Trematoda Trematoda

Botulus microporus, a giant digenean parasite from the intestine of a lancetfish

The Trematoda is a class within the phylum Platyhelminthes that contains two groups of parasitic worms, commonly referred to as flukes.

Taxonomy and biodiversity The Trematoda are estimated to include 18 000[1] to 24 000[2] species, and are divided into two subclasses. Nearly all trematodes are parasites of mollusks and vertebrates. 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. Formerly the Monogenea were included in the Trematoda on the basis that these worms are also vermiform parasites, but modern phylogenetic studies have raised this group to the status of a sister class within the Platyhelminthes, along with the Cestoda. Life cycles Almost all trematodes infect mollusks as the first host in the life cycle, and most have a complex life cycle involving other hosts. Most trematodes are monoecious and alternately reproduce sexually and asexually. The two main exceptions to this are the Aspidogastrea, which have no asexual reproduction, and the schistosomes, which are dioecious. In the definitive host, in which sexual reproduction occurs, eggs are commonly shed along with host feces. Eggs shed in water release free-swimming larval forms that are infective to the intermediate host, in which asexual reproduction occurs. A species that exemplifies the remarkable life history of the trematodes is the bird fluke, Leucochloridium paradoxum. The definitive hosts, in which the parasite multiplies, are various woodland birds, while the hosts in which the parasite grows (intermediate host) are various species of snail. The adult parasite in the bird's gut produces eggs and these eventually end up on the ground in the bird's faeces. Some very fortunate eggs get swallowed by a snail and here they hatch into tiny, transparent larva (miracidium). These larvae grow and take on a sac-like appearance. This stage is known as the sporocyst and it forms a central body in the snail's digestive gland that extends into a brood sac in the snail's head, muscular foot and eye-stalks. It is in the central body of

the sporocyst where the parasite replicates itself, producing lots of tiny embryos (redia). These embryos move to the brood sac and mature into cercaria. Infections Main article: Trematode infection Human infections are most common in the Orient, Africa, South America, or the Middle East. However, trematodes can be found anywhere that human waste is used as fertilizer. Etymology Trematodes are commonly referred to as flukes. This term can be traced back to the Old English name for flounder, and refers to the flattened, rhomboidal shape of the worms. The flukes can be classified into two groups, on the basis of the system which they infect in the vertebrate host.

Tissue flukes infect the bile ducts, lungs, or other biological tissues. This group includes the lung fluke, Paragonimus westermani, and the liver flukes, Clonorchis sinensis and Fasciola hepatica. Blood flukes inhabit the blood in some stages of their life cycle. Blood flukes include species of the genus Schistosoma.

They may also be classified according to the environment in which they are found. For instance, pond flukes infect fish in ponds.[3] Trematodes are flukes of the class Trematoda; phylum Platyhelminthes. Important ones affecting man belong to the genera Schistosoma (blood fluke), Echinostoma (intestinal fluke), Fasciolopsis (liver fluke), Gastrodiscoides (intestinal fluke), Heterophyes (intestinal fluke), Metagonimus (intestinal fluke), Clonorchis (Asiatic liver fluke), Fasciola (liver fluke), Dicrocoelium (liver fluke), Opisthorchis (liver fluke), and Paragonimus (lung fluke). Man usually becomes infected after ingesting insufficiently cooked fish, crustaceans, or vegetables that contain their larvae. The cycle begins when larvae are released into freshwater by infected snails. The free-swimming larvae can then directly penetrate the skin of humans while swimming or be ingested after encycsting in or on various edible vegetation, fish, or crustaceans. The oval-shaped fluke (sometimes called a flatworm) has a tough outer body layer called a tegument that covers layers of circular, longitudinal, and diagonal muscles that protects it from the human digestive tract. Some can inhabit the liver, bile duct, or lymph vessels. They can be several inches long, an inch or so wide, and only thick enough to hold themselves together. Below are just a very few examples of the thousands known. Blood flukes: Schistosoma japonicum, S. mansoni, S. haematobium are three species of blood flukes (schistosomes) that cause the disease schistosomiasis, which infects about 200 million people worldwide. One of the three types of disease, S. japonicum is found in Asia; S. mansoni occurs in Africa, the Eastern Mediterranean, the Caribbean, and South America; the third, S. haematobium is found in Egypt. Freshwater snails play intermediate host in the life cycle development of these blood flukes. The snails release larvae into the water, where they can penetrate the skin of swimmers or bathers. The parasites burrow into the skin, and then are carried into the bloodstream to be taken to the liver, intestines, or bladder. There are two forms of schistosomiasis. With one, inflammation begins when the worms lodge in the lining of the intestine or liver. With the other form, the bladder and urinary tract can become fatally infected by worms as they lodge in the walls. Travellers to Africa, especially, are warned not to bath, wade, or swim in fresh water because of possible infestations blood flukes. Infection causes fever and chills, but also elevates the number of white blood cells (eosinophils), as well as producing

abdominal pain resulting from enlargements of the liver and spleen. Often, these symptoms do not show up for four to eight weeks after exposure, and, therefore, may not be associated with the possibility of parasite infestation while on vacation. Liver fluke: Clonorchis sinensis is common in the Orient and Hawaii, and is transmitted through the ingestion of raw, dried, salted, pickled, or undercooked fish. Snails, carp, and forty additional fish species have been known to play the intermediate host to this fluke. In humans, it inhabits the bile ducts of the liver, causing it to enlarge and become tender, as well as producing chills, fever, jaundice, and a type of hepatitis. Oriental lung fluke: Paragonimus westermani is found mainly in the Far East, where it enters the body, producing the disease called paragonimiasis. Humans acquire the fluke ingesting infected crabs and crayfish that have not been sufficiently cooked or are served raw. The adult worms go to the lungs, and, sometimes, the brain, where seizures similar to epilepsy can occur. Symptoms include an occasional mild cough, producing a peculiar rusty brown sputum. The lung fluke can perforate lung tissue and deplete oxygen supplies to the entire bloodstream. Symptoms often resemble those of pulmonary tuberculosis. Sheep liver fluke: Fasciola hepatica is more common in Central and South America, parts of Africa, Asia, and Australia. Infection is usually acquired from eating the larva worms encysted on such aquatic vegetation as watercress. Worms migrate to the liver and bile ducts, where they produce upper right quadrant abdominal pain, liver abscesses, and fibrosis. Intestinal fluke: Fasciolopsis buski is more common in Southeast Asia, Australia, and Latin America. Transmission occurs when individuals bite into the unpeeled outer skin of plants that harbor encycsted larvae. Such plants can be water chestnuts, bamboo shoots, and lotus plant roots because they are often cultivated in ponds and streams infected by animal waste. Adult flukes live in the duodenum (the shortest and widest part of the small intestine) and jejunum (connects the duodenum and the ileum, which opens into the large intestine), where they cause ulceration. Symptoms include the following: diarrhea, nausea, vomiting, abdominal pain, as well as facial and abdominal edema.

Fasciola hepatica Common liver fluke

Fasciola hepatica - adult worm Scientific classification Kingdom: Animalia Phylum: Class: Platyhelminthes Trematoda

Subclass: Digenea

Order: Family: Genus: Species:

Echinostomida Fasciolidae Fasciola F. hepatica

Binomial name Fasciola hepatica (Linnaeus, 1758) Fasciola hepatica, also known as the common liver fluke or sheep liver fluke, is a parasitic flatworm of the class Trematoda, phylum Platyhelminthes that infects liver of various mammals, including humans. The disease caused by the fluke is called fascioliasis (also known as fasciolosis). F. hepatica is worldwide distributed and causes great economic losses in sheep and cattle.

Life cycle In order to complete its life cycle, F. hepatica requires an aquatic snail as an intermediate host such as Galba truncatula, in which the parasite can reproduce asexually. From the snail, minute cercariae emerge and swim through pools of water in pasture, and encyst as metacercariae on near-by vegetation. From here, the metacercariae are ingested by the ruminant, or in some cases, by humans eating un-cooked foods such as watercress. Contact with low pH in the stomach causes the early immature juvenile to begin the process of excystment. In the duodenum, the parasite breaks free of the metacercariae and burrows through the intestinal lining into the peritoneal cavity. The newly excysted juvenile does not feed at this stage, but once it finds the liver parenchyma after a period of days, feeding will start. This immature stage in the liver tissue is the pathogenic stage, causing anaemia and clinical signs sometimes observed in infected animals. The parasite browses on liver tissue for a period of up to 56 weeks and eventually finds its way to the bile duct where it matures into an adult and begins to produce eggs. Up to 25,000 eggs per day per fluke can be produced, and in a light infection, up to 500,000 eggs per day can be deposited onto pasture by a single sheep. Disease biology

Egg of F. hepatica In the United Kingdom, Fasciola hepatica is a frequent cause of disease in ruminants - this is most common between March and December. Cattle and sheep are infected when they consume the infectious stage of the parasite from low-lying, marshy pasture. The effects of liver fluke are referred to as fascioliasis, and include anaemia, weight loss and sub-mandibular oedema. Diarrhea is only an occasional consequence of liver fluke.

Liver fluke is diagnosed by yellow-brown eggs in the faeces. They are not distinguishable from the eggs of Fascioloides magna, although the eggs of F. magna are very rarely passed in sheep, goats or cattle. A serious consequence of the liver damage caused by fascioliasis is that latent Clostridium novyi spores can be activated by the low oxygen conditions in the damaged tracts the parasite forms in the liver - this can lead to "black disease", caused by Clostridium novyi type B or immune-mediated haemolytic anaemia (IMHA) leading to haemoglobinuria caused by Clostridium novyi type D. Treatment

Slide showing its internal organs The drug of choice in the treatment of fasciolosis is triclabendazole, a member of the benzimidazole family of anthelmintics. The drug works by preventing the polymerization of the molecule tubulin into the cytoskeletal structures, microtubules. However, resistance of F. hepatica to triclabendazole has already been recorded in Australia[1] and Ireland.[2] Artemether has been shown to be effective in a rat model of fascioliasis.[3]

Schistosoma
Schistosoma

Schistosoma mansoni egg

Scientific classification Kingdom: Animalia Phylum: Class: Order: Family: Platyhelminthes Trematoda Strigeidida Schistosomatidae

Subclass: Digenea

Genus:

Schistosoma
Weinland, 1858

A genus of trematodes, Schistosoma spp., commonly known as blood-flukes and bilharzia, cause the most significant infection of humans by flatworms (schistosomiasis) and are considered by the World Health Organization as second in importance only to malaria, with hundreds of millions infected worldwide. Adult worms parasitize mesenteric blood vessels. Eggs are passed through urine or feces to fresh water, where larval stages can infect a new host by penetrating the skin.

History
The eggs of these parasites were first seen by Theodor Maximilian Bilharz, a German pathologist working in Egypt in 1851 who found the eggs of Schistosoma haematobium during the course of a post mortum. He wrote two letters to his former teacher von Siebold in May and August of 1851 describing his findings. von Siebold wrote a paper (published in 1852) summarizing Bilharz's findings. Bilhart's wrote a paper in 1856 describing the worms more fully and he named them Distoma haematobium. Their unusual morphology meant that they could not be comfortably included in Distoma so in 1856 Meckel von Helmsback created the genus Bilharzia for them. In 1858 Weinland proposed the name Schistosoma (Greek: 'split body') after the male worms morphology. Despite Bilharzia having precedence the genus name Schistosoma was officially adopted by the International Commission on Zoological Nomenclature. The term Bilharzia to describe infection with these parasites is still in use in medical circles. Bilharz also described Schistosomum mansoni but this species was redecribed by Louis Westenra Sambon in 1907 at the London School of Tropical Medicine who named it after his teacher Patrick Manson. In 1898 all the then known species were placed in a subfamily by Stiles and Hassel. This was then elevated to family status by Looss in 1899. Poche in 1907 corrected a grammatical error in the family name. The life cycle was determined by da Silva in 1908.

Evolution
The origins of this genus remain unclear. For many years it was believed that this genus had an African origin but DNA sequencing suggests that the hippo (Hippopotamus amphibius) species (S. edwardiense and S. hippopotami) may be basal. Since hippos were present in both Africa and Asia during the Cenozoic era the genus may have originated as parasites of hippos.[1] The original hosts for the South East Asian species were probably rodents. The sister group to Schistosoma is a genus of elephant-infecting schistosomes - Bivitellobilharzia. Another mammalian genus - Orientobilharzia is also closely related. The cattle, sheep, goat and cashmere goat parasite Orientobilharzia turkestanicum appears to be related to the African schistosoma. Within the haematobium group S. bovis and S. curassoni appear to be closely related as do S. leiperi and S. mattheei.

S. mansoni appears to have evolved in East Africa 0.43-0.30 million years ago. S. incognitum and S. nasale are more closely related to the African species rather than the japonicum group. S. sinensium appears to have radiated during the Pliocene. S. mekongi appears to have invaded South East Asia in the mid-Pleistocene. Estimated speciation dates for the japonicum group: ~3.8 million years ago for S. japonicum/South East Asian schistosoma and ~2.5 million years ago for S. malayensis/S. mekongi.

Taxonomy
The genus Schistosoma as currently defined is paraphyletic so revisions are likely. Currently twenty one species are recognised within this genus. The genus has been divided into four groups - indicum, japonicam, haematobium and mansoni. The affinities of the remaining three species are still being clarified. Twelve species are found in Africa. Eleven of these are divided into two groups - those with a lateral spine on the egg (mansoni group) and those with a terminal spine (haematobium group). The four mansoni group species are: S. edwardiense, S. hippotami, S. mansoni and S. rodhaini. The eight haematobium group species are: S. bovis, S. curassoni, S. intercalatum, S. guineensis, S. haematobium, S. leiperi, S. margrebowiei and S. matthei. S. spindale is widely distributed in Asia but is also found in Africa. The other species occur in Asia and India The indicum group has three species: S. indicum, S. nasale and S. spindale. This group appears to have evolved during the Pleistocene. All use pulmonate snails as hosts. S. indicum is found in India and Thailand. The japonicum group has three species: S. japonicum, S. malayensis and S. mekongi. S. sinensium is a sister clade to the S. japonicum group and is found in China. S. ovuncatum forms a clade with S. sinensium and is found in northern Thailand. The definitive host is the rat (Rattus rattus) and the intermediate host is the snail Tricula bollingi. This species is known to use snails of the family Pomatiopsidae as hosts. S. incognitum appears to be basal in this genus. It may be more closely related to the African/Indian species than to the South East Asian group. This species uses pulmonate snails as hosts.

Species infecting humans

Parasitism of humans by Schistosoma appears to have evolved at least three occasions in both Asia and Africa.

S. guineensis, a recently described species, is found in West Africa. Known snail intermediate hosts include Bulinus forskalii. S. haematobium, commonly referred to as the bladder fluke, originally found in Africa, the Near East, and the Mediterranean basin, was introduced into India during World War II. Freshwater snails of the Bulinus genus are an important intermediate host for this parasite. Among final hosts humans are most important. Other final hosts are rarely baboons and monkeys.[2]. S. intercalatum. The usual final hosts are humans. Other animals can be infected experimentally.[2] S. japonicum whose common name is simply blood fluke is found widely spread in Eastern Asia and the southwestern Pacific region. In Taiwan this species only affects animals, not humans. Freshwater snails of the Oncomelania genus are an important intermediate host for S. japonicum. Final hosts are humans and other mammals including cats, dogs, goats, horses, pigs, rats and water buffalo.[2] S. malayensis This species appears to be a rare infection in humans and is considered to be a zooenosis. The natural vertebrate host is von Muller's rat (Rattus muelleri). The snail host(s) are not yet known. S. mansoni, found in Africa, Brazil, Venezuela, Suriname, the lesser Antilles, Puerto Rico, and the Dominican Republic. It is also known as Manson's blood fluke or swamp fever. Freshwater snails of the Biomphalaria genus are an important intermediate host for this trematode. Among final hosts humans are most important. Other final hosts are baboons, rodents and raccoons.[2] S. mekongi is related to S. japonicum and affects both the superior and inferior mesenteric veins. S. mekongi differs in that it has smaller eggs, a different intermediate host (Neotricula aperta) and longer prepatent period in the mammalian host. Final hosts are humans and dogs.[2] The snail Tricula aperta can also be experimentally infected with this species. Human Schistosomes Scientific Name First Intermediate Host Bulinus forskalii Bulinus spp West Africa Africa Africa, Middle East China, East Asia, Philippines South East Asia Africa, South America, Caribbean, Middle East South East Asia Endemic Area

Schistosoma guineensis Schistosoma intercalatum

Schistosoma haematobium Bulinus spp. Schistosoma japonicun Schistosoma malayensis Schistosoma mansoni Schistosoma mekongi Oncomelania spp. Not known Biomphalaria spp. Neotricula aperta

Species infecting animals other than humans

S. indicum, S. nasale, S. leiperi are all parasites of ruminants. S. edwardiense and S. hippopotami are parasites of the hippo.

Morphology

Adult schistosomes share all the fundamental features of the digenea. They have a basic bilateral symmetry, oral and ventral suckers, a body covering of a syncytial tegument, a blind-ending digestive system consisting of mouth, oesophagus and bifurcated caeca; the area between the tegument and alimentary canal filled with a loose network of mesoderm cells, and an excretory or osmoregulatory system based on flame cells. Adult worms tend to be 10-20 mm long and use globins from their hosts' hemoglobin for their own circulatory system.

Reproduction
Unlike other trematodes, the schistosomes are dioecious - i.e., the sexes are separate. The two sexes display a strong degree of sexual dimorphism, and the male is considerably larger than the female. The male surrounds the female and encloses her within his gynacophoric canal for the entire adult lives of the worms, where they reproduce sexually.

Schistosomiasis(Bilharziasis)

Schistosomiasis is infection with blood flukes of the genus Schistosoma, which are acquired transcutaneously by swimming or wading in contaminated waters. The organisms infect the vasculature of the GI or GU system. Acute symptoms are dermatitis, followed several weeks later by fever, chills, nausea, abdominal pain, diarrhea, malaise, and myalgia. Chronic symptoms vary with species but include bloody diarrhea and hematuria. Diagnosis is by identifying eggs in stool, urine, or biopsy specimens. Serologic tests are sensitive and specific. Treatment is with praziquantel. Etiology and Pathophysiology Schistosomiasis is by far the most important trematode infection. Schistosoma is the only trematode that invades through the skin; all other trematodes infect only via ingestion. About 200 million people are infected worldwide. The risk of infection is spreading as new dams are built in endemic areas. There are 5 species of schistosomes, all with similar life cycles involving freshwater snails. S. haematobium, which causes urinary tract disease, is widely distributed over the African continent with smaller foci in the Middle East and India. The other Schistosoma sp cause intestinal disease. S. mansoni is widespread in Africa and is the only species in the Western Hemisphere, endemic in Brazil, Surinam, Venezuela, and on some Caribbean islands. S. japonicum is present only in Asia, mainly in China and the Philippines. S. mekongi is in Laos and Cambodia; S. intercalatum is in Central Africa. The disease may be imported in travelers and immigrants from endemic areas, but transmission does not occur within the US and Canada. Adult worms live and copulate within the veins of the mesentery or bladder, depending on the species. Some eggs penetrate the intestinal or bladder mucosa and are passed in stool or urine; other eggs remain within the host organ or are transported through the portal system to the liver, and occasionally to other sites (eg, lungs, CNS, spinal cord). Excreted eggs hatch in freshwater, liberating miracidia that enter snails. After multiplication, thousands of free-swimming

cercariae are released. These penetrate human skin within a few minutes after exposure and transform into schistosomulae, which travel through the bloodstream to the lungs, where they mature in about 6 wk. Subsequently they migrate to their ultimate home in the intestinal veins or the venous plexus of the GU tract. Eggs appear in stool or urine 1 to 3 mo after cercarial penetration. Estimates of the adult worm life span range from 3 to 37 yr. Symptoms and Signs Schistosome dermatitis is a pruritic papular rash where the cercariae penetrate the skin (see also Dermatitis Caused by Avian and Animal Schistosomes, below) in previously sensitized people. Acute schistosomiasis (Katayama fever) occurs with onset of egg laying, typically 2 to 4 wk after heavy exposure. Symptoms include fever, chills, nausea, abdominal pain, malaise, myalgia, urticarial rashes, and marked eosinophilia, resembling serum sickness. Manifestations are more common and usually more severe in visitors than in residents of endemic areas and typically last for several weeks. Chronic schistosomiasis results mostly from host responses to eggs retained in tissues. Early on, intestinal mucosal ulcerations caused by S. mansoni or S. japonicum may bleed and produce bloody diarrhea. As lesions progress, focal fibrosis, strictures, fistulas, and papillomatous growths may develop. With S. haematobium, ulcerations in the bladder wall may cause dysuria, hematuria, and urinary frequency. Over time, chronic cystitis develops. Strictures may lead to hydroureter and hydronephrosis. Papillomatous masses in the bladder are common, and squamous cell carcinoma may develop. Blood loss from both GI and GU tracts frequently results in anemia. Secondary bacterial infection of the GU tract and persistent Salmonella septicemia associated with S. mansoni are also common. Several species, notably S. haematobium, can cause genital disease in both men and women, resulting in numerous symptoms including infertility. Granulomatous reactions to eggs of S. mansoni and S. japonicum in the liver usually do not compromise liver function but may produce fibrosis and cirrhosis, which can lead to portal hypertension and subsequent hematemesis from esophageal varices. Eggs in the lungs may produce granulomas and focal obliterative arteritis, which may cause pulmonary hypertension and cor pulmonale. Eggs lodged in the spinal cord can cause transverse myelitis, and those in the CNS can cause seizures. Diagnosis Eggs are sought in the stool (S. japonicum , S. mansoni , S. mekongi , S. intercalatum) or urine (S. haematobium and occasionally S. japonicum). Repeated examinations using concentration techniques may be necessary. Geography is a primary determinant of species, so a history of exposure should be communicated to the laboratory. If the clinical picture suggests schistosomiasis but no eggs are found on repeated examination of urine or feces,

intestinal or bladder mucosa can be biopsied for eggs. Serologic tests are highly sensitive and specific for infection but do not provide information on worm burdens, clinical status, or prognosis. Treatment and Prevention Single-day oral treatment with praziquantel Some Trade Names BILTRICIDE Click for Drug Monograph (20 mg/kg bid for S. haematobium , S. mansoni, and S. intercalatum; 20 mg/kg tid for S. japonicum and S. mekongi) is recommended. However, treatment does not affect developing schistosomulae and thus may not abort an early infection. Adverse effects are generally mild and include abdominal pain, diarrhea, headache, and dizziness. Therapeutic failures have been reported, but it is difficult to determine whether they are due to reinfection or drug-resistant strains. Oxamniquine (not available in the US) is effective only against S. mansoni. African strains are more resistant to this drug than South American strains and require larger doses (30 mg/kg po once/day for 1 or 2 days vs 15 mg/kg once). Oxamniquine-resistant cases have been observed. Patients should be examined for living eggs 3 and 6 mo after treatment. Retreatment is indicated if egg excretion has not decreased markedly. In the future, antigen detection tests may supplant quantitative egg counts as tools to monitor response to chemotherapy. Scrupulously avoiding contact with contaminated water prevents infection. The sanitary disposal of urine and feces reduces the likelihood of infection. Adult residents of endemic areas are more resistant to reinfection than children, suggesting the possibility of acquired immunity. Vaccine development is under way. Dermatitis Caused by Avian and Animal Schistosomes (Cercarial Dermatitis; Swimmers' Itch; Clam Diggers' Itch) Cercarial dermatitis is a skin condition that develops when Schistosoma sp that cannot develop in humans penetrate the skin. Cercariae of Schistosoma sp that infect birds and mammals other than humans can penetrate the skin. Although the organisms do not develop in humans, humans may become sensitized and develop pruritic maculopapular skin lesions at the site of penetration. Skin lesions may be accompanied by a systemic febrile response that runs for 5 to 7 days and resolves spontaneously. Saltwater schistosome dermatitis (clam diggers' itch) occurs on all Atlantic, Gulf, Pacific, and Hawaiian coasts. It is very common in muddy flats off Cape Cod. Freshwater schistosome dermatitis (swimmers' itch) is common in lakes of northern Michigan, Wisconsin, and Minnesota. Diagnosis is based on clinical findings. Most cases do not require medical attention. Treatment is symptomatic with cool compresses, baking soda, or antipruritic lotions. Topical corticosteroids can also be used.

Integrity

Service

Excellence

Chapter 6.

The Trematodes (Flukes)

6.1

Infections of the Alimentary Canal and Associated Organs

Introduction
The trematodes (or flukes) are leaf shaped with an outer cover called the tegument which may be smooth or spiny. There are two suckers or attachment organs, an anterior oral sucker and a posterior ventral sucker. The suckers form a characteristic feature of the group, from which the name Trematode is derived from the Greek word for hole. They can occur in a variety of host environments, with the majority being endoparasites but some are found to be ectoparasitic. Most trematodes are hermaphroditic and most of the body consists of reproductive organs and their associated structures. The digestive system is well developed; they generally feed on intestinal debris, blood, mucus and other tissues, depending on the host environment.

Illustration 6-1. Trematode Eggs Found in Stool Specimens of Humans. (SOURCE: CDC/Adapted from Melvin, Brooke, and Sadun, 1959)

Species Trematodes Schistosoma mansoni

Size

Shape

Color

Stage of Development When Passed

Specific Features and Variations

140 m x 66 m. Range, 114-180 m x 45-73 m.

Elongated with prominent lateral spine near posterior end. Anterior end tapered and slightly curved.

Yellow or yellow brown.

Embryonated. Contains mature miracidium.

Lateral spine. Found in feces; in rare cases, in urine also. Eggs are discharged at irregular intervals and may not be found in every stool specimen. Are rare in chronic stages of infection. Found in feces. Often coated with debris and may be overlooked.

Schistosoma japonicum

90 m x 70 m. Range, 68-100 m x 45-80 m.

Oval. Small lateral spine is often seen or may appear as a small hook or "knob" located in a depression in the shell. Elongated with rounded anterior end and terminal spine at posterior end.

Yellow or yellow brown.

Embryonated. Contains mature miracidium.

Schistosoma haematobium

143 m x 60 m. Range, 112-170 m x 40-70 m. 175 m x 60 m. Range, 140-240 m x 50-85 m.

Yellow or yellow brown.

Embryonated. Contains mature miracidium.

Terminal spine. Found in urine, occasionally in feces. Egg often covered with debris. Terminal spine long, slender with bent tip. Resembles S. haematobium egg except it is longer, is thinner, and has a longer spine. Found in feces. May have debris adhering to shell. Found in feces. Closely resembles S. japonicum egg except it is smaller. May be coated with debris.

Schistosoma intercalatum

Elongated with tapered anterior end and terminal spine. Sometimes "spindleshaped."

Yellow or yellow brown.

Embryonated. Contains mature miracidium.

Schistosoma mekongi

69 m x 56 m* Range, 51-73 m x 39-66 m.

Spherical. Small lateral spine, not always visible or may appear as a small "knob" in a depression in the shell.

Yellow or yellow brown.

Embryonated. Contains mature miracidium.

Clonorchis sinensis

30 m x l6 m. Range, 27-35 m x 11-20 m.

Small, ovoidal, or elongated with broad rounded posterior end and a convex operculum resting on "shoulders." A small "knob" may be seen on the posterior end. Elongated with operculum on anterior end and pointed terminal "knob" on posterior end. Small, elongated or slightly ovoidal. Operculum. Slight "knob" at posterior end.

Yellow brown.

Embryonated. Contains mature miracidium.

Small size, operculum and "knob" on posterior end. Shell often is covered by adhering debris.

Opisthorchis felineus

30 m x 12 m. Range, 26-30 m x 11-15 m. 28 m x 15 m. Range, 28-30 m x 15-17 m. 28 m x 17 m. Range, 26-30 m x 15-20 m.

Yellow brown.

Embryonated. Contains mature miracidium.

Lacks prominent shoulders characteristic of Clonorchis and has more tapered end.

Heterophyes heterophyes

Yellow brown.

Embryonated. Contains mature miracidium.

Resembles Clonorchis egg but with less distinct shoulders. Operculum is broader than in Clonorchis. Resembles Clonorchis and Heterophyes eggs. Shell is slightly thinner than Heterophyes. Operculum is broader than Clonorchis. Found in sputum, occasionally in feces. Resembles egg of D. latum but is larger, slightly asymmetrical and the operculum is smaller and flatter. The widest part of the Paragonimus egg is usually anterior to the center ; in a D. latum, the widest area is around the center. Large size. Broadly oval eggs.

Metagonimus yokogawai

Small, elongated or ovoidal. Operculum. No "shoulders" at anterior end. Small "knob" often seen on posterior end. Ovoidal or elongate with thick shell. Operculum is slightly flattened and fits into shoulder area of shell. Posterior end is thickened. Egg often asymmetrical with one side slightly flattened.

Yellow or yellow brown.

Embryonated. Contains mature miracidium.

Paragonimus westermani

85 m x 53 m. Range, 68-118 m x 39-67 m.

Yellow brown to dark brown.

Unembryonated. Filled with yolk material in which a germinal cell is imbedded. Cells are irregular in size.

Fasciola hepatica

145 m x 80 m. Range, 120-150 m x 63-90 m.

Ellipsoidal, thin shell. Small, indistinct operculum.

Yellow to light brown.

Unembryonated. Filled with yolk cells in which an indistinct germinal cell is imbedded. Unembryonated. Filled with yolk cells in which an indistinct germinal cell is imbedded.

Fasciolopsis buski

140 m x 80 m. Range, 130-159 m x 78-98 m.

Ellipsoidal, thin shell. Small, indistinct operculum.

Yellow brown.

Large size. Resembles F. hepatica egg and cannot be easily distinguished from Fasciola.

Table 6-1. Differential Morphology of the Diagnostic Stages of Helminths Found in Humans: Eggs (Trematodes) (SOURCE: CDC)

Trematodes require an intermediate host in their life cycle with vertebrates being the definitive host. Larval stages may occur in either invertebrate or vertebrate hosts. There are three groups of trematodes:

Monogenea, which typically are external parasites of fish with direct life cycles Aspidogastrea, these are endoparasites with the entire ventral surface as an adhesive organ Digenea, these are endoparasites with simpler adhesive organs and life cycles involving one or more intermediate hosts (indirect life-cycle). This section concentrates on the Digenean

trematodes. Most Digenean trematodes inhabit the alimentary canal of vertebrates and many of the associated organs, such as the liver, bile duct, gall bladder, lungs, bladder and ureter. These organs are rich in cavities containing food such as blood, mucus, bile and intestinal debris. The Digenean trematodes have a complex life cycle, with rare exceptions, always involve a mollusk host. There may be six larval stages the miracidium, sporocyst, redia, cercaria, mesocercaria (rare) and the metacercaria (the majority have 4 or 5 stages). Trematode eggs have a smooth hard shell and the majority of them are operculate.

Fasciola species
Introduction
Fasciola, Fasciolopsis and Echinostoma species are trematodes which parasitize the liver and intestines of a variety of vertebrates. They are hermaphroditic and their distinguishing characteristics are shown in Table 6-2. Fasciola hepatica trematodes are not thought to infect man but in fact man is not an unusual host, with infections being reported in many countries including Europe and the USA. The eating of unwashed watercress appears to be the source of infection, with them ending up in the liver. The most common host is sheep where they can cause severe disease. Fasciolopsis buski (giant intestinal fluke) is a duodenal parasite infecting both man and pigs. They are found widespread in Asia and China, but they have been found to be endemic in Taiwan, Thailand, Bangladesh and India. Night soil (human excreta) is used as a fertilizer in these countries on plants such as water chestnut and caltrops. The snails graze on these crops and also the definitive hosts eat them raw and unwashed, peeling the edible water plants with their teeth. Infection with Echinostoma species is thought to be contracted by ingestion of fresh water snails containing metacercaria. Such as Echinostoma ilocannum which occurs in the Philippines. The metacercariae infect the large snail Piola luzionica and in return are eaten raw. Despite the large numbers of these flukes they are of little medical importance, the most important being F. buski. Location of adult in host Bile Ducts Bile Ducts

Species Fasciola hepatica Fasciola gigantica

Geographic Distribution Cosmopolitan Africa, the Orient and Hawaiian Islands

Reservoir Hosts Sheep Camels, Cattle and Water Buffalo

130-1

1601

Fasciolopsis buski Echinostoma species

Far-East and Indian Subcontinent South East Asia and Japan

Pigs, Dogs and Rabbits Variety of Mammals

Intestine Intestine

1301

881

Table 6-2. Table describing the characteristics which differentiate the various Fasciola species which are important to man.

Life Cycle and Transmission

The life cycles of Fasciola, Fasciolopsis and Echinostoma species are complex, requiring more than one intermediate host.

Adult worms inhabit the liver or bile ducts of the definitive host (human), where they lay many eggs which are deposited into the environment in the feces. They are immature when passed. If they are passed into water they become mature in nine to 15 days at the optimum temperature of 22-25C.

Illustration 6-2. The general life cycle of Fasciola, Fasciolopsis and Echinostoma species. Immature eggs

are discharged in the biliary ducts and in the stool . Eggs become embryonated in water , eggs release miracidia , which invade a suitable snail intermediate host , including many species of the genus Lymnae. 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 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 (Fasciola hepatica: up to 30 m by 13 m; F. gigantica: up to 75 m) reside in the large biliary ducts of the mammalian host. Fasciola hepatica infect various animal species, mostly herbivores. The life cycle of the Echinostomes differs by one minor point: the cercariae encyst wither within the

tissues of the intermediate host in which sporocysts and rediae develop, or penetrate and encyst in other animals such as amphibians or fish. (SOURCE: PHIL 3393 - CDC/Alexander J. da Silva, PhD/Melanie Moser)

Morphology
The morphology of the adult flukes of Fasciola, Fasciolopsis and Echinostoma species is well documented. They are large leaf-shaped parasites about 23cm long. There are two suckers, an anterior oral sucker surrounding the mouth and a ventral sucker (acetabulum) on the ventral surface.

Image 6-1. Adult fluke of a Fasciola Trematode. Their morphology shows a large leaf-shape about 23cm long with two suckers, an oral and a ventral one. (SOURCE: CDC)

The outer tegument is covered in tiny spines which face backwards enabling them to attach themselves along with their suckers to the tissues. Ova are all thin shelled, ellipsoid, quinone colored (bile stained) with an operculum that is often inconspicuous. Although ova of Echinostoma species can usually be differentiated by size due these flukes being much smaller in size than F. Buski and F. hepatica, there is much cross-over in the size of Fasciola and Fasciolopsis species.

Pathogenesis
Light infections due to Fasciola hepatica may be asymptomatic. However, they may produce hepatic colic

with coughing and vomiting; generalized abdominal rigidity, headache and sweating, irregular fever, diarrhea and anemia.

Image 6-2. Ova of Fasciola are ovoid in shape, quinone color and often showing an inconspicuous operculum. Fasciola hepatica ova measure 130 - 150m by 63 - 90m. There is much cross-over in ova size between all of the Fasciola species. (SOURCE: PHIL 1540 - CDC/Dr. Mae Melvin)

Infections due to Fasciola gigantica occur mainly in cattle raising areas and cause clinical symptoms similar to those of Fasciola hepatica although human infections are less common. The adult flukes of Fasciolopsis buski attach to the intestine, resulting in local inflammation and ulceration. Heavier infections may subsequently lead to abdominal pain, malabsorption and persistent diarrhea, edema and even intestinal obstruction. Marked eosinophilia may be seen. The adult flukes of Echinostoma species attach to the intestine resulting in little damage to the intestinal mucosa. Light infections are generally asymptomatic and heavy infections may produce light ulceration, diarrhea and abdominal pain.

Laboratory Diagnosis
Definitive diagnosis is made by observing the ova in feces, since the flukes are very prolific any significant infection will be easily picked up. Where identification cannot be made from the size of the ova, clinical information and the source of infection may help to provide a diagnosis. Serological techniques are available for the diagnosis of Fasciola hepatica.

Clonorchis sinensis

Introduction
Clonorchis sinensis, also known as the Chinese (aka Oriental) liver fluke is a narrow elongate liver fluke found in the Far East, mainly Japan, Korea, China, Taiwan and Vietnam. It belongs to the group of Oriental liver flukes where there are three main species which commonly infect man. The other two species are Opisthorchis felineus and Opisthorchis viverrini. (Table 6-2) The three species are so similar in their morphology, life cycles and pathogenicity that they are very rarely discussed as separate species. All members of this group are parasites of fish-eating mammals, particularly in Asia and Europe. Man is the definitive hosts and water snails and fish are the intermediate hosts. Infections can be easily avoided by man not eating raw fish since this is the only way that infection can be passed on. Clonorchis sinensis parasitize the biliary duct in humans who become infected by eating raw or undercooked fish. Dogs and cats are the most important reservoir hosts.

Life Cycle and Transmission

Illustration 6-3. Diagram illustrating the life cycle of Clonorchis sinensis (Chinese Liver Fluke). This parasite requires the involvement of two intermediate hosts (fresh water snails and fish) to complete the life cycle. Embryonated eggs are discharged in the biliary ducts and in the stool . Eggs are ingested by a suitable snail intermediate host ; there are more than 100 species of snails that can serve as intermediate hosts. 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, where they encyst as metacercariae . Infection of humans 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 one month. The adult flukes (measuring 10 to 25 m by 3 to 5 m) reside in small and medium sized biliary ducts. In addition to humans, carnivorous animals can serve as reservoir hosts. (SOURCE: PHIL 3385 CDC/Alexander J. da Silva, PhD/Melanie Moser)

Morphology
The adult flukes measure 1120m by 34.5m and are lanceolate in shape, translucent and brownish in color. They are all hermaphroditic. Keeping in common with other flukes they possess two suckers.

Image 6-3. Diagram illustrating the internal morphology of the Oriental liver fluke, Clonorchis sinensis. (SOURCE: SFSU.EDU)

The ova of Clonorchis sinensis contain fully developed miracidia and possess prominent opercular shoulders (flask shaped egg) and are operculate. They are bile stained and measure 29m by 16m. In wet mounts they are transparent and you can quite easily see their anatomy. There can be up to 6,000 worms present and a daily egg output of 1,000 eggs per microliter of bile or 600 per gram of feces.

Image 6-4. Ova of Clonorchis sinensis. Showing the prominent opercular shoulders which makes identifying this trematode easy. They are described as flask shaped, bile stained. (SOURCE: PHIL 695 CDC/Dr. Mae Melvin)

The cercariae possess eyespots, the penetration and cystogenous glands are also well developed.

Image 6-5. Saline smear showing the characteristic flask shape of the Clonorchis sinensis ova. They are bile stained with a smooth outer coat. (SOURCE: PHIL 4845 CDC)

Pathogenesis
Many millions of people become infected every year but only a minority suffers from any illness. The pathology is related to the number of parasites present. Light infections of up to 50 eggs or more are usually asymptomatic. A heavy infection of 500 or more eggs may cause serious illness. Acute infections may be characterized by fever, diarrhea, epigastric pain, enlargement and tenderness of liver and sometimes jaundice. The invasion by these worms in the gall bladder may cause cholecystitis, due to flukes becoming impacted in the common bile duct.

Laboratory Diagnosis
Definitive diagnosis is made by observing the characteristic ova in feces following an iodine stained, formol-ether concentration method of the feces or from duodenal aspirates when there is

complete obstructive jaundice or from the Entero-Test.

Heterophyes heterophyes Geographic distribution Location of adult in host

Far East

Metagonimus yokogawai
Far East

Opisthorchis viverrini
Thailand

Dic de

Small intestine

Small intestine

Liver and bile ducts

Li

Size of ova

26.5-30m by 15-17m

26.5-30m by 15-17m

26.7m by 15m

Shape of ova

Prominent opercular shoulders Bile stained

Prominent opercular shoulders Bile stained

Prominent opercular shoulders Bile stained

Dark she

Infection acquired by

Eating raw or pickled fish

Eating raw or pickled fish

Eating raw fresh water fish

Ea

Symptoms

Occasionally diarrhea and vomiting

Occasionally diarrhea and vomiting

Malaise and right upper quadrant pain

dige

Table 6-2. Table summarizing the less common flukes that are known to infect man. (CDC)

Dicrocoelium dendriticum
Far East Liver and bile ducts 38-45m by 22-30m Dark brown, thick shelled and large operculum Eating infected ants

Biliary and digestive problems

Paragonimus westermani
Introduction
Paragonimus westermani is a lung fluke found in both humans and animals. The adults are 12m long and are found in capsules in the lung. Although they are hermaphroditic, it is necessary for worms to be present in the cyst for fertilization to occur. The disease is seen in the Far East, China, South East Asia, and America.

Life Cycle

Illustration 6-4. Diagram of the general life cycle of the lung fluke, Paragonimus westermani. 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

. Human infection with P. westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite . 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 to 12 m by 4 to 6 m). 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. (SOURCE: PHIL 3415 - CDC/Alexander J. da Silva, PhD/Melanie Moser)

Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P. westermani.

Morphology
The adult worm is an ovoid, reddish brown fluke about 12m long. The eggs are ovoid, brownish yellow, thick shelled and operculated. They measure 80-100m by 45-65m and may be confused with the ova of Diphyllobothrium latum.

Image 6-6. Saline smear of Paragonimus westermani egg. The egg shells are thick and operculated. (SOURCE: PHIL 1541 CDC/ Dr. Mae Melvin)

Clinical Disease
As the parasites grow in the lung cyst, inflammatory reaction and fever occurs. The cyst ruptures and a cough develops resulting in an increase in sputum. The sputum is frequently blood tinged and may contain numerous dark brown eggs and Charcot-Leyden crystals. Hemoptisis may occur after paroxysms of coughing. Dyspnea and bronchitis develop with time. Bronchiectasis may occur and pleural effusion is sometimes seen. The disease resembles pulmonary tuberculosis. Cerebral calcification may also occur.

Laboratory Diagnosis
Diagnosis is based on finding the characteristic eggs in brown sputum. The eggs can also be found in the feces due to swallowing sputum. A chest x-ray may show cystic shadows and

calcification. Serological tests, in particular, the ELISA method, are useful diagnostic tests.

Schistosomes
Introduction
The Schistosomes are blood trematodes belonging to the Phylum Platyhelmintha. They differ from other trematodes in that they have separate sexes. The male worms resemble a rolled leaf where they bear the longer and more slender female in a ventral canal (the gynaecophoric canal). They require definitive and intermediate hosts to complete their life cycle. There are five species of Schistosomes responsible for human disease; S. mansoni, S. haematobium and S. japonicum with S. mekongi and S. intercalatum being less common. They are the only trematodes that live in the blood stream of warm-blooded hosts. The blood stream is rich in glucose, and amino acids, so along with the plasma and blood cells, it represents an environment which is suitable for egg producing trematodes. Over 200 million people are infected over at least 75 countries with 500 million or more people exposed to infection. With the disease spreading due to improved water supplies being created therefore, forming potentially new habits for snails. The disease caused is called schistosomiasis or Bilharzia and is the most important of helminth diseases. Infection by the three most common species is the same in both sexes and in all age groups. Though, S. mansoni and S. haematobium is seen to occur more often and most heavily in teenagers especially males.

Life Cycle
Adult worms of S. mansoni live in the plexus of veins draining the rectum and colon, and in branches of the portal vein in the liver.

Illustration 6-5. Diagram illustrating the general life cycle of the Schistosomes. Eggs are eliminated with feces 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 . 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 (size 7 to 20 m; males slightly smaller) 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 . 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. (SOURCE: CDC)

Adults of S. japonicum live in the anterior mesenteric blood vessels and in the portal vein in the liver; while the adults of S. haematobium live in the vesical plexus draining the bladder. Once the eggs are laid by the adult female worms the majority of them first pass through the veins of the blood vessel in which the worm is living, and then into the lumen of the intestine and are passed in the feces (S. mansoni and S. japonicum), or into the lumen of the bladder, and are then passed in the urine ( S. haematobium). Those eggs that reach fresh water hatch, releasing a miracidium which, to develop further must infect a snail of the correct species within 24 hours. The eggs of each species are markedly different but each produce virtually identical miracidium. Asexual multiplication takes place in the snail, and results in the release of cercariae (minute in size with forked tails, 200m long) into the water about 36 weeks later. Cercariae actively swim around and when they have located, or come into contact with, a definitive host they actively penetrate the skin. They can stay active looking for a host for 2448 hours after which if they dont find a host they will die. The head of the cercariae migrates to the liver and develops into either adult male or female worms (flukes), here they pair up and then migrate to their region of the venous blood system (species specific sites). The females leave the males and moves to smaller venules closer to the lumen of the intestine or bladder to lay her eggs (about six weeks after infection). The majority of adult worms live from 24 years, but some can live considerably longer.

Schistosoma mansoni
Introduction
S. mansoni occurs in West and Central Africa, Egypt, Malagasy, the Arabian Peninsula, Brazil, Surinam, Venezuela and the West Indies. The intermediate host is an aquatic snail of the genus Biomphalaria. Man is the most common definitive host, occasionally baboons and rats are infected. The adult worms live in smaller branches of the inferior mesenteric vein in the lower colon.

Morphology
The adult males measure up to 15 millimeters in length and females up to 10m. The schistosomes remain in copula throughout their life span, the uxorious male surrounding the female with his gynaecophoric canal. The male is actually flat but the sides roll up forming the groove. The cuticle of the male is covered with minute papillae. The female only posses these at the anterior and posterior end as the middle section being covered by the male body. Oral and ventral suckers are present, with the ventral one being lager serving to hold the worms in place, preventing them being carried away by the circulatory current.

The ova of S. mansoni are 114-175m long by 45-68m wide. They are light yellowish brown, elongate and possess a lateral spine. The shell is acid fast when stained with modified Ziehl-Neelsen Stain.

A non-viable egg is dark colored and shows no internal structural detail or flame cell movement. Eggs can become calcified after treatment and are usually smaller, appear black and often distorted with a less distinct spine.

Image 6-7. Micrograph of a S. mansoni ova, clearly showing its lateral spine which is a good distinguishing factor when identifying Schistosome ova. They range in size between 114-175m long by 45-68m wide. (SOURCE: PHIL 4841 CDC)

The schistosomes differ from other trematodes in that they are dioecious, digenetic, their eggs are not operculate and infection is acquired by penetration of cercaria through the skin.

Clinical Disease
The clinical disease is related to the stage of infection, previous host exposure, worm burden and host response. Cercarial dermatitis (swimmers itch) follows skin penetration and results in a maculopapular rash which may last 36 hours or more.
After mating, the mature flukes migrate to the venules draining the large intestine. Their eggs are laid and they penetrate the intestinal wall. They are then excreted in the feces, often accompanied by blood and mucus. It is the eggs and not the adult worms, which are responsible for the pathology associated with S. mansoni infections. The adult flukes acquire host antigen which protects them from the host's immune response. The host's reaction to the eggs which are lodged in the intestinal mucosa, leads to the formation of granulomata and ulceration of the intestinal wall. Some of the eggs reach the liver via the portal vein. The granulomatous response to these eggs can result in the enlargement of the liver with fibrosis, ultimately leading to portal hypertension and ascites. The spleen may also become enlarged. Other complications may arise as a result of deposition of the eggs in other organs e.g. lungs. Katayama fever is associated with heavy primary infection and egg production. Clinical features include high fever, hepatosplenomegaly, lymphadenopathy, eosinohilia and dysentery. This syndrome occurs a few weeks after primary infection.

Laboratory Diagnosis Microscopy

Laboratory confirmation of S. mansoni infection can be made by finding the eggs in the feces after an iodine stained, formol-ether concentration method. When eggs cannot be found in the feces, a rectal biopsy can be examined.

Serology
Serological tests are of value in the diagnosis of schistosomiasis when eggs cannot be found. An enzyme linked immunosorbent assay (ELISA) using soluble egg antigen, is employed at HTD.

Schistosoma japonicum

Introduction
Schistosoma japonicum is found in China, Japan, the Philippines, and Indonesia. It causes disease of the bowel with the eggs being passed out in the feces. It differs form S. mansoni and S. haematobium in that it is a zoonosis in which a large number of mammals serve as reservoir hosts; cats, dogs and cattle playing major roles in the transmission of the disease. The life cycle is not very different from that of S. mansoni, the intermediate hosts are from the subspecies Oncomelania hupensis. Sexual maturity is reached in about four weeks and eggs may be seen in the feces as quickly as five weeks. The worms live coupled together in the superior, mesenteric veins and deposit 15003500 eggs per day in the vessels of the intestinal wall. The eggs infiltrate through the tissues and are passed in the feces.

Morphology
The adult worms are longer and narrower than the S. mansoni worms. The ova are about 55-85m by 4060m, oval with a minute lateral spine or knob.

Clinical Disease
The main lesions are again due to the eggs, occurring in the intestine and liver. The eggs which are sequesters in the intestine mucosa or submucosa initiate granulomatous reactions, resulting in the formation of pseudotubercles.

Image 6-8. Unstained micrograph of a S. japonicum ova. They are oval in shape with a minute lateral spine or knob. (SOURCE: PHIL 649 CDC/Dr. Moore)

Due to the number of eggs released by the females the infection is more severe than one with S. mansoni. This is also due to the parasite being less well adapted to man, therefore, the circumoval granuloma is very large. The initial illness can be prolonged and sometimes fatal.

Laboratory Diagnosis Microscopy

Laboratory confirmation of S. japonicum infection can be made by finding the eggs in the feces after an iodine stained, formol-ether concentration method. When eggs cannot be found in the feces, a rectal biopsy can be examined.

Other Intestinal Schistosome species

Other Schistosome species which are responsible for human disease are S. mekongi and S. intercalatum. These two species cause similar symptoms to that of S. mansoni and can be summarized in Table 6-3.

S. mekongi Geographic location Diagnostic specimen Egg size Egg shape Mekong River basin Stool, rectal biopsy, serology 30-55m by 60-65m Oval, minute lateral spine or knob

S. intercalatum Central and west Africa

Stool, rectal biopsy, serolog 140-240m by 50-85m Elongate, terminal spine

Table 6-3. Table describing the other less common intestinal Schistosome species that are known to cause disease in man. (SOURCE: CDC)

Schistosoma haematobium
Introduction
Schistosoma haematobium is different from the other two species previously mentioned in that it causes urinary schistosomiasis. It occurs in Africa, India and the Middle East. The intermediate host is the Bulinus snail. Just like S. mansoni, its distribution runs parallel to the irrigation projects and in areas which favor the intermediate hosts. They are exclusively parasites of man. The mature worms live in copula mainly in the inferior mesenteric veins and the females deposit their eggs in the walls of the bladder and finally making their way into the urine. The life cycle is very similar to that of S. mansoni, with sexual maturity being reached within 45 weeks, but eggs may not appear in the urine until 1012 weeks or even later.

Morphology
The adult worms are longer than those of S. mansoni. The ova are relatively large, measuring 110170m in length and 40-70m in width. They have an elongated ellipsoid shape with a prominent terminal spine.

Image 6-9. Schistosoma haematobium eggs are elongated with a prominent terminal spine. The larva inside the egg produces an enzyme that passes through the egg-shell. (SOURCE: PHIL 4843 CDC)

Clinical Disease
The clinical disease is related to the stage of infection, previous host exposure, worm burden and host response. Cercarial dermatitis (Swimmers Itch) following skin penetration, results in a maculopapular rash and can last 36 hours or more. The mature flukes of S. haematobium migrate to the veins surrounding the bladder. After mating, the eggs are laid in the venules of the bladder and many penetrate through the mucosa, enter the lumen of the bladder and are excreted in the urine accompanied by blood. Thus hematuria and proteinuria are characteristic, though not invariable features of urinary schistosomiasis.

As with all Schistosoma species, it is the eggs and not the adult worms which are responsible for the pathology associated with S. haematobium. In chronic disease, eggs become trapped in the bladder wall resulting in the formation of granulomata. Following prolonged infection, the ureters may become obstructed and the bladder becomes thickened resulting in abnormal bladder function, urinary infection and kidney damage. Chronic urinary schistosomiasis is associated with squamous cell bladder cancer. Heavy infections in males may involve the penis resulting in scrotal lymphatics being blocked by the eggs.

Laboratory Diagnosis
The definitive diagnosis of urinary schistosomiasis is made by finding the characteristic ova of S. haematobium in urine. Terminal urine should be collected as the terminal drops contain a large proportion of the eggs. The urine can either be centrifuged and the deposit examined microscopically for ova. Eggs can sometimes be found in seminal fluid in males.

A bladder biopsy is seldom necessary to make the diagnosis. A rectal snip may show the presence of ova as they sometimes pass into the rectal mucosa.
Serological tests can be of value when eggs cannot be found in clinical samples. An enzyme linked immunosorbent assay using soluble egg antigen to detect antischistosome antibody is most sensitive.

There is a marked periodicity associated with the time when most eggs are passed out. Higher numbers of eggs are encountered in urine specimens passed between 1000 and 1400 hours, presumably as a result of changes in the hosts metabolic and physical activities.