Chapter 8




8.1.1 GENERAL INFORMATION Classification

There are two main subclasses of the class Trematoda: 

A. Monogenea - the monogenetic trematodes

These are the fluke parasites of fishes, amphibia and reptiles. None of them occur in domestic animals. This is the last we will speak of MONOGENETIC TREMATODES. 

B. Digenea - the digenetic trematodes

These are the flukes that parasitize our domestic animals. Their life cycles require one, two, or more intermediate hosts. THE FIRST INTERMEDIATE HOST OF ANY DIGENETIC FLUKE IS USUALLY A SNAIL! Terms used in Relation to Trematodes:


Individual containing gonads of both sexes, i.e hermaphroditic.


Condition where male and female gonads are found in different individuals Operculum a lid-like structure covering certain cestode adn most tremtode eggs.


The ciliated larva which hatches out from the trematode egg.


Young flukes which develop from germ cells in sporocyst and redia.


Stage in which the cercaria becomes encysted.


A larval stage which is sac like and containing germinal cells which give either to a second generation of sporocyst or to redia.


A larval stage which is sac like but with a pharynx and a rudimentary intestine. It contains germinal cells which give rise to a second generation of redia or to cercaria.


Adhesive organs. There are generally 2 suckers, oral and ventral.


Ventral sucker with well developed muscles


The male copulatory organ.

Cirrus pore

The opening through which the cirrus is protruded

Cirrus pouch

A hollow organ surrounding the introverted cirrus.

Vas deferens

Canal connecting vas efferens to cirrus.

Vas efferns

A canal extending from a testis to the vas dferens

Seminal receptacle

A dilated organ in the female genital tract which stores sperms

Seminal vesicle

The dilated lower part of the vas deferens which opens into cirrus.


Is the fertilizing chamber where the ovum is fertilized by the spermatozoon.

Laurer’s canal

A tubular structure connecting the oviduct with the exterior. Also known as the copulatory canal.

Meblis’ gland

A unicellular gland which encircles the ootype. Its function is not known.

Vitelline glands

The glands which provide substances for development of the egg and the formation of the shell.

Common genital pore

The common opening formed by the fusion of the male genital duct and the uterus. This is usually enclosed in a small chamber.

Flane cell

An excretory cell with a tuft of cilia, whose beating resembles the flickering of a flame. The flame cells open into a collecting tubule. Also known as solenocyte.


A loose collection of ells and fibers Morphological features of flukes (Figure 3.2)

  • A. The flukes are usually dorsoventrally flattened. Some are long and narrow, some are leaf shaped, while some have thick fleshy bodies. The schistosomes are long and wormlike,
  • B. They have a tegument. This tegument may be smooth or it may be spiny.


  • C. They have two organs of attachment:
    • 1. an anterior sucker called the ORAL SUCKER

      2. a ventral sucker called the ACETABULUM

  • D. They have a digestive system that begins with a mouth surrounded by an oral sucker. There is a muscular pharynx then an esophagus which leads to two blind ceca. The ceca may be unbranched (simple) or highly branched. There is no anus.
  • E. Fluke have an excretory system.
  • F. Flukes have a nervous system
  • G. With the exception of the Schistosomes, digenetic flukes are hermaphroditic the flukes will possess complete functioning sets of both male and female sex organs. Self fertilization usually takes place.

1. Male Sex Organs:

Two testes, two vasa efferentia, a vas deferens, a vesiculum seminalis, a pars prostatica, a cirrus, a cirrus sca, a genital pore.

2. Female Organs:

One vary, a seminal receptacle, vitelline or yolk glands, vitelline duct, an ootype(where the eggs are formed), Mehlis’ glands (surrounding the ootype), a uterus, a genital pore.

II. Developmental forms in the life cycel of trematodes (Figure 3.3 and 3,4)

  • A. trematodes, as do all parasites, have a tremendous reproductive capacity. The developmental stages in the life cycle of a fluke are:


Egg --> Miracidium --> Sporocyst --> Redia --> Cercaria--> Metaceracaria --> Adult Fluke


  • B. The operculated egg has an operculum (door) on one pole. The egg contains the embryonic fluke.
  • C. A miracidium emerges out the open end of egg. It is triangular in shape, the anterior end is broad. It is covered with cilia. On its anteior end is a spine which it uses to bore into a snail, the first intermediate host. A snail is usually the first intermediate host for any digenetic flukes.
  • D. Following penetration the ciliated coat is lost and the miracidium develop into a sporocyst within the snail. The sporocyst is an undifferentiated mass of cells. It is within the snail. 

 * The reproductive potential in the trematode life cycle is enormous; millions of cercariae may be produced from a single miracidium.
* This is a generalized life cycle of a "typical fluke. Every fluke that exists has its own variation of this life cycle. There are many variations for this generalized life cycle.


Figure 3.3 : Developmental Forms in the life Cycle of Trematodes

 Figure 3.4: Some variations in the life cycles of Digenetic Trematodes

  • E. With in the sporocysts germinal cells multiply and become rediae. The redia has an oral sucker, a pharynx, an intestine and a birth pore. The redial stage occurs within the snail.
  • F. The redia "gives birth" to cercariae. Cercariae escape from the snail and escape into the environment (e.g.water). The cercaria has suckers, an intestine, an excretory system and a nervous system. It also has a tail for propelling itself through the water after escaping from the snail. Cercaroae usually encyst within a second intermediate host or they encyst upon vegetation. Some cercariae may penetrate the host directly.
  • G. The encysted from undergoes physiological maturation to produce the infective stage, the metacercaria. The metacercaria is the final larval stage. It has to reach the definitive host to complete the life cycle. The metaceraria may enter the dfinitive host passively on contaminated herbage or within a second intermediate host.
  • H. When the encysted metaceraria is ingested by the final host it excysts in the intestine of the host. The immature stage migrates to its predilection site, and becomes an adult fluke.


8.1.2 THE DIGENETIC TREMATODES (FLUKES) FASCIOLA HEPATICA (Figure 3.5) Importance of Fasciola hepatica:

  • 1. Important parasite of cattle in the United States
  • 2. Major cause of liver condemnation; it causes "liver rot" or "liver fluke disease" in ruminants
  • 3. Best-known of the trematodes Host and Habitat

This fluke is found in the bile ducts of sheep, goat, ox and other ruminants; it also occurs in rabbits. Flukes feed on the lining of the bile ducts. Identification

  • 1. F. hepatica has measurements in the range of 30 by 13 mm. It is leaf-shaped, broader on its anterior end than on its posterior end, and has an anterior cone-shaped projection which is followed by a pair of prominent "shoulders".
  • 2. The ventral sucker, at the level of the shoulder, is about as large as the oral sucker.
  • 3. The tegument is armed with sharp spines
  • 4. the branching of the internal organs is important
    • a. intestinal ceca
    • b. testes
    • c. ovary
  • 5. Vitelline glands take up the lateral fields. The uterus lies anterior to the testes. The operculated eggs are from 130 to 150 microns by 63 to 90 microns. Life cycle

The eggs enter the duodenum with the bile and leave the host in the feces. The eggs hatch and the miracidium emerges from the egg. The miracidium penetrates an aquatic snail of the genus Lymanae and develops into sporocyst. Each sporocyst produces 5 to 8 rediae. The rediae produce cercariae. These cercariae emerge from the snail. The cercaria will swim using its tail and settles on vegetation below the water level. It soon sheds its tail and produces a transparent cyst around itself; this cyst stage is called a metacercaria. Metacercariae are swallowed by the definitive host when the host eats the vegetation. The metacercariae excyst in the duodenum and become juvenile flukes. They immediately penetrate the intestinal wall, enter the body cavity and creep over the viscera until they contact the capsule f the liver. They burrow into the liver parenchyma and wander for about two months. They feed, grow and enter bile ducts. Flukes become sexually mature in another month and begin producing perculated eggs. Pathogenesis 

The pathological effects of F. hepatica depend upon the number of metacercariae ingested. No damage results from passage of the juvenile flukes through the intestinal wall or peritoneal cavity. The primary lesions occur in the liver parenchyma or bile ducts.

The disease may exist as two syndromes: Acute fascioliasis

  • 1. Acute fascioliasis is seen in sheep. It is not as common as chronic fascioliasis. It is a traumatic bepatitis caused by migration of large numbers of juvenile trematodes (greater than 10,000 metacercariae must be ingested). There is intensive destruction of liver parenchyma and marked hemorrhage. When large numbers immature flukes penetrate the liver, rupture of the liver capsule may occur. The liver may become enlarged, pale and friable and show numerous hemorrhagic tracts on its surface and throughout the parenchyma.


Figure 3.5: Fasciola Hepatica


  • In less acute forms of the disease, the liver is covered with migratory tracts but an infiltration of white cells is more evident. Early fibrosis may be sen.
  • The clinical entity of the acute and subacute forms is seen in animals of all kinds and in all states of nutrition. Death may occur rapidly or after several days. Animals are disinclined to move, are anorexic and demonstrate a painful abdomen when touched.
  • A complication of the acute condition is "BLACK DISEASE" caused by Clostridium novyi. This is an anaerobic bacterium which proliferates in the anaerobic lesions induced by the migrating immature trematodes. The organism occurs in normal sheep; the clinical entity occurs only after liver damage has been produced by some other agent. Sheep aged 2 to 4 years are usually affected. A vaccine is available for "black disease". Chronic fascioliasis

  • 2. Chronic fascioliasis is the more common form of the disease in sheep and cattle. Major consequence of F. hepstica is hepatic fibrosis. Migration of immature flukes in the liver produces migratory tracts. There is traumatic destruction of liver parenchyma, hemorrhage and necrosis. Migration of the flukes also results in thrombus formation in the hepatic veins and liver sinusoids. These thrombi obstruct blood flow and cause an ischemic coagulative necrosis in the liver parenchyma. Healing and regeneration of these lesions begins, collagen is laid down and fibrosis occurs. This scar tissue contracts and distorts the hepatic architecture.
  • The presence of adult flukes in the bile ducts causes a hyperplastic cholangitis. At first, the epithelium of the bile duct undergoes hyperplasia. The spines and suckers of the flukes denude the bile duct epithelium. There is fibrosis of the lamina propria of the bile duct and the surrounding tissues. Fluke eggs also lodge in the smaller bile ducts. The hyperplastic biliary mucosa becomes permeable to plasma proteins, particularly albumin. This together with the blood feeding activity of the adult flukes, produces a hypoablbuminemia and a hypoproteinemia.
  • In cattle, calcification of the fibrotic lesions develops and complete casts of the bile ducts are formed. The walls of the ducts are commonly calcified, protrude markedly from the surface, and are difficult to cut with a knife. They resemble the stem of a clay pipe, resulting in the "pipestem liver effect". Clinical signs

  • 1. The animals exhibit a profound anemia due to changes in serum proteins. The anemia is due to intrabiliary hemorrhage from the blood feeding activity of the adults (0.5 ml of blood/adult fluke/day). Plasma proteins are lost due to blood feeding activity of the adults and leakage of protein through the bile duct epithelium.
    • a. Acute fascioliasis of sheep
      • 1. the animal dies suddenly.
      • 2. Blood-stained froth appears at the nostrils and blood is discharged from the anus.
    • b. Chronic fascioliasis
      • 1). Sheep: Signs are first seen when the young flukes burrow through the liver parenchyma. The animals lack vigor. There is diminished appetite. The mucous membranes are pale and edema develops. Edema may appear in the intermandibular space, producing "bottle jaw". The wool is dry and brittle and falls out in patches. Sheep are debilitated, emaciated and generally depressed. Death may ensue.
      • 2) Cattle: Cattle affected by chronic fascioliasis demonstrate digestive disturbances. They are often constipated nd pass dry hard feces. Some diarrhea may be seen. Calves are often emaciated, dull and weak. Diagnosis

Demonstration of the operculated ova in the feces. The egg of Fasciola hepatica has a yellow shell and an indistinct operculum. Treatment

  • 1. Carbon tetrachloride has been used for more than 50 years.*
  • 2. Hexachloroethane
  • 3. Hexachlorophene

*Not recommended for use in cattle. Use caution in sheep: POISON

  • 4. Hetol
  • 5. Bithionol
  • 6. Diamphenethide
  • 7. Oxyclozanide Control

  • 1. Treat infected animals
  • 2. Control the snail intermediate host
    • a. Eliminate snail bahitats by draining areas and fencing off areas.
    • b. Molluscicides such as copper sulfate may be used.

    Caution: these may be toxic to fish. Do not graze stock on treated pastures until a rain has fallen.

    • c. Biological control using ducks and frogs FASCIOLOIDES MAGNA (Figure 3.6) Host and Habitat

This parasite occurs in the liver (rarely the lungs) of cattle, horses, sheep and pigs in North America. The infection is quite common in the mouse, white-tailed deer, mule deer and elk. This parasite is found in the Gulf Coast states and the southeastern US. Idnetification

These flukes are oval and are thick and flesh-colored. They are 23 to 100 mm long, 11 to 26 mm wide and 2 to 4.5 mm thick. They have no distinct anterior cone-like projection. The eggs are 109 to 168 by 75 to 96 microns. Life Cycle

The life cycle is very similar to that of F. hepatica. The egg hatches and the miracidium penetrates an aquatic snail. In 7 to 8 weeks, cercariae have developed. The cercariae are liberated and encyst on vegetation. On ingestion by the definitive host, the juvenile parasites migrate through the intestinal wall and peritoneal cavity to the liver.

Two variations may occur in the life cycle of F. magna:

  • 1. Members of the family Cervidae (the deer family) are considered to be normal definitive hosts of F. magna. In deer, the young fluke migrates extensively in the liver. The flukes form capsules that connect to the bile ducts. Eggs are passed from the flukes in their capsules and through their connections with bileduct. Eggs are passed into the feces. In North America, the white-tailed deer is the usual definitive host of F. magna; in the US,13-60% of white-tailed deere are infected with F. magna.


Figure 3.6: Fascioloides magna


  • 2. The larger Bovidae (cattle, bison and yak) and pigs are aberrant hosts. F. magna mgrates in the liver but becomes encapsulated in closed cysts. Eggs are not passed out of the liver and into the feces.
  • 3. In sheep which are also aberrant hosts, there is an uninterrupted migration through the liver. Encapsulation is rarely seen. Sheep are usually killed by the uninterrupted migration that occurs. Pathogenesis

1. Deer 

Parasites are found in thin-walled, connective tissue cysts up to 4 cm diameter. The bile ducts connect to the cyst and serve as an exit avenue for eggs.

2. The larger Bovidae

The parasites are enclosed in a thick-walled fibrous tissue capsule. The bile ducts are occluded. Cysts are filled with black fluid containing the parasites, bile pigments and eggs. The liver may have evidence of migration, hemorrhage, hematoma, infarction, necrosis but the animals show no ill health. Black iron porphyrin pigment accumulates in the liver, omentum, kidney and other organs. 

3. Sheep

Death. The uninterrupted migration produces extensive liver damage hemorrhage and necrosis. Diagnosis

  • 1. Deer - obsevation of typical ova on fecal floatation
  • 2. Bovidae - Clinical signs, necropsy and (rarely) observation of typical ova on fecal floatation.
  • 3. Sheep - Clinical signs and necropsy. Treatment

  • 1. Oxyclozanide
  • 2. Rafoxanide
  • 3. Nitroxynil
  • 4. Clioxanide
  • 5. Diamphenethide
  • 6. Albendzole Control

  • 1. Sheep and cattle should not be raised on land inhabited by deer.
  • 2. Use of molluscicides DICROCOELIUM DENDRITICUM -The Lancet Fluke(Figure 3.7) Hosts and Habitat

This small fluke occurs in the bile ducts of sheep, goat, ox, deer, pig, donkey, and man. Identification

This is a small fluke, it is 6 to 10 mm long and 1.5 to 2.5 mm wide. Life Cycle

The adult flukes are found in the bile duct. The operculated eggs are voided in the feces. The first intermediate host is a land snail (Cionella lubrica). The miracidia do not hatch out of the eggs until the eggs have been swallowed by the intermediate host. The miracidia migrate to the mesenteric gland of the snail and develop into sporocysts. These produce a second generation of sporocysts (Rediae are not formed). Within the second generation sporocysts are cercariae. These cercariae emerge from the sporocysts only in damp weather following a dry spell. They migrate to the pulmonary chamber of te snail and clump together in masses called slime balls. When a drop in temperature occurs, the slime balls are expelled from the snail and adhere to vegetation. The slime balls are eaten by ants of the genus Formica. Metacercaia are produced in the abdominal cavity. Some metacercaria will enter the brain of the ant causing tetanic spasm of the mouthparts when environmental temperatures dr. Affected ants attach to herbage overnight and are available to grazing animals in the early morning. The definitive hosts are infected by swallowing infected ants. The metacercaria enter the bile ducts and grow to adults. Pathegenesis and Clinical signs

These flukes attach to the lingings of the fine branches of the bile ducts. The number of parasites per infected animal may be as many as 2000 to 14,000 adults/infected animal. 

Advanced infection will produce extensive cirrhosis and scarring of the liver surface, distension of th bile ducts, and marked proliferation of the bile duct glandular epithelium. Clinically one sees anemia, edema and emaciation. Many cases, however, will show no clinical signs. 5 Diagnosis

The demonstration of the operculated ova in the feces. Treatment

  • 1. Hetolin -19-22 mg/kg
  • 2. Albendazole - 15 mg/kg or 7.5 kg/kg in two does two to three weeks apart.
  • 3. Cambendazole - 25 mg/kg
  • 4. Fenbendazole - 150 mg/kg
  • 5. Thiabendzole - 200-300 mg/kg
  • 6. Praziqauantel - 50 mg/kg Control

  • 1. Treat infected animals
  • 2. Land snails are difficult to control because they are less vulnerable to molluscidies. Domestic poultry may be used as biological controls.
  • 3. Disrupt ant nests in pastures.


Figure 3.7: Dicrocoelium Dendriticum PLATYNOSOMUM FASTOSUM - the lizard poisoning fluke of cats(figure 3.8) Host and Habitat

This fluke is found in the liver and bile ducts of cats in Florida and other southern states. Identification

These flukes are 4 to 8 mm by 1.5 to 2.5 mm. This fluke is morphologically similar to Dicrocoelium dendriticum except that the testes are horizontal in position rather than tandem. The eggs are brown, operculated, and measure 34 to 50 by 20 to 35 microms.


Figure 3.8: Platynosomum fastosum Life cycle

Eggs are voided in the feces and are ingested by land snails. Cercariae are produced. The snail is eaten by a lizard of the genus Anolis. Metacercariae encyst in the bile duct of the lizard. Cats become infected by eating lizards. The fluke excysts and enters the bile duct of the cat. Pathogenesis and clinical signs

P. fastosum does not normally cause severe disease in cats. Frequently the cat will exhibit a temporary inappetance due to hepatic dysfunction. Grossly the bile ducts may be dilated and the duct epithelium desquamated. Clinical signs observed are diarrhea, vomiting, icterus, and death. Infection with this fluke may be referred to as LIZARD POISOBNING. Diagnosis

Demonstration of the operculated ova in the feces Treatment

  • 1. Praziquantel 20 mg/kg
  • 2. Nitroscanate 100 mg/kg Control

Prevent cats from ingesting lizards PARAMPHISTOMUM SPP. AND COTYLOPHORON SPP. - Rumen Flukes(Figure 3.9). Host and Habitat

  • 1. Paramphistomum spp: rumen, reticulum of cattle and sheep
  • 2. Cotylophoron spp: rumen, reticulum of cattle, sheep, and goats. Idnetification 

These genera are similar morphologically. Living flukes are cone-shaped or pear-shaped and frequently are light red. They may be 5-13 mm long and 2-5 mm wide. These flukes characteristically have a large posterior, subterminal sucker in addition to the oral sucker. The eggs are from 144 to 176 by 73 to 100 microns. Their eggs are easily confused with those of Fasciola hepatica. Life Cycle

Eggs are passed in the feces. Miracidia penetrate the snail intermediate host. Cercariae emerge from the snail and encyst on vegetation. The metacercariae are ingested along with food and water. The immature flukes attach to the mucosa of the small intestione. They are embedded in the mucosa and are plug feeders. They draw pieces of mucosa into the suckers, which pinch off plugs, causing necrosis and hemorrhage. After 6 to 8 weeks, the flukes migrate forward through the reticulum to the rumen. Pathogenesis and Clinical Signs

The immature flukes are a considerable irritant to the intestinal mucosa, especially of the duodenum. A catearrhal or hemorrhagic enteritis may occur throughout the upper small intestine. Infected animals lose appetite and condition. They are dull, weak, and anemic. Adult flukes do not seem to be pathogenic. 


Figure 3.9: Paramphistomum spp. and Cotylophoron spp. Diagnosis

  • 1. Fecal examination-their eggs are easily confused with those of F. hepatica.
  • 2. Demonstration of adult flukes or immature flukes at necropsy. Treatment

  • 1. Resorantel
  • 2. rafoxanide
  • 3. oxyclosanide
  • 4. niclofolan
  • 5. bithionol
  • 6. hexachlorophene . ALARIA SPP. (FIGURE 3.10) Host and Habitat.

These flukes are found in the intestines of dogs, cats, coyotes, foxes and other animals in North America. Identification

These flukes are 2 to 5 mm in length. They have a flat expanded anterior part and a posterior cylindrical part. At the anterior lateral part are two ear-like projections. The suckers are very small. The eggs are yellow-brown and are from 98 to 134 by 62 to 68 microns. Life Cycle

The egg is voided in the feces. It hatches in two weeks and the miracidium penetrates a second intermediate host such as a tadpole or frog. This larval stage is called a mesocercaria. The mesocercaria is similar to themetacercaria of other flukes. The final host is infected by ingestng the amphibian containing the mesocercaria. The fluke migrates through the abdominal and thoracic cavities to the lungs or migrates via the circulation to the lungs. It then passes to the small intestine via the trachea and pharynx.

Paratenic hosts may also be involved in the life cycle. Mice, rats, snakes and birds may eat frogs or toads and become infected with the mesocercariae. These serve as paratenic hosts and are a source of infective mesocercariae if eaten by the definitive host.


Figure 3.10: Alaria spp.  Pathogenensis

Heavy infections may cause a catarrhal duodenitis, but the majority of infections are usually nonpathogenic.

Man may act as a paratenic host, but this role may prove fatal. A man in the wilderness ate inadequately cooked frogs legs. Several thousand mesocercariae were found in the peritoneal cavity, brain, heart, kidneys, liver, lungs, lymph nodes, pancreas, spinal cord, spleen and stomach. Death was from asphyxiation due to extensive pulmonary hemorrhage. Diagnosis

  • 1. Identification of eggs on fecal flotation
  • 2. Demonstration of adults at necropsy Treatment

  • 1. Bithionol
  • 2. Praziquantel
  • 3. Albendazole
  • 4. Fenbendazole Control

Since this fluke is nonpathogenic, treatment or other types of control are seldom attempted. NANOPHYETUS SALMINCOLA (also known as Troglotrema salminocla)--the salmon poisoning fluke(Figure 3.11) Host and Habitat

This fluke occurs in the small intestine of the dog, cat, fox, coyote, raccoon, opossum, otter, mink, lynx, etc., in the Pacific Northwest. Identification

This is a minute fluke. It is only 0.5 to 1 mm in length. The worms are creamy white. The eggs are from 52 to 82 by 32 to 56 microns. Life Cycle

The raccoon and the spotted skunk are the principal definitive hosts in the US. Eggs are passed in the feces, hatch and release miracidia. The miracidium penetrates the first intermediate host, a stream snail. The cercaria develops, is liberated and penetrates through the skin of a fish in the family Salmonidae, the second intermediate host. Metacercariae are found in the muscle, kidney, eye and other organs of the fish. The dog becomes infected by ingesting the organs of the fish. Pathogenesis

In dogs, the trematodes penetrate deeply into the mucosa of the duodenum or attach to the mucosa of other parts of the small or large intestine. In large numbers, a superficial enteritis is produced which may lead to a hemorrhagic enteritis. This fluke serves as a vector for Neorickettsia helminthoeca, a rickettsial agent which causes "salmon poisoning" in dogs and another rickettsia which causes "Elokomin fluke fever".

Only members of the family Canidae are susceptible to "salmon poisoning". The clinical signs are sudden onset of fever and a complete loss of appetite. Within a few days, vomiting is marked and there is profuse diarrhea which may be hemorrhagic. Mortality is high (50 to 90%). Recovered animals are immune to reinfection.

"Elokomin fluke fever" is also caused by a rickettsial agent and affects a wider host range (dogs, foxes, coyotes, bears, raccoon, ferrets, and man). Clinical signs are similar to "salmon poisoning" (i.e., fever, lymphadenopathy, vomiting, diarrhea, dehydration, and ocular discharge). In dogs, morbidity is high and mortality is low. Diagnosis

  • 1. Eggs are detected in the feces
  • 2. rickettsiae can be demonstrated in fluid aspirated from the mandibular lymph nodes.
  • 3. History of travel from the Pacific Northwest also aids in the diagnosis of "Salmon Poisoning". Treatment

  • 1. Treat the animal symptomatically; i.e., relieve the vomiting, diarrhea, and dehydration.
  • 2. Treat the rickettsiae with tetracyclines, sulfonamides and chloramphenicol. Glozxazone is also effective. Control

No Salmonid fish should be fed in a raw or undercooked state. If such a fish is eaten, administer apomorphine.


Figure 3.11: Nanophyetus salmincola PARAGONIMUS KELLICOTTI - the lung fluke of dogs and cats (Figure 3.12) Hosts and Habitat

This fluke is found in the lungs of dogs and cats. Identification

The adult flukes live in cysts in the lungs. The parasite is red-brown and is from 7.5 to 16 by 4 to 8 mm. The cuticle is spiny. The eggs are yellow-brown and are from 75 to 118 by 42 to 67 microns. They have an operculum and the shell is thickened at the pole opposite the operculum. Life Cycle

Adult flukes live in cysts in the lungs. Eggs are laid in the cysts and escape through connecting channels into the bronchi. The cysts may also rupture and release eggs. The eggs pass up from thelung in the sputum which has a characteristic rusty color. Animals swallow the mucus, and eggs are found in the feces. The miracidium hatches from the egg and penetrates an aquatic or land snail. Sporocysts, rediae, and cercariae develop in the snail. The cercariae escape from the snail and swim in the water. They penetrate a crayfish and encyst within it. The final host becomes infected by eating the crayfish. The young fluke is liberated in the intestine, penetrates the diaphragm and enters the lungs from the pleural cavity. The parasite penetratesthe pulmonary parenchyma, a cystic cavity is formed and the parasite mature to the adult stage. The cyst usually contains two parasites surrounded by a purulent fluid mixed with bood and eggs. The flukes have also been known to wander to aberrant sites such as the brain Pathogenesis and Clinical Signs

Migrating immature flukes causes an eosinophilic peritonitis, pleuritis, myositis and multifocal pleural hemorrhage. Adult flukes produce a chronic bronchiolitis, hypeplasia of bronchiolar epithelium and a chronic eosinophilic granulomatous pneumonia.

Infected animals are lethargic and have an intemittent cough. Dyspnea or pneumothorax may be seen in cats. Parasites lodged in the brain can cuase problems.


Fig 3.12: Paragonimus Kellicotti Diagnosis

  • 1. Finding eggs in the sputum or feces
  • 2. Lesions may also be detected by radiography (signet ring effect). The lesions are most frequent in the right caudal lobe. Treatment

  • 1. Albendazole (5-1 mg/kg/day for 14-21 days)
  • 2. Bithionol (1 mg/kg/day for seven days or on alternate days for 3 days.
  • 3. Fenbendazole 5-1 mg/kg/day in two divided doses for 1 to 14 days
  • 4. Niclofolan 1 mg/kg/day for three days or two doses of 2 mg/kg on alternate days. Control

  • 1. Prevent dogs and cats from ingesting freshwater crustaceans.
  • 2. Eliminate snails! PROSTHOGONIMUS MACRORCHIS -the oviduct fluke(Figure 3.13) Host and Habitat

This fluke is found in the bursa of Fabricius and oviduct of domestic and wild birds of North America. Identification

This oval fluke is 5 to 7 mm in length and the testes are large; hence, the species name macrorchis (big testes). Life Cycle

Two intermediate hosts are required; the first is a water snail and the second is a dragonfly nymph (a naiad). Sporocysts are formed which produce cercariae. These cercariae are liberated from the snail and swim about in the water. They are drawn into the anal openings of a dragonfly naiad. The tail of the cercaria is lost and the metacercaria penetrates into the muscles of the naiad and encysts. The definitive host is infected by eating either the dragonfly naiad or the adult dragonfly. The juvenile fluke migrate to the cloaca and the bursa of Fabricius, where they become adult flukes. The bursa of Fabricius is atrophied in mature birds, so the flukes enter oviduct. Pathogenesis and Clinical Signs

This is the most pathogenic fluke of poultry in North America. The flukes produce an acute inflammation of the oviduct. This results in the production of abnormal eggs and discharge of egg albumin from the cloaca. The irritated oviduct performs retroperistaltic movements, and broken yolks, egg albumin, bacteria and parasite material enter the peritoneal cavity. A fatal peritonitis usually results. Infected birds become inactive and lose their appetite. Egg production drops and those eggs that are produced, have thin shells or no shells at all.

Figure 3.13: Prosthogonimum Macrorchis Diagnosis

  • 1. The eggs may be found in large numbers in the cloacal discharges.
  • 2. Adult flukes may be identified on necropsy.
  • 3. On rare occasions, adult flukes may be found in the eggs laid by infected chickens. Treatment

Albendazole and praziquantel may be effective anthelmintics. Control

  • 1. Snail control should be practiced.
  • 2. Birds should have limited access to wet marshy land where dragonflies are common. ECHINOSTOMA REVOLUTUN(Figure 3.14) Host and Habitat

This fluke occurs in the rectum and ceca of the duck, goose and other aquatic birds. Identification

It is 10 to 22 mm long and up to 2.25 mm broad. On its anterior end is a head crown which bears 37 spines. The eggs are from 90 to 126 by 59 to 71 microns. Life Cycle

The eggs are voided in the feces and hatch, releasing a miracidium. The miracidium penetrates an aquatic snail, the first intermediate host. Cercariae are produced in the snail. These cercariae either encyst in the same snail or they escape and enter another snail of the same or different species. An alternate second intermediate host is the tadpole . The final host becomes infected by ingesting these snails and the flukes grow to the adult stage in 15 to 19 days. Pathogenesis and Clinical Signs

In light infections, the flukes produce little pathology. Heavy fluke infections may cause severe enterits, hemorrhagic diarrhea and progressive emaciation.


figure 3.14: Echinostoma Revolutun Diagnosis

Diagnosis is made by finding the eggs of the worms in the feces of the host or by finding adult flukes in the intestine at necropsy. Treatment

  • 1. Brotianide
  • 2. Oxyclozanide
  • 3. Rafoxanide
  • 4. flubendazole Control

  • 1. Consider snail control
  • 2. Prevent chickens' access to wet marshy areas. SCHISTOSOMA SPP. (also known Bilharzia spp.) (Figure 3.15) General information concerning the schistosomes:

  • 1. These flukes inhabit the blood vessels of their hosts.
  • 2. Remember that flukes are usually hermaphroditic. Schistosomes are the exception to that rule. They are not hermaphroditic. There are both male and female schistosomes.
  • 3. The schistosomes resemble the 'roundworms'; they do nto look like flukes.
  • 4. The females is a very slender worm. She is carried, especially during copulation, in the gynecophoric canal of the male (gyneco - female; - phoric - to carry). The gynecophoric canal is formed by the incurved lateral edges of the male's body.
  • 5. The eggs are thin-shelled and have no operculum. Some schistosome eggs have a lateral or terminal spine.
  • 6. Schistosoma spp. are important parasites of man and domestic animals. Hosts:

  • 1. Schistosoma hematobium - parasite of man; adult flukes reside in the posterior mesenteric arteries. Eggs are laid in the walls of the bladder, ureters and urethra.
  • 2. Schistosoma mansoni - parasite of man; occurs in the mesenteric veins of man.
  • 3. Schistosoma japonicum - occurs in the portal and mesenteric veins of man and domestic animals in the Far East.
  • 4. Schistosoma bovis - occurs in the portal and mesenteric veins of cattle, sheep and goats, in Central, East and West Africa, the Mediterranean and the Middle East. Identification

Schistosoma bovis males are 9 to 22 mm long and 1 to 2 mm wide. The female is 12 to 28 mm long. The eggs are usually spindle shaped and measure 187 by 60 microns. Eggs of human schistosomes have a lateral or terminal spine. Life Cycle

The female schistosome, containing her eggs, penetrates deeply into the small vessels of the mucosa or submucosa of the intestine and lays her eggs in the capillaries. The eggs pass through the intestinal wall and out with the feces. The mechanism by which this "escape" is achieved is not at all clear and has been the subject of much speculation. The spines on the eggs are often credited with contribution to the expulsion. The eggs hatch after contact with water and release the miracidium. Miracidia penetrate the tissues of aquatic snails and develop through two generations of sporocysts. The second generation of sporocysts forms cercariae. These cercariae are called furcocercous (or fork-tailed) cercariae. They emerge from the snail and swim about in the water. Infection of the definitive host (man) is by active skin penetration. Cercariae of Schistosoma do nto encyst and they do nto develop through a second intermediate host. They pnetrate the skin of the definitive host by digesting the skin tissue. The cercariae then lose their tails and transform to structures called schistosomulae. Schistosomulae are nothing more than young flukes. They mature in the blood vesselts of the lungs. They are then carried to the liver, presumably via the bloodstream, and are found in the portal veins of the liver. The worms pair together and migrate to the mesenteric veins. Pathogenesis (S. bovis)

Two clinical syndromes are seen in animals infected with schistosomes: Acute intestinal schistosomiasis

It is seen in heavily infected animals and begins when female worms pass large number of eggs, at 7 to 9 weeks after infection. The duration of the syndrome depends upon the intensity of infection. Recovery is usually spontaneous. With this syndrome, histopathology reveals severe hemorhagic lesions in the intestinal mucosa, particularly the small intestine and the cecum. The intestinal mucosa is edematous and covered wit hemorrhagic foci, 1 to 10 mm in diameter. Large numbers of eggs will be found in the mucosa and in the blood-stained mucus covering the intestinal surface. There is a marked granulomatous response to eggs laid in the submucosa. The eggs gradually disintegrate and there is infiltration with epithelioid cells, fibroblasts and fibrous tissue formation. Longstanding infections are manifested by granulomatous


Figure 3.15: Schistosoma spp.


lesions in the mucosa, submucosa and muscularis mucosa. There is prominent fibrous thickening of the intestnal wall and intestinal catarrh.

Adult parasites cause phlebitis in the mesenteric veins and there is proliferation of the tunica intima with a partial occlusion of the lumen. Adult worms may then move from their predilection sites in the veins of the intstine and move to other organs of the body (pancreas, lungs, and mesenteric lymph nodes). Chronic hepatic schistosomiasis

Chronic hepatic schistosomiasis occurs in schistosome-infected animals, particularly those exposed to heavy infections. Animals develop granulomatous lesions and periportal inflammation. There is progressive portal fibrosis. Lymphoid nodules and follicles develop around dead parasites in the liver. In heavy infections, there may be massive thrombosis of the portal veins and hepatic infarction.

This is an immunological disease resulting from the host's cell-mediated immune response to schistosome eggs in the liver. Remember that eggs are usually laid in mesenteric capillaries. Some eggs may be swept back in the portal circulation. They lodge in the portal venules. This lodging of eggs has little effect on the portal blood supply, but soluble antigens begin to escape through pores in the egg shell and stimulate lymphocytes, macrophages, and eosinophils to accumulate around the egg. An avascular granuloma forms which may reach 100 times the size of the egg. The inflammatory reaction will become chronic and is characterized by the formation of epithelioid cells, giant cells, and fibroblasts. The egg is destroyed. Healing occurs and collagen and fibrous tissue may be laid down. In heavy infections, the development and healing of large numbers of egg granulomas causes massive fibrosis in the portal triads. One may see "clay-pipestem" fibrosis. The development of fibrous scar tissue causes obstruction of the venous blood supply. Clinical signs of S. bovis

  • 1. The migration of large numbers of schistosomulae through the lungs may cause a temporary cough (this is RARE).
  • 2. Acute intestinal schistosomiasis - profuse diarrhea, dehydration and anorexia. Anemia and hypoalbuminemia are present, sometimes with edema. There is a marked decrease in production, or a weight loss.
  • 3. Chronic hepatic schistomiasis - emaciation, eosinophilia, anemia, hypoalbuminemia and hypergammaglobulinemia. Neurological signs may be seen. Diagnosis

  • 1. Fecal examination may reveal the eggs of the parasites mixed with blood and mucus (bovine).
  • 2. Biopsies (human and bovine)
  • 3. Serological tests for animals are not reliable.
    • a. intradermal skin testing
    • b. complement-fixation test
    • c. circumoval precipitin reaction
    • d. cercarienhullien reaction (CHR) Treatment

  • 1. Praziquantel is the drug of choice for schistosomiasis in man. Dose at 6 mg/kg or three doses of 2 mg/kg four hours apart. Side effects of this drug are nausea, vomiting and dizziness.
  • 2. Schistosomiasis in animals- Take care. Many of the drugs kill all the adult schistosomes at the same time. These become emboli in the portal veins and portal occulusion and hepatic infarction may occur and result in hepatic failure.
    • a. Stibophen
    • b. Hycathone
    • c. Niridazole
    • d. Trichlorophon. Control

  • 1. Control the snail intermediate host using molluscicides.
  • 2. Fence off lakes and ponds. Provide water in watering troughs. Clean water troughs.
  • 3. Human schistosomiasis - reduce contact with contaminated water by providing piped water to houses, laundry units and swimming pools. Do not defecate in streams. If people must work around water provide protective clothing.

*Item of Interest! Schistosome cercarial dermatitis - "swimmer's itch"

Several species of bird schistosomes are disturbed throughout the world and cuase "swimmer's itch" when their cercariae attack anyone on whose skin the organisms land.

The guilty genera Trichobilharzia, Gigantobilharzia, Ornithobilarzia and Microbilharzia.

The skin reaction is a product of sensitization with repeated infections causing increasingly severe reactions. The cercariae penetrate the skin of the human. They cannot complete their migration, and the host's immune responses rapidly kill them. When the cercariae die, they release substances that cause inflammation and a pus-filled pimple. An itching rash may be produced all over the body. This swimmer's itch is not a serious threat to health, but is annoying -much like poison ivy. This condition is most common in the Great Lakes Area, but it has been reported from every state in the United States. HETEROBILHARZIA AMERICANA - the blood fluke of dogs Host and Habitat

This fluke is found in the mesenteric veins of the small and large intestines and probably the portal veins of the dog, bobcat and raccoon along the coast of the Gulf of Mexico. It is found in the Lousiana swamplands and the mudflats of the Mississippi delta. Identification

These flukes have separate sexes. The female is slender and may be 9 mm long. The male worm is about 6.5 mm long and has a gynecophoric canal. The egg is 8 x 5 microns, has no spine, and contains a miracidium. Life Cycle

Eggs hatch immediately after deposition if they contact water. The miracidium enters an aquatic snail, the first intermediate host. Mature cercariae are produced in 25 days. The cercariae penetrate the skin of th definitive host, migrate to the lung, then to the liver and to the mesenteric vein. Pathogenicity and Clinical Signs

At the site of penetration by the cercariae, the develops a marked itching skin rash with pustular eruptions. The animal may exhibit an intermittent diarrhea with mucus, Infected dogs show emaciation, anorexia, and diarrhea, and may develop a terminal coma accompanied by bloody diarrhea. Diagnosis

Identification of eggs in the feces. Control

Restrict access to marsh lands and swamps. Treatment is not usually attepted. Calamine lotion may alleviate te pruritus. Vvulifer Amblophitis (FIGURE 3.17)

BLACK SPOT of fishes is due to Vvulifer amblophitis, a parasite of the kingfisher, a fish-eating bird distributed widely across the US. The adult fluke is found in the small intestine of the bird. Eggs are voided in the feces. The miracidum hatches and penetrates an quatic snail. The parasite goes through two sporocyst stages in the snail and emerges as cercariae. These cercariae rise to the surface of the water, where they are sensitive to the passing of a fish, particularly a perch or centrarchid. If they contact a fish, they drop their tails and penetrate the fish. Once inside the dermis of the fish, the cercariae change into neascus metacercariae. The fish (the second intermediate host) responds to the neascus by laying down layers of melanin granules, causing a conspicuous black spot. Kingfishers become infected when they eat such a fish. It is permissible for a human to eat the fish as long as it is cooked well. CLINOSTOMUM SP (FIGURE 3.17)

YELLOW GRUB of fishes is caused by Clinostomum sp. The adult flukes are found in the mouth and throat of the definitive host. Eggs are dropped out of the mouth while the bird is drinking. Eggs may also be swallowed and passed in the feces. The first intermediate hosts are snails in which wsporocysts and redia are produced. Cercariae are released and they penetrate the second intermediate host, a fish. Metacercariae are found subcutaneously in the muscles of bass, perch and trout. Metacercariae are unsightly yellow cysts ("yellow grubs"). The heron becomes infected by eating infected fish.

Note: A case of larynogopharyngitis due to ingestion of fish infected with Clinostomum has been recorded in man.


Figure 3.16: Uvulifer ambloplitis