Download 7.Medical Helminthology flatworms

Medical Helminthology.
Flatworms - human parasites
Professor Fedonyuk L. Ya.
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According to the way of development parasites
are classificated into biohelminthes and
geohelminthes.
 Geohelminthes develop without intermediate
hosts. Soil is the best environment for their egg's
development. Humans are infected through dirty
fruits and vegetables, which contain
geohelminthe's eggs (Ascaris lumbricoideus).
 Biohelminthes have complete life cycle with
intermediate hosts. There are trophycal
connections between definitive and intermediate
hosts (for example, Taenia solium).
General characteristic of Flatworms (Phylum
Plathelminthes)
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The flatwotms consists of some 12, 200 species, including classes of
parasitic worms: Trematoda, Cestoda
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All flatworms
symmetrical.

flattened dorsoventrally
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they have a definite head at the anterior end.
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Their bodies are solid: the only internal space consists of the
digestive cavity. They have no anus; a single opening to the digestive
system serves as both mouth and anus.
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Wastes probably move out of flatworms mostly by diffusing across
the general body surface.
The most of flatworm species, in all three classes, are
hermaphrodites. A single individual generally cannot fertilize itself,
although exceptions do exist.

are
acoelomate,
triploblastic,
and
bilaterally
General characteristic of Class Trematoda
- Flattened dorsoventrally (leaflike).
- Unsegmented.
- Body is covered by cuticle.
- Organs of fixation: oral sucker,
ventral sucker.
- Organs and systems: digestive
system, excretory system, nervous
system.
Genital
system:
Trematodes are hermaphrodites
except genus Schistosoma.
-The life cycle is passed in two hosts
(alternation of hosts) and has
sexual and asexual stages.
BLOOD FLUKES - genus
SCHISTOSOMA

Distribution: Africa, Asia, Middle
East, Latin America.
 Schistosoma mansoni and
Schistosoma japonicum cause
Hepatosplenic Schistosomiasis.
 Schistosoma haematobium causes
Urinary Schistosomiasis.
 Localization: venous vessels of bowel,
liver, and bladder.
 Morphology: atypical trematodes
which the adult female nesting within
a specialized groove in the body of
the larger male.
BLOOD FLUKES

Transmission: infection
through skin of larvae
from snail hosts.

Infective stage: cercariae.
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Intermediate host: snail.
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Definitive host: man.
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Mode of transmission:
penetration of skin by
cercarie.
BLOOD FLUKES
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Clinical
manifestations
of
Hepatosplenic Shistosomiasis:
 eosinophilia,
 granulomatous polyps in colon,
 Fever,
 anorexia, weight loss,
 anemia,
 portal hypertension,
 dysentery and cirrhosis of liver,
 pruritic skin rash.
 Eggs go back through portal
circulation to liver, causing
hepatomegaly, liver tenderness.

Clinical manifestations of
Urinary Schistosomiasis:
 eosinophilia,
 hematuria,
 terminal
dysuria (pain,
difficulty at the end of
urination);
 obstructed urine flow.
BLOOD FLUKES

Laboratory
diagnostics
of
Hepatosplenic Schistosomiasis: eggs
with lateral spine in feces.
 Laboratory diagnostics of Urinary
Schistosomiasis: eggs with terminal
spine in urine

Prevention: involves proper
disposal of human waste and
eradication of the snail host when
possible.
 Swimming in endemic areas should
be avoided.
LUNG FLUKE: PARAGONIMUS
WESTERMANI –
an agent of paragonimiasis
 Distribution:
Far East,
Central America,
Africa, and India.
 Morphology: an egglike form of the body,
from 7,5 to 16 mm.
LUNG FLUKE
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Mode of transmission:
ingestion of metacercarial
cysts in crabs or crayfish.
Final hosts: carnivorous
mammals, pigs, humans.
Intermediate hosts:
1) snail (sporocyst, redia,
cercaria);
2) crabs or crayfish
(metacercaria).
Infective stage:
metacercariae
LUNG FLUKE
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Clinical disease: a chronic cough with
bloody sputum, dyspnea, pleuritic chest
pain, and pneumonia.
 Laboratory diagnosis: eggs in sputum or
feces.
 Prevention: cooking crabs and crayfish
properly.
BILIARY (LIVER) FLUKES

CLONORCHIS
SINENSIS – oriental
small biliary (liver)
fluke, causes
Clonorchiasis.

Distribution:
endemic in Far East,
China, Japan, and
Vietnam.
CLONORCHIS SINENSIS
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Localization: bile
ducts, gallbladder,
and pancreas.
 Morphology: the
adult worms are 1 to
2 cm; the eggs are
small, brownish.
CLONORCHIS SINENSIS
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Transmission: fecal-oral
(ingestion of contaminated raw,
frozen, dried, pickled, and salted
fish, which contain
metacercariae).
Infective stage:
metacercariae.
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Intermediate hosts:
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1- snail (miracidium, sporocyst,
rediae, cercariae),
2 - fish Cyprinidae genus- the
family that includes carp and
goldfish (metacercariae).
Final hosts: carnivorous
mammals and humans.
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CLONORCHIS SINENSIS
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Clinical disease:
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cholecystitis and cholelithiasis,
hepatic colic, associated with profound weight
loss and diarrhea.
An individual fluke may live for 15-30 years in
the liver. In humans a heavy infestation of liver
flukes may cause cirrhosis of the liver and death.
Laboratory diagnosis: immature eggs in
feces, in fluid from biliary drainage, or duodenal
aspirate.
Prevention: adequate cooking of fish and
proper disposal of human waste
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FASCIOLA HEPATICA
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an agent of fascioliasis.
Distribution: endemic in
Far East.
Localization: bile ducts,
gallbladder, and pancreas.
Morphology: large size (3-5
cm) and conical form of the
body; possess sucking disks (oral
and abdominal) that provide
them motion.
Multibranched uterus is situated
under the abdominal sucking
disk.
Testis are branched too and
situated in the middle part of the
body.
FASCIOLA HEPATICA
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Life-cycle:
Final host - herbivorous
mammals
humans.
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(horses)
and
Intermediate host — the
snail Limnea truncatula.
 Transmission: fecal-oral
(ingestion of water , some nonwater plants and vegetables,
which contain adolescariae).
 Invasive
stage:
adolescariae.
FASCIOLA HEPATICA
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Clinical disease: Parasites
obstruct bile ducts and lay eggs
within
them,
leading
to
cholelithiasis
(gallstones).
Biliary obstruction can occur,
sometimes
causing
biliary
cirrhosis.
 Diagnosis: immature eggs in
feces. An egg has large sizes,
thin membrane, yellow color
and small cover in one pole.
 Prevention: involves not
eating wild aquatic vegetables.
OPISTHORCHIS FELINEUS
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small biliary fluke, causing
Opisthorchiasis.
Distribution: Siberia.
Morphology:
flat, the length of the body 4-13
mm.
In the middle part of the body
there is a branched uterus.
Behind it there is a round ovary.
There is a roseolla-like testis in
the back of the uterus - a
diagnostic sign of this worm.
OPISTHORCHIS FELINEUS
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Life-cycle:
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Final host - carnivorous
mammals and humans.
Intermediate host 1) snail Bithynia leachi genus
2) - fish.
Transmission: ingestion of
contaminated raw, frozen,
dried, pickled, and salted fish,
which contains metacercariae.
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Invasive stage:
metacercariae cysts in fish
muscles.
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Localization: bile ducts,
gallbladder, liver.
OPISTHORCHIS FELINEUS
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Clinical disease: cholecystitis and cholelithiasis, hepatic
colic, cirhosis. Clinical picture is very similar to Clonorhis
infection. Infection can lay dormant for several years before
presenting clinically.
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Diagnosis: immature eggs in feces, in fluid from biliary
drainage, or duodenal aspirate. Eggs are 15-30 mcm in
sizes, have oval form and yellow color. The outer
membrane is thick, and there is a cover in the front of the
egg. The internal structure of the egg is microgranular.

Prevention involves not eating undercooked or
contaminated raw, frozen, dried, pickled, and salted fish;
eradication of snail hosts when possible.
DICROCOELIUM LANCEATUM
– causes Dicrocoeliasis.
 Distribution: worldwide.
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Localization: bile ducts, gallbladder and
liver of mammals (cattle, horses).
Very rare in humans.
Morphology: the worms are 1 cm long
with lanceolate form of the body;
the
intestine
(gut)
has
two
nonbranched channels which are
situated in the lateral sides of the
body.
Two round testis are situated in the
front of the body - the diagnostic sign
of this worm.
Transmission: ingestion of plants with
the
ants,
which
contain
metacercariae.
DICROCOELIUM LANCEATUM
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Invasive stage: metacercariae.
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Life-cycle:
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Final host - herbivorous mammals (cattle,
horses).
intermediate host
1- the snail of Zebrina and Helicela genus,
2- the ants Fornica genus.
Clinical disease: is similar to fascioliasis.
Diagnosis: immature eggs in feces. An egg
have oval form, smooth membrane, brown
color, a cover is present in the front end.
Prophylactics: eradication of the snails, ants
when possible; dehelmithization of cattle.
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Tapeworms
(Cestoda)
consist of a rounded head, called a scolex, and
long strobila or chain of proglottids (multiple
segments) of varying stages of maturity.
They have no digestive tract of its own at any
point in its life cycle.
The cestodes receive all of its nutrients be the
nonciliated tegument.
The scolex has specialized means of attaching to
the intestinal wall, namely suckers, hooks, or
sucking grooves.
The worm grows by adding new proglottids
from its germinal center next to the scolex.
The oldest proglottids at the distal end are
gravid and produce many eggs, which are
excreted in the feces and transmitted to various
intermediate hosts. Humans usually acquire the
infection when undercooked flesh containing
the larvae is ingested. All cestodes have stage of
larva and stage of oncosphere in the life cycle.
Taenia solium

The adult form of T. solium
causes taeniasis solium. T. solium
larvae cause cysticercosis.
 Distribution Teniasis and
cysticercosis occur worldwide but
is endemic in areas of Asia, South
America, and eastern Europe
 Morphology T. solium can be
indentified by its scolex with 4
suckers and circle of hooks and
by its gravid proglottids, which
have 7-12 primary uterine
branches.
 Larva
of
T.solium
called
cysticercus. A cysticercus consist
of a pea-sized fluid-filled bladder
with an invaginated scolex.
Taenia solium
Life cycle
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Transmittion: fecal-oral
Invasive stage: cysticerci.
Definitive hosts – humans
Intermediate hosts - pigs
Humans can be infected by
eating raw or undercooked pork
containing the larvae
cysticercus.
In the small intestine, the larvae
attach to the gut wall and take
about 3 months to grow into
adult worm.
The gravid terminal proglottids
detach daily, are passed in the
feces.
Taenia solium

The cysticerci can become large in eye,
subcutaneous tissue, brain, lung, heart,
and muscle. In the brain, they manifest as
a
space-occupying
lesion.
Living
cysticerci do not cause inflammation, but
when they die they can release substansis
that provoke an inflammatory response.
Taenia saginata

causes taeniasis saginata.
Distribution: occur worldwide
but is endemic in areas of Asia,
South America, and eastern
Europe.
 Morphology. T. saginata can be
indentified by its scolex with 4
suckers without
hooklets. Its
gravid proglottids have 17-35
primary uterine branches. Larva
of T.saginata called cysticercus.
 Transmittion: fecal-oral
 Invasive stage: cysticerci

Life cycle.
 Definitive hosts -humans
 Intermediate hosts - cattle Humans
can be infected by eating raw or
undercooked beef containing larvae.
Laboratory diagnosis: gravid proglottids
(with 17-35 uterine branches) may be
found in the stools.
 Prevention. Prevention of taeniasis
saginata involves cooking beef
adequately and preventing cattle from
ingesting human feces by disposing of
waste properly.
 Clinical
manifestation of teniasis
saginata:
 abdominal pain,
 nausea,
 diarrhea,
 weight loss,
 infection may by asymptomatic.
 In some, proglottids appear in the
stools and may even protrude from
the anus.
Diphyllobothrium latum, the fish tapeworm,
causes diphyllobothriasis
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Distribution: Scandinavia, northern
Russia, Japan, Canada, USA.
Morphology. Diphyllobothrium latum
can be indentified by its scolex with 2
elongated sucking grooves by which
the worm attaches to the intestinal
wall.
The proglottids are wider than they
are long, and the gravid uterus is in
the form of a rosette.
Adult worm is the longest of the
tapeworms, measuring up to 13 m.
Larva called plerocercoid.
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Transmittion: fecal-oral.
Invasive stage:
plerocercoid.
Definitive hosts- humans
.
Intermediate hosts
-1)copepod crustacea
-2) freshwater fish
Humans infected by
eating
raw
or
undercooked
fish
containing plerocercoids
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Clinical disease: infection by D.latum causes little
damage in the small intestine.
In some individuals, megaloblastic anemia occurs as
a result of vitamin B12 deficiency caused by
preferential uptake of the vitamin by the worm.
Most patients are asymptomatic, but abdominal
discomfort and diarrhea can occur.
Diagnosis depends on finding the typical eggs, oval,
yellow-brown eggs with an operculum (lidlike
opening) at one end, in the stools.
Prevention involves adequate cooking of fish and
proper disposal of human feces.
Hymenolepis nana (dwarf tapeworm) is found
worldwide, commonly in the tropics.
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Morphology. It is only 2-3 cm in
length. Scolex has round form and
contain suckers and hooks.
A neck is very long and thick.
Strobila has 200 proglottides.
The uterus has an excretory ostium.
Eggs are released from it into the
feces.
Transmission: fecal-oral (by the
ingestion
of
eggs
from
contaminated food or water).
Invasive stage: egg.

Life cycle.
 The eggs of H. nana are directly
infectious for humans;
 ingested eggs can develop into adult
worms without an intermediate host.
 Within the duodenum, the eggs hatch
and differentiate into cysticercoid
larvae and then into adult worms.
 Gravid proglottids detach,
disintegrate, and release fertilized
eggs.
 The eggs either pass in the stool or
can reinfect the small intestine
(autoinfection). A lot of H.nana
worms (sometimes hundreds) are
found.

Clinical disease: asymptomatic, but diarrhea
and abdominal cramps may be present.
 Diagnosis can be proved by observing eggs in
stool.
 Prevention consists of good personal hygiene
and avoidance of fecal contamination of food
and water.
Echinococcus granulosus (dog tapeworm)

is found primarily in shepherds living in the
Mediterranean region, the Middle East, and
Australian, USA (western states).
 Morphology. Worm is up to 3-5 mm. Scolex has
suckers and hooks. A neck is short. Strobila has 35 proglottides. Posterior segment (mature) is the
largest and contains uterus with the haustrums,
genital pore situated in the back of the proglottid.


Transmission: fecal-oral
Invasive stage: egg
 Life cycle.
 Definitive hosts: dogs.
 Intermediate hosts: sheep,
humans.

Diagnosis: made by Clinical
manifestations. asymptomatic,
but liver cysts may cause hepatic
dysfunction. Cysts in the lungs
can erode into a bronchus,
causing bloody sputum, end
cerebral cysts can cause
headache and focal neurologic
sings.
 Diagnosis: made by routine Xray, observation of eosinophilia,
serologic tests.
 Prevention of human disease
involves not feeding the entrails
of slaughtered sheep to dogs.
Echinococcus multilocularis

Distribution: is found in
northern Europe, Siberia,
Canada, the USA.
 Many of the features of this
organism are the same as those
of E. granulosus,
 but the definitive hosts are
mainly foxes and the
intermediate hosts are various
rodents. Humans are infected
by accidental ingestion of food
contaminated with fox faeces.

The disease occurs primarily in
hunters and trappers. Within
the human liver, the larvae
form multiloculated cysts with
few protoscoleces, proliferate,
producing a honeycomb effect
of hundreds of small vesicles
(without fluid).
 The clinical picture usually
involves jaundice and weight
loss. The prognosis is poor.
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