Trematodes

Veterinary Parasitology V.M 343

 Trematodes Cestodes Nematodes Protozoa

Platyhelminthes
Multi-cellular worms
flattened dorsoventrally incomplete (or no) digestive system.

Body is not truly segmented. Three main groups that are parasitic
Monogenes and Aspidobothrea Trematodes (flukes) Cestodes (Tapeworms)

Class Trematoda
Subclass Monogenea
not important in veterinary medicine

Subclass Digenea
includes all flukes parasitic in domestic animals life cycle requires 1 or more intermediate hosts
first intermediate host usually a mollusk

Monogene

Digenes

Cestodes

Digenetic trematodes

monostome

distome

amphistome

Features of digenetic trematodes

Body is flattened dorso-ventrally
non-segmented leaf-like shape Vary in size from 1 mm to several cms

External covering or tegument

metabolically active (absorption/secretion) often has spines has a glycocalyx or CHO coat

Features of digenetic trematodes

Lack a body cavity
organs suspended in parenchyma

Muscle layers beneath tegument

sluggish locomotion

Usually possess two suckers for attachment to host

anterior = oral sucker ventral = acetabulum

Features of digenetic trematodes

Most are hermaphroditic
a few have separate sexes usually undergo self-fertilization dense eggs detected by sedimentation

Life cycle has up to five larval stages

miracidium sporocyst (+ daughter sporocysts) redia (+ daughter redia) cercaria metacercaria

Digene Life Cycle

Complex life cycles with at least two hosts and several life cycle stages First Intermediate Host is almost always a snail. Some have another aquatic animal or plant as a second intermediate host. Definitive host is usually eats the second intermediate host.
Except Schistosoma sp.

Digene Life Cycle - Egg

Not an ovum but a developing embryo
Already fertilized and ready to hatch into new organism

Most digene eggs have an operculum

Except Schistosoma

Digene Life Cycle Miracidium

Covered in cilia, slipper shaped Leaves the egg, swims around looking for first intermediate host, a snail. Burrows into the first intermediate host and loses the cilia
Turns into a sporocyst or redia

Digene Life Cycle - Sporocyst

When miracidium finds a snail, it penetrates its mantle and turns into a sporocyst Sac of embryos; it releases embryos into the snail Embryos can become sporocyst, redia, or cercaria

Digene Life Cycle - Redia

Similar to a sporocyst but has a pharynx and small digestive system More mobile than sporocyst Makes embryos which can turn into redia or cercaria

Digene Life Cycle - Cercaria

Leaves the snail to find next host Looks like a miniature adult with a tail Tail for swimming
Loses tail as it penetrates next host Schistosoma cercaria have forked-tails

Digene Life Cycle - Metacercaria

Resting stage of the life cycle Miniature adult curled up in a tissue cyst.
Looks like a bubble on body wall

Waiting for intermediate host to be eaten by definitive host.

Digene Life Cycle - Adult

Typical digene adults are flat, leaf-shaped
Male and female organs in same individual

Adult Schistosoma are round

Sexes are separate Males are larger than females
Arrows point to female

Digene Life Cycle

Egg Adult Miracidium Metacercaria Daughter sporocyst Cercaria Daughter Redia Redia Sporocyst

Fasciola hepatica

Definitive Host: Herbivorous mammals. Occasionally humans. First Intermediate Host: Aquatic snails Lymnea cailliaudi and L. stagnalis Second Intermediate Host: None. Metacercaria form on aquatic plant or water column.

Fasciola hepatica

Geographic Distribution: Cosmopolitan. Transmission to D.H.: Ingestion of metacercaria. Human infections usually come from ingestion in water or on water cress. Location in Definitive Host: Liver, particularly bile duct.

Fasciola hepatica Life Cycle

Adult in liver Penetrates intestinal wall and migrates Excysts D.H. ingests metacercaria
Metacercaria on vegetation or in water column

Eggs go out in feces

Miracidium hatches in water

Penetrates a snail Sporocyst Mother Redia Daughter Redia

Leaves snail

Cercaria

Pathogenesis - F. hepatica
Associated with larval migration
damage cumulative (esp. small ruminants) severity determined by numbers
hemorrhage + death if high number of larvae penetrate liver capsule

migration in liver destroys parenchyma & produces hemorrhagic tracts that become fibrotic ( liver rot ) reduced capacity to produce albumin

Pathogenesis - F. hepatica
Associated with adults in bile ducts:
Anemia
Blood-sucking activity Produce proline that inhibits erythropoiesis

Damage bile duct epithelium

due to fluke activity (movement, spines) causes leaky epithelium that results in:
additional blood loss (RBCs and plasma proteins) anemia, hypoproteinemia, hypoalbuminemia

bile duct hyperplasia, fibrosis and calcification ( pipestem liver )

Clinical signs- F. hepatica

Acute fascioliasis
associated with massive larval migration in liver anorexia, depression, weakness
possible sudden death in < 48 hrs after onset of signs

more common in small ruminants seasonal

Clinical signs - F. hepatica

Chronic fascioliasis: adults in bile ducts
anemia, pale mucous membranes + icterus submandibular edema ( bottle jaw ) disrupted digestion p poor-doer
loss of condition, decreased production, etc.

possible death-more likely in sheep cattle more resistant than sheep NON-seasonal
liver damage cumulative

Fasciola hepatica

Diagnosis: Eggs in feces, ELISA test. Treatment: Rafoxanide is drug of choice for livestock and humans. Clorsulon combined with Ivermectin or Albendazole. *bithinol *periodic ivomic is advisable

Fasciola hepatica Notes

Pasture rotation important to reduce infection of livestock. A closely related species, F. gigantica, also infects humans and cattle.

Dicrocoelium lanceatum
Definitive Hosts: Sheep, cattle, goats, pigs and cervids.
Humans rarely infested. 45% of cattle in Switzerland infected

First Intermediate Hosts: Land snails Second Intermediate Host: Ants Geographic Distribution: Throughout Europe and Asia.
Few pockets in U.S. and Australia (recent introduction)

Dicrocoelium lanceatum

Location in DH: Bile Ducts. Transmission to D.H.: D.H. eats infected ant. Pathology and Symptoms: Can cause bile duct obstruction and typical liver problems. Diagnosis: Egg is in feces. Treatment: bithionol and thiabendazole in sheep, Praziquantel in humans.

Adult in bile duct

Egg out in feces

Eggs eaten by snail

Miracidium hatches in snail Sporocyst

D.H. ingests ant with grass Ant climbs to top of grass blade Few encyst in ants brain Metacercaria in hemocoel

Dicrocoelium dendriticum Life Cycle

Daughter sporocyst Cercaria

Ant eats delectable slime ball

Released in slime ball

Migrates to antle cavity

Clinical signs and lesions

Hosts develop little immunity
can accumulate >50,000 adults

Lesions
Bile ducts thickened and distended Liver cirrhosis pcondemned at slaughter

Usually no clinical signs

can develop anemia, emaciation and edema with large numbers of parasites

Diagnosis, treatment & control of D. dendriticum Usually diagnosed at necropsy or slaughter Treatment
nothing approved for use albendazole or clorsulon only products with efficacy against flukes
efficacy against D. dendriticum unknown

Heterophyes heterophyes
D.H: humans and other fisheating mammals First I.H.: Aquatic snails Second I.H.: Fish or amphibians Geographic Range: Middle East, northern Africa, Asia Minor, Far East including Korea, China, Japan, Taiwan, and Philippines

Heterophyes heterophyes
Mode of Transmission: Eating undercooked or raw fish Location in D.H.: Small intestines. Pathology: Mild inflammatory response. Heavy infections damage the mucosa and can penetrate it. Then eggs go to other locations, including heart, brain, lymph nodes, etc.

Heterophyes heterophyes
Symptoms: Heavy infections can cause intestinal pain and mucous diarrhea.
Eggs in heart cause tissue reactions that can lead to valve damage and cardiac arrest
14.6% of cardiac arrest in Philippines due to this worm

Eggs in brain and spinal cord can also be fatal. Adult worms have also been reported in heart and brain.

Diagnosis: Difficult. Eggs resemble other intestinal species. Need adult worm. Treatment: Praziquantel Notes: All species of Heterophyes are infective to humans

Adult in small intestine Matures Excyst in duodenum

Egg out in feces

Eggs eaten by snail

Miracidium hatches in snail Sporocyst Redia

Heterophyes heterophyes Life Cycle

Daughter redia

Fish eaten by D.H. Metacercaria in muscle Cercaria burrows into skin of fish Hangs in water column

Cercaria

Leaves snail

Echinostoma revolutum

Definitive Host: Ducks, goose, aquatic birds, pigeon and rarely human. First Intermediate Host: Snails, fish, or frogs. Second Intermediate Host: Fish and tadpoles

Echinostoma sp.

Geographic Distribution: world wide and present in the Middle East. Location in intermediate host: intestines or bile duct. Pathology and Symptoms: harmless unless heavily infested.

Echinostoma sp.

Life cycle Eggs 3w----Miracidium snail or fish----host swallow infected snail or fish. Diagnosis ----eggs in feces Treatment Oxycyclozanide Bithianol

Rumen flukes
Digenetic trematodes: paramphistomids Paramphistomum cervi
cattle, wild cervids more common in deer and moose

Cotylophoron spp.
sheep, goats

Structure
~1 cm long with sucker at each end Attach to host with ventral sucker Body
pinkish when fresh stout & conical, or globular look like large rice krispies

Life cycle - paramphistomes

Adults
attached to mucosa of rumen or reticulum Eggs passed in feces hatch to miracidium

Enter snail intermediate for asexual reproductionpcercaria emerge encyst on vegetation as metacercaria
ingested by new host

Life cycle - paramphistomes

In definitive host:
Metacercaria excysts in duodenum Enters duodenal mucosa Emerges to lumen and migrates cranially to rumen/reticulum mature to egg-laying adults

Clinical signs
immature stages migrate in gut mucosa
cause inflammation, hemorrhage, diarrhea, anemia, dehydration, possible death

Diagnosis of rumen flukes

Detect eggs in feces by sedimentation Very similar to eggs of Fasciola hepatica Rumen fluke eggs are:
Large, ellipsoidal with operculum at 1 end larger than liver fluke eggs (160Q vs. 140Q) pale grey-green
liver fluke eggs are golden yellow brown

Treatment of rumen flukes

Not usually treated unless also infected with liver flukes Albendazole & clorsulon only anthelmintics effective against flukes
not effective against paramphistomes if treat dual fluke infection and recheck fecal may think liver flukes were not eliminated

Schistosoma

Very different from most sp. digenes

Sexes are separate Adults are round, not flat Eggs have no operculum Cercaria have forked tail

But have some characteristics of digenes

Two suckers Same integument Incomplete digestive tract Snail Intermediate host Same life cycle stages
Except no metacercaria or redia

Schistosoma sp.
Schistosoma haematobium Schistosoma mansoni Schistosoma japonicum

Schistosoma mansoni

Definitive Hosts: Humans, and many wild mammals including monkeys and rodents. First Intermediate Host: Aquatic snails Second Intermediate Host: None Geographic Distribution: Africa and South America.
Spread to South America with the slave trade.

Schistosoma mansoni

Transmission to D.H.: Cercaria burrow into the skin. Location in D.H.: Portal veins of the large intestine. Pathology: Most pathology is due to the body s inflammatory response to the eggs. Eggs have a sharp lateral spine so they tend to lodge in the liver. The body walls them off in granulomas, reducing liver function.

Schistosoma mansoni

. Symptoms: Causes Schistosomiasis. Three Phases

Migratory cercaria migrating to right place Usually asymptomatic Acute Adults start making eggs Fever, chills, fatigue, headache, malaise, muscle aches, and gastrointestinal discomfort. Chronic Occurs where parasite is endemic. Ascites, enlargement of spleen and liver, dwarfism

Diagnosis: Eggs with lateral spine in the feces, usually in float. ELISA test Treatment: Praziquantel Prevention: Proper sanitation, killing snail host, staying out of water.

Adults in veins of the large intestine Mature

Eggs go out in feces

Eggs hatch in water

Miracidium Penetrates snail

Large Intestines Liver Heart

Schistosoma mansoni Life Cycle

Goes to peripheral blood vessels Penetrates skin of D.H. Leaves snail

Sporocyst

Daughter Sporocyst

Cercaria

Schistosoma haematobium
Definitive Hosts: Humans. Very host specific with no known reservoir hosts. First Intermediate Host: Aquatic snails Second Intermediate Host: None Geographic Distribution: northern Africa and small area of Middle East. Transmission to D.H.: Cercaria burrow into the skin.

Control of Schistosomiasis
Education
Educate the people to the danger Try to keep them from defecating/urinating in the same water they bathe in

Chemotherapy
Praziquantel can help prevent infections as well as cure them

Vector control
Mostly focused on eliminating the snail Snail-eating fish, competitor snails, chemical molluscicides Better environmental practices

Vaccination
Still in the developmental stages