FREE ESSAY ON PARASITIC FLATWORMS

PARASITIC FLATWORMS

INTRODUCTION
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.