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