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Parasitology

 

 


 

Volume 6.  The Trematodes

 

 

 

 

 

 

 

 

Co- Authors:  M. Arcari 1, A. Baxendine 1 and C. E. Bennett2

 

1. Diasys Ltd    2. University of Southampton 


CONTENTS

 

          Helminth Parasites                                                            

                                    

5.        Infections of the alimentary tract and associated organs-

          Part One – The Trematodes                                                        1

          Fasciola species                                                                           3

          Clonorchis sinensis                                                                       8

          The Schistosomes                                                                        12          Schistosoma mansoni                                                                  13

Schistosoma japonicum                                                                16

Schistosoma haematobium                                                           18      

 

          References


6. Infections of the Alimentary Canal and asociated organs. Part One - The Trematodes

 

The trematodes (or flukes) are leaf shaped and can outer cover called the tegument which may be smooth or spiny. There are 2 suckers or attachment organs, an anterior oral sucker and a posterior ventral sucker.  The suckers form a characterisitic feature of the group, from which the name Trematode is  derived from (trematodes is a Greek word for meaning holes). They can occur in a variety of host environments, with the majority being endoparasitic but some are found to be ectoparasitic.

 


Most trematodes are hermaphroditic and most of their body consists of the reproductive organs and their associated structures. (Fig. 1) The digestive system is well developed, they generally feed on intestinal debris, blood, mucus and other tissues, depending on the host environment.


 

Text Box: Excretory bladder

 

Figure 1.  A generalised diagram of the Trematode anatomy. (Adapted and redrawn from Smyth, J.D, 1994)

 

 

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: The Monogenea, which typically are external parasites of fish with direct life cycles. The Aspidogastrea, these are endoparasites with the entire ventral surface as an adhesive organ. Finally the third group is the 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 mollusc 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 parasitise the liver and intestines of a variety of vertebrates. They are hermaphroditic and their distinguishing characteristics are shown in Table 1.

 

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 is used as a fertiliser 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 injestion 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.

 

 

Species

 

Geographic Distribution

Reservoir Hosts

Location of adult in host

Size of Ova

Fasciola hepatica

Cosmopolitan

Sheep

 

 

Bile Ducts

130 - 150mm

by

63 - 90mm

Fasciola

gigantica

Africa, the Orient and Hawaiian Islands

Camels, Cattle and Water Buffalo

Bile Ducts

160 – 190mm

by

70 - 90mm

Fasciolopsis buski

Far-East and Indian Sub-continent

Pigs, Digs and Rabbits

Intestine

130 – 140mm

by

80 - 85mm

Echinostoma species

South East Asia and Japan

Variety of Mammals

Intestine

88 – 116mm

by

58 - 69mm

 

Table1. 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.  (Fig. 2)

 

Adult worms inhabit the liver or bile ducts of the definitive host (human), where they lay many eggs which are deposited into the environmnent in the faeces. They are immature when passed.  If they are passed into water they become mature in 9 to 15 days at the optimum temperature of 22 - 25°C.

 

 

 

 

 

 

 

 

 

 

 


 

 


Figure 2. The general life cycle of Fasciola, Fasciolopsis and Echinostoma species. They all involve one or more intermediate hosts.

 

 

The larvae (miracidia) develop within the eggs and hatch out into water, where they then penetrate the snail (intermediate host). The miracidia must find a snail within 8 hours of hatching out of the egg. Each species of fluke favours one particular intermediate host; F. hepatica invade snails from the genus Lymnaea, the most important being Lymnaea truncatula and F. buski invade snails of the family Planorbidae, e.g. Segmentina hemisphaerula.

 

Within the snails the miracidia mature into sporozoites and then into redia and cercariae. This development takes 1 to 2 months according to the temperature. (In summer there is only one redial generation but in cooler weather there are two redial generations.)

 

The cercariae leave the snail, usually at night: they then swim around for several hours and then encyst (forming a resistant external wall) on submerged vegetation or fresh water fish.

 

If the cysts are ingested by a definitive host, the metacercariae excyst in the duodenum. They then migrate through the intestinal wall and either reach the liver tissue and bile ducts via the body cavity or via the lymphatics and the circulation. They require 2 to 3 months to reach maturity.

 

The life cycle of the Echinostomes differs by one minor point: the cercariae encyst wither within the tissues of the same molluscan host in which sporocysts and rediae develop, or penetrate and encyst in other animals such as amphibians or fish.

 

Morphology

The morphology of the adult flukes of Fasciola, Fasciolopsis and Echinostoma species is well documented. (Fig. 3)They are large leaf-shaped parasites about 2 –3 cm long.  There are two suckers, an anterior oral sucker surrounding the mouth and a ventral sucker (acetabulum) on the ventral surface.

 


 

Figure 3.  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.

 

 

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 coloured (bile stained) with an operculum that is often inconspicuous. (Fig. 4 & 5) Although ova of Echinostoma species can usually be differentiated by size due these flukes beign much smaller in size than F. Buski and F. hepatica, there is much cross-over in the size of Fasciola and Fasciolopsis species as shown in

Table 1.

 

Pathogenesis

Light infections due to Fasciola hepatica may be asymptomatic.  However, they may produce hepatic colic with coughing and vomiting; generalised abdominal rigidity, headache and sweating, irregular fever, diarrhoea and anaemia.

 


 

Figure 4.  Diagram illustrating the morphology of a Fasciola ova, the miracidium develops within the egg. (Drawn and adapted from Smyth, J.D, 1994)

 


 

Figure 5.  Ova of Fasciola are ovoid in shape, quinone colour and often showing an inconspicuous operculum. Fasciola hepatica ova measure 130 - 150mm by 63 - 90mm. There is much cross-over in ova size between all of the Fasciola species.

 

 

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 diarrhoea, oedema 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, diarrhoea and abdominal pain.

 

Laboratory diagnosis

Definitive diagnosis is made by observing the ova in faeces, 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 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. 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 sinenesis parasitise 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

The adult flukes are found in the bile ducts and gall bladder where they deposit eggs. (Fig. 6) The eggs are passed out into the environment in faeces, having

 


 

 


Figure 6.  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.

 

 

 

Entered the gut in the bile. Further development can only take place if they are eaten by appropriate species of water snails (intermediate hosts), e.g. Bulimus fuchsianus. Within the snails body the miracidium (which hatched out of the operculated egg) matures into a sporocyst and then a redia (both are asexual replicative stages). Within the redia, several cercariae develop with unforked tails. These escape into the surrounding water when the redia finally bursts. They can live in the water for 1 – 2 days waiting to come in contact with a suitable species of fish (over 80 species have been recognised as susceptible hosts), they force their way in through the scales, lose their tails and encyst as infective metacercariae.

 

Humans become infected when they eat raw or slightly pickled fish, the metacercariae excyst in the duodenum and descend the bile ducts. There they develop into adult flukes within 4 weeks.

 

From infection of the snail to the formation of the infective metacercariae takes about 8 weeks.

 

 

Morphology


The adult flukes measure 11 – 20mm by 3 – 4.5mm and are lanceolate in shape, translucent and brownish in colour. (Fig. 7) They are all hermaphroditic. Keeping in common with other flukes they possess two suckers.


Figure 7. Diagram illustrating the internal morphology of the Oriental liver fluke, Clonorchis sinensis. (Adapted and redrawn from Smyth, J.D, 1994)

 

 


The ova of Clonorchis sinensis contain fully developed miracidia and possess prominent opercular shoulders (flask shaped egg) and are operculate. (Fig. 8 & 9) They are bile stained and measure 29mm by 16mm. 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 microlitre of bile or 600 per gram of faeces.


 

Text Box: Figure 8. Ova of Clonorchis sinensis, showing the prominent opercular shoulders which makes identifying this trematode easy, they are described as flask shaped. They are bile stained and measure 29mm by 16mm.  (Adapted and redrawn from Smyth, J.D, 1994)
The cercariae possess eyespots, the penetration and cystogenous glands are also well developed.

 


 

Figure 9. Saline smear showing the characteristic flask shape of the Clonorchis sinensis ova. They are bile stained with a smooth outer coat.

 

 

 

 

 

 

 

 

Pathogenesis

Many millions of people become infected every year but only a minority suffer 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 characterised by fever, diarrhoea, 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 faeces following concentration of the faeces (refer to volume 1) or from duodenal aspirates when there is complete obstructive jaundice or from the Entero-Test.

 

 

 

Heterophyes heterophyes

Metagonimus yokogawai

Opisthorchis viverreni

Dicrocoelium dendriticum

Geographic distribution

Far East

Far East

Thailand

Far East

Location of adult in host

Small intestine

Small intestine

Liver and bile ducts

Liver and bile ducts

Size of ova

26.5- 30mm by     15 – 17mm

26.5- 30mm by     15 – 17mm

26.7 by 15mm

38 – 45mm by    22 – 30mm

Shape of ova

Prominent opercular shoulders Bile stained

Prominent opercular shoulders Bile stained

Prominent opercular shoulders Bile stained

Dark brown, thick shelled and large operculum

Infection

acquired by

Eating raw or pickled fish

Eating raw or pickled fish

Eating raw fresh water fish

Eating infected ants

Symptoms

Occasionally diarrhoea and vomiting

Occasionally diarrhoea and vomiting

Malaise and right upper quadrant pain

Biliary and digestive problems

 

Table 2. Table summarising the less common flukes that are known to infect man.


Paragonimus westermanni

 

Introduction

Paragonimus westermanni is a lung fluke found in both humans and animals.  The adults are 12mm 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 fertilisation to occur.  The disease is seen in the Far East, China, South Eat Asia and America.

 

 

Life cycle

Humans become infected by ingestion of insufficiently cooked crayfish or crabs containing metacecariae which excyst in the intestine, penetrate through the wall into the peritoneal cavity and make their way through the diaphragm and pleura into the lungs.  (Fig. 10)

 

The lung cysts in which the worms most commonly occur usually contain 1 – 3 flukes. The eggs become freed into the bronchial tubes and pass out with sputum, but they may also appear in the faeces in large numbers, as a result of being swallowed.

 

Sporocyst and 2 redia generations occur, giving rise to creeping cercariae. These penetrate a number of fresh-water crustaceans, in which they encyst invarious sites such as gills, muscles, heart and liver. Encysted metacercariae are not immediately infective but have to undergo further maturation.

 

Mammalian hosts ingest the cysts, which are then ingested in the duodenum and the freed metacercariae penetrate through the intestinal wall into the body cavity to reach the pleural cavity in about 4 days and the lungs in about 14 – 20 days. In the lungs, a fibrous capsule is formed by the host, after about 6 weeks the worms mature and produce eggs, which characteristically appear in the sputum.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Figure 10. Diagram of the general life cycle of the lung fluke, Paragonimus westermanni.

 

 

Morphology

The adult worm is an ovoid, reddish brown fluke about 12 mm long. 

 

The eggs are ovoid, brownish yellow, thick shelled and operculated.  They measure 80 – 100mm by 45 - 65mm and may be confused with the ova of Diphyllobothrium latum. (Fig. 11)

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 


 

 


Figure 11. Saline smear of Paragonimus westermanni egg. The egg shells are thick and operculated, measuring approximately 80 – 100mm by 45 - 65mm.

 

 

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.  Haemoptisis may occur after paroxysms of coughing.  Dyspnoea 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 faeces 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.

 

 


The 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 5 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. (Fig. 12)


 


Figure 12. Diagram illustrating the general life cycle of the Schistosomes. These trematodes are different from all of the others previously mentioned in that they have separate sexes and inhabit the blood stream of warm-blooded hosts.

Adults of S. japonicum live in the anterior mesenteric blood vessels and in the portal vein in the liver. Whilst 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 faeces (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, 200mm 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 6 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 geuns 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 millimetres in length and females up to 10 mm.  The schistosomes remain in copula throughout their life span, the uxorious male surrounding the female with his gynaecophoric canal. (Fig. 13) 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.

 


 

Figure 13. Diagram showing the coupling of the adult male and female S. mansoni worms as they would be in the inferior mesenteric veins of the lower colon. The males hold the females within the gynaecophoric canal.

 

The ova of S. mansoni are 114-175mm long by 45-68mm wide.  They are light yellowish brown, elongate and possess a lateral spine. (Fig. 14 & 15) The shell is acid fast when stained with modified Ziehl-Neelsen Stain.


 


 

 


 

 


A non-viable egg is dark coloured 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.

 

 


 

 


Figure 15. Saline smear of a S. mansoni ova showing clearly 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.

 

 

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 faeces, 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, eosinophilia 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 faeces.  When eggs cannot be found in the faeces 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 faeces.

 

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 reach in about 4 weeks and eggs may be seen in the faeces as quickly as 5 weeks.

 

They worms live coupled together in the superior, mesenteric veins and desposit 1500 – 3500 eggs per day in the vessels of the intestinal wall. The eggs infiltrate through the tissues and are passed in the faeces.

 

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. (Fig 16)

 

 

 

 

 

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 submucsa initiate granulomatous reactions, resulting in the formation of pseudotubercles.

 

 

 


 

Figure 16. Saline smear of a S. japonicum ova. They range in size between 55 - 85mm by 40 - 60mm, oval in shape with a minute lateral spine or knob. (Fig 14)

 

 

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 intial 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 faeces.  When eggs cannot be found in the faeces 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 2 species cause similar symptoms to that of S. mansoni and can be summarised in Table 3.

 

 

S. mekongi

S. intercalatum

Geographic location

Mekong River basin

Central and west Africa

Diagnostic specimen

Stool, rectal biopsy, serology

Stool, rectal biopsy, serology

Egg size

30-55 by 50-65mm

140-240 by50-85mm

Egg shape

Oval, minute lateral spine or knob

Elongate, terminal spine

 

Table 3. Table describing the other less common intestinal Schistosome species that are known to cause disease in man.

 

 

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 favour 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 110mm - 170mm in length and 40mm - 70mm in width.  They have an elongated ellipsoid shape with a prominent terminal spine. (Fig. 17)


 

Figure 17. Schistosoma haematobium eggs are elongated (110-170 by 40-70 microns) with a prominent terminal spine.  The larva inside the egg produces an enzyme that passes through the egg-shell,

 

 

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 maculo-papular 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 haematuria 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 10 am and 2pm, presumably as a result of changes in the host’s metabolic and physical activities.


 


 References

 

Murray, PR, Drew, WL, Koyayashi, GS & Thomson, JH: Medical Microbiology. Mosby Books Inc., New York (1990)

 

Peters, W & Gilles, HM: Tropical Medicine & Parasitology. Wolfe Medical Publications Ltd.

 

Jeffrey & Leach: Atlas of Medical Helminthology and Protozoology. E & S Livingstone Ltd.

 

Ash, LR & Orihel, TC: Atlas of Human Parasitology. ASCP Press, Chicago.

 

Garcia, LS & Bruckner, DA: Diagnostic Medical Parasitology. Elsevior Science Publishing Co. Inc.

 

Muller, R & Baker, JR: Medical Parasitology. Gower Medical Publishing.

 

Snell, JJS, Farrell, ID & Roberts, C: Quality Control, Principles and Practice in the Microbiology Laboratory. Public Health Laboratory Service. ISBN 0 901 144 312.

 

Brown, VC. A Longitudinal study of the prevalence of intestinal helminths in baboons (Papio doguera) from Tanzania. (1994) Thesis, Liverpool.