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Intestinal Flukes

  • Author: Joseph Adrian L Buensalido, MD; Chief Editor: Michael Stuart Bronze, MD  more...
 
Updated: Jul 14, 2016
 

Background

Numerous trematodes cause disease in humans. These include the schistosomes, which live in the gastrointestinal and genitourinary tracts, various liver flukes (eg, Clonorchis sinensis,Opisthorchiasis species), and the intestinal trematodes (flukes). These trematodes are included in the World Health Organization (WHO) list of neglected tropical diseases (NTDs) that prevail in tropical and subtropical conditions in 149 countries and affect more than one billion people, costing developing economies billions of dollars every year.[1] This article focuses on intestinal trematodes, although clonorchiasis and opisthorchiasis are also discussed despite being liver fluke infections, since their respective pathogens migrate through the intestine before ending up in the liver.

Intestinal trematodes can be classified into at least 14 families (with their corresponding sources of infection found below), as follows:[2]

  • Brachylaimidae (from terrestrial snails)
  • Cathaemasiidae (from a yet unknown source)
  • Diplostomidae (from snakes, frogs, and tadpoles)
  • Echinostomatidae (from freshwater fish, frogs, mussels, snails, and tadpoles)
  • Fasciolidae (from aquatic vegetables and contaminated water)
  • Gastrodiscidae (from aquatic vegetables, crustaceans, molluscs, and amphibians)
  • Gymnophallidae (from oysters)
  • Heterophyidae (freshwater fishes)
  • Lecithodendriidae (from dragonflies)
  • Microphallidae (from shrimps and crabs)
  • Nanophyetidae (from salmonid fishes)
  • Paramphistomidae (from aquatic plants)
  • Plagiorchiidae (from insect larvae)
  • Strigeidae (from a yet unknown source)

Intestinal trematodes are flat hermaphroditic worms that vary in length from a few millimeters to many centimeters (see the image below). Of the approximately 70 species known to colonize the human intestine, only a few species are known to cause actual infection. Globally, it is likely that more than the estimated 40-50 million people are infected with intestinal trematodes, primarily infected via the foodborne route. Populations in Southeast Asia appear to be most vulnerable. An exhaustive 2009 review of these infections in this region provides detailed information on the large number of species infecting humans, their pathogenicity, diagnostic issues, and treatments.[3]

In 2012, the various manifestations, methods of diagnosis, and management of foodborne trematodiasis, which include the intestinal flukes, were detailed in the British Medical Journal[4] and the European Journal of Microbiology and Infectious Diseases[5] . In the former, the species of intestinal flukes considered to be of public importance include the following:

  • Echinostoma species
  • Fasciolopsis buski
  • Gymnophalloides seoi
  • Haplorchis species
  • Heterophyes species
  • Metagonimus species
Adult fluke of Fasciolopsis buski. Image reproduce Adult fluke of Fasciolopsis buski. Image reproduced from the Division of Parasitic Diseases, Centers for Disease Control and Prevention (CDC), Atlanta, GA.

The most common human intestinal trematode was said to be Fasciolopsis buski, which causes fasciolopsiasis,[6] and should be differentiated from Fasciola hepatica and Fasciola gigantica, which are liver flukes that cause fascioliasis. Infection involving the other 3 trematodes—Heterophyes heterophyes, Metagonimus yokogawai, and Echinostoma species—results in a presentation that is clinically similar to that of malabsorptive illness.

In the genus Echinostoma, Echinostoma ilocanum is the most common organism that causes infection in humans. However, there are 500 species of echinostomatid flukes, with 20 species from 8 genera that can cause human infection. The genus Echinostoma is considered the largest, which includes Echinostomahortense, Echinostomaangustitestis, Echinostomacinetorchis, Echinostomaechinatum, E ilocanum, Echinostomamacrorchis, and Echinostomarevolutum.[7]

H heterophyes and M yokogawai are less-common causes of human intestinal fluke infection.

Other intestinal flukes that rarely cause human intestinal infection include Gastrodiscoides hominis, Phaneropsolus bonnei, and Prosthodendrium molenkampi. Intestinal flukes have likely infected humans for hundreds of years, if not longer. Evidence of Gymnophalloides seoi infection has been traced back to the 17th century based on discovery of G seoi eggs in a Korean mummy.[8]

See Common Intestinal Parasites, a Critical Images slideshow, to help make an accurate diagnosis.

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Pathophysiology

Intestinal flukes cause inflammation, ulceration, and mucous secretion at the site of attachment. Severe infections may also cause intestinal obstruction or malabsorption, leading to hypoalbuminemia, protein-losing enteropathy, and impaired vitamin B-12 absorption. Foodborne illness has been associated with the ingestion of many different types of potentially infected foods, such as different types of both freshwater and brackish-water fish and snails, reptiles (amphibians and certain snakes), aquatic plants, and insects.[3]

Fasciolopsis buski

F buski, which causes fasciolopsiasis, attaches to the duodenal and jejunal mucosa; however, in severe infections, it may attach to the ileum or colon.

In London, Busk first described F buski in 1843 after finding it in the duodenum of a sailor. In 1925, Barlow first determined its life cycle in humans. A well-known illustrative life cycle schematic is shown below.

Life cycle of Fasciolopsis buski. Image reproduced Life cycle of Fasciolopsis buski. Image reproduced from the Division of Parasitic Diseases, Centers for Disease Control and Prevention (CDC), Atlanta, GA.

The immature eggs (see the images below) are discharged from human feces and reach fresh water, hatching after 3-7 weeks and forming miracidia.

The life cycle of Fasciolopsis. Immature eggs are The life cycle of Fasciolopsis. Immature eggs are discharged into the intestine and stool and become embryonated in water. The eggs then release miracidia, which invade a suitable snail intermediate host, in which the parasites undergo several developmental stages (sporocysts, rediae, cercariae). The cercariae are released from the snail and encyst as metacercariae on aquatic plants, which are eaten by mammalian hosts (humans and pigs), who become infected. After ingestion, the metacercariae excyst in the duodenum and attach to the intestinal wall, where they develop into adult flukes (20-75 mm X 8-20 mm) in approximately 3 months and attach to the intestinal wall of the mammalian hosts. The adults have a life span of about one year. Image reproduced from the Division of Parasitic Diseases, Centers for Disease Control and Prevention (CDC), Atlanta, GA.
Egg of Fasciolopsis buski. Images reproduced from Egg of Fasciolopsis buski. Images reproduced from the Division of Parasitic Diseases, Centers for Disease Control and Prevention (CDC), Atlanta, GA.

Upon contact with host snails, the miracidia penetrate the soft tissues and form sporocysts, first- and second-generation rediae, and, lastly, cercariae. The cercariae encyst on various plants such as water caltrop, water chestnut, lotus (on the roots), water bamboo, and other aquatic vegetables. Humans are infected by consuming these raw vegetables.

In the human duodenum, the metacercariae attach to the walls and become adult worms in approximately 3 months. The adult worm (see image below) causes traumatic, toxic, and obstructive damage to the intestinal mucosa. Deep inflammatory ulcerations develop at the site of attachment. Large numbers of worms provoke excess mucous discharge and can obstruct the lumen. The adult worm metabolites can also cause intoxication and sensitization when absorbed via the lumen. A recent case report provides evidence of heavy infestation as a risk factor for intestinal perforation.[9]

Adult fluke of Fasciolopsis buski. Image reproduce Adult fluke of Fasciolopsis buski. Image reproduced from the Division of Parasitic Diseases, Centers for Disease Control and Prevention (CDC), Atlanta, GA.

Echinostoma species

In 1907, in Manila, Garrison first noted the genus Echinostoma, which is reported to have 12 species that may cause disease in humans. The most common species is E ilocanum, which has a characteristic horseshoe-shaped collar of 1-2 rows of straight spines that surround the dorsal and lateral sides of the oral sucker. E ilocanum flukes are small and elongated, measuring 5-15 mm in length and 1-2 mm in width. The most well-studied human-infecting species is E hortense.[10]

The adult worm, attached to the intestinal wall of humans, produces eggs that are passed in the feces. The eggs reach water, and miracidia develop and penetrate the first intermediate hosts—snails. During the course of 6-7 weeks inside the host snails, they develop into sporocysts, mother rediae, daughter rediae, and cercariae.

The cercariae leave the snails to encyst in the second intermediate hosts, which can be freshwater snails, fish, tadpoles, or vegetables. Humans are infected by ingesting raw or undercooked second intermediate hosts. Although not directly applicable to the human host, data in rodents suggest that, depending on trematode species, host species, and strain, primary expulsion of the fluke may occur.[11, 12] Inside human hosts, the flukes then attach to the small intestinal mucosa and, depending on the severity of infection, can produce shallow ulcers with mild inflammation and/or local necrosis. Mild infections do not cause symptoms, but heavy infections produce diarrhea, flatulence, and intestinal colic similar to fasciolopsiasis.

Disease manifestations in humans likely result from two pathogenetic mechanisms, including fluke-induced mechanical irritation and/or the related allergic reaction to various toxic metabolites.[10] Humoral responses to echinostomal infections may include elevated serum and gut-associated immunoglobulin A (IgA), immunoglobulin G (IgG), and immunoglobulin M (IgM) levels, as demonstrated by studies involving Echinostoma caproni.[13]

The intestinal epithelium appears to provide an important mechanism in mucosal defense. Its rapid epithelial cell turnover seems to facilitate the rejection of intestinal helminths. In rats, it has been shown that E caproni infection stimulates the augmented renewal of the intestinal epithelium, preventing the parasite from establishing itself in the host, resulting in clearance of the helminth.[14]

Various animals may be definitive hosts for differ Various animals may be definitive hosts for different Echinostoma species, such as aquatic birds, carnivores, rodents, and humans. Unembryonated eggs are passed in stool (1), and development occurs in the water (2). The miracidium takes an average of 10 days to mature and then hatches (3), penetrating the first intermediate host, a snail (4). Snails, in general, serve as the first intermediate host. The intramolluscan stages are as follows: sporocyst (4a); rediae (4b); and cercariae (4c). Cercariae may then encyst as metacercariae in the same first intermediate host or leave to penetrate a new second intermediate host (5). Several animals may become the second intermediate host, such as other snails, bivalves, fish, and tadpoles. The definitive host gets infected after eating infected second intermediate hosts (6). The metacercariae excyst in the duodenum (7). Adults then live in the small intestine (8). Image reproduced from the Division of Parasitic Diseases, Centers for Disease Control and Prevention (CDC), Atlanta, GA.

Heterophyes heterophyes

H heterophyes is the most common of the 10 species that compose the genus Heterophyes. H heterophyes is a small fluke, measuring 1-1.8 mm in length and 0.3-0.7 mm in width, with a broadly rounded posterior end. The oral sucker is subterminal and is one third the size of the ventral sucker.

H heterophyes are observed in the human intestine, jejunum, and ileum. The illustrative life cycle schematic for H heterophyes is shown below. These worms produce eggs, which are excreted in the feces and into the water. The first intermediate hosts, the snails, ingest the eggs. In the snails, the eggs hatch and undergo their developmental cycle, forming cercariae, which emerge from the snails and encyst on the second intermediate hosts—brackish or freshwater fish. In the second intermediate hosts, the cercariae are transformed into metacercariae, which infect humans upon ingestion of raw or undercooked fish. See the image below.

The life cycle of Heterophyes. The adult parasites The life cycle of Heterophyes. The adult parasites release embryonated eggs (each with a fully developed miracidium), which are then passed in the host's feces. After ingestion by a suitable snail (first intermediate host), the eggs hatch and release miracidia, which penetrate the snail's intestine. Snails of the genera Cerithidea and Pirenella are important hosts in Asia and the Middle East, respectively. The miracidia undergo several developmental stages in the snail (sporocysts, rediae, cercariae). Many cercariae are produced from each redia. The cercariae are released from the snail and encyst as metacercariae in the tissues of a suitable freshwater or brackish-water fish (second intermediate host). The definitive host becomes infected by ingesting undercooked or salted fish that contains metacercariae. After ingestion, the metacercariae excyst, attach to the mucosa of the small intestine, and mature into adults (measuring 1-1.7 mm X 0.3-0.4 mm). Heterophyes heterophyes infects humans, various fish-eating mammals (eg, cats, dogs), and birds. Image reproduced from the Division of Parasitic Diseases, Centers for Disease Control and Prevention (CDC), Atlanta, GA.

In humans, the flukes attach to the small bowel and cause shallow ulcers, mild inflammation, and/or superficial necrosis. Clinical presentation includes diarrhea, dyspepsia, and intestinal colic. Because of their small size, the eggs, and sometimes the adult flukes, enter blood vessels and embolize to the brain, producing symptoms similar to cerebral hemorrhage. Eggs may also enter the mesenteric lymphatics and travel to the heart, causing myocarditis, chronic congestive heart failure, and death.

Metagonimus yokogawai

M yokogawai, which is closely related to H heterophyes, is another important parasite. M yokogawai measures 1-2.5 mm in length and 0.4-0.75 mm in width. The ventral sucker is located to the right of the midline.

M yokogawai has a life cycle similar to that of H heterophyes, in which the adult worm in the human intestine produces eggs that are excreted in the feces. The illustrative life cycle schematic for M yokogawai is shown below. The eggs enter the water and infect the first intermediate hosts, the snails, where the eggs undergo their developmental cycle and become cercariae. Cercariae infect the second intermediate hosts, freshwater fish, and become metacercariae. Metacercariae infect humans after ingestion of raw or undercooked fish. The flukes then invade the mucosa of the small intestines, causing inflammation and ulcerations. Flukes eventually become encapsulated.

See the image below.

Life cycle of Metagonimus. The adult parasites rel Life cycle of Metagonimus. The adult parasites release fully embryonated eggs (each with a fully developed miracidium), which are then passed in the host's feces. After ingestion by a suitable snail (first intermediate host), the eggs hatch and release miracidia, which penetrate the snail's intestine. Snails of the genus Semisulcospira are the most common intermediate host for Metagonimus yokogawai. The miracidia undergo several developmental stages in the snail (sporocysts, rediae, cercariae). Many cercariae are produced from each redia. The cercariae are released from the snail and encyst as metacercariae in the tissues of a suitable freshwater or brackish-water fish (second intermediate host). The definitive host becomes infected by ingesting undercooked or salted fish that contains metacercariae. After ingestion, the metacercariae excyst, attach to the mucosa of the small intestine, and mature into adults (measuring 1-2.5 mm X 0.4-0.75 mm). M yokogawai infects humans, fish-eating mammals (eg, cats, dogs), and birds. Image reproduced from the Division of Parasitic Diseases, Centers for Disease Control and Prevention (CDC), Atlanta, GA.

As in infection with H heterophyes, M yokogawai occasionally embolize to other organs. Patients infected with M yokogawai present with mucous, diarrhea, and vague abdominal symptoms. Prognosis is usually good, except in cases of embolization. Fortunately, health studies performed in 2006 indicate that M yokogawai species and infections have become less endemic in certain regions.[15]

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Epidemiology

Frequency

United States

Infection with intestinal flukes affects only immigrants from endemic areas.

International

Intestinal flukes are endemic in the Far East and Southeast Asia. H heterophyes can also be found in the Nile delta region of Egypt. The movement of migrant workers within and across various East Asian countries has led to an increase in the prevalence of intestinal flukes parasites (mainly F buski) into regions that were not previously endemic for intestinal flukes. The list of countries where human trematode infections have been reported is long, with several studies indicating variable incidence rates.[16, 17, 18, 3, 19, 20, 21, 7, 22, 23, 24]

Multiple families of trematodes cause intestinal infections, and most of them are found in Asia. The Brachylaimidae family can be found in Oceania. The families found in Africa include Echinostomatidae, Gastrodiscidae, Heterophyidae, and Paramphistomidae. Those that have been reported in Europe include Echinostomatidae, Gastrodiscidae, Heterophyidae, and Nanophyetidae. A minority are present in the Americas, particularly Heterophyidae and Paramphistomidae.[2]

The largest human outbreaks of Fasciola species infection have occurred in the Gilan Province of Iran, affecting more than 15,000 people.[25]

Bihar, East India, was recently found to be endemic for fasciolopsiasis, especially since this area is generally poor, with both villagers and local medical practitioners lacking awareness about the parasite.[26]

In Boseong River, Gokseong-gun, South Korea, it has been shown that the eggs of M yokogawai and other Metagonimus species could be found in 24.3% of residents.[27]

China, Japan, and South Korea are considered high prevalence areas for human E hortense infections. This is especially true in Koje-myon, Kochang-gun, Kyongsangnam-do Province of South Korea, where prevalence has been reported to be up to 9.5%.[28]

In Xieng Khouang Province, Lao PDR (a country close to Myanmar), Cambodia, China, Thailand, and Vietnam, the rate of positivity for small trematode eggs was 4.4%, including Opisthorchis viverrini, heterophyids, and lecithodendriids.[29]

Mortality/Morbidity

Death from infection is rare and usually occurs only in persons with a heavy worm burden who present with severe cachexia and prostration. Other intercurrent infection may also cause death. In cases of infection with H heterophyes or M yokogawai, death may occur after embolization of the eggs to the heart or brain. Embolization to the brain and spinal cord can also cause focal neurologic disease.

Race

Intestinal flukes are endemic in Asia and in some parts of North Africa, affecting groups who live in these areas.

Sex

Intestinal flukes have no predilection for either sex.

Age

Intestinal flukes can affect both children and adults, but children are affected more severely. These intestinal infections are important public health problems, particularly among school children in developing countries.[30]

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Contributor Information and Disclosures
Author

Joseph Adrian L Buensalido, MD Clinical Associate Professor, Section of Infectious Diseases, Department of Medicine, Philippine General Hospital, University of the Philippines Manila College of Medicine

Joseph Adrian L Buensalido, MD is a member of the following medical societies: American Society for Microbiology, Infectious Diseases Society of America, Philippine Medical Association, Michigan Infectious Disease Society, Philippine College of Physicians

Disclosure: Nothing to disclose.

Coauthor(s)

Marja Arcangel Bernardo, MD Fellow, Section of Infectious Diseases, Department of Medicine, University of the Philippines-Philippine General Hospital

Marja Arcangel Bernardo, MD is a member of the following medical societies: Philippine College of Physicians

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American Medical Association, Oklahoma State Medical Association, Southern Society for Clinical Investigation, Association of Professors of Medicine, American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Additional Contributors

Chi Hiong U Go, MD Assistant Professor, Department of Internal Medicine, Texas Tech University Health Science Center at Odessa

Chi Hiong U Go, MD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine

Disclosure: Nothing to disclose.

Thomas E Herchline, MD Professor of Medicine, Wright State University, Boonshoft School of Medicine; Medical Director, Public Health, Dayton and Montgomery County, Ohio

Thomas E Herchline, MD is a member of the following medical societies: Alpha Omega Alpha, Infectious Diseases Society of Ohio, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Burke A Cunha, MD Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital

Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Asim A Jani, MD, MPH, FACP Clinician-Educator and Epidemiologist, Consultant and Senior Physician, Florida Department of Health; Diplomate, Infectious Diseases, Internal Medicine and Preventive Medicine

Asim A Jani, MD, MPH, FACP is a member of the following medical societies: American Association of Public Health Physicians, American College of Physicians, American College of Preventive Medicine, American Medical Association, American Public Health Association, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Paul Chen University of Texas Southwestern Medical School

Disclosure: Nothing to disclose.

Acknowledgements

The author would like to acknowledge Paul Chen, BS, ScM (2008) in Genetic Epidemiology, Johns Hopkins University Bloomberg School of Public Health, whose contributions and insights were invaluable for the revision of this article.

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Life cycle of Fasciolopsis buski. Image reproduced from the Division of Parasitic Diseases, Centers for Disease Control and Prevention (CDC), Atlanta, GA.
The life cycle of Fasciolopsis. Immature eggs are discharged into the intestine and stool and become embryonated in water. The eggs then release miracidia, which invade a suitable snail intermediate host, in which the parasites undergo several developmental stages (sporocysts, rediae, cercariae). The cercariae are released from the snail and encyst as metacercariae on aquatic plants, which are eaten by mammalian hosts (humans and pigs), who become infected. After ingestion, the metacercariae excyst in the duodenum and attach to the intestinal wall, where they develop into adult flukes (20-75 mm X 8-20 mm) in approximately 3 months and attach to the intestinal wall of the mammalian hosts. The adults have a life span of about one year. Image reproduced from the Division of Parasitic Diseases, Centers for Disease Control and Prevention (CDC), Atlanta, GA.
Egg of Fasciolopsis buski. Images reproduced from the Division of Parasitic Diseases, Centers for Disease Control and Prevention (CDC), Atlanta, GA.
Adult fluke of Fasciolopsis buski. Image reproduced from the Division of Parasitic Diseases, Centers for Disease Control and Prevention (CDC), Atlanta, GA.
The life cycle of Heterophyes. The adult parasites release embryonated eggs (each with a fully developed miracidium), which are then passed in the host's feces. After ingestion by a suitable snail (first intermediate host), the eggs hatch and release miracidia, which penetrate the snail's intestine. Snails of the genera Cerithidea and Pirenella are important hosts in Asia and the Middle East, respectively. The miracidia undergo several developmental stages in the snail (sporocysts, rediae, cercariae). Many cercariae are produced from each redia. The cercariae are released from the snail and encyst as metacercariae in the tissues of a suitable freshwater or brackish-water fish (second intermediate host). The definitive host becomes infected by ingesting undercooked or salted fish that contains metacercariae. After ingestion, the metacercariae excyst, attach to the mucosa of the small intestine, and mature into adults (measuring 1-1.7 mm X 0.3-0.4 mm). Heterophyes heterophyes infects humans, various fish-eating mammals (eg, cats, dogs), and birds. Image reproduced from the Division of Parasitic Diseases, Centers for Disease Control and Prevention (CDC), Atlanta, GA.
Life cycle of Metagonimus. The adult parasites release fully embryonated eggs (each with a fully developed miracidium), which are then passed in the host's feces. After ingestion by a suitable snail (first intermediate host), the eggs hatch and release miracidia, which penetrate the snail's intestine. Snails of the genus Semisulcospira are the most common intermediate host for Metagonimus yokogawai. The miracidia undergo several developmental stages in the snail (sporocysts, rediae, cercariae). Many cercariae are produced from each redia. The cercariae are released from the snail and encyst as metacercariae in the tissues of a suitable freshwater or brackish-water fish (second intermediate host). The definitive host becomes infected by ingesting undercooked or salted fish that contains metacercariae. After ingestion, the metacercariae excyst, attach to the mucosa of the small intestine, and mature into adults (measuring 1-2.5 mm X 0.4-0.75 mm). M yokogawai infects humans, fish-eating mammals (eg, cats, dogs), and birds. Image reproduced from the Division of Parasitic Diseases, Centers for Disease Control and Prevention (CDC), Atlanta, GA.
Various animals may be definitive hosts for different Echinostoma species, such as aquatic birds, carnivores, rodents, and humans. Unembryonated eggs are passed in stool (1), and development occurs in the water (2). The miracidium takes an average of 10 days to mature and then hatches (3), penetrating the first intermediate host, a snail (4). Snails, in general, serve as the first intermediate host. The intramolluscan stages are as follows: sporocyst (4a); rediae (4b); and cercariae (4c). Cercariae may then encyst as metacercariae in the same first intermediate host or leave to penetrate a new second intermediate host (5). Several animals may become the second intermediate host, such as other snails, bivalves, fish, and tadpoles. The definitive host gets infected after eating infected second intermediate hosts (6). The metacercariae excyst in the duodenum (7). Adults then live in the small intestine (8). Image reproduced from the Division of Parasitic Diseases, Centers for Disease Control and Prevention (CDC), Atlanta, GA.
Table 1. Common Intestinal Trematode Infections*
Infection Source Geographic Distribution
Fasciolopsiasis Freshwater plants (water caltrop, water chestnut) China, Thailand, Bangladesh, India
Echinostomiasis Tadpoles, freshwater snails, fish, frogs Indonesia, Philippines, Taiwan, Thailand
Heterophyiasis Fish Egypt, Iran, Tunisia, Turkey
Metagonimiasis Fish (cyprinid) Far East, Spain, Eastern Europe
*Adapted with permission from Tribble D, Wagner KF. Trematode infections. Infectious Disease Practice. 1996;20:69-73.
Table 2. Commonly Associated Exposures and Clinical Features of Certain Intestinal Trematodes*
Infection Source Clinical Features
Alaria americana Undercooked frog legs Disseminated fatal thoracic, gastrointestinal, retroperitoneal, and CNS manifestations; intraocular infections
Echinostomiasis (16 species) Freshwater fish, aquatic plants, clams, snails, mollusks, contact with aquatic birds May be asymptomatic; mild abdominal pain, bloating, dyspepsia, diarrhea, eosinophilia
Fibricola species Tadpoles Abdominal pain, diarrhea, fever, eosinophilia
Fasciolopsis species Water chestnut, water calthrop, water bamboo, water morning glory lotus and water hyacinth May be symptomatic; may be subclinical; gastritis, nausea, diarrhea, eosinophilia; generalized edema in persons with heavy infection burden
Gastrodiscoides species Vegetables, aquatic plants Often asymptomatic; may manifest as abdominal pain and diarrhea in severe cases
Watsonius watsoni Water bamboo Severe diarrhea
Fischoederius elongates Aquatic plants Epigastric pain and vomiting
Heterophyes species Mullets, fish; brackish water May be asymptomatic; intestinal mucosal disease, ulcer-related abdominal pain, dyspepsia, nausea, vomiting, diarrhea, weight loss
Gymnophalloides seoi Oysters Fever, abdominal pain, anorexia, weight loss, diarrhea, pancreatitis
Carneophallus brevicaeca Shrimp Fatal when infection involves CNS and heart
Brachylaima ruminae Poultry, rats Abdominal pain, diarrhea
Metagonimiasis species Fish (ayu, golden carp) May be asymptomatic; intestinal mucosal disease, ulcer-related abdominal pain, dyspepsia, nausea, vomiting, diarrhea, weight loss
Nanophyetus salmincola Undercooked fish (eg, salmon, trout, steelhead) May be symptomatic; mild diarrhea, abdominal pain
*Adapted from Berger SA, Marr JS. Human Parasitic Diseases Sourcebook. 1st ed. Sudbury, MA: Jones and Bartlett; 2006.
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