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
Introduction
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)
Morphology
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.
Prevention
1.
Safe disposal of dog faeces.
2.
Education to prevent feeding uncooked offal to
dogs.
Echinococcus
multilocularis
Introduction
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.
Morphology
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.
Diagnosis
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
Introduction
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.
Diagnosis
There are no serological tests available.
Capillaria
philippensis
Introduction
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.
Morphology
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
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.
