PHYLUM PLATHYHELMINTHES. CLASS TREMATODA.
CLASS CESTODA
Helminth Parasites
The word “worm” is used loosely to describe organisms with elongated bodies and a more or less creeping habit.
The word “Helminth” does mean “worm”, but in zoological terms it is more restricted to members of the phyla Platyhelminths, Nematoda and Acanthocephala.
There are three groups of medically important helminthes: Cestodes (tapeworms), Nematodes (roundworms) and Trematodes (flukes).
These parasites live in both the body spaces (gut lumen, bile ducts, lungs, oral cavity, etc.) and in tissues (blood, muscles and skin).
According to the way of development parasites are classificated into biohelminthes and geohelminthes.
Geohelminthes develop without intermediate hosts. Soil is the best environment for their egg’s development. Humans are infected through dirty fruits and vegetables which contain geohelminthe’s eggs (for example, Ascaris lumbricoideus).
Biohelminthes have complete life cycle with intermediate hosts. There are trophycal connections between definitive and intermediate hosts (for example, Taenia solium).
General characteristic of Flatworms (Phylum Plathelminthes).
The flatwotms (phylum Platyhelminthes) consists of some 12, 200 species. These ribbon-shaped, soft-bodied animals are also called because they are flattened dorsoventrally, from top to bottom. Flatworms are among the simplest of bilaterally symmetrical animals, but they have a definite head at the anterior end. Their bodies are solid: the only internal space consists of the digestive cavity. Flatworms are acoelomates (have no body cavity), usually hermaphroditic, and a digestive canal is present. Trematode eggs are excreted in the stool, urine, or sputum of the definitive host. All flukes require a mollusk as their first intermediate host. The larval stage that escapes from the mollusk may then enter a second intermediate host. The larval stage that escapes from the mollusk may then enter a second intermediate host (fish, crustacean), encyst on vegetation, or penetrate directly into the skin of the definitive host. Infection generally results from the ingestion of insufficiently cooked fish, crustaceans, and vegetation.
Phylum Plathelminthes includes classes:
1) Class Trematoda;
2) Class Cestoda.
General characteristic of Class Trematoda (Flukes):
1) Flattened dorsoventrally (leaf-like).
2) Unsegmented.
3) Body is covered by cuticle.
4) Organs of fixation: oral sucker, ventral sucker.
5) Organs and systems of Flatworms: digestive system, excretory system, nervous system, genital system: Trematodes are hermaphrodites except genus Schistosoma.
6) The life cycle is passed in two hosts (alternation of hosts) and has sexual and asexual stages.
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 organs of attachment, 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 (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. The digestive system is well developed; they generally feed on intestinal debris, blood, mucus and other tissues, depending on the host environment.
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 organisms are founf mostly 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.
Liver Flukes:
Clonorchis sinensis, Opisthorchis species, and Dicrocoelium dendriticum
Classification. Helminths. Phylum Platyhelminths. Trematodes.
Diseases. Clonorchiasis (Chinese liver fluke infection), Opisthorchiasis, Dicrocoeliasis.
Geographic Distribution
China, Taiwan, Japan, Korea, Vietnam (Clonorchis); Thailand and Lao People’s Democratic Republic (O. viverrini); Eastern Europe and former USSR (O. felineus); Europe, former USSR, northern Africa, northern Asia, areas of the Far East, and the western hemisphere (Dicrocoelium).
Location in Host. Bile ducts of the liver.
Morphology
Adult Worms. Adult Clonorchis are flattened and spatulate, measuring
10-25 mm long and 3-5 mm wide. They are hermaphroditic, with a single, rounded ovary situated anterior to the two extensively branched testes. Adults of O. felineus from humans are usually smaller, 7-12 mm long, and their slightly lobed testes are posterior to the oval or lobed ovary. Dicrocoelium adults measure
5-15 mm long and 1,5-2.5 mm in width, and their paired, slightly lobed testes are immediately behind the ventral sucker and anterior to the ovary.
Eggs
The ovoid, yellow-brown eggs of Clonorchis have a moderately thick shell and a seated operculum that results in its prominent “shoulders” appearance; they measure 27-35 μm and 12-19 μm. There is usually a small knob at the abopercular end. These eggs contain a miracidium when passed in feces. Eggs of O. viverrini and O. felineus are similar in morphology and size, measuring 19-29 μm long and 12-17 μm in width. Operculate Dicrocoelium eggs are thick-shelled, have a deep golden brown color, contain a miracidium, and measure 38-45 μm long and 22-30 μm in width.
Life Cycle
Clonorchis and Opisthorchis have similar life cycles involving appropriate freshwater snails as the first intermediate hosts and many fish as second intermediate hosts. Metacercariae encyst under the scales or skin of fish. Infection is acquired by ingestion of raw or inadequately cooked infected fish. Clonorchis metacercariae, ingested by a mammalian host, migrate to the bile ducts of the liver via the common bile duct and mature in 3 to 4 weeks. The life span of adult Clonorchis may be 20 to 25 years. Cats and dogs serve as animal reservoirs for human infection. Dicrocoelium has a markedly different life cycle that involves the use of appropriate terrestrial snails as first intermediate hosts. Large numbers of cercariae are released from snails and agglomerate within the mucus of molluscs to form “slime balls” that are deposited on soil or grass. These slime balls are ingested by ants that serve as the second intermediate host; infection is acquired by the ingestion of ants harboring metacercariae. Sheep, cattle, deer, and other herbivores are the usual hosts for this parasite, but human infections are common in many areas.
Diagnosis. Detection of characteristic eggs in feces.
Diagnostic Problems
Clonorchis eggs sometimes are confused with heterophyid eggs but generally are somewhat larger and have a prominent seated operculum, whereas heterophyid eggs usually have an inconspicuous operculum flush with its shell surface. Although Clonorchis eggs typically have a knob or hooklike protrusion at the abopercular end, it is often difficult to see or may be absent. Although Opisthorcbis eggs are quite similar to those of Clonorchis, the shoulders of these eggs are not usually as prominent. Ingestion of infected livers from herbivorous animals may result in spurious passage of Dicrocoelium eggs in human feces.
Comments
Clonorchis infections occurring in residents of Hawaii and the west toast of the United States who have not been to the Orient probably are caused by eating of imported pickled fish containing still-viable metacercariae. In Canada, a related liver fluke, Metorchis conjunctus, has been found to cause clinical illness (abdominal pain, anorexia, and liver function abnormalities) in people eating raw fish, in particular the while sucker, Catostomus commersoni. Eggs of this parasite measure approximately 28 μm in length by 16 μm in width and are morphologically indistinguishable from the eggs of Opisthorchis species.
FASCIOLA HEPATICA – an agent of fascioliasis. It is a biliary (liver) fluke. Relatively common large fluke.
Distribution: endemic in Far East.
Localization: bile ducts, gallbladder, pancreas.
Morphology: large sizes (3-5 cm) and conical form of the body; possess sucking disks (oral and abdominal) that provide them motion. Multibranched uterus is situated under the abdominal sucking disk. Testis are branched too and situated in the middle part of the body;
Embryonated egg capsule of Fasciola hepatica.
Transmission: fecal-oral (ingestion of water, some non-water plants and vegetables, which contain adolescariae).
Invasive stage: adolescariae.
Clinical disease: Parasites obstruct bile ducts and lay eggs within them, leading to cholelithiasis (gallstones). Biliary obstruction can occur, sometimes causing biliary cirrhosis.
Life-cycle: Final host – herbivorous mammals (horses, pigs) and humans. Intermediate host — the snail Limnea truncatula. Eggs are excreted in feces of infected host. Egg hatches and forms a miracidium in water. It penetrates a snail host. In snail, after such stages as sporocyst and redia, free-swimming cercariaes are released to water. Cercariaes lose their tails and are covered by thick membrane and transform into adolescariae. They collect on watercress plants. Adolescariae are ingested by humans (final host), where they transform into juvenile and then — adult fluke.
Diagnosis: immature eggs in feces. An egg has large sizes, thin membrane, yellow color and small cover in one pole.
Prevention: involves not eating wild aquatic vegetables.
OPISTHORCHIS FELINEUS – small biliary fluke, causing Opisthorchiasis.
Distribution: Siberia.
Localization: bile ducts, gallbladder, liver.
Morphology: flat, the length of the body 4-13 mm. In the middle part of the body there is a branched uterus. Behind it there is a round ovary. There is a rosella-like testis in the back of the uterus – a diagnostic sign of the Opisthochis felineus.
Transmission: ingestion of contaminated raw, frozen, dried, pickled, and salted fish, which contains metacercariae.
Invasive stage: metacercariae cysts in fish muscles.
Clinical disease: cholecystitis and cholelithiasis, hepatic colic, cirhosis. Clinical picture is very similar to Clonorhis infection. Infection can lay dormant for several years before presenting clinically.
Life-cycle: Final host – carnivorous mammals and humans. First intermediate host – the snail Bithynia leachi genus, second – fish. Life cycle of Opisthochis felineus is the same as of Clonorshis sinensis.
Diagnosis: immature eggs in feces, in fluid from biliary drainage, or duodenal aspirate. Eggs are 15-30 mcm in sizes, have oval form and yellow color. The outer membrane is thick, and there is a cover in the front of the egg. The internal structure of the egg is microgranular.
Prevention involves not eating undercooked or contaminated raw, frozen, dried, pickled, and salted fish; eradication of snail hosts when possible.
DICROCOELIUM LANCEATUM – causes Dicrocoeliasis.
Distribution: worldwide.
Localization: bile ducts, gallbladder and liver of herbivorous mammals (cattle, horses). Very rare in humans.
Morphology: the worms are 1 centimeter long with lanceolate form of the body;
the intestine (gut) has two nonbranched channels which are situated in the lateral sides of the body. Two round testis are situated in the front of the body – the diagnostic sign of the Dicrocoelium lanceatum.
Transmission: ingestion of plants with the ants, which contain metacercariae.
Invasive stage: metacercariae.
Clinical disease: is similar to fascioliasis.
Life-cycle: Final host – herbivorous mammals (cattle, horses). First intermediate host — the snail of Zebrina and Helicela genus, second intermediate host — ants Fornica genus.
Diagnosis: immature eggs in feces. An egg have oval form, smooth membrane, brown color, a cover is present in the front end.
Prophylactics: eradication of the snails, ants when possible; dehelmithization of cattle.
Clonorchis sinensis
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.
Clonorchis sinensis
The other two species are Opisthorchis felineus and Opisthorchis viverrini. 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 maot 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.
Definitive diagnosis is made by observing the characteristic ova in feces following concentration of feces or from duodenal aspirates when there is complete obstructive jaundice or from the Entero-Test.
Table summarising the less common flukes that are known to infect man
|
|
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 |
Metagonimus yokogawai
Classification. Helminths. Phylum Platyhelminthes. Trematodes.
Diseases. Metagonimiasis.
Geographic Distribution
Metagonimus yokogawai is found in China, Japan, south-eastern Asia, and the Balkan states. On a worldwide basis, these intestinal fluke typically have highly localized geographic distributions.
Location in Host. This intestinal fluke lives in the crypts and lumen of the small intestine.
Morphology. Adult Flukes
M. yokogawai are minute, pyriform-.shaped organisms, measuring 1.0-2.5 mm long and 0.3-0.7 mm wide. Characteristically they have a fleshy collar at the anterior end that is provided with spines and partially surrounds the oral sucker.
Eggs
Eggs are small, ovoid, operculate, and yellow-brown, measuring 20-30 μm by 15—17 μm. They contain a miracidium when discharged in feces. With most of the genera listed above, the sizes of their embryonated eggs overlap considerably, generally between 20-30 μm in length. M. yokogawai eggs resemble the eggs of Fasciola and Fasciolopsis in shape but are considerably smaller, measuring 80-115 μm by 58-70 μm. These eggs are thin-shelled, unembryonated when laid, and have an inconspicuous operculum. Frequently, they have a roughening or slight thickening of their shell at the abopercular end.
Life Cycles
Intestinal flukes use fresh-water snails and fish as first and second intermediate hosts, respectively. In fish, the metacercarial stages typically are encysted under the scales or in the skin, and humans become infected by eating raw or inadequately cooked fish. In some instances, marine bivalves such as clams and oysters serve as intermediate hosts. The prepatent period is usually short, from 1 to 3 weeks, and the normal life span is up to several months.
Diagnosis. Presence of characteristic eggs in feces.
Diagnostic Problems
Because the egg-laying capacity of M. yokagawai and other small intestinal flukes is limited, sedimentation concentration procedures may be needed to demonstrate eggs in light infections. Accurate species identification is often difficult because the eggs of most of these flukes are similar in size and morphology; without knowledge of the types of intestinal flukes occurring in the animals in any geographic area a specific identification is frequently impossible.
Eggs of many of the intestinal flukes may be confused with those of the liver flukes, Cionorchis sinensis and Opisthorchis species. Usually the eggs of the liver flukes are somewhat larger (27-35 μm by 12-19 μm), have a seated operculum, and a knob at the abopercular end.
Comments
The presence of this infection in humans, as well as other infections caused by related, small intestinal flukes, are generally a result of the lack of host specificity by parasites. In a particular geographic region where fish are eaten raw or inadequately cooked, birds, rodents, dogs, cats, and other mammals often serve as reservoirs for human infections. In addition to the trematodes described above, numerous other small flukes of animals in south-eastern Asia occasionally have been reported from humans.
Pathology caused by this small intestinal fluke is usually limited to mild inflammatory changes resulting from the attachment of the parasites to the mucosal epithelium. Mild, intermittent mucous diarrhea and colicky pain are often associated with these infections, but these symptoms are usually limited to a period of several months to 1 year, because of a short life span of the adult worms.
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.
Morphology
The adult worm is an ovoid, reddish brown fluke about 12 mm long.
Clinical Signs of Disease
As the parasites grow in the lung cyst, inflammatory reaction and fever occurs. The cyst ruptures and cough develops resulting in the increase of sputum. The sputum is frequently blood tinged and may contaiumerous 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.
The Schistosomes
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 the environment, 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. Improved water supplies promote spread of disease, forming potentially new habits for snails.
The disease caused is called schistosomiasis or Bilharzia and is the most important of helminthic 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.
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 pass in feces (S. mansoni and S. japonicum), or into the lumen of the bladder, and are then excreted in the urine (S. haematobium). Those eggs that reach fresh water hatch, releasing a miracidium, which 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 move to smaller venules closer to the lumen of the intestine or bladder to lay their 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, Malaysia, 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. 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 flow.
The ova of S. mansoni are 114-175mm long and 45-68mm 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 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.
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 Signs of Disease
The clinical sigs of disease are 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 for 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 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, 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 feces. When eggs cannot be found in feces rectal biopsy can be indicated.
Schistosoma mansoni eggs
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
Schistosoma japonicum is found in China, Japan, the Philippines and Indonesia. It causes disease of the bowel with the eggs being passed out in feces.
It differs form S. mansoni and S. haematobium that is called zoonosis, in which a large number of mammals serve as reservoir hosts, cats, dogs and cattle play 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 4 weeks and eggs may be seen in the feces as quickly as 5 weeks after.
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 feces.
Morphology
The adult worms are longer and narrower than the S. mansoni worms. The ova are about 55 – 85mm and 40 – 60mm, oval with a minute lateral spine or knob.
Clinical Signs of Disease
The main lesions appear due to the presence of 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 pseudotubercules.
Due to the number of eggs released by the females the infection is more severe than one with S. mansoni. This is also happens due to the better adaptation of the parasite 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 feces. When eggs cannot be found in feces rectal biopsy can be indicated.
Schistosoma japonicum egg
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 summarised in the table.
Table describing other less common intestinal Schistosome species that are known to cause disease in man
|
|
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 |
Schistosoma haematobium
Schistosoma haematobium differs from the other two species previously mentioned and 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.
Schistosoma haematobium egg
Clinical Signs of Disease
The clinical signs of disease are 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 for36 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 2 pm, presumably as a result of changes in the host’s metabolic and physical activities.
Prevention: involves proper disposal of human waste and eradication of the snail host when possible. Swimming in endemic areas should be avoided.
Tapeworms (Cestoda)
Tapeworms (Cestoda) consist of a rounded head, called a scolex, neck and long strobila or chain of proglottids (multiple segments) of varying stages of maturity.
The scolex has specialized means of attaching to the intestinal wall, namely suckers, hooks, or sucking grooves.
The worm grows by adding new proglottids from its germinal center next to the scolex. The oldest proglottids at the distal end are gravid and produce many eggs, which are excreted in the feces and transmitted to various intermediate hosts. Humans usually acquire the infection when undercooked flesh containing the larvae is ingested. In certain instances, eg, cysticercosis and hydatid disease, the eggs are ingested and the resulting larvae cause the disease. All cestodes have stage of larva and stage of oncosphere in the life cycle.
Adult Parasites of class Cestoda are hermaphroditic and live in the intestinal lumen of vertebrate hosts. Those that can infect man include Diphyllobothrium latum, Taenia saginata, Taenia solium, Hymenolepis nana.
Larval stages of Echinococcus granulosus and Taenia solium (hydatid, cysticercus) may be found in various organs and tissues of man and other intermediate hosts.
The cestodes (or tapeworms) form a group of worms, exhibiting two unmistakable morphological features; they all possess flat, ribbon like bodies and lack an alimentary canal.
Adult tapeworms usually inhabit the alimentary canal of their hosts (though they occasionally are found in the bile or pancreatic ducts) and attach themselves to the mucosa by means of a scolex. Despite the lack of a digestive system they do absorb food from the hosts intestine; thereby providing the tapeworms a habitat that is associated with high nutritional levels, feeding the tapeworms high growth rate.
Larvae on the other hand show a wide range of habitat preferences, being found in almost any organ of both vertebrate and invertebrate hosts. Though most larval species show a preference for a particular site.
This lack of an alimentary canal markedly separates tapeworms from nematodes and trematodes. The outer tegument of the body must serve not only as a protective coating but also as a metabolically active layer through which nutritive material can be absorbed, along with secretions and waste material to be transported out of the body.
The body consists of a chain of segments or proglottids, which can be immature, mature or gravid; the latter of which contain a fully developed uterus packed with eggs. Therefore, each tapeworm is made up of a ‘string of individuals’ having a complete set of reproductive organs in progressive degrees of sexual maturity and budding off from a body attached to the host tissue by a head or scolex.
Except for Hymenolepis nana, which can develop directly in the same host, the lifecycle of tapeworms involves both an intermediate and definitive host.
Taenia species
Taenia species are the most common cestode parasites of humans. More than 60 million people are infected with T. saginata (“beef” tapeworm) world wide and about 4 million are infected with T. solium (“pork” tapeworm).
T. saginata has a comsmopolitan distribution, but is more common in developing countries where hygiene is poor and the inhabitants have a tendency of eating raw or insufficiently cooked meat. T saginata is the most common adult tapeworm found in man. T solium is virtually extinct in Europe and the USA. \
The adults of both species live in the small intestine of man, the definitive host The gravid segments are very active and escape through the anus, releasing large numbers of eggs in the perianal region or on the ground where they can survive for long periods. When ingested by pigs or catle, the eggs hatch, each releasing an oncosphere, which migrates through the intestinal wall and blood vessels to reach striated muscle within which it encysts, forming cysticerci.
When inadequately cooked meat containing the cysts is eaten by man, the oncospheres excyst, settle in the small intestine and develop there into adult cestodes over the next 3 months or so. The segments of T. solium are somewhat less active than those of the beef tapeworm but its eggs, if released in the upper intestine, can invade the host (auto-infection), setting up the potentially dangerous larval infection known as cysticercosis in muscle of any other site.
Both humans and cattle or pigs are necessary to the complete life cycle of Taenia species. (In Europe and the USA cattle are the normal intermediate hosts, but in the tropics several other ruminants, e.g. goat, sheep llama and giraffe, may serve as the intermediate hosts.) Eggs ingested by the intermediate hosts usually contain oncospheres. The oncospheres then hatch out in the duodenum, pass into the intestine where they penetrate the intestinal wall and are then carried by the circulation to be deposited in tissues (usually muscle). There they develop into cysticerci larva, which are white and ovoid, measuring approximately 8 x 5mm.
Humans become infected by ingesting inadequately, cooked beef or pork with cysticerci, containing an invaginated protoscolex.
The protoscolexes evaginate and pass into the small intestine where they attach themselves to the mucosa and develop into adult worms.
Eggs and proglottids are passed out in the faeces, and are then eaten by the intermediate host, thus, perpetuating the life cycle.
Larval Cestodes, which Infect Man
Infections in man with Echinococcus granulosus, Echinococcus multilocularis and Multiceps multiceps are caused by an accidental ingestion of eggs, which are excreted by the definitive animal host. The disease that developes due to the invasion of these parasites is caused by the larval stages or hydatid cyst, and is known as hydatid disease or hydatidosis.
Each cestode possesses an elongated tape-like body, which lacks an alimentary canal. The adult tapeworms are strings of individuals having a complete set of reproductive organs (proglottids) in progressive degrees of sexual maturity and budding off from a body attached to the host tissue by a head or scolex.
The larval stage, show a wide variation being found in almost any organ of both vertebrate and invertebrate hosts.
Echinococcus granulosus
Echinococcosis or Hydatid disease in man is caused by the larval stage of the dog tapeworm, Echinococcus granulosus. Hydatid disease is most extensively found in East Africa, North Africa, South Africa, the Middle East and parts of South America and Australia. The intermediate hosts are cattle, sheep, pigs, goats or camels and the definitive host for this disease is the dog or other canids.
Life cycle of the cestode
Larval infection in man causes hydatid disease.
Adult worms are only seen in the definitive hosts, dogs, they cannot develop in man. Man is an accidental intermediate host of hydatid disease. When the ova are ingested by a suitable intermediate host, they hatch in the duodenum and the oncosphere migrates to the blood stream where it is carried to the liver, lungs and other organs of the body. Here it develops into a hydatid cyst, which consists of an outer thick laminated cyst wall, and an inner, thiucleated germinal layer. From the inner layer brood capsules are produced which contain protoscoleces. The brood capsules detach from the germinal layer, releasing free protoscoleces. Hydatid sand is the name given to the fluid in the cysts, which consists of protoscoleces, tissue debris, and sometimes free hooklets. Here, the life cycle stops in humans, but is continued when a hydatid cyst containing protoscoleces egg in sheep liver, is ingested by a suitable canine host where the protoscoleces develop into adult worms.
Morphology
The adult worm measures approximately 3 – 8.5 mm long. The scolex has 4 suckers and a rostellum with hooks, the latter becoming tightly inserted into the crypts of Lieberkühn. The mature strobila has only 3 – 4 proglottids, one is immature, one is mature and the final one is gravid; when gravid the eggs are expelled in the faeces.
Due to the close similarity of the eggs to other Taenia species found in dogs they were until recently thought to be morphologically indistinguishable.
The larvae in man develop into a unilocular cyst which gives rise to unilocular hydatid disease.
This is characterised as having only one bladder or many completely isolated bladders, each enclosed in its own well-developed envelope. The latter consists of several layers, the most prominent being the laminated layer. Within this again is the germinal membrane from which the brood capsules arise inside and develop thousands of larvae or protoscoleces, the whole being suspended in a hydatid fluid.
Clinical Signs of Disease
Hydatid disease in humans is potentially dangerous depending on the location of the cyst. During first period of disease is asymptomatic, but liver cysts may cause hepatic dysfunction. Some cysts may remain undetected for many years until they become large enough to affect other organs. Symptoms are then of a space occupying lesion. Lung cysts are usually asymptomatic until there is a cough, shortness of breath or chest pain. Hepatic cysts result in pressure on the major bile ducts or blood vessels. Expanding hydatid cysts cause necrosis of the surrounding tissue.
Slow leakage of the hydatid fluid results in eosinophilia and rupture of an abdominal hydatid cyst results in severe allergic symptoms.
Symptoms may not manifest themselves for 5 – 20 years after the infection.
Cysts in the lungs can erode into a bronchus, causing bloody sputum; end cerebral cysts can cause headache and focal neurologic sings. If the cysts rupture spontaneously or during trauma or surgical removal, life-threatening anaphylaxis can occur (the cyst fluid contains parasite antigens, which can sensitize the host).
Laboratory Diagnosis
1. Imaging and serodiagnosis are the mainstay of diagnosis. Serological tests include Enzyme linked immunosorbent assay (ELISA), an indirect haemagglutination test a complement fixation test and a Western Blot system.
2. Microscopic examination of the cyst fluid to look for the characteristic protoscoleces, which can be either invaginated or evaginated. The cyst fluid will also reveal free hooklets and tissue debris. 1% eosin may be added to the fluid to determine the viability of the protoscoleces. Viable protoscoleces exclude eosin whereas nonviable protoscoleces take up the eosin.
3. Histological examination of the cyst wall after surgical removal.
Western Blots
One serological test, which is proved to be of value to diagnosing Hydatid disease, is the Western Blot. The test presents a definitive means for detection of human antibodies to the cestode E. granulosus.
Diagnosis can be made using the Western Blot assay for the detection of IgG antibodies in serum reactive with E. granulosus antigens present on a membrane. Field studies support a sensitivity of 80% and specificity of 100% in patients with hepatic cysts.
This assay is known as the Qualicode Hydatid Disease Kit, the principle behind the test is that it is a qualitative membrane-based immunoassay manufactured from E. granulosus proteins. The E. granulosus proteins are fractionated according to molecular weight by electrophoresis on a ployacrylamide slab gel (PAGE) in the presence of sodium dodecyl sulfate (SDS). The separated E. granulosus proteins are then transferred via electrophoretic blotting from the gel into strips for testing of individual samples.
During the procedure, the strips containing the E. granulosus proteins are incubated with serum specimens and washed to remove unbound antibodies.
Visualisation of human immunoglobulins specifically bound to E. granulosus proteins is performed by sequential reaction with goat anti-human immunoglobulin-alkaline phosphatase conjugate and BCIP/NBT substrate. Bands corresponding to the positions of the resoled E. granulosus proteins will be visualized on the strip, indicating the presence in the serum sample of IgG antibodies directed against
E. granulosus antigens. Band positions are compared to those on a reference strip developed using Hydatid disease positive control.
Prevention
1. Safe disposal of dog feces.
2. Education to prevent feeding uncooked offal to dogs.
Echinococcus multilocularis
The larvae of Echinococcus multilocularis is a particularly dangerous species causing multilocular (alveolar) hydatid disease in man and animals and is common in the highlands of Europe i.e. Switzerland and Germany, in Canada, Alaska and Northern Russia. The most common definitive hosts are foxes and wolves in addition to domestic cats and dogs when they have access to infected rodents.
Life cycle
Foxes are the primary definitive hosts, although, under domestic circumstances dogs can act as the definitive host. Rodents are the intermediate hosts. Man is an accidental host by the ingestion of eggs where multilocular cysts are formed. In these cysts, the limiting membrane is thin, and the germinal epithelium may bud off externally resulting in proliferation in any direction.
Metastases may occur. Unlike E. granulosus, there is little fluid in the cysts of E. multilocularis.
Morphology
The morphology is in general very similar to that of E. granulosus, but the adults are much smaller.
Unlike E. granulosus, cysts of E. multilocularis in man do not contain daughter cysts with scolices. Instead, the larval cyst, or as it is referred to as an alveolar or multilocular hydatid cyst, forms a multicystic structure made up of proliferating vesicles embedded in a dense fibrous stroma, which is often mistaken for a hepatic sarcoma. In older cysts the hydatid fluid is replaced by a jelly-like mass.
Clinical Signs of Disease
Cysts are formed primarily in the liver and their growth in the vena cava or portal vein results in metastases in the lung or brain. Clinical signs of disease are similar to that of E. granulosus.
Diagnosis
1. Laboratory diagnosis can be made by ELISA.
2. Clinical diagnosis is made by ultrasound.
Differences between the hydatid cysts of E. granulosus and E. multilocularis
|
Echinococcus granulosus |
Echinococcus multilocularis |
|
Slow development of cyst |
Rapid development of cyst |
|
Cysts have thick-walled chambers |
Cyst has thin-walled chambers |
|
Separated by connective tissue |
Not separated by connective tissue |
|
Cyst is fluid filled |
Cyst is gelatinous filled |
|
Cyst is free of host material |
Cyst is contaminated by host material |
The Cestodes
The cestodes (or tapeworms) form a group of worms, exhibiting two unmistakable morphological features; they all possess flat, ribbon-like bodies and lack an alimentary canal.
Adult tapeworms usually inhabit the alimentary canal of their hosts (though they occasionally are found in the bile or pancreatic ducts) and attach themselves to the mucosa by means of a scolex. Despite the lack of the digestive system they do absorb food from the hosts intestine; thereby providing the tapeworms a habitat that is associated with high nutritional levels causing the tapeworms high growth rate.
Larvae on the other hand show a wide range of habitat preferences, being found in almost any organ of both vertebrate and invertebrate hosts. Though, most larval species show a preference for a particular site.
This lack of the alimentary canal markedly separates tapeworms from nematodes and trematodes. The outer tegument of the body must serve not only as a protective coating but also as a metabolically active layer through which nutritive material can be absorbed, along with secretions and waste material to be transported out of the body.
The body consists of a chain of segments or proglottids, which can be immature, mature or gravid; the latter contains a fully developed uterus packed with eggs. Therefore, each tapeworm is made up of a ‘string of individuals’ having a complete set of reproductive organs in progressive degrees of sexual maturity and budding off from a body attached to the host tissue by a head or scolex.
Except for Hymenolepis nana, which can develop directly in the same host, the lifecycle of tapeworms involves both an intermediate and definitive host.
Taenia species
Taenia species are the most common cestode parasites of humans. More than 60 million people are infected with T. saginata (“beef” tapeworm) world-wide and about 4 million are infected with T. solium (“pork” tapeworm). T. saginata has a comsmopolitan distribution, but is more common in developing countries where hygiene is poor and the inhabitants have a tendency of eating raw or insufficiently cooked meat. T saginata is the most common adult tapeworm found in man. T solium is virtually extinct in Europe and the USA.
The adults of both species live in the small intestine of man, the definitive host. The gravid segments are very active and escape through the anus, releasing large numbers of eggs in the perianal region or on the ground where they can survive for long periods. When ingested by pigs or cattle, the eggs hatch, each releasing an oncosphere, which migrates through the intestinal wall and blood vessels to reach striated muscle within which it encysts, forming cysticerci. When inadequately cooked meat containing the cysts is eaten by man, the oncospheres excyst, settle in the small intestine and develop there into adult cestodes over the next 3 months or so. The segments of T. solium are somewhat less active than those of the beef tapeworm but its eggs, if released in the upper intestine, can invade the host (auto-infection), setting up the potentially dangerous larval infection known as cysticercosis in muscle of any other site. (Peters & Gilles, 1995)
Both humans and cattle or pigs are necessary to the complete life cycle of Taenia species. (In Europe and the USA cattle are the normal intermediate hosts, but in the tropics several other ruminants, e.g. goat, sheep, llama and giraffe, may serve as the intermediate hosts.) Eggs ingested by the intermediate hosts usually contain oncospheres. The oncospheres then hatch out in the duodenum, pass into the intestine where they penetrate the intestinal wall and are then carried by the circulation to be deposited in tissues (usually muscle). There they develop into cysticerci larva, which are white and ovoid, measuring approximately 8 x 5mm.
Humans become infected by ingesting inadequately cooked beef or pork with cysticerci, containing an invaginated protoscolex. The protoscolexes evaginate and pass into the small intestine where they attach themselves to the mucosa and develop into adult worms.
Eggs and proglottids are passed out in feces, and are then eaten by the intermediate host, thus, perpetuating the life cycle.
Morphology
Ova of Taenia species are spherical, yellowish brown and measure 31 – 34mm in diameter. The shell is thick and radially striated. Within the shell, the onchosphere has 3 pairs of hooklets. However, the microscopical appearance of the ova of T. saginata and T. solium are identical.
The length of the adult T. saginata is 4 – 8 meters long and that of T. solium is 3 – 5metres long. The proglottids of Taenia species can be identified by the number of uterine branches; 7 – 13 for T. solium and 15 – 20 for T. saginata. If the scolex is recovered, the 4 suckers and rostellum of hooklets of T. solium will distinguish it from T. saginata, which has 4 suckers but no hooklets.
Clinical Signs of Disease
The presence of the adult worm rarely causes symptoms apart from slight abdominal irritation with diarrhoea, constipation or indigestion. The accidental ingestion of the embryonated ova of T. solium may result in cysticercosis in man. An infection due to an adult Taenia, in man or animals, is referred to as taeniasis.
T. saginata (the “beef” tapeworm) does not cause human cysticercosis.
When the embryonated eggs are ingested, the embryos hatch out, migrate through the intestinal wall and are carried around the body in the circulation and deposited in various tissues. Muscle and subcutaneous tissues are usually infected, but cysticerci can infect most organs and tissues. Human cysticercosis is usually asymptomatic unless the infection is particularly heavy or cysticerci are formed in some vital area e.g. the brain, resulting in neurological sequelae.
Comparison of T.saginata and T.solium
|
Characteristic |
Taenia saginata |
Taenia solium |
Intermediate host |
Cattle, reindeer |
Pig, wild boar |
|
Site of development |
Muscle, viscera |
Brain, skin, muscle |
|
Scolex: adult worm |
No hooks |
Hooks |
|
Scolex: cysticercus |
No rostellum |
Rostellum & hooks |
|
Proglottis: uterine branches |
23 (14 – 32) * |
8 (7 –11) * |
|
Passing of proglottids |
Single, spontaneous |
In groups, passively |
|
Ovary |
2 lobes |
3 lobes |
|
Vagina: sphincter muscle |
Present |
Absent |
* No universal agreement to the number of uterine branches in these 2 species. As a rough guide, specimens with more than 16 branches are likely to be those of T. saginata and those with less than 10 branches are ikely to be of T. solium.
Laboratory diagnosis
Diagnosis of intestinal taeniasis can be made by recovery of the characteristic ova in stool. However, the ova of T. solium and T. saginata are identical and diagnosis is made by the recovery of the segments or scolex.
The diagnosis of cysticercosis depends upon serology. MRI scans may reveal the presence of lesions in the brain. Calcified cysticerci are less often seen in the brain: in about one-third of cases, 10 years or more after infection. Occasionally, the diagnosis is made histologically on surgical specimens. Calcification in muscles usually appears 3 – 5 years after initial infection, and are most typically seen as spindle-shaped calcifications, most numerous in the thighs.
Western Blots
Various Immunodiagnostic tests appear to give good results on serum or CSF.
Diagnosis using an immunodiagnostic test can be made using in vitro qualitative assay for the detection of IgG antibodies in serum reactive with T. solium antigens present on the membrane.
Infected individuals develop a predominately IgG response to the parasite. ELISA has been used as a screening test, but low sensitivity and frequent artifactual crossreactions, or crossreactions with antibodies from other parasitic infections, limit its usefulness as a confirmatory diagnostic test. The Western Blot assay (U.S Patent No. 5,354,660) developed by Tsang et al, at the U.S. Centers for Disease Control has been shown to provide a reliable method for evaluation of sera from patients with clinically diagnosed active cysticercosis. Field studies support a sensitivity of 98% and specificity of 100% for this assay.
This assay is known as the QualiCode Cysticercosis Kit, the principle behind the test is that it is a qualitative membrane-based immunoassay manufactured from T. solium proteins. The T. solium proteins are fractionated according to molecular weight by electrophoresis on a polyacrylamide slab gel (PAGE) in the presence of sodium dodecyl sulfate (SDS). The separated T. solium proteins are then transferred via electrophoretic blotting from the gel to a nitrocellulose membrane. This antigen-bearing membrane has been cut into strips for testing of individual samples. Sera are tested at 100X dilution.
Intersep is now the leading suppliers of Qualicode Western Blot Kits.
Intersep now supply the kits for cysticercosis, hydatid disease, babesiosis, human granulocytic ehrlichiosis, canine and human lymes disease.
The Qualicode line of immunoassay kits is used to detect the presence of antibody (either IgG or IgM) to a specific infectious disease agent. These qualitative assays have the sensitivity and specificity of confirmatory tests. The kits are designed for batch testing any number of samples from 1 – 24. Interpretation is simplified by including Reference Strips, Positive and Negative Controls and a Record sheet with every kit.
All reagents to perform the assay are provided along with three 8-channel incubation trays.
During the procedure, the strips containing the T. solium proteins are incubated with serum specimens and washed to remove unbound antibodies. Visualisation of human immunoglobulins specifically bound to T. solium proteins is performed by sequential reaction with goat anti-human immunoglobulin-alkaline phosphatase conjugate and BCIP/NBT substrate. Bands corresponding to the positions of the resoled T. solium proteins will be visualised on the strip, indicating the presence in the serum sample of IgG antibodies direct against Taenia antigens. Band positions are compared to those on a reference strip developed using the cysticersosis positive control.
Hymenolepis nana
Hymenolepis nana, the dwarf tapeworm, is the smallest tapeworm to infect humans. This cestode belongs to a large family known as Hymenolepididae.
The diagnostic features of this family are: scolex armed with one circlet of five hooks; 1 – 3 large testes and sacciform uterus. In addition to the H.nana, three other species, H. diminuta, H. microstoma and H. citelli have been used extensively for studies on cestodes.
Hymenolepis nana has a cosmopolitan distribution and is thought to be the most common tapeworm throughout the world. The infection is more frequently seen in children although adults are also infected, causing hymenolepiasis.
Life cycle
The life cycle of H. nana does not require an intermediate host; complete development occurs within the villi of a single host, resulting in a ‘direct’ life cycle. Though it can also utilise an insect as an intermediate host.
The eggs that are released from mature proglottids in the upper ileum are usually passed out in feces. If swallowed by another human they develop into hexacanth oncospheres and burrow into the villi of the small intestine.
This is where they develop into tailless cysticercoids and then migrate towards the ileum and attach thear for proglottids formation. The eggs, which are ingested by insects, such as fleas, beetles or cockroaches hatch to form tailed cysticercoids, which remain unmodified as long as they are inside the insect. If they are accidentally swallowed by a human they pass down to the ileum and establish themselves. (Peters & Gilles, 1995)
Morphology
The egg containing the oncosphere bears three pairs of hooklets and is surrounded by a membrane. This membrane has 2 polar thickenings from which arise threadlike filaments extending into the space between the membrane and the colourless hyaline shell, unlike those of H. diminuta, which do not possess any filaments.
The adult tapeworm is normally 2.5 – 4cm long. The scolex is knob like in shape, has a rostellum with hooklets and 4 suckers. The segments are wider than they are long. Ova are spherical or ovoid measuring 30 – 47mm in diameter. This is what distinguishes it morphologically from H. diminuta.
Clinical Signs of Disease
Infections due to H. nana may cause no symptoms even with heavy worm burdens. However, symptoms of restlessness, irritability, anorexia, abdominal pain and diarrhoea have been reported. Heavy worm burdens may be caused by autoinfection, which can be a problem in the immunocompromised.
Laboratory Diagnosis
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Diagnosis is based on recovery and identification of the characteristic ova in a formol-ether concentrate of feces. Adult worms and proglottids are rarely seen in stool samples.
Diphyllobothrium latum
Members of this order, commonly known as pseudophyllids, are chiefly parasites of fish-eating mammals, birds and fish. They typically are found with a scolex which is characterised by two shallow elongated bothria situated with one dorsally and one ventrally. The proglottids are flattened dorsoventrally.
Diphyllobothrium latum is an intestinal tapeworm, known as the human ‘broad’ tapeworm. It is the largest tapeworm found in man. The term ‘broad’ relates to the fact that the proglottids are generally wider than longer. It is an important human parasite. The adult worms of two other species of the genus, D. dendriticum and D. ditremum are chiefly parasite of fish-eating birds and mammals.
The tapeworm, D. latum has a wide distribution, occurring especially in countries bordering on the Baltic Sea (Finland, Sweden etc.): and also in Russia, Switzerland and North America. It is in these countries where the populations are known to eat uncooked or partly cooked (i.e. smoked) fish.
Apart from man they are found in many other hosts, especially the dog, cat and pig. This is due to the host countries allowing the domestic animals access to the offal from the infected fish.
The life cycle of this tapeworm requires two intermediate hosts.
The eggs are passed out in human faeces, once in water they hatch out into small ciliates coracidium larvae, which swim until ingested by Copepods. It is in these intermediate hosts that growth and development of the 1st larval stage are completed (they are now known as procercoids). When these crustaceans (fresh water) are eaten by fish, the procercoid larvae continue to develop in the flesh of fish and become known as plerocercoid larvae. It is this stage of the larvae, which develops in man when they eat undercooked fish and they grow into adult worms in the small intestine.
Morphology
The egg is usually ovoid and has a small knob at the opercular end and is yellowish-brown in colour with a smooth shell, of moderate thickness. They measure 58 – 75mm by 40 – 50mm in size.
Adult worms can reach up to a length of 10 metres or more and may contain up to 3,000 proglottids. The scolex is spatulate with no rostellum or hooklets. It has 2 shallow grooves or bothria, which are unlike the typical 4 suckers seen on the Taenia species. The proglottids measure 3mm long and 11mm wide and have a rosette shaped central uterus.
Clinical Signs of Disease
The infection caused by D. latum is due to the ingestion of raw, poorly cooked or pickled fresh water fish. The symptoms associated with D. latum infection may be absent or minimal with eosinophilia. There may be occasional intestinal obstruction, diarrhoea, and abdominal pain. The most serious symptom is the onset of pernicious anaemia. This is due to vitamin B12 deficiency, caused by excessive absorption of the vitamin by the adult worm and the absorption of cobalamins from the host intestine (occurring only in a small percentage of people).
Laboratory diagnosis
Laboratory diagnosis depends on the recovery of characteristic eggs from a formol ether concentrate of feces. Proglottids may also be seen in fecal samples usually in a chain of segments from a few centimeters to about 0.5 meters in length.
Taenia solium.
The adult form of T. solium causes taeniasis solium. T. solium larvae cause cysticercosis. Teniasis and cysticercosis occur worldwide but is endemic in areas of Asia, South America, and Eastern Europe.
Morphology. T. solium can be identified by its scolex with 4 suckers and circle of hooks and by its gravid proglottids, which have 7-12 primary uterine branches. Larva of T.solium called cysticercus. A cysticercus consists of a pea-sized fluid-filled bladder with an invaginated scolex.
T. solium cysticercus.
T. solium scolex
T. solium scolex
Life cycle. Humans are infected by eating raw or undercooked pork containing the larvae (fecal-oral way of transmittion).
In the small intestine, the larvae attach to the gut wall and take about 3 months to grow into adult worms measuring up to 5 m. The gravid terminal proglottids detach daily, are passed in the feces, and are accidentally eaten by pigs. A 6-hooked embryo (oncosphere) emerges from each egg in the pig’s intestine. The embryos burrow into a blood vessel and are carried to skeletal muscle. They develop into cysticerci in the muscle, where they remain until eaten by a human. Humans are the definitive hosts, and pigs are the intermediate hosts.
A different and far more dangerous sequence occurs when a person ingests the eggs in food or water that has been fecally contaminated or ingestion of T. solium eggs after vomiting (in patient with taeniasis). The cysticerci can become large in eye, subcutaneous tissue, brain, lung, heart, and muscle. In the brain, they manifest as a space-occupying lesion. Living cysticerci do not cause inflammation, but when they die they can release substances that provoke an inflammatory response.
Clinical manifestation of teaniasis solium: abdominal pain, nausea, diarrhea, weight loss, infection may by asymptomatic.
Clinical manifestation of cysticercosis in the brain: headache, meningoencephalitis, vomiting, and seizures; in the eyes: uveitis, retinitis.
Diagnosis of teaniasis solium: gravid proglottids (with 7 – 12 uterine branches) may be found in the stools.
Diagnosis of cysticercosis depends on demonstrating the presence of the larvae of T.solium in tissue by x-ray, or computed tomography scan.
Prevention of taeniasis involves cooking pork adequately and preventing pigs from ingesting human feces by disposing of waste properly.
Prevention of cysticercosis consists of treatment of patients to prevent autoinfection plus observation of proper hygiene, including hand washing, to prevent contamination of food with the eggs.
Taenia saginata causes taeniasis saginata.
Taeniasis saginata occur worldwide but is endemic in areas of Asia, South America, and Eastern Europe.
Morphology. T. saginata can be indentified by its scolex with 4 suckers but in contrast to T.solium, no hooklets.
Its gravid proglottids have 17-35 primary uterine branches. Larva of T.saginata called cysticercus.
Life cycle. Humans are infected by eating raw or undercooked beef containing larvae (fecal-oral way of transmission). In the small intestine, the larvae attach to the gut wall and take about 3 months to grow into adult worms measuring up to 10 m. The gravid terminal proglottids detach, are passed in the feces, and are eaten by cattle.
Embryos (oncospheres) emerge from the eggs in the cow’s intestine and burrow into a blood vessel, where they are carried to skeletal muscle. They develop into cysticerci in the muscle. The cycle is completed when the cysticerci are ingested. Humans are the definitive hosts, and cattle the intermediate hosts.
Clinical manifestation of teniasis saginata: abdominal pain, nausea, diarrhea, weight loss, infection may by asymptomatic. In some, proglottids appear in the stools and may even protrude from the anus.
Laboratory diagnosis: gravid proglottids (with 17-35 uterine branches) may be found in the stools.
Prevention. Prevention of taeniasis saginata involves cooking beef adequately and preventing cattle from ingesting human feces by disposing of waste properly.
Diphyllobothrium latum, the fish tapeworm, causes diphyllobothriasis.
The disease is found worldwide but is endemic in areas where eating raw fish is the custon, such as Scandinavia, northern Russia, Japan, Canada, USA (northern Michigan, Minnesota).
Morphology. Diphyllobothrium latum can be indentified by its scolex with 2 elongated sucking grooves by which the worm attaches to the intestinal wall.
The proglottids are wider than they are long, and the gravid uterus is in the form of a rosette.
Scolex of D. latum
Adult D.latum is the longest of the tapeworms, measuring up to 13 m. Larva of D.latum called plerocercoid.
Life cycle.
Humans are infected by eating raw or undercooked fish containing larvae (fecal-oral way of transmittion). In the small intestine, the larvae attach to the gut wall and develop into adult worms. Gravid proglottids release fertilized eggs, and the eggs are then passed in the stools. The immature eggs must be deposited in fresh water for the life cycle to continue. The embryos emerge from the eggs and are eaten by tiny copepod crustacea (first intermediate hosts). There, the embryos differentiate and form procercoid larvae in the body cavity. When the copepod is eaten by freshwater fish, eg, pike, trout, and perch, the larvae differentiate into plerocercoids in the muscle of the fish (second intermediate host). The cycle is compelled when raw or undercooked fish is eaten by humans (definitive hosts).
Clinical disease: infection by D.latum causes little damage in the small intestine. In some individuals, megaloblastic anemia occurs as a result of vitamin B12 deficiency caused by preferential uptake of the vitamin by the worm. Most patients are asymptomatic, but abdominal discomfort and diarrhea can occur.
Diagnosis depends on finding the typical eggs, oval, yellow-brown eggs with an operculum (lidlike opening) at one end, in the stools.
Prevention involves adequate cooking of fish and proper disposal of human.
