Platyhelminthes (flat worms) as parasites of medical interest

Platyhelminthes (flat worms) as parasites of medical interest

Type of parasites Protozoa Helminths Arthropods Nematodes Trematodes Cestodes Platyhelminthes

A simplified classification of flat worms Platyhelminthes Trematoda Planaria Monogenea Digenea Cestoda

Trematodes General features

Trematodes (or flukes) Nearly all trematodes are parasites of mollusks and vertebrates. The trematodes are estimated to include 18.000 to 24.000 species, and are divided into two subclasses. The smaller Aspidogastrea, comprising about 100 species, are obligate parasites of mollusks and may also infect turtles and fish, including cartilaginous fish. The Digenea, which constitute the majority of trematode diversity, are obligate parasites of both mollusks and vertebrates, but rarely occur in cartilaginous fish.

Trematodes (or flukes) All digenea are parasitic. Dorso-ventrally flattened worms with simple anatomy and without segmentation. No coelom, but animals are filled with mesodermal parenchyma. No blood vessels.

Trematodes (or flukes) Simple ladder nervous system. The nervous system includes anterior cerebral ganglia, longitudinal nerve cords, and some lateral nerves. The brain consists of a pair of ganglia in the head region, from which two or three pairs of nerve cords run down the length of the body. Trematodes generally lack any specialised sense organs, although some ectoparasitic species do possess one or two pairs of simple ocelli. Most free living planarians and parasitic larval forms possess a variety of sensory organs.

Trematodes (or flukes) Digenea posses two suckers (oral and ventral acetabulum) which they use to attach within the host. The mouth is located at the forward end of the animal, and opens into a muscular, pumping pharynx. The pharynx connects, via a short oesophagus, to one or two blind-ending caeca, which occupy most of the length of the body.

Trematodes (or flukes) In some species, the caeca are themselves branched. As in other flatworms, there is no anus, and waste material must be expelled through the mouth. Muscular pharynx permits the worm to pump food into the blind ending gut.

Trematodes (or flukes) Most trematodes are hermaphrodites (but there are important exceptions, e.g. Schistosoma sp). Most are capable of some form of asexual reproduction (e.g. many turbellarians reproduce by fission). Most flatworms are hermaphroditic; however, they often pair with other individuals to exchange gametes

Trematodes (or flukes) Although the excretion of nitrogenous waste occurs mostly through the tegument, trematodes do possess an excretory system, which is instead mainly concerned with osmoregulation. This consists of two or more protonephridia (flame cells), with those on each side of the body opening into a collecting duct. The excretory system is a network of water collecting tubules adjacent to flame cells. The two collecting ducts typically meet up at a single bladder, opening to the exterior through one or two pores near the posterior end of the animal.

Trematodes (or flukes) When cilia beat they move water into the tubules and out the body through pores called nephridiopo res.

Trematodes (or flukes) Also the tegument ( skin ) plays an important role active in nutrient uptake. The epidermis consists of a single cell: a syncytium formed by fusion of multiple cells. The tegument s cell bodies and nuclei underlie the two muscle layers.

Digenea important in human parasitology Opistorchis, Clonorchis, Fasciola, Dicrocoelium Biliary duct Paragonimus Lung Schistosoma Blood vessels

Biliary duct

Life cycle of Opistorchis

Opistorchiasis Causal Agent: Opisthorchis viverrini (Southeast Asian liver fluke) and O. felineus (cat liver fluke). Geographic Distribution: O. viverrini is found mainly in northeast Thailand, Laos, and Kampuchea. O. felineus is found mainly in Europe and Asia, including the former Soviet Union.

Opistorchiasis Life cycle: The adult flukes deposit fully developed eggs that are passed in the feces. After ingestion by a suitable snail (first intermediate host), the eggs release miracidia, which undergo in the snail several developmental stages (sporocysts, rediae, cercariae). Cercariae are released from the snail and penetrate freshwater fish (second intermediate host), encysting as metacercariae in the muscles or under the scales. The mammalian definitive host (cats, dogs, and various fish-eating mammals including humans) become infected by ingesting undercooked fish containing metacercariae. After ingestion, the metacercariae excyst in the duodenum and ascend through the ampulla of Vater into the biliary ducts, where they attach and develop into adults, which lay eggs after 3 to 4 weeks. The adult flukes (O. viverrini: 5-10 mm by 1-2 mm; O. felineus: 7-12 mm by 2-3 mm) reside in the biliary and pancreatic ducts of the mammalian host, where they attach to the mucosa.

Opistorchiasis Clinical Features: Most infections are asymptomatic. In mild cases, manifestations include dyspepsia, abdominal pain, diarrhea or constipation. With infections of longer duration, the symptoms can be more severe, and hepatomegaly and malnutrition may be present. In rare cases, cholangitis, cholecystitis, and chlolangiocarcinoma may develop. In addition, infections due to O. felineus may present an acute phase resembling Katayama fever (schistosomiasis), with fever, facial edema, lymphadenopathy, arthralgias, rash, and eosinophilia. Chronic forms of O. felineus infections present the same manifestations as O. viverrini, with in addition involvement of the pancreatic ducts.

Opistorchiasis Laboratory Diagnosis: Diagnosis is based on microscopic identification of eggs in stool specimens. However, the eggs of Opisthorchis are practically indistinguishable from those of Clonorchis. Treatment: Praziquantel is the drug of choice to treat opisthorchiasis. Embryonated egg

Life cycle of Clonorchis

Clonorchiasis Causal Agent: Clonorchis sinensis (Chinese or oriental liver fluke). Geographic Distribution: Endemic areas are in Asia including Korea, China, Taiwan, and Vietnam. Clonorchiasis has been reported in non endemic areas (including the United States). In such cases, the infection is found in Asian immigrants, or following ingestion of imported, undercooked or pickled freshwater fish containing metacercariae.

Life Cycle: Clonorchiasis Embryonated eggs are discharged in the biliary ducts and in the stool. Eggs are ingested by a suitable snail (first intermediate host). Each egg releases a miracidia, which go through several developmental stages (sporocysts, rediae and cercariae). The cercariae are released from the snail and after a short period of free-swimming time in water, they come in contact and penetrate the flesh of freshwater fish (second intermediate host), where they encyst as metacercariae. Infection of humans (definitive host) occurs by ingestion of undercooked, salted, pickled, or smoked freshwater fish. After ingestion, the metacercariae excyst in the duodenum and ascend the biliary tract through the ampulla of Vater. Maturation takes approximately 1 month. The adult flukes (measuring 10-25 mm by 3-5 mm) reside in small and medium sized biliary ducts. In addition to humans, carnivorous animals can serve as reservoir hosts.

Clonorchiasis Clinical Features: Most pathologic manifestations result from inflammation and intermittent obstruction of the biliary ducts. In the acute phase, abdominal pain, nausea, diarrhea, and eosinophilia can occur. In long-standing infections, cholangitis, cholelithiasis, pancreatitis, and cholangiocarcinoma can develop, which may be fatal.

Clonorchiasis Laboratory Diagnosis: Microscopic demonstration of eggs in the stool or in duodenal aspirate is the most practical diagnostic method. The adult fluke can also be recovered at surgery. Treatment: Praziquantel or albendazole* are the drugs of choice. Embryonated egg Adult fluke

Life cycle of Fasciolia

Fascioliasis Causal Agents: Fasciola hepatica (the sheep liver fluke) and Fasciola gigantica, parasites of herbivores that can infect humans accidentally. Geographic Distribution: Fascioliasis occurs worldwide. Human infections with F. hepatica are found in areas where sheep and cattle are raised, and where humans consume raw watercress, including Europe, the Middle East, and Asia. Infections with F. gigantica have been reported, more rarely, in Asia, Africa, and Hawaii.

Fascioliasis Life Cycle: Immature eggs are discharged in the biliary ducts and in the stool. Eggs become embryonated in water and release miracidia, which invade a suitable snail intermediate host (Galba, Fossaria and Pseudosuccinea). In the snail the parasites undergo several developmental stages (sporocysts, rediae and cercariae). The cercariae are released from the snail and encyst as metacercariae on aquatic vegetation or other surfaces. Mammals (definitive hosts) acquire the infection by eating vegetation containing metacercariae. Humans can become infected by ingesting metacercariae-containing freshwater plants, especially watercress. After ingestion, the metacercariae excyst in the duodenum and migrate through the intestinal wall, the peritoneal cavity, and the liver parenchyma into the biliary ducts, where they develop into adults. In humans, maturation from metacercariae into adult flukes takes approximately 3 to 4 months. The adult flukes (F. hepatica up to 30 mm by 13 mm; F. gigantica up to 75 mm) reside in the large biliary ducts of the mammalian host. F. hepatica infect various animal species, mostly herbivores.

Fascioliasis Clinical Features: During the acute phase (caused by the migration of the immature fluke through the hepatic parenchyma), manifestations include abdominal pain, hepatomegaly, fever, vomiting, diarrhea, urticaria and eosinophilia, and can last for months. In the chronic phase (caused by the adult fluke within the bile ducts), the symptoms are more discrete and reflect intermittent biliary obstruction and inflammation. Occasionally, ectopic locations of infection (such as intestinal wall, lungs, subcutaneous tissue, and pharyngeal mucosa) can occur.

Fascioliasis Laboratory Diagnosis: Microscopic identification of eggs is useful in the chronic (adult) stage. Eggs can be recovered in the stools or in material obtained by duodenal or biliary drainage. They are morphologically indistinguishable from those of Fasciolopsis buski. Unembryonated egg Antibody detection tests are useful especially in the early invasive stages, when the eggs are not yet apparent in the stools, or in ectopic fascioliasis.

Fascioliasis Laboratory Diagnosis: False fascioliasis (pseudofascioliasis) refers to the presence of eggs in the stool resulting not from an actual infection but from recent ingestion of infected livers containing eggs. This situation (with its potential for misdiagnosis) can be avoided by having the patient follow a liver-free diet several days before a repeat stool examination.

Fascioliasis Treatment: Unlike infections with other flukes, Fasciola hepatica infections may not respond to praziquantel. The drug of choice is triclabendazole with bithionol as an alternative.

Life cycle of Dicrocoelium

Dicrocoeliasis Causal Agent: Dicrocoelium dendriticum, the lanceolate fluke. Geographic Distribution: Europe, northern Asia, America and northern Africa.

Dicrocoeliasis Life Cycle: Ruminants are the usual definitive hosts for D. dendricitum, although other herbivorous animals, carnivores, and humans can serve as definitive hosts. Embryonated eggs are shed in feces. The eggs are ingested by a snail. When the miracidia hatch, they migrate through the gut wall and settle into the adjacent vascular connective tissue, where they become mother sporocysts. The sporocysts migrate to the digestive gland where they give rise to several daughter sporocysts. Inside each daughter sporocyst, cercariae are produced. The cercariae migrate to the respiration chamber where they are shed in slime ball from the snail. Many species of snail may serve as the first intermediate host (Zebrina spp. and Cionella spp.). After a slime ball is ingested by an ant, the cercariae become free in the intestine and migrate to the hemocoel where they become metacercariae. Many ants may serve as the second intermediate host, especially members of the genus, Formica. After an ant is eaten by the definitive host, the metacercariae excyst in the small intestine. The worms migrate to the bile duct where they mature into adults. Humans can serve as definitive hosts after accidentally ingesting infected ants.

Dicrocoeliasis Clinical Features: Most infections are light and asymptomatic. In heavier infections, symptoms may include cholecystitis, liver abscesses and upper abdominal pain. Laboratory Diagnosis: Microscopic identification of eggs in the stool or duodenal fluid. If eggs are found only in stool, it could represent spurious passage following the ingestion of infected animal liver. Additional specimens should be collected to confirm a true infection. Treatment: Praziquantel* is the drug of choice. Embryonated egg

Lung

Life cycle of Paragonimus

Paragonimiasis Causal Agent: More than 30 species of the genus Paragonimus have been reported which infect animals and humans. Among the more than 10 species reported to infect humans, the most common is Paragonimus westermani, the oriental lung fluke. Geographic Distribution: Paragonimus spp. are distributed throughout the Americas, Africa and southeast Asia. P. westermani is distributed in southeast Asia and Japan. P. kellicotti is endemic to North America.

Paragonimiasis Life Cycle: The eggs are excreted unembryonated in the sputum, or alternately they are swallowed and passed with stool. In the external environment, the eggs become embryonated and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues. Miracidia go through several developmental stages inside the snail: sporocysts, rediae, with the latter giving rise to many cercariae, which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host.

Paragonimiasis Life Cycle: Human infection with P. westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite. Animals such as pigs, dogs, and a variety of feline species can also harbor P. westermani. The metacercariae excyst in the duodenum, penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults (7.5-12 mm by 4-6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycles is not achieved, because the eggs laid cannot exit these sites. Time from infection to oviposition is 65 to 90 days. Infections may persist for 20 years in humans.

Paragonimiasis Clinical Features: The acute phase (invasion and migration) may be marked by diarrhea, abdominal pain, fever, cough, urticaria, hepatosplenomegaly, pulmonary abnormalities, and eosinophilia. During the chronic phase, pulmonary manifestations include cough, expectoration of discolored sputum, hemoptysis, and chest radiographic abnormalities. Extrapulmonary locations of the adult worms result in more severe manifestations, especially when the brain is involved.

Paragonimiasis Laboratory Diagnosis: Diagnosis is based on microscopic demonstration of eggs in stool or sputum, but these are not present until 2 to 3 months after infection. Eggs are also occasionally encountered in effusion fluid or biopsy material. Concentration techniques may be necessary in patients with light infections. Biopsy may allow diagnostic confirmation and species identification when an adult or developing fluke is recovered. Treatment: Unembryonated egg Praziquantel* is the drug of choice to treat paragonimiasis. Bithionol is an alternative drug for treatment of this disease.

Blood vessels

Life cycle of Schistosoma

Schistosomiasis Causal Agents: Schistosomiasis is caused by digenetic blood trematodes. The three main species infecting humans are Schistosoma haematobium, S. japonicum and S. mansoni. Two other species, more localized geographically, are S. mekongi and S. intercalatum. In addition, other species of schistosomes, which parasitize birds and mammals, can cause cercarial dermatitis in humans. Geographic Distribution: S. mansoni is found in parts of South America and the Caribbean, Africa, and the Middle East. S. haematobium in Africa and the Middle East. S. japonicum in the Far East. S. mekongi and S. intercalatum are found focally in Southeast Asia and central West Africa, respectively.

Schistosomiasis Life Cycle: Eggs are eliminated with faeces or urine. Under optimal conditions the eggs hatch and release miracidia, which swim and penetrate specific snail intermediate hosts. The stages in the snail include 2 generations of sporocysts and the production of cercariae. Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host and shed their forked tail becoming schistosomulae. The schistosomulae migrate through several tissues and stages to their residence in the veins. Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species.

Schistosomiasis Life Cycle: For instance, S. japonicum is more frequently found in the superior mesenteric veins draining the small intestine and S. mansoni occurs more often in the superior mesenteric veins draining the large intestine. However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. S. haematobium most often occurs in the venous plexus of bladder, but it can also be found in the rectal venules. The females deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S. mansoni and S. japonicum) and of the bladder and ureters (S. haematobium), and are eliminated with feces or urine, respectively.

Trematodes of the Schistomatidae family have separate sexes (unusual for Platyhelminthes). The males are shorter and fatter than the females, and have a ventral groove (gynecophoric canal) along their body into which the female can fit. male

Mating

Schistosomiasis Clinical Features: Pathology of S. mansoni and S. japonicum schistosomiasis includes: Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension and occasional embolic egg granulomas in brain or spinal cord. Pathology of S. haematobium schistosomiasis includes: Hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, hourse and goats, serve as reservoirs for S. japonicum, and dogs for S. mekongi.

Clinical Features: Many infections are asymptomatic. Schistosomiasis Acute schistosomiasis (Katayama's fever) may occur weeks after the initial infection, especially by S. mansoni and S. japonicum. Manifestations include fever, cough, abdominal pain, diarrhea, hepatosplenomegaly, and eosinophilia. Occasionally central nervous system lesions occur: cerebral granulomatous disease may be caused by ectopic S. japonicum eggs in the brain, and granulomatous lesions around ectopic eggs in the spinal cord from S. mansoni and S. haematobium infections may result in a transverse myelitis with flaccid paraplegia. Continuing infection may cause granulomatous reactions and fibrosis in the affected organs, which may result in manifestations that include: colonic polyposis with bloody diarrhea (S. mansoni mostly); portal hypertension with hematemesis and splenomegaly (S. mansoni, S. japonicum, S. mansoni); cystitis and ureteritis (S. haematobium) with hematuria, which can progress to bladder cancer; pulmonary hypertension (S. mansoni, S. japonicum, more rarely S. haematobium); glomerulonephritis; and central nervous system lesions.

Skin vesicles on the foot, created by the penetration of Schistosoma

boy infected with Schistosoma japonicum schisto liver granuloma Portal hypertension

Schistosomiasis Laboratory Diagnosis: Microscopic identification of eggs in stool or urine is the most practical method for diagnosis. Stool examination should be performed when infection with S. mansoni or S. japonicum is suspected, and urine examination should be performed if S. haematobium is suspected. Eggs can be present in the stool in infections with all Schistosoma species. The examination can be performed on a simple smear (1 to 2 mg of fecal material). Since eggs may be passed intermittently or in small amounts, their detection will be enhanced by repeated examinations and/or concentration procedures (such as the formalin-ethyl acetate technique). In addition, for field surveys and investigational purposes, the egg output can be quantified by using the Kato-Katz technique (20 to 50 mg of fecal material) or the Ritchie technique.

Schistosomiasis Laboratory Diagnosis: Eggs can be found in the urine in infections with S. haematobium (recommended time for collection: between noon and 3 PM) and with S. japonicum. Detection will be enhanced by centrifugation and examination of the sediment. Quantification is possible by using filtration through a Nucleopore membrane of a standard volume of urine followed by egg counts on the membrane. Tissue biopsy (rectal biopsy for all species and biopsy of the bladder for S. haematobium) may demonstrate eggs when stool or urine examinations are negative.

Lateral spine Schistosomiasis

Schistosomiasis Treatment: Safe and effective drugs are available for the treatment of schistosomiasis. The drug of choice is praziquantel for infections caused by all Schistosoma species. Oxamniquine has been effective in treating infections caused by S. mansoni in some areas in which praziquantel is less effective.