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Video Endoscopic Sequence 1 of 19.
Trichuris Trichuris (whipworm).
A female Trichuris has been found in the cecum that is the normal habitat of this worms.
Trichuriasis is an intestinal infection found in human beings which is caused by Trichuris trichiura, more commonly known as whipworm because of its whip-like appearance. It is characterized by the invasion of the colonic mucosa by the adult Trichuris and produces minor inflammatory changes at the sites of localization. It is prevalent throughout the world, especially in tropical areas. Its diagnosis is usually made by identification of the typical eggs in the stool; adult whipworm is rarely seen during colonoscopy. Colonoscopy can directly diagnose trichuriasis, confirming the threadlike form of worms with an attenuated end. The worms can be overlooked, particularly if colon preparation is imperfect. Attenuated whip-like ends of whipworms, which are embedded in the colonic mucosa, were removed with biopsy forceps.
Download the video clip by clicking on the endoscopic image. If you wish to observe in full screen, wait to be downloaded complete then press Alt and Enter. Configure the windows media in repeat is optimal. All endoscopic images shown in this Atlas contains video clips. Medline.
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Video Endoscopic Sequence 2 of 19.
This worm seem to be a female, Note : A filariform anterior part. See the histopathologic below.
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Video Endoscopic Sequence 3 of 19.
The worm derives its name (whipworm) from its characteristic whiplike shape; the adult (male - 30-45 mm, female - 35-50 mm) with males being somewhat smaller than females. Buries its thin, threadlike anterior half into the intestinal mucosa, After 10-14 days in soil, eggs become infective. Soil-containing eggs must be swallowed. no tissue migratory phase occurs. Larvae hatch in the small intestine, where they grow and molt, finally taking up residence in the large intestine. The time from ingestion of eggs to development of mature worms is approximately 3 months. Adult females lay eggs for up to 5 years.
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Video Endoscopic Sequence 4 of 19.
Another trichuris is observed in the appendicular hole. This worm seem to be a male, Note : A filariform anterior part and coiled posterior end. More than 700 million people are infected worldwide. The adult worms (approximately 4 cm in length) live in the cecum and ascending colon. The adult worms are fixed in that location with the anterior portions threaded into the mucosa. Most cases are asymptomatic. Heavy parasite loads cause diarrhea, anemia and pain.
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Video Endoscopic Sequence 5 of 19.
One of the worm was taken with the biopsy forceps, see below the sequences of video clips and pictures of this whipworm.
Eosinophilia is uncommon; however, when present, it ranges from 5-20%.
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Video Endoscopic Sequence 6 of 19.
A video clip and a image of the whipworm.
Macroscopic and histopatologic images are displayed in this sequence, see below.
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Video Endoscopic Sequence 7 of 19.
Caudal aspect of female Trichuris trichura. ( Stereoscopic view).
The history of T. Trichuria dates back to the times of prehistoric man; however, the first written record of T. trchiura appeared in 1740 when an Italian scientist by the name of Morgani discovered the residence of adult T. trichiura worms in the colon. In 1761 Roedere, a German physician, gave a report of the exact morphologic description and provided accurate drawings of the parasite. The organism received its taxonomy classification in the 18th C.
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Video Endoscopic Sequence 8 of 19.
Cephalic part of the Trichuris trichura separated from the body. To the left there is a portion of caudal part of the parasite. The mouth is a simple opening, lacking lips. The buccal cavity is tiny and is provided with a minute spear.
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Video Endoscopic Sequence 9 of 19.
Stereoscopic view of the body of the parasite.
The esophagus is very long, occupying about two thirds of the body length and consists of a thin-walled tube surrounded by large, unicellular glands, the stitchocytes.
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Video Endoscopic Sequence 10 of 19.
Sections of the worm, demonstrated a gravid female adult nematode with numerous immature ova.
This is a longitudinal section of Trichuris trichura, showing eggs in the uterus. Female worms in the cecum shed between 3,000-20,000 eggs per day.
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Video Endoscopic Sequence 11 of 19.
A complete section of the uterus with numerous eggs.
Life cycle of T.trichiura: Eggs, after are discharges with the feces, require between 12 days and several weeks (based on the environment condition) for development of larvae. When infective eggs are ingested, the larvae hatch in the small intestine, and migrate to the lower intestine and colon, and enters the epithelium of the intestine. They become sexually mature in about 3 months. The larvae bore into the mucosa with the slender anterior part of the body.
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Video Endoscopic Sequence 12 of 19.
Characteristic eggs of Trichuris trichura with typical extremes.
Each worm causes an estimated 5 mL of blood loss every day. Heavy infections are required to cause anemia
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Video Endoscopic Sequence 13 of 19.
A 10x view of eggs into the uterus.
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Video Endoscopic Sequence 14 of 19.
A 4x view of eggs.
Whipworm infections transpire as a result of accidental ingestion of Trichuris trichiura eggs or embryos. After they are swallowed, the eggs move to the host's small intestine, where they develop into juveniles. The young worms then move to the large intestine and attach their anterior ends to the intestinal wall. After approximately three months, the parasite becomes a sexually mature adult, females producing up to 10,000 eggs per day, which are passed out of the host's system with digestive wastes. The eggs need a warm moist environment to survive outside the body and become infective in about three weeks. Since whipworms do not actually multiply inside a host, each individual worm represents a separate incident of infection.
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Video Endoscopic Sequence 15 of 19.
Colonic mucosa with erosion and chronic inflammatory changes, and hemorrhages, 10x.
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Video Endoscopic Sequence 16 of 19.
The colonia mucosae shows chronic inflamation and superficial hemorrage.(Low power 4x).
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Video Endoscopic Sequence 17 of 19.
Low power,4x, of colonic mucosa with inflamatory changes. There are superficial erosions.
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Video Endoscopic Sequence 18 of 19.
Low power, 4x, of colonic mucosa with inflamatory changes.
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Video Endoscopic Sequence 19 of 19.
Same picture of colonic mucosa at 10x.
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Video Endoscopic Sequence 1 of 9.
Schistosoma Mansoni in the Cecum
Magnification Colonoscope.
This 34 year-old male, a routine colonoscopy was performed a Schistosoma Mansoni was found at the cecum.
In the Republic of El Salvador no cases of Schistosoma Mansoni have been reported previously, in this atlas we presented two cases of Schistosoma Mansoni found them at the cecum.
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Video Endoscopic Sequence 2 of 9.
High Magnification Image and Video Clip.
The Schistosome Egg is Responsible For Most of the Pathology Associated with Schistosomiasis.
Schistosome eggs, which may become lodged within the hosts tissues, are the major cause of pathology in schistosomiasis, which takes a number of forms. Onset of egg laying in humans is sometimes associated with an onset of fever (Katayama fever). This "Acute Schistosomiasis" is not however as important as the chronic forms of the disease. For S. mansoni and S. japonicum these are "Intestinal" and "Hepatic Schistosomiasis", associated with formation of granulomas around trapped eggs lodged in the intestinal wall or in the liver respectively. The hepatic form of the disease is the most important, granulomas here giving rise fibrosis of the liver and hepatosplenomegaly in severe cases.
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Video Endoscopic Sequence 3 of 9.
Schistosomiasis (ie, bilharziasis) is a human disease syndrome caused by infection from one of several species of parasitic trematodes of the genus Schistosoma. Schistosomiasis is a major source of morbidity and mortality for developing countries in Africa, South America, the Caribbean, the Middle East, and Asia. Tourism to and immigration from endemic areas can result in schistosomiasis cases presenting anywhere in the developed world.
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Video Endoscopic Sequence 4 of 9.
Most human schistosomiasis is caused by Schistosoma haematobium, Schistosoma mansoni, or Schistosoma japonicum. Less prevalent species such as Schistosoma mekongi and Schistosoma intercalatum also may cause systemic human disease. Less importantly, other schistosomes with avian or mammalian primary hosts can cause severe dermatitis in humans (eg, swimmer's itch secondary to Trichobilharzia ocellata).
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Video Endoscopic Sequence 5 of 9.
After malaria, schistosomiasis is the second most prevalent tropical disease in the world. In some parts of the world, it also is known as bilharzia in honor of Theodore Bilharz. He first identified the etiological agent for Schistosoma hematobium in Egypt in 1851.
The pathophysiology of schistosomiasis is due to the immune response against the schistosome eggs. The clinical manifestations depend on the species of parasite, intensity of worm burden, and immunity of the person to the parasite. Recent World Health Organization (WHO) reports estimate that 500-600 million people in 74 tropical and subtropical countries are at risk for schistosomiasis. Over 200 million people in these countries are infected. Of these, 120 million are symptomatic, with 20 million having severe clinical disease.
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Video Endoscopic Sequence 6 of 9.
The life cycle of the flatworms that cause human schistosomiasis involves a sexual stage in the human and an asexual stage in the fresh water snail host. The adult worms are small, 12-26 mm long and 0.3-0.6 mm wide, and vary with the different species. S hematobium lives in the venous plexus near the urinary bladder and ureters, S mansoni lives in the inferior mesenteric vein, and S japonicum lives in the superior mesenteric vein of both the large and small intestines.
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Video Endoscopic Sequence 7 of 9.
Adult worms mate and lay eggs. The eggs are nonoperculate, possess a spine, and contain a miracidium. The microscopic appearance of the egg allows diagnostic differentiation of the 5 species. An adult S hematobium produces 20-200 round, terminally spined eggs per day; S mansoni produces 100-300 ovoid, laterally spined eggs per day; and S japonicum produces 500-3500 round, small, laterally spined eggs per day. The eggs of S intercalatum have prominent terminal spines, and S mekongi have small lateral spines.
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Video Endoscopic Sequence 8 of 9.
Pathophysiology: The pathophysiology of infection correlates with the life cycle of the parasite, as follows.
.Cercariae: Skin penetration of cercariae produces an allergic dermatitis at the site of entry. With prior sensitization, a pruritic papular rash occurs. This also is observed with nonhuman avian schistosomes.
Schistosomula: These are tailless cercariae that are transported through blood or lymphatics to the right side of the heart and lungs. Heavy infection can cause symptoms such as cough and fever. Eosinophilia may be observed.
Adult worm: Adult worms do not multiply inside the human body. In the venous blood, adult male and female worms mate, and the female lays eggs 4-6 weeks after cercarial penetration. Adult worms rarely are pathogenic. The female adult worm lives for approximately 3-8 years and lays eggs throughout her life span.
Eggs: They cause Katayama fever and schistosomiasis.
- · Katayama fever: The exact pathophysiology is not known. It occurs 4-6 weeks after infection, at the time of the initial egg release. It is reported most commonly with S japonicum but also has been reported with S mansoni. Katayama fever is believed to be due to the high worm and egg antigen stimuli that result from immune complex formation and lead to a serum sickness–like illness. This syndrome is not due to granuloma formation.
- · Schistosomiasis: It is due to immunological reactions to Schistosoma eggs trapped in tissues. Antigens released from the egg stimulate a granulomatous reaction comprised of T cells, macrophages, and eosinophils that results in clinical disease. Symptoms and signs depend on the number and location of eggs trapped in the tissues. Initially, the inflammatory reaction is readily reversible. In the latter stages of the disease, the pathology is associated with collagen deposition and fibrosis, resulting in organ damage that may be only partially reversible.
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Video Endoscopic Sequence 9 of 9.
The geographic distribution and pathophysiology of schistosomiasis reflect the unique life cycle of these parasites. Schistosomes infect particular species of susceptible freshwater snails in endemic areas. The infected snails release cercariae, which are fork-tailed free -swimming larvae approximately 1 mm in length. The cercariae survive in freshwater up to 48 hours, during which time they must attach to human skin or to that of another susceptible host mammal or die.
Cercariae attach to human hosts utilizing oral and ventral suckers. They then migrate through intact skin to dermal veins and, over the next several days, to the pulmonary vasculature. During this migration, the cercariae metamorphose, shedding tails and outer glycocalyces while developing double-lipid-bilayer teguments that are highly resistant to host immune responses.
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Video Endoscopic Sequence 1 of 2.
Trichuris Trichuris (whipworm).
This parasite is prevalent in the tropics, larvae penetrate the intestinal mucosa, and reattach as adults to the mucosa of the cecum wall of the colon. The mucosa becomes edematous and friable. Bleeding from friable mucosa can result in anemia.
This parasite, which only infect human, found in most parts of the world, but mostly in worm and humid areas. The infection is mostly found from children and infection rates as high as 90% has been reported from many areas.
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Video Endoscopic Sequence 2 of 2.
Trichuris Trichuris (whip worm) at the cecum.
The adult worm usually reaches 3-5 cm in length and has a lifespan of 1-3 years.
Humans are the only known host of T trichiura. The organism is spread via the fecal-oral route. Potential hosts ingest the embryonated (mature) eggs. The eggs hatch in the small intestine, and the larvae attach to and penetrate the small intestinal mucosa, where they begin to mature. After approximately 1 week, the immature worms move passively to the large intestine and proximal colon. The worms' anterior portions penetrate the mucosal epithelium, and the worms can imbed over one half of their length into the mucosal surface.
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Video Endoscopic Sequence 1 of 9.
Melanosis Coli and Schistosoma Mansoni
This 63 year-old female a colonoscopy was performed due to an abdominal pain.
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Video Endoscopic Sequence 2 of 9.
In spite of to have tried to move the parasite with the pressure of the water spurt, but this action was impossible.
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![The eggs, which are highly antigenic and can induce an intense granulomatous response, migrate through the bowel or bladder wall to be shed via feces or urine. During this time (approximately 10 d) they begin to mature into miracidia. Eggs that are not shed successfully may remain in the tissues or be swept back to the portal circulation (from the mesenteric vessels) or to the pulmonary circulation (from the vesicular vessels via the inferior vena cava [IVC]). The free-swimming miracidia that are shed into freshwater survive 2-3 weeks, during which time they must infect a susceptible snail to complete the life cycle. Within the infected snail, 2 generations of sporocysts multiply, mature into free-swimming cercariae, and exit the snail to seek a human host and begin a new cycle. The eggs, which are highly antigenic and can induce an intense granulomatous response, migrate through the bowel or bladder wall to be shed via feces or urine. During this time (approximately 10 d) they begin to mature into miracidia. Eggs that are not shed successfully may remain in the tissues or be swept back to the portal circulation (from the mesenteric vessels) or to the pulmonary circulation (from the vesicular vessels via the inferior vena cava [IVC]). The free-swimming miracidia that are shed into freshwater survive 2-3 weeks, during which time they must infect a susceptible snail to complete the life cycle. Within the infected snail, 2 generations of sporocysts multiply, mature into free-swimming cercariae, and exit the snail to seek a human host and begin a new cycle.](../../../TricocefMelanosis3.jpg) |
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Video Endoscopic Sequence 3 of 9.
The eggs, which are highly antigenic and can induce an intense granulomatous response, migrate through the bowel or bladder wall to be shed via feces or urine. During this time (approximately 10 d) they begin to mature into miracidia. Eggs that are not shed successfully may remain in the tissues or be swept back to the portal circulation (from the mesenteric vessels) or to the pulmonary circulation (from the vesicular vessels via the inferior vena cava [IVC]).
The free-swimming miracidia that are shed into freshwater survive 2-3 weeks, during which time they must infect a susceptible snail to complete the life cycle. Within the infected snail, 2 generations of sporocysts multiply, mature into free-swimming cercariae, and exit the snail to seek a human host and begin a new cycle.
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Video Endoscopic Sequence 4 of 9.
Acute Schistosomiasis - Also called 'Katayama' fever. This is associated with the onset of the female parasite laying eggs, (approximately 5 weeks after infection), and granuloma formation around eggs trapped in the liver and intestinal wall. It resembles 'serum sickness' (i.e. acute immune complex disease), with hepatosplenomegaly, and leucocytosis with eosinophilia. This phase of the infection is often asymptomatic, but when symptoms do occur they include fever, nausea, headache, an irritating cough and, in extreme cases diarrhoea accompanied with blood, mucus and necrotic material. These symptoms , if present, last from a few weeks, to several months. It is not as commonly associated with S. mansoni infections compared with those of S. japonicum.
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Video Endoscopic Sequence 5 of 9.
The Chronic Phase of Infection.
- This is the more important aspect of Schistosoma mansoni pathology, and may be divided into two areas Intestinal Schistosomiasis - This and the hepatic schistosomiasis detailed below, manifest a number of years after infection. The pathogenic reaction is a cellular, granulomatous inflammation around eggs trapped in the tissues, with subsequent fibrosis. All areas of both the small and large intestine may be involved, with the large intestine showing the most severe lesions, whereas severe pathology in the small intestine is only rarely observed, even though large numbers of eggs may be deposited here. Colonic polyps are also sometimes seen, especially in Egypt (Cheever et al 1978). The reasons for the high prevalence of this aspect of pathology in Egypt are not clear.
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Video Endoscopic Sequence 6 of 9.
Hepatosplenic Schistosomiasis - Again, this aspect of the disease is only seen a few years after infection. The pathology is similar to that seen in the intestine, with a cellular, granulomatous inflammation around eggs trapped in the liver, leading to fibrosis and hepatosplenic disease. Other organs may more rarely also contain granulomas around eggs, particularly the lungs.
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Video Endoscopic Sequence 7 of 9.
Pathology Associated with Infection by Other Species of Schistosome.
S. japonicum Infection
The primary cause of pathology here is a granulomatous reaction to egg trapped in the liver, and both the acute and chronic aspects of the disease are similar to that of S. mansoni infections, although the acute disease Katayama fever, is more common here than for S. mansoni . The chronic stage of the disease may also be more severe, owing to the greater egg output and longevity of S. japonicum females compared with those of S. mansoni.
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Video Endoscopic Sequence 8 of 9.
Schistosoma Mansoni in the cecum
S. haematobium Infection
Adult parasites are found in small venules around the bladder and ureter, with the majority of egg deposition in the tissues of these organs, as eggs pass through the bladder wall, to leave the body in the urine. The disease cause is chronic in nature, with the most frequently affected organ being the urinary bladder, where calcification of eggs trapped in the tissues often occurs. The disease is characterised by blood in the urine (haematuria ), hence the infection is often refered to as 'Urinary Schistosomiasis '. Cancer of the bladder is an important complication of infection with S. haematobium. Eggs may be deposited in the liver, often in high numbers, and granuloma formation may occur, but this is much less severe than with S. mansoni.
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Video Endoscopic Sequence 9 of 9.
Minor species
- S. Intercalatum infection.
- This is diagnosed by the presence of terminally spined eggs in the faeces, (the other terminally spined schistosome eggs, those of S. haematobium , are only found in the urine). Blood may be seen in the faeces, and diarrhoea may occur. However the portal hypertension . seen in S. mansoni infections has not been reported, and infections are often asymptomatic.
- S. mekongi infection.
- This has not been greatly studied, but the pathology appears to be similar to that of S. japonicum.
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