Volume 8.  Larval Cestodes and Nematodes which Infect Man


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


1. Intersep Ltd    2. University of Southampton


More information can be obtained on www.intersep.com and www.soton.ac.uk/~ceb/, Ectoparasites and Endoparasites.







8.       Larval Cestodes which Infect Man

                    Echinococcus granulosus

                    Echinococcus multilocularis

                    Multiceps multiceps

                    Capillaria philippensis






Larval Cestodes which Infect Man


Infections in man with Echinococcus granulosus, Echinococcus multilocularis and Multiceps multiceps are caused by the accidental ingestion of eggs which are excreted by the definitive animal host.  The disease that is produced due to the invasion of these parasites is caused by the larval stages or hydatid cyst, 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.


Liife cycle of the cestode, Echinococcus granulosus. 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, thin nucleated 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 eg. in sheep liver, is ingested by a suitable canine host where the protoscoleces develop into adult worms. (Fig. 1)



The adult worm measures approximately 3 – 8.5mm 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. (Fig. 2 & 3)








Figure 2. Diagrammatic representation of the mature proglottid of Echinococcus granulosus





Figure 3. Adult female worm of Echinococcus granulosus. The mature strobila has only 3 – 4 proglottids; one is immature, one is mature and the final one is gravid. The eggs are released from the gravid proglottid 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 which develop thousands of larvae or protoscoleces, the whole being suspended in a hydatid fluid. (Figure 4, 5 & Table 1)




Figure 4. A diagrammatic representation of the tranverse section of a hydatid cyst of Echinococcus granulosus.


Figure 5. Unilocular cyst of Echinococcus granulosus. This is characterised as having only one bladder or many completely isolated bladders, each enclosed in its own well-developed envelope. Inside which develop thousands of larvae or protoscoleces, the whole being suspended in a hydatid fluid.  These cysts in man give rise to unilocular hydatid disease.




Clinical disease

Hydatid disease in humans is potentially dangerous depending on the location of the cyst.  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.


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 has 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 achieved 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 QualicodeŌ 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 visualised on the strip, indications the presence in the serum sample of IgG antibodies direct against E. granulosus antigens. Band positions are compared to those on a reference strip developed using the Hydatid disease positive control.



1.   Safe disposal of dog faeces.

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 in 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.



The morphology is in general very similar to that of E. granulosus, but the adults are much smaller. (Fig. 6 & Table 1)


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.



Figure 6. Diagrammatic representation of the adult worm if Echinococcus multilocularis.




Clinical Disease

Cysts form primarily in the liver and growth in the vena cava or portal vein results in metastases in the lung or brain.  Clinical disease is similar to that of E. granulosus. 



1.     Laboratory diagnosis is can be made by ELISA.

2.     Clinical diagnosis is made by ultrasound.




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


Table 1. Differences between the hydatid cysts of E. granulosus and E. multilocularis.


Multiceps multiceps



Multiceps multiceps, is a cestode of cosmopolitan distribution and causes coenuriasis in man. The dog is the common definitive host in the USA and UK. With the intermediate stages developing in many ungulates, especially sheep.


Life cycle

The adult worm is found in dogs and other canidae. The intermediate hosts comprise of a number of herbivorous animals, where the cysts develop in the brain and spinal cord causing a disease called ‘staggers’, which affects the balancing powers of the animals.  Man becomes infected by the accidental ingestion of eggs.  The oncosphere hatches and penetrates the intestinal wall and the embryo is carried by the blood stream to various parts of the body including the central nervous system where it lodges and the cyst or coenurus develops. (Fig. 7) Multiple scolices burst from the inner surface of the cyst wall.  The cyst resembles that of a cysticercus (Cysticercus cerebralis).  It is filled with fliud, semi-transparent and glistening white. The cysticercus possesses unusual asexual multiplication, forming a bladder (or coenurus) which gives rise to hundreds of daughter protoscoleces directly from its inner wall. It therefore differs from a hydatid cyst.



Figure 7. Diagrammatic representation of a Multiceps multiceps coenurus cyst. Hundred of daughter protoscoleces are released from the cyst, therefore differing from a hydtatid cyst.



Clinical Disease

In humans, coenuri are most frequently found in the brain and spinal cord but also in the subcutaneous tissue.  Symptoms include headache, vomiting, paraplegia seizures and eye problems. The coenurus may cause serious damage or even death, but only a few have ever been reported.



There are no serological tests available.




Capillaria philippensis



Intestinal capillariasis was first observed in the Philippines in 1962 and since then it has been noted, although less frequently in Thailand, with scattered reports from Taiwan, Japan, Egypt, and Iran. Capillaria philippensis is a small nematode which when in its human host burrows into the intestinal mucosa.


Man and fish eating birds become infected when eaten uncooked or poorly cooked fish. Therefore, infections are seen in endemic proportions where uncooked fish is seen as a delicacy.


Life cycle

The complete life cycle is not known however human infection is initiated by the consumption of raw fish.  The infective larvae are found in the intestine of the fish. When infective fish are eaten by humans, the larvae mature and the adult worms live in the intestinal mucosa, mainly in the jejunum, where they are usually present in large numbers.  Larval stages, oviparous and larviparous females are also found in the host's intestine, which suggests that the nematode multiplies in the intestine resulting in auto-infection as in Strongyloides infection.  The eggs are passed out in the faeces and embryonate in the soil, a process which takes about 12 days.  The eggs are ingested by fresh-water fish, they hatch and develop into the infective form in the intestine of the fish. (Fig.8)




Figure 8. Diagram of the life cycle of Capillaria philippensis. Humans become infected from eating infected fish. The disease in man is known as Capillariasis.




If man ingests the eggs, the resultant larvae migrate from the intestine to the liver where they form adults and cause hepatic capillariasis.




The adult female worm measures 2.5 - 4.3mm, whilst the males are marginally smaller measuring 2.3 -3.2mm.  Adult females can produce immature and mature ova as well as free larvae that can auto-infect. (Fig. 9)




Figure 9. Adult female worm of Capillaria philippensis. They measure approximately 2.5-4.3 mm in length. Anterior part contains the esophagus and "stichosome". Posterior part contains the intestine and reproductive system. (www.medicine.cmu.ac.th)


The eggs measure 45mm x 21mm, and resemble those of Trichuris but have less prominent polar plugs.  They have a thick striated shell. (Fig. 10)



Figure 10. Egg of Capillaria philippensis. They are oval in shape measuring 45mm by 21mm. They closley resemble the eggs of Trichuris but have less prominent plugs. (www.medicine.cmu.ac.th)

Clinical Disease

Many cases may be asymptomatic but by in large, the symptoms are related to the worm burden. The most common symptoms are watery stools with large fluid loss, anorexia, nausea, vomiting, and hypotension.  Abdominal distension and oedema may also develop.  Death can ensue from pneumonia, cerebral oedema, hypokalemia and heart failure.  The large worm burden can cause electrolyte imbalance, plasma protein imbalance, and fluid loss, proving fatal within 4 – 6 months if untreated.  Villi blunting leads to malabsorption but eosinophilia is not a feature of this disease.



Diagnosis depends on finding the characteristic eggs or larvae in the faeces. Pulmonary capillariasis diagnosis relies on finding adult worms or eggs in lung biopsies.



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