Parasitic Flatworms Essay, Research Paper
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 glycolipidlike molecules to the surface of co-cultured Schistosomula. (p.599).