Parasitic Flatworms
Imagine going to the doctor for a simple check up. Sure you've had some
minor
problems- indigestion, lack of energy, weight loss, and a bit of gas-
but that's
not out of the ordinary....or is it? In most cases you would be
correct...but
today is your unlucky day. The doctor has just informed you
that you have a
tapeworm parasite. PARASITIC CHARACTERISTICS By definition, a
parasite is an
organism that lives either in or on another organism. Infected
organisms that
are carrying a parasite are called host organisms- or hosts.
This parasitic
relationship can vary from benign to harmful- and sometimes
even fatal. There
are two main types of parasites: endoparasites and
exoparasites, however
endoparasites will be the focus of this paper, and
flatworms in particular.
Endoparasites are parasites that live inside the
host organism. Endoparasites
that inhabit vertebrates or invertebrates live
off the nutrients in the food
host organisms eat as well as the tissue of the
host. These parasites not only
live in the cavities of hollow organs but can
also live within the tissue.
Endoparasites can range from microscopic in
size to 25 feet or more in length.
Many worms are antiparasitic. Some
live in the host's digestive tract feeding
off the host's blood. Others, such
as trichinosis, enter the host through the
digestive tract and then migrate
throughout the body tissue. Most microscopic
worms secrete toxins into the
hosts blood stream which then circulates and often
causes damage to
surrounding systems and tissue. The life cycle of endoparasites
is as varied
as the parasites themselves. Some parasites are permanent fixtures
in a
host's body, while others only live within the host for a limited amount
of
time. For example, parasitic worms can live within a host for up to 30
years!
The host not even being aware of this fact because there are
little or no
symptoms of the invasion. Not only are life cycles varied for
parasites but the
number of hosts they live in are as well. Sometimes
parasites live in only one
host for their entire life- known as autecious -
while others change hosts-
known as heteroecious. In relation to the life
cycle of parasitic worms, there
are also different reproductive methods. Many
parasites do not reproduce within
their host, or reproduce to a limited
degree. They are more likely to reproduce
eggs that enter another host before
they develop in the final host. These
parasites just use their fist host as
an intermediatory step in completing their
life cycle. The species
schistosoma ( Refer to Figure 1 ) from the class
trematoda is an example of
such a parasite. These parasites go through a life
cycle in which they use an
invertebrate, usually a snail as an intermediatory
host. ( Refer to Figure 1a
) FLATWORM CHARACTERISTICS Flatworms from the phylum
Platyhelminthes, are
parasites that live within the intermediatory host but
usually complete their
sexual maturity within a vertebrate. They are broken into
three major
classes: Turbellaria, the most primitive, free-living class that
resides
either in or on a host, they generally live in a marine
environment.
Trematoda which is the small parasitic flatworm ( most of
which are called
flukes) has disk like suckers which attach to the outside or
internal organs of
their host, and the class Cestoda which consist of the
parasitic flatworm known
as the tapeworm. ( Refer to Figure 2 ) Tapeworms
have no true digestive tract,
therefore they live inside the digestive tract
of vertebrates and some
invertebrates, absorbing food through their body
wall. They latch onto the walls
of their host's digestive tract with suckers
and hooks, located at their head,
which is called a scolex. The phylum
platyhelminthes are one of interest when
discussing parasitic flatworms that
infect vertebrates and invertebrates.
INFECTION Humans and animals are in
continuous contact with microorganisms,
because of this relationship there
are numerous ways in which infection of
flatworms can occur. Organisms that
transmit parasites are known as vectors.
Some vectors transmit parasites
when they are eaten by the hosts. An example of
this would be a flea eaten by
a dog or cat. When the animal eats the flea, the
immature form of the
tapeworm emerges from the fleas body and later develops
into a mature
tapeworm. Another way animals can become infected is by eating
feces of
infected animals which carry the eggs of the parasites. Pigs and cattle
are
known for this type of infection. Humans can become infected by
larva
penetrating the skin, when walking barefoot on infected soil. An
example of this
would be the species schistosoma which has a complex life
cycle. One being the
infection of a snail (intermediatory hosts ) to the
later infection of a human (
primary hosts). Humans can also become infected
by eating undercooked beef,
pork, fish or other flesh foods contaminated with
larvae cyst. The eggs then
hatch in the intestinal tract and release larval
forms, which burrow into the
tissues of the host and form cysts. The flatworm
then seeks the alimentary canal
and develops there. The larvae often exhibits
specific selection of tissues in
encysting, for example, one species attacks
the liver in humans and dogs whereas
others attack the brain in sheep.
Development of the tapeworm in encysted meat
is stimulated by the gastric
juices of the host. The adults then attach
themselves to the intestinal tract
(small intestine) of their host by the scolex
and absorb partially digested
food through their body wall. The relationship
between the host and parasite
is a delicate one, since each modifies the
activities and functions of the
other. The outcome of host parasite interaction
depends on the pathogenicity
and the relative degree of resistance or
susceptibility of the host. It was
found that "Like all free-living
species, parasites are subject to selection
pressure to ensure optimum
exploitation of their environment and survival of
the genes" ( D. Wakelin.,
1993, p. 488 ). However the animal or human
wants to defend itself against the
parasites that have pathogenic potential
at different stages. Host defenses
include completely preventing the
infection, or if an infection does occur
actions can be taken against the
parasite before and infection is apparent to
the host. However there are time
when the defenses needed to stop the parasite
are not effective until it's to
late. Nevertheless, in some instances the
defense system completely over
looks the parasite and is not aware of its
presence. Therefore " The
parasites may successfully colonize a
well-defended host by evading
recognition and thus preventing an effective
immune response from ever being
mounted" ( Eric S. Loker, 1994, p. 730 ).
EVASIVE TECHNIQUES OF THE
PARASITIC FLATWORM For millions of years now,
parasites and hosts have been
playing an intense game of chess, seeing who will
gain possession of the
ultimate board. " Survival of parasites in their
natural host is bound up
with their ability to evade the responses that their
presence evokes. This
may be achieved using a variety of mechanisms." (
Waekelin. D, 1984, p.
639 ). Parasites are able to with stand many hostile or
lethal factors within
their hosts. Therefore, the survival mechanisms must be a
highly
sophisticated repertoire of evasive strategies. The concept of
antigen
sharing, or disguise, is probably the most accepted. " The idea that
cross
reacting host and parasite antigens might be in part responsible for
parasite
survival was first proposed in the early 1960s by Sprent (1962) and
elaborated
upon by Damian (1964), Capron, Biguet, Vernes & Afschan (1968)
and Smither,
Terry & Hockley (1968,1969)" ( D. J. Mclaren, 1988, p.
597 ). Shared
and synthesized Determinants There have been examples of
antigen synthesis by
the flatworm ( trematodes ). However, evidence to
support the data obtained has
not been overwhelming. As far as trematode are
concerned, it has been shown that
adult schistosomes recovered from either
mice or monkeys, express an antigenic
determinant on their surface which
cross reacts with mouse a2- macroglobulin.
This shows that, " since the
antisera used in these study gave no cross-
reactions between murine and
rhesus monkey a2-macroglobulin , the mouse -like
determinant was suggested to
be synthesized by the parasite." ( D. J
McLaren, 1988, p. 598 ). Evidence
to support this hypothesis was gathered by
using an immunoelectron microscopy
to confirm the location of the cross-reacting
parasite. However criticisms
for this hypothesis stems from the lack of
generality (these results were
taken from rodents and not humans). Generality is
an important factor because
S. mansoni ( parasitic Schistosoma flatworm ) is
primarily a parasite of
humans. It is certain that some parasitic flatworms can
synthesize shared
determinants, however it still remains uncertain wether these
synthesized
epitopes grant survival value of the parasite. Acquired Host
Determinants
Blood Group Antigens Another concept believed to be utilized by the
parasitic
flatworm is the masquerading of itself as a "host" to evade
the host immune
response. It has been shown with various experiments done by
Damian,
Damian, Greene & Hubbard ( as cited in Parasitology 1988) commented
on by
D. J Mclaren, noted that : Adult schistosomes recovered form mice
were
rapidly killed following transfer into monkeys that had been
previously
immunized against mouse cells. In contrast mouse worms
transplanted into normal
monkeys suffered a temporary setback, but then
continued to develop and lay eggs
in a normal fashion . . . an immune maker
confirmed that mouse antigens were
indeed present on the surface of the
mouse- derived schistosomes prior to
transfer... and further demonstrated
that the immune attack mounted against the
parasite by the ant-mouse monkey
was surface directed. (P.599) Other studies
have shown familiar results, both
in vivo and in vitro. The host molecules
acquired by the schistosomes were in
fact surface components of the erythrocyte;
A, B, H, And Lewis b+
antigens were acquired by parasitic flatworm. Even more
interesting was the
fact that A and B antigens could be acquired from the serum
of A or B
positive donors in the absence of homologous erythrocytes,
irrespective of
the secretor status of the donor. This provided information that
the blood
group substances were taken up as glycolipids rather then
glycoproteins. This
proof was derived from an experiment done by Goldring, Kusel
and Smithers (
as cited in Parasitology 1988 ) as mentioned by D. J
McLaren.
Schistosomula grown in vitro with a megalolipid extract of the A
blood group
antigen expressed A antigen on their surfaces and secondly,
erythrocytes whose
surface carbohydrates were radio-isotope labeled were
found to transfer only
labeled glycolipid like molecules to the surface of
co-cultured Schistosomula.
(p.599). The molecular interdigitation of the
glycolipid with the parasites
tegumental outer membrane, to leave the
haptenic carbohydrate portion of the
molecule exposed is another view of the
acquired host antigens with the parasite
surface. Proof of such association
is evident in other experiments done. It has
been shown that, "Lewis blood
group glycolipids have been shown to transfer
from serum to co-cultured
deficient erythrocytes" ( D. J. McLaren 1988,
p.599 ). Histocompatibility
Agents An additional way that the parasite evades
the immune response is by
the uptake of other host molecules taken up as
glycoproteins. As described, "
The existence of contaminating antigens of
host origin in parasites... made
it necessary to introduce and define a new term
"eclipsed antigen" for an
antigenic determinant of parasite origin
which resembles an antigenic
determinant of its host" ( Damien 1964 p.130
). Therefore the host will not
be able to recognize a parasite as foreign, thus
not producing antibodies to
evoke an attack. It has been shown that
Schistosomula posses
serologically detectable alloantigens on their surface: the
major
determinants of immunological recognition of self. Gene products of the
K,
D and Ia regions of the MHC were demonstrated by experimental
techniques. ( D.J
Mclaren, 1988 )These MHC-coded antigens were further
shown to be acquired in
vitro following co-culture of lung stage parasites
with allogeneic lymphocytes,
and that reinjection in vivo , using these
allogeneic recipients showed that an
exchange of the acquired alloantigens
can be exchanged within 87 hrs.
Demonstrating that the MHC antigens can
be acquired by lung stage Schistosomula
following culture in the presence of
human platelets. Its has also been noted
that MHC-encode alloantigens were
detected on the surface of older larvae ( 21
days ), and adult worms. Thus
showing that he alloantigens can be acquired
through various stages of the
Schistosomula stages of life. Evidence gathered
has shown that the
schistosome can acquire the MHC gene products from the host
and does not
synthesize them itself. Information gathered from researchers such
as,
Simpson, Singer, McCutchan, Sacks and Sher, have shown that there is
DNA
sequences in the parasite genome homologous to class MHC antigens. It is
also
notable to state here that certain regions of the MHC are known to
selectively
shed, in association with membrane lipids. These host lipids are
known to
"associate readily with the schistosomular surface, a mechanism for
the
transfer of MHC antigens to the parasite can thus be envisioned."
(D.J
McLaren 1988, p.601) Intracellular Substance Agents Intracellular
substance
antigens, with specifications confined to the tegument of certain
skin cells,
have also been detected on the surface of skin-penetrated
schistosomlua. These
antigens were not present when cercariae were
transported by mechanical means
into the host, nor were they present in
Schistosomula recovered from the lung of
an animal on day 5. This information
brings about some doubt as to the long term
value of the intracellular
substance antigens in the disguise process. It is
perhaps a characteristic
used only to evade and gain entrance into the host, and
once within, the
parasite loses this antigen. immunoglobulins An area of
interest to numerous
researchers is the acquisition of host immunoglobulin by
the parasite. In
schistosomes it has been noted that there was a presence of
IgG1, IgG2a,
IgG2b, IgG3, IgA, and IgM on the surface of the worm. It has been
shown that
these antibodies are to be hetrospecific rather than the classical
blocking
antibodies. They are also noted to be bound to the surface of the
parasite
via Fc receptors on the tegumental outer membrane. However in
adults,
experiments done by Torpier, Carpon & Ouaissi have shown that (
as cited in
Parasitology 1988 ) Rosetting techniques have failed to
confirm the presence of
Fc receptors on adult schistosomes....Fc with
human receptors with specificity
to human b2-microglobulin were detected on
the surface of skin-penetrated
Schistosomula using this technique (p.602)
Thus giving the parasite a cloak
against the immune response of the host.
Protection According to Age of The
Flatworm As it has been shown, a
considerable amount of effort has been devoted
to the location and
identification of host molecules on the tegumental surface
of the parasite.
Even though most information gathered has not been able to
conclusively prove
that shared determinants serve as a disguise of the parasites
flatworm to the
host immune system, another alternative may be that may serve as
a different
but as important function. It is conceivable that the parasite
does
synthesize a molecule that mimics a host immunoregulatory protein There
has been
a certain evidence that has shown that " murine protein and the
worm
synthesized determinant share physicochemical and
immunological
characteristics...and function to inhibit T-cell induced
lymphocyte
blastogenesis" ( D. J Mclaren, 1988 p.604 ). The stage at which
the
flatworm is in would seem apparently important as some experiments have
shown.
It seems that the older schistosome rely exclusively upon their
disguise for
protection against the immune response of the host, but the
younger stages have
additional mechanisms of protection, termed intrinsic
This intrinsic mechanism
reportedly in the young is shown to be of some
interest. Resistance against
immune attack has been reported by some authors
to develop in the absence of
host molecules, but the general consensus of
opinion is that protection proceeds
faster and more efficiently if the worms
were given access to mammalian serum.
In this context the young
schistosome has been shown to selectively incorporate
host lipids and to be
capable of performing a limiting range of interconversions.
These changes
in lipid composition have been correlated with increased
protection against
both complement mediated and eosinophil-mediated cytotoxicity.
In other
experiments it was shown that modulation of cell surface lipids were
known to
alter the susceptibility of the cell to complement lysis. Therefore it
seems
that the lipid exchange between the young schistosome and its host serves
to
secure the tegumental membrane and supplement the protection afforded by
the
acquired host antigen disguise. It has also been suggested that
the
immunoglobulin absorbed by schistosomes play an important role in
membranes
modulation. This was demonstrated when " rabbit antibody was
complexed to
mouse immunoglobulin on the parasite surface, that particular
immunoglobulin was
shed from the tegumental outer membrane very quickly" (
D.J McLaren 1988,
p.607 ). This suggests that when the outer membrane was
damaged a quick turnover
of the membrane was noticed. Effectively protecting
it from further damage from
the host immune system. SUMMARY The Balance We
have taken a look at a few ways
in which the flatworm parasite can evade its
host immune system. It is obvious
that the outer tegumental membrane of the
parasite is a crucial element in the
survival of the evasive flatworm. Strong
evidence indicating that acquired blood
group determinants and incorporation
of host lipids help in this protection.
Though the offense of the
parasite may be strong, a balance between the host and
parasite must be
reached. "Each host-parasite relationship is a unique
product of the
particular individual involved...there is therefore a complex
trade off for
both partners between the beneficial and harmful effects of the
host
response" ( Wakelin 1993, p. 493 ) The interactions between the two
will be
dependent on one another, the complexity of the genetically
determined
response of the host immune system on the parasite, and the
intricate strategies
employed by the parasite. The parasite does not want to
be terminated nor
expelled by the immune response of the host, however to
much taken from the host
and the parasite finds itself in is situation where
the host is incapable of
providing nutrients for both the parasite and
itself, thus destroying both
individuals. A balance must be found for a
successful existence, between the
host and parasite. One could almost
consider the interaction of the parasite and
host to lead to coevolutionary
arms race, in which an evolutionary progress in
one side provokes a further
response in the other side. The host should evolve
defensive means to reduce
the impact of paratism, while the parasite should
evolve mens to counter the
host defense. Evasive techniques applied by humans It
is impossible to avoid
all situations that could lead to parasitic infection.
There are however
a few basic precautions that can serve as a guidelines to
better protect
oneself. Drinking pure clean water, always washing produce
(especially
vegetables), cooking meat thoroughly, and maintaining a healthy
lifestyle
that includes keeping fit. A strong body makes for a great line of
defense
against parasites.