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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.
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 )
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.
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 ).
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.
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.
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.
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