Platyhelminthes/cestoda: Class Trematoda, Order Echinostomatida Flashcards
Describe trematodes broadly. (4)
called Flukes
Oval or leaf-like body.
Length from few mm to few cm.
Tegument with small spines.
Trematoda Attachment organs
muscular suckers
(oral sucker and ventral sucker)
Trematode Gastrointestinal tract
Starts with mouth, followed by muscular pharynx and esophagus.
Intestine is ring-like or consists of two blind-ending branches.
Digested material is expelled through mouth.
Excretory system – two longitudinal canals.
Products are excreted through excretory pore.
Describe trematode Reproductive system
occupies most of the body – hermaphrodites
define Heteroxenous life cycle
The indirect parasite life cycle is known as the heteroxenous life cycle. Here, the parasite has a definite host and an intermediate host.
So reproduction and maturation happen within the definitive host, while the intermediate stage is the carrier stage, in which the parasite is trematodes typically undergo a series of developmental stages.
These stages may involve the formation of larval forms known as cercariae, which emerge from the intermediate host and seek out the definitive host for further development and reproduction.
Within the intermediate host, these larvae may migrate through various tissues or organs, potentially causing damage or pathology depending on the species and location within the host’s body.
In the Heteroxenous life cycle with intermediate hosts - what are they typically?
molluscs as intermediate host
Flukes or trematodes typically invade what organs of their mammalian hosts?
Parasites of intestine, liver, bile, lungs, bladder and blood vessels.
Causes trematodoses.
Trematoda life cycle.
Egg hatches a miracidium (larva)
The larva enters a snail host
Develops into sporocyst within snail
Becomes another form of larva (redia)
Transforms into cercaria (swimming form of larva)
Leaves the snail, finds some herbage to hang out on
Becomes a metacercaria while it waits to be eaten by a ruminant
Eaten by sheep in which it then becomes adult fluke and can produce eggs
miracidium
sporocyst
cercaria
metacercaria
Trematode life cycle forms:
miracidium - I stage larva
sporocyst - II stage larva
cercaria – III stage larva
metacercaria - encysted cercaria
then becomes adult
Genus Fasciola, Fascioloides:
Class
Order
Family
Trematoda:
Order Echinostomatida
Family Fasciolidae
Genus Fasciola, Fascioloides
Fasciolosis is a parasitic disease caused by the common liver fluke from the
family
Fasciolidae, which occurs mainly in ruminants and is common in moist, swampy areas.
The course of the disease is acute or chronic.
Three important tremtode genera:
Fasciola
Fascioloides (magna)
Fasciolopsis (buski)
Name 2 main species of Fasciola genera flukes.
Fasciola hepatica
F. gigantica
Other genera:
(Fascioloides magna)
(Fasciolopsis buski)
Final hosts of flukes:
mainly ruminants
Other may serve as reservoirs (e.g. horses, donkeys)
Intermediate host of flukes:
mud-snail (genus Lymnaea)
Fasciola hepatica aka common liver fluke:
Life cycle dependent on the presence of?
The incidence of fasciolosis is highest…?
Life cycle dependent on the presence of the snail and on the climate.
The incidence of fasciolosis is highest in years with heavy rainfall.
Fasciola hepatica aka common liver fluke:
Distribution:
Seasonality:
Distribution: Worldwide
Seasonality outbreaks, highest in years with heavy rainfall.
Fasciola hepatica aka common liver fluke:
Habitat in final host?
Habitat in final host: Liver bile ducts, ruminants.
Transmission of Fasciola hepatica aka common liver fluke:
Ruminants ingest parasite larva (metacercaria) from off plants.
What is meant by summer infection of the snail?
Summer infection is more important than winter infection.
Rainy summer - high development
Larvae ingested by sheep in August
Acute disease in early autumn, can cause sudden deaths.
What is meant by winter infection of the snail?
Summer infection is more important than winter infection.
Winter: Rainy autumn - many larvae in spring
Larvae ingested in late spring
Disease in late summer versus acute disease in autumn caused by summer infection.
Liver fluke Development inside final host:
- After ingestion flukes penetrate intestinal wall - enter peritoneal cavity and migrate to liver.
- Young flukes migrate in liver parenchyma for 6-8 weeks.
- Then mature and produce eggs in bile ducts.
Fasciola hepatica aka common liver fluke:
Prepatent period
Patent period
Complete life cycle takes at least
Prepatent period 2-3 months
Patent period 5 months to years
Complete life cycle takes at least 3-4 months
Fasciola hepatica aka common liver fluke pathogenesis depends on:
Number of metacercariae ingested
Parasite developmental stage
Species of host
Two-fold pathogenesis:
Young parasite migration causes liver damage.
Adult parasite in the bile ducts causes:
- haematophagic activity
- biliary mucosa damage
Describe acute Fascioliasis. (5)
Require ingestion of very large numbers of larvae.
Disease occurs 2-6 weeks after infection.
Destruction of the liver parenchyma and blood vessels by migrating flukes occurs.
In autumn or early winter – sudden death.
Concurrent secondary infection with Clostridium novyi – „black disease“.
Describe subacute Fascioliasis. (4)
Parasites ingested over a longer period.
Some larvae migrating and some in bile ducts.
Symptoms occur 6-10 weeks after infection - anemia (which is why the famacha conjunctiva color guide is used), hypoalbuminaemia.
Occurs in Late autumn or winter.
Describe chronic Fascioliasis.
Most common form.
Symptoms seen 4-5 months after ingestion of larvae.
Late winter or early spring typically.
Clinical signs of acute fascioliasis.
Often seen in sheep, llamas, alpacas.
Subclinical in cattle
Acute signs:
sudden death during autumn
weakness
pale mucous membranes, anemia (famacha)
dyspnea
enlarged liver upon palpation
painful abdomen
Clinical signs of chronic fascioliasis.
progressive loss of condition
anemia (famacha)
lowered appetite - indigestion
reduced milk production
„bottle-jaw“ - submandibular oedema due to loss of plasma protein (hypoalbuminemia)
wool problems
Primarily later autumn/winter.
bottle jaw due to hypoalbuminemia
What species quire resistance to fascioloiasis?
sheep do not appear to develop resistance but cattle seem to acquire partial resistance.
Post-mortem findings in fascioloiasis?
I phase: migrating flukes destruction of liver tissue; Internal hemorrhages
II phase: adults in bile duct; Ingestion of blood; damaging mucosa of ducts
Acute dz
liver enlarges, fibrinous deposits
Chronic dz
Cirrhosis, thickened, large bile ducts;
2/3 liver damage results in liver
condemnation in slaughterhouses
„Bottle-jaw“ differential diagnoses other than liver flukes: (4)
Heart failure
Abscesses
Tumors
Other parasites, mainly nematodes
Describe liver fluke eggs.
Shape:
Content:
Shell:
Color:
Size:
Shape: ellipsoidal, operculated
Content: granular, larva inside
Shell: thin shell
Colour: yellow brown
Size: 130-150 µm
Examination of blood/serum in fascioliasis may reveal: (2)
Raised liver enzymes (GLDH and GGT).
Serology - bulk tank milk ELISA for herd screening. (Enables detection 2-4 weeks post infection.)
Serology - copro antibody ELISA (Enables detection 6-8 weeks p.i.).
Methods for Detecting the eggs of liver flukes?
Faecal sedimentation method
NB: no eggs in faeces in acute fascioliosis!
Can detect only patent infection
Treatment of liver flukes.
Various flukicides or broad-spectrum antihelminthics.
Such as:
Triclabendazole
Albendazole
Clorsulon + Ivermectin
Have Varying efficacy against different
stages of parasite.
Prevention and control of liver flukes.
Reduction of snail populations with Strategic drenching
Meteorological forecasting
- avoid grazing during high risk period
- fencing snail habitats
Metaphylaxis with anthelmintics
- Animals in high risk areas
- Early Spring - adult stages
- Late Autumn - juvenile stages
Forms of disease in F.hepatica.
acute
subacute
chronic
sheep, alpacas, llamas prone to acute/subacute
cattle prone to chronic
2 main families belonging to fluke order echinostomatida?
fasciolidae &
paramphistomatidae
rumen fluke infection also known as?
Paramphistomiosis - rumen fluke infection
Paramphistomosis is a parasitic disease caused by the young forms of Paramphistomum cervi (rumen fluke), that migrate in
the mucosa of the small intestine and forestomach of ruminants, and by the adults that attach to the wall of the foregut.
The disease is common in moist pastures.
Rumen fluke caused by?
Paramphistomum cervi
(Synonym: P. explanatum)
Final hosts of Paramphistomum cervi/rumen fluke? (2)
ruminants, wild cervids
Intermediate hosts of Paramphistomum cervi/rumen fluke?
aquatic snails: Planorbidae and Lymnaeidae
Morphology of Paramphistomum fluke spp.
Non-typical trematode, conical and maggot-like.
Adults pear-shaped.
Size:
adults up to 15mm
juveniles 1-3mm long
Color is pink when young, brownish when adult.
Epidemiology/seasonality of Paramphistomum fluke spp. (rumen fluke)
More prevalent in tropical regions.
Mostly prevalent in moist, swampy pastures.
More at the end of rainy summers.
Eggs destroyed during winter, but in snails the larva can winter successfully.
Prevalence increases with age in sheep and goats.
Predilection site Paramphistomum fluke spp. (rumen fluke):
adults in
juveniles in
adults in forestomach
juveniles in duodenum
Life cycle of the rumen fluke is similar to that of the…?
Life cycle similar to liver fluke.
The time from egg hatching to a mature adult releasing eggs is about 95 days.
Life cycle of Paramphistomum fluke spp. (rumen fluke):
Different development in the final host:
* Young flukes remain in small intestine for 3-6 weeks.
* Then travel to forestomach to mature while burrowed into mucosa.
Prepatent period 7-14 weeks
Clinical signs Paramphistomum infection (rumen fluke):
Uncommon in domestic livestock. Signs seen in young cattle with heavy infection.
Signs 1 month after infection:
severe enteritis
profuse diarrhea
anorexia
polydipsia
unthriftiness
edemas
Paramphistomum juveniles burrowing into the
mucosal and submucosal layers of the duodenum can cause
necrosis & hemorrhage which contribute to the clinical signs of enteritis, diarrhea etc.
identify these eggs
left: F.Hepatica, liver flukes
right: P. cervi, rumen fluke
Eggs detected by fecal sedimentation method.
Significant Order belonging to Trematoda other than Echinostomatida?
Order Plagiorchiida
Trematode family to belong to Order Plagiorchiida
Family Dicrocoelidae
(Genus Dicrocoelium)
Dicrocoeliosis is a chronic parasitic disease caused by
a small lancet fluke (Dicrocoelium dendriticum) that mainly parasitizes the bile ducts and gall bladder of ruminants, and is common in hilly and dry pastures.
Geographical distribution of lancet fluke/Dicrocoelium dendriticum
Worldwide (except South Africa and Australia)
target organs of lancet fluke/Dicrocoelium dendriticum
Biliary and pancreatic ducts of their final hosts (mainly ruminants)
Final hosts of lancet fluke/Dicrocoelium dendriticum
mainly ruminants (Occasionally others)
possible zoonosis
Intermediate hosts of the lancet fluke/Dicrocoelium dendriticum
I * land snail (Zebrina detrita)
II * brown ant (Formica fusca)
possible zoonosis
Transmission of the lancet fluke/Dicrocoelium dendriticum.
Ingestion of metacercaria in ants
Life cycle of the lancet fluke/Dicrocoelium dendriticum.
- Egg hatches inside snail
- Snail produces slime balls with larvae
- Larvae mass ingested by ants
- Inside the ant body cavity/brain larva develops
Transmitted to final ruminant host via ingestion of infected ants
In final host
* Young flukes migrate from small intestine to bile ducts
* No parenchymal migration
Life cycle around 6 months
Patent period several years
Clinical signs of Dicrocoelium dendriticum infection.
Often absent in cattle and sheep. No immune reaction in cattle, sheep, goats thus accumulate flukes.
Severe signs in older sheep, alpacas & llamas:
Acute decline in condition
Anemia
Edema
hypothermia
Emaciation
Reduced wool growth
Decreased lactation
Weight loss
Post mortem signs of Dicrocoelium dendriticum infection.
Livers relatively normal because absence of migration in the liver parenchyma, does not suck blood.
In Severe cases:
Liver fibrosis or cirhoses, thickened bile ducts, abscesses, granulomas
Describe the eggs of Dicrocoelium dendriticum.
Shape:
Content:
Shell:
Color:
Size:
Shape: asymmetrical, oval one
side flattened, with operculum
Content: larva (miracidium)
Shell: thick shell
Colour: dark brown
Size: 35-40 µm
Diagnostic methods for diagnosing Dicrocoelium dendriticum infection. (2)
Faecal flotation method (ZnSO4)
Sedimentation method
Treatment of Dicrocoelium dendriticum.
Higher doses of anthelmintics:
Albendazole
Netobimin
Praziquantel
Prevention and control of Dicrocoelium dendriticum.
Difficult to control, because of the longevity of the eggs, they also survive drying of hay.
Also, Wide distribution of intermediate hosts and plenty of reservoir hosts.
Prevention:
Snail chemical control with molluscicides are ecologically not recommended. Instead keeping ducks, turkeys, chickens to eat snails.
Covering ant nests with tree branches.
Preventing animals from grazing early morning and late evening.
Dicrocoelium dendriticum size
Really small flukes
Name the 4th important order of Trematoda that is not listed here,
Echinostomatida
Plagiorchiida
Strigeidida
Opisthorchiida
Opisthorchiosis is a parasitic disease caused by trematodes from the genus Opisthorchis, which mainly parasitize the
bile ducts and gall bladder of carnivores, and is characterized by chronic inflammation of the bile ducts tissue and liver.
Cat liver fluke in latin?
+ alt. name?
Opisthorchis felineus
Cat liver fluke = siberian liver fluke
Final host of Opisthorchis felineus
This is the Cat liver fluke.
Final host: humans, dogs, cats
Intermediate host of Opisthorchis felineus
This is the Cat liver fluke.
Intermediate hosts:
1. IM host: freshwater snail
2. IM host: freshwater fish (carp)
Transmission of the Cat liver fluke.
Infection by eating infected raw fish.
Distribution of the cat liver fluke.
worldwide
Opisthorchis felineus also present in Europe.
Other species prevalent in Asia/India.
Opisthorchis felineus location inside final/paratenic host:
cat liver fluke
Location in final/paratenic host:
- biliary or pancreatic ducts
- small intestine
Clinical signs of cat liver fluke in cats & dogs:
Can be mild to severe, depends on the infection duration.
In chronic and severe cases:
epithelial hyperplasia
mild to severe fibrosis
carcinomas in the liver/pancreas
cholecystitis
diarrhea or constipation
weakness to exhaustion
coma, death
Diagnostic methods for detection of Opisthorchis felineus/cat liver fluke.
fecal sedimentation method
Treatment for Opisthorchis felineus/cat liver fluke
praziquantel or fenbendazole
- for 6 days and 3x10 days interval
Describe the eggs of Opisthorchis felineus/cat liver fluke.
Shape:
Content:
Shell:
Colour:
Size:
Shape: flattened one end with
operculum, knob on other side
Content: larva (miracidium)
Shell: thick dark shell
Colour: light brown
Size: 30x15 µm
Alariosis is a parasitic disease of the
small intestine of
carnivores, caused by worms of the genus Alaria, in which gastro-intestinal inflammation and lung damage occur.
Alaria alata can cause what disease?
Alariosis
Definitive hosts of Alaria alata:
wolves, foxes, dogs
(Common in feral animals)
Intermediate hosts of Alaria alata:
- IM hosts: freshwater snails
- IM hosts: tadpoles
Reservoir hosts of Alaria alata:
snakes, mice, birds
Dead-end hosts of Alaria alata:
humans
Alaria alata Localisation in the final host:
small intestine.
Young flukes migrate to the diaphragm &
lungs causing pulmonary hemorrhages.
Definitive/final hosts: wolves, foxes, dogs
