Medical Helminthology. Flatworms - human parasites.

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Medical Helminthology. Medical Helminthology. Flatworms - human parasites Flatworms - human parasites

Transcript of Medical Helminthology. Flatworms - human parasites.

Page 1: Medical Helminthology. Flatworms - human parasites.

Medical Medical Helminthology.Helminthology. Flatworms - human Flatworms - human

parasitesparasites

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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).

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GGeneral characteristic of Flatworms (Phylum eneral characteristic of Flatworms (Phylum

Plathelminthes)Plathelminthes) The flatwotms consists of some 12, 200 species, including classes of

parasitic worms: Trematoda, Cestoda

All flatworms are acoelomate, triploblastic, and bilaterally symmetrical.

flattened dorsoventrally

they have a definite head at the anterior end.

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.

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.

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General characteristic of Class Trematoda General characteristic of Class Trematoda   - Flattened dorsoventrally

(leaf-like).  - 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.

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BLOOD FLUKESBLOOD FLUKES - - genus genus

SCHISTOSOMASCHISTOSOMA 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.

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BLOOD FLUKESBLOOD FLUKES Transmission: infection

through skin of larvae from snail hosts.

Infective stage: cercariae.

Intermediate host: snail.

Definitive host: man.

Mode of transmission: penetration of skin by cercarie.

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BLOOD FLUKESBLOOD FLUKES 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.

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BLOOD FLUKESBLOOD 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.

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LLUNGUNG FLUKE FLUKE:: PARAGONIMUS PARAGONIMUS WESTERMANI – WESTERMANI –

an agent of paragonimiasisan agent of paragonimiasis Distribution: Far East, Central

America, Africa, and India.Morphology: an egg-like form

of the body, from 7,5 to 16 mm.

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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

LLUNGUNG FLUKE FLUKE

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LLUNGUNG FLUKE FLUKE

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.

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BILIARY (LIVER) BILIARY (LIVER) FLUKESFLUKES CLONORCHIS

SINENSIS – oriental small biliary (liver) fluke, causes Clonorchiasis.

Distribution: endemic in Far East, China, Japan, and Vietnam.

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CLONORCHIS SINENSISCLONORCHIS SINENSIS Localization: bile

ducts, gallbladder, and pancreas.

Morphology: the adult worms are 1 to 2 cm; the eggs are small, brownish.

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CLONORCHIS SINENSISCLONORCHIS SINENSIS Transmission: fecal-oral

(ingestion of contaminated raw, frozen, dried, pickled, and salted fish, which contain metacercariae).

Infective stage: metacercariae.

Intermediate hosts: 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 SINENSISCLONORCHIS SINENSIS Clinical disease: 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 HEPATICAFASCIOLA HEPATICA 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.

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FASCIOLA HEPATICAFASCIOLA HEPATICA Life-cycle: Final host - herbivorous

mammals (horses) and humans.

Intermediate host — the snail Limnea truncatula.

Transmission: fecal-oral (ingestion of water , some non-water plants and vegetables, which contain adolescariae).

Invasive stage: adolescariae.

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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.

FASCIOLA HEPATICAFASCIOLA HEPATICA

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OPISTHORCHIS FELINEUSOPISTHORCHIS FELINEUS 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.

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OPISTHORCHIS FELINEUSOPISTHORCHIS FELINEUS Life-cycle: 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.

Invasive stage: metacercariae cysts in fish muscles.

Localization: bile ducts, gallbladder, liver.

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OPISTHORCHIS FELINEUSOPISTHORCHIS FELINEUS 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.

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.

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DICROCOELIUM LANCEATUM DICROCOELIUM LANCEATUM – – causes Dicrocoeliasis.causes Dicrocoeliasis. Distribution: worldwide.

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.

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DICROCOELIUM LANCEATUMDICROCOELIUM LANCEATUM Invasive stage: metacercariae. Life-cycle: 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)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.

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Taenia soliumTaenia 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.

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Taenia soliumTaenia soliumLife cycle 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.

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Taenia soliumTaenia 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.

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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

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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.

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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.

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Diphyllobothrium latum, the fish tapeworm, causes diphyllobothriasis

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.

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Hymenolepis nana (dwarf tapeworm) is found

worldwide, commonly in the tropics. 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.

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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.

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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.

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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 3-5 proglottides. Posterior segment (mature) is the largest and contains uterus with the haustrums, genital pore situated in the back of the proglottid.

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Transmission: fecal-oral Invasive stage: egg Life cycle. Definitive hosts: dogs. Intermediate hosts: sheep,

humans.

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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 X-ray, observation of eosinophilia, serologic tests.

Prevention of human disease involves not feeding the entrails of slaughtered sheep to dogs.

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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.

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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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