-based
transmission is common.
The snail hosts that harbor S. mansoni are the genera: Biomphalaria
(B. glabrata) and Trobicorbis. These have oval shells.

Morphology
Male: The male ranges in size from 1-1.4 cm in length and the body
is covered by coarse tubercles. It has 6-9 testes
Female:The female is 1.5-2.0 cm in length. The ovary is present in the
anterior third and Vitelline glands occupy the posterior two-thirds. It
lays about 100-300 eggs daily. The uterus is short containing few ova.

URINARY SCISTOSOMIASIS
Etiology - Schistosoma haematobium
Habitat - The worm lives in the veins of the bladder of humans.
The peak prevalence is the 10-14 year age group. The snail hosts that
harbor S. haematobium are the genera Bulinus (Bulinus africanus, B.
truncatus) and Physopsis.

Male:The male ranges in size from 1-1.5 cm in length. The body is

covered by fine tubercles. It has 4-5 testes.

Female:The female ranges in size from 2-2.5 cm in length. The ovary

is present in the posterior third. Vitelline glands occupy the posterior
thirds. Uterus is long containing many ova. It lays about 20-200 eggs
daily.
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SCHISTOSOMA JAPONICUM

The female adult worm lays about 500-3500 eggs daily. The eggs are
ovoid, bearing only a minute lateral spine or a small knob postero-
laterally. It is found in Japan, China, and Philippines, etc.

SCHISTOSOMA INTERCALATUM

This is the rarest and least pathogenic schistosome that matures in

man. It is found in Western and Central Africa. The daily egg output is
about 300. The eggs have a terminal spine.

LIFE CYCLE OF SCHISTOSOMES

Adult worms reside in pairs: the female lying in the gynecophoral

canal of the male. After fertilization, eggs are passed into the venules.
A larval form – the miracidium - develops within the egg. Its lytic
enzymes and the contraction of the venule rupture the wall of the
venule liberating the egg into the perivascular tissues of the intestine
(S. mansoni) or urinary bladder (S. haematobium). The eggs pass into
the lumens and organs and are evacuated in the feces (S. mansoni) or
the urine (S. haematobium). On contact with fresh water the
miracidia hatch from the eggs and swim about until they find the
appropriate snail, which they penetrate. After two generations of
sporocyst development and multiplication within the snail, the fork-
tailed cercariae emerge. Infection to man takes place during bathing
or swimming. The cercariae penetrate the skin, are carried into the
systemic circulation and pass through to the portal vessels. Within
the intrahepatic portion of the portal system, the worms feed and
grow to maturity.
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Figure 1.1. Life cycle of schistosomes

Symptoms and complications

Patients infected with S. haematobium suffer from terminal

haematuria and painful micturition. There is inflammation of the
urinary bladder (cystitis), and enlargement of spleen and liver.

Patients infected with S. mansoni suffer from cercarial dermatitis

(swimmers itch) and dysentery (mucus and blood in stool with tenesmus)
as well as enlargements of the spleen and liver.
S. haematobium causes squamous cell carcinoma in the bladder.

Laboratory Diagnosis
S. mansoni
 Microscopic examination of the stool for eggs after
concentration by sedimentation method. The egg has
characteristic lateral spine.
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 Rectal snip

S. haematobium:
 Examination of the urine after allowing it to sediment in a conical
urinalysis glass. A drop from the sediment is taken and examined
for eggs. Egg has terminal spine.
 Biopsy from bladder

Figure 1.2. Eggs of S. mansoni and S. haematobium

Treatment:
Praziquantel: single oral dose of 40 mg/kg divided into two doses.

Prevention:
1. Health education:
A. On use of clean latrines and safe water supply
B. Avoid urination and defecation in canals, avoid contact
with canal water
2. Snail control:
A. Physical methods:
i. Periodic clearance of canals from vegetations.
ii. Manual removal of snails and their destruction.
B. Biological methods: Use of natural enemies to the snails
such as Marisa.
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C. Chemical methods: Molluscides are applied in the

canals to kill the snails. e.g. Endod

1.2. INTESTINAL FLUKES

 Fasciolopsis buski: These giant intestinal flukes (2-7.5 cm in

length) are found in some Asian countries.
 Heterophyids: Minute flukes acquired by ingestion of raw fresh
water fish. They are found in Asian countries.

1.3. LIVER FLUKES

 Clonorchis sinensis: Chinese liver fluke - adult worms live in bile

ducts.
 Faciola hepatica: Sheep liver fluke - is a common parasite,
cosmopolitan in distribution. It is large (3 cm in length). Adult
worms reside in the large biliary passages and gall bladder.
 Other: Faciola gigantica: lives in the liver of cattle. Human
infections are very rare.

1.4. LUNG FLUKES

At least eight different species of lung flukes, all belonging to the

genus Paragonimus, are known to infect man. Paragonimus
westermani, best known species, affects man causing
paragonimiasis (lung disease). It is found in Asia (China, India,
Indonesia, Malaya etc) and some African countries.