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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)

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.  

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 22-25°C.

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 µm by 13 µm; F. gigantica: up to 75 µm) 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 2–3cm 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 2–3cm 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 - 150µm by 63 - 90µm. 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 µm by 3 to 5 µm) 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 11–20µm by 3–4.5µm 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 29µm by 16µm. 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.    

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

Paragonimus westermani

Introduction

Paragonimus westermani is a lung fluke found in both humans and animals.  The adults are 12µm 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 µm by 4 to 6 µm).  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 12µm long. 

The eggs are ovoid, brownish yellow, thick shelled and operculated.  They measure 80-100µm by 45-65µm 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 µm; 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, 200µm long) into the water about 3–6 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 24–48 hours after which if they don’t 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 2–4 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 10µm.  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 114-175µm long by 45-68µm 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 114-175mm long by 45-68mm 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 1500–3500 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 55-85mm by 40-60mm, 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.  

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 4–5 weeks, but eggs may not appear in the urine until 10–12 weeks or even later.

Morphology

The adult worms are longer than those of S. mansoni. The ova are relatively large, measuring 110-170mm in length and 40-70mm 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 (Swimmer’s 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 host’s metabolic and physical activities.