3. Digenea, cestoda, acanthocephala

THEORY

1.    Morphology, classification and life cycle of DIGENEA and MONOGENEA.  Platyhelminthes, classification, characteristics, life cycle 

Phylum: Plathyhelminthes (20 000 species of flatworms)

Subphylum: Trematoda,

Class: Monogenea, Cestoda

Subclass: Digenea

DIGENEA - trematodes, parasitic flukes/flatworms.

Morphology:

• dorsoventrally flattened, oval/round, ranges in size from 1-2 mm up to 10-15 cm.

• oral and abdominal (acetabulum) suckers for attachment.

• Most are hermaphrodites - few exceptions like schistosoma (separate sexes).

  • both sexes - male has 2 testes, female has one ovary, short oviduct and uterus. Yolk is stored in vitelline cells - glands.

• Tegument for nutrient absorption, ladder-like nervous system, incomplete digestive system. Diffusion breathing (circulatory, resp. system missing). Excretory by flame cells + coll. ducts

Location: Endoparasites. Found in most vertebrate groups, often in the GIT, liver or bile duct. Worldwide.

Digenea Life cycle: complex, one or more IH (typ. mollusk as the first (aquatic). FH usually eats IM.

• asexual reproduction - IM

• Sexual reproduction - FH

• eggs are often unembryonated, develops outside host.

• Digenea larval stages:

  1. Miracidium - ciliated larvae that seeks mollusk host

  2. sporocyst

  3. rediae - within mollusk

  4. cercariae - juvenile form with a tail

  5. metacercariae - encysted stage infective to FH

     • absent in blood flukes (schosoma) - cercaria have forked-tails.

• Digenea development:

  1. Embryogony: egg → miracium

  2. Parthenogony: asexual reproduction within IM host. From miracidium → sporocyst, rediae and cercariae.

  3. Cystogony: development of metacercariae.

  4. Maritogony: final maturation in FH.

MONOGENEA

Genra: Gyrodactylus, Dactylogyrus, Diplozoon

• Mainly on fisk gills, skin and fins of fish (ectoparasites) - some can be endo (bladder, mouth)

• Morphology: spindle shaped/circular. Dorsoventrally flattened, divided into anterior and posterior. Attaches to host by opisthaptor with hooks (hooks/suckers). Oral sucker (prohaptor) is anterior.

• hermaphroditic.

Location: Ectoparasites, worldwide.

Life cycle: Direct, with a single host.

• Oviparous monogens → Embryonated eggs released into water → develops → ciliated cycle (oncomiracidium) can be completed on single host.

• Viviparous monogenes release live larvae → attach to some host

2.    Fasciolosis of mammals (Fasciola, Fascioloides, Fasciolopsis). 

Class: Digenea

Order: Echinostomida

Suborder: Fasicolata

Family: Fasicolidae

Genus: Fasciola, Fasciolides, Fasciolopsis

Species: Fasciola hepatica, gigantica, Fascioloides magna, Fasciolopsis buski.

Geographical distribution: worldwide (F. gigantica and buski more in Asia, F. magna more in America)

Morphology: leaf-shaped, broad anterior end, 3 cm-10 cm (F. magna), covered in spines. Testes are branched and located in the back part, uterus in the front. Yolk glands are along the entire body. Significant oral and ventral sucker (acetabulum).

Egg: large, oval, symmetrical, two thin shells with operculum, unembryonated, yellow/brown

FH: mostly ru, some eq and man, F. buski in pigs and man

IH: Lymnaea truncatula (water snail)

Location in FH: bile ducts, liver

Life cycle:

1) unembryonated eggs are shed in feces

2) exogenous embryogony

3) miracidium hatch and penetrates snail mucosa

4) miracidium develops into sporocyst → produce rediae → produce cercaria → released to environment

5) cercaria encysts to metacercaria on plants and is eaten by FH

6) excyst in the small intestine and migrate through the liver parenchyma (juvenile) until it reaches the bile ducts and matures.

Pathogenesis and clinical signs:

Clinical signs of F. hepatica: release cathepsin and damage the liver tissue causing liver inflammation. Bleeding, rupture of bv, weight loss, non-specific, anemia, edema, emaciation, hemorhage.

Diagnosis: sedimentation, made by clinical signs, microscopy of eggs, serology or post-mortem pathology.

Treatment: triclabendazole, closantel, praziquantel (fasciolopsis spp) - heat treatment of plants. remove animal from grazing area.

3. Dicrocoeliosis of ruminants (Dicrocoelium, Eurytrema, Platynosomum)

Class: Digenea

Order: Plagiorchida

Family: Dicrocoelidae

Genus: Dicrocoelium, Eurytrema, Platynosomum

Morphology: Adults are small to medium, 6-10mm in length. Their suckers are well developed. Cirrus pouch anterior to the acetabulum. Ovary posterior to the testes. The uterus has ascending and descending limbs, folded and filling most of the body behind the gonads. Vitellaria fairly well developed, lateral to the ceca in the middle region. Eggs are always embryonated. They do not have spines on tegument. 2/3 of the body contains the uterus with eggs. The eggs can be differentiated from others by miracidium spots. Eggs are small, oval, asymmetrical, have operculum, 2 hard shells and miracidium is dark brown. This fluke is slender and more transparent and smaller than F. hepatica.

Acetabulum - testes - ovary - uterus (diff from fasicola).

Geography: All over the world.

Epidemiology: 50% in cattle, common parasite. IM host does not require a moist environment, the eggs can survive up to one year on dry pasture. Massive infection of snails and ants usually occur in summer, autumn and spring – grazing season.

Location: liver, gall bladder, bile duct and pancreatic duct

FH: Reptiles, birds and mammals (including humans, Zoonotic potential!). Most often sheep.

IM: 1: land snails, 2: insects (ants, grasshopper)

Pathogenesis and clinical signs: The flukes in the bile duct cause inflammation, formation of fibrinotic tissue, edematous bile duct, mucosa with cellular infiltration. Symptoms are usually not observed unless there are large numbers of worms, no specific symptoms. In heavy infection, the bile ducts becomes very large and one can see the fibrinolytic layer.

If signs do occur, very similar to F. hepatica. Anemia, emaciation, decreased milk and wool production.

Diagnosis: Sedimentation method.

Treatment: Same as other trematodes (triclabendazole). No immunity post infection, reinfection can occur. One can try to control the land snails population on the pastures.

Dicrocoelium dendriticum – inhabits the bile duct of sheep. 6-10mm, spear shape. Eggs are dark brown with operculum, small, 2 thin shells, asymmetrical and embryonated in fresh feces. Juvenile is found in small bile ducts ad adults in large bile ducts and gall bladder. LC: Eggs in the feces of the host are eaten by land snails and hatch in the intestine, where miracidia penetrate the gut wall. Mother sporocysts produce daughter sporocysts in which cercariae develop. Cercariae leave the daughter sporocysts and accumulate in the mantle chamber where mucous secreted from the snail envelopes hem and form “slime balls”, which are deposited on the vegetation as the snail moves. Slime balls contain many hundreds of cercariae and are eaten by ants, they look like berries. Cercariae penetrate the wall of GIT and then into the abdominal cavity, where 1-2 cercariae penetrate the brain and metacercariae encyst there, altering the ants behavior so when the temperature drops in the evening, infected ants climb to the tips of the grass and hang by their mandibles, allowing FH to more easily ingest them while grazing. They never migrate to the liver of FH. Migrate to bile ducts by ductus choledochus. Prepatent period is 7-9 weeks and whole life cycle takes about 6 months.

No rediae!

Eurytrema pancreaticum – found in pancreatic and bile ducts (sometimes duodenum) of herbivores in subtropical countries. They are oval to fusiform in shape. Suckers are large, oral sucker larger than ventral sucker. The eggs are embryonated in uterus. Second IH host is a grasshopper. FH are ruminants. Life cycle, pathogenesis is the same.

Platynosomu fastosum–FH: cats, especially outdoor cats. IM host: snails, and 2: lizards, toads, geckoes and shinks. Found in bile duct and pancreatic duct of cats. Cat will exhibit temporary inappetence due to hepatic dysfunction. The bile ducts may be dilated as the flukes attach to mucosa. Clinical signs are non-specific – diarrhea, vomiting, icterus and death.Diagnosisis made by sedimentation method and can betreatmentwith praziquantel and Nitroscanate.

4. Prosthogonimosis + and other trematodonoses in birds

Class: Digenea

Order: Plagiorchida

Family: Prosthogonimidae

Genus: Prosthoonimus

 

Important species:

P. pellucidus – in bursa fabricii, oviduct and posterior intestine, in North America,

P. macrorchis – in burs fabricii of domestic poultry and ducks in North America. Cause damage to organs and prevet egg laying in some cases.

P. ovatus – bursa fabricii, oviduct of fowl, geese ad wild birds in Europe, Africa and America.

P. cutaneous and P. anatinus – duck and goose, found in Europe.

Morphology: Adult body is flat and transparent with spines on the cuticle. They have an oval/pear shape. Posterior end appear broader than anterior end. The uterus occupies about half of the body at the posterior end, ovary contains multiple lobes and is between ventral sucker and testes. Misalignment of the testicles in many species.

Location: Live in oviducts of avian species, environment most suitable during reproduction

FH: ducks, chickens, sparrows, and crows

IM: 1: water snail, 2: dragonfly nymph

Life cycle: Unembryonated eggs are released into the water and ingested by water snail and hatch into miracidium - transform to sporocyst - cercariae, drawn into the anal openings of dragonfly nymph by breathing movements of these insects. Dragonfly metamorphoses into adult and is eaten by FH. Metacercariae encyst the small intestine and migrates to cloaca and bursa fabricii or oviduct in birds without bursa, where it reaches sexual maturity. Causes atrophy of bursa. Occurs during end of winter – middle of march.

Pathogenesis: Prostogonimus spp. are considered to be the most pathogenic trematode of poultry in Europe and America. They cause irritation in the oviduct, resulting in acute inflammation. The irritated oviduct readily performs retroperistaltic movements, causing broken yolk, albumen, bacteria and parasite to enter the abdominal cavity, where they cause peritonitis, usually with fatal results.

Clinical signs: At first, general health is not disturbed, but hens may begin to lay eggs with soft or without any shell. There is a tendency of hens to sit on the nest. Discharge from cloaca, irritated oviduct passes the eggs rapidly with no shell deposited. The birds become listless, abdomen is pendulous and the legs are held widely apart in walking. The feathers around the cloaca are soiled with albumen. If peritonitis develops, the comb and wattles become cyanotic and the birds will die. Post mortem findings: inflammation of oviduct with dirty, cheesy mass in the lumen (yolk and albumin), dirty fluid in abdomen if peritonitis and organs are stuck together by cheesy mass. Serous membranes show marked congestion and hemorrhages may be present.

Diagnosis: coprological examination and finding the eggs in feces, post mortem

Treatment: albendazole, fenbendazole, praziquantel.

OTHERS (from lecture/practical on moodle):
INTESTINAL FLUKES:
- Echinostoma revolutum: Rectum, cecum. L, eliptical, asymmetrical, 2 thin shells, operculum, unembryonated, light grey
- Plagiorchis arcuatus:bursa fabrici, oviduct
- Triglotrema acutum:bone perforation, penetarte into brain
- Opistorchis (simulans, geminus):Geese and duck gall bladder. 

BLOOD FLUKES:
- Bilharziella polonica:Water poultry (geese, ducks) (cercarial dermatitis - called swimmer´s itch)
- Trichobilharzia ocellata: Furkocercariae

5. Paramphistomatidosis of ruminants. 

Class: Digenea

Order: Amphistomida

Family: Paraphisomidae

Genus: Paramphistomum, Calicophoon, Cotylophoron, Gigatocotyle, Orthocoelium

Main species: P. cervi, P. daubnei, P. ichikawai, P. microbothrium

Morphology: They have two suckers on the anterior and posterior site, the acetabulum is very large. They are pear-shaped, small in size, 1-1,5m, light pink to red in color due to hemoglobin. Same organs as rest of Digenea class. Eggs are oval with operculum, similar to F. hepatica but they are a bit longer. Eggs are L, two shells, unembryonated and colorless. They are hermaphrodites with complete reproductive system.

Location: Adults in mucosa of rumen, juvenile in abomasum and duodenum. Depending on species, can also be found in liver.

Geography: Europe

Etiology: Paramphistomum cervi (most prevalent), P. daubneyi, P. icikawai, P. microbothroides are the most pathogenic. Infection is severe in all ruminants. Young calves and lambs are most susceptible. Prepatent period is 3-5 months.

Epidemiology: very common in ruminants. These parasites may survive for years in humid environments, metacercariae has a resistant shell. There is a constant source of infection for generation of snails, they breed and ensure a widespread availability of the snails within infested areas.

FH: Ruminants

IM: Water snail, family Planorbidae

Life cycle: Same as F. hepatica. Cattle shed embryonated eggs in feces, dependent on higher temperatures of 25 C otherwise embryonoy goes slowly. Whole life cycle takes 10-12 months.

Pathogenesis: Adults are located in rumen mucosa and acetabulum sicks mucosa and form necrosis which lead to erosion and bleeding. The juvenile in small intestine cause local hemorrhage and bleeding - holes in the tissue - form fibrinotic tissue instead, which is not good for intestines as they need mucosa with microbes. Duodenitis, enteritis. The adults forms nodules in the rumen wall and destroy papilla, decrease digestion and appetite – papilla atrophy.

Clinical signs: Diarrhea, weight loss, weakness. No good condition, increased temperature, no special signs. Acute – extensive diarrhea, anorexia, thirst, anemia, hypoalbuminemia, edema, emaciation, death, submandibular edema. Chronic – symptoms usually absent

Diagnosis: sedimentation methods and finding eggs in the feces, ELISA – finding antigens or post-mortem inspection.

Treatment: Trichlabendazole is very effective against juvenile. Closantel, oxyclosanid and albendazole can also be used. Control of snails is very difficult. Pasture control can also work to a certain degree.

Only a small amount of immunity after infection, like F. hepatica.

 

Gigantocotyle explanatum– found in biliary duct of large ruminants (wild and domestic). Recently come to Europe (Italy), originally found in Asia, Africa and south America. Life cycle is the same.

Class: Digenea

Order: Opistorchiida

Family: Opistorchiidae

Genus: Opistorchis

 

Important species:

Opistorchis felineus – Europe and Asia

O. viverrine

Clonorchis sinensis

Morphology: Suckers are weakly developed and testes are posterior and tandem. Ovary is pretesticular, genital pole is located just anterior to acetabulum. Vitelline follicles are large, lateral and usually anterior to the gonadal region. Adults are similar to, but often smaller than, Clonorchis sinensis, but differ in shape of testes and distribution of vitelline follicles. 10-25mm in length. C. sinensis have teticles formed as a tree, meanwhile O. felineus have lobed testes posterior.

Epidemiology: Consumption of uncooked fish – sushi.

Location: Inhabit liver, bile ducts and gall bladder. Zoonotic!

FH: Fish-eating mammals and humans

IM: 1: water snails, 2: fish and sometimes amphibians

Life cycle: Embryonated eggs with miracidium are excreted in feces and ingested by snail. Asexual reproduction in snail results in daily release of thousands of cercariae 1-2 months after infection of snail. Free-swimming cercariae penetrate - infective metacercariae under the fish`s skin or muscle after 21 days. Metacercariae hatch and migrate to bile ducts and mature (1 month prepatent period). Humans can get infected when ingesting fish.

Pathogenesis: Can see enlarged bile ducts. Juvenile stages – liver parenchyma migration = hepatitis. Adult flukes cause cholagitis, pericholangitis. Pancreas damage.

Clinical signs: Liver is painful and enlarged, ascites and icterus. Clinical manifestation in moderate infection.

Diagnosis: Identification of eggs in feces.

Therapy: Praziquantel 

Class: Digenea

Order: Opistorchiida

Family: Heterophyidae

Genus: Heterophyes + Metagonimus   

Species:

Heterophyes Heterophyes 

Metagonimus yokogawai

(H)

(M)  

Heterophyes heterophyes

Morphology: small intestine trematode. Spined tegument. They have a small oral sucker, pharynx and simple intestinal system and ceca. Ventral sucker is strong and has 70 spines. They do not have cirrus pouch. Reproductive organs are grouped except for a separate genital sucker with may chitinous rodlets, characteristic seminal vesicle and uterus. Number and location of testes are different according to genra. Teardrop shape.

Epidemiology: People at high risk or infection are those who live by bay waters including fishermen. Infection is acquired by eating raw fish. It is common that people defecate in the water while fishing.

Location: small intestine

FH: Fish eating mammals and humans.

IM: 1. Snails, 2. fish

Life cycle: Indirect. Eggs contain miracidia. Embryonated eggs released by FH in feces -> snail host ingest eggs. Miracidium emerge from eggs and penetrate snails intestine. Miracidium -> sporocyst -> rediae -> cercariae released from snail and penetrate skin of fish and encyst as metacercariae in tissue of fish. FH become infected wen ingesting undercooked fish containing metacercariae. Metacercariae excyst in small intestine and mature as adults.

Pathogenesis and clinical signs: Mild inflammatory reaction. Intestinal pain and mucosa diarrhea in heavy infections. Eggs can also migrate to brain and spinal cord and cause neurological disorders. Diarrhea and colicky abdominal pain. Migration of eggs to the heart, resulting in fatal myocardial and valvular damage.

Diagnosis: Detection of eggs in feces

Treatment: Praziquantel

Family: Heterophyidae

Metagonimus yokogawai

Morphology: Spined tegmentum. Have genital pore. They have a scaly surface. Abdominal sucker is more ventral from midline.

Location: Small intestine

FH: Dogs, cats, humans, rats and pigs. Zoonotic!

IM: 1. Water snail. 2, sweet fish/cyprinid fish

Life cycle: Similar to H. heterophyes. But metacercariae cause damage in small intestine and release toxins in FH -> severe local inflammation shown as abdominal pain and diarrhea.

Pathogenesis: Invade intervillous space of small intestine, toxic effect.

Clinical signs: Same as H. heterophyes

Diagnosis: Detection of eggs in feces

Treatment: Praziquantel