Parasitic wasps Essay Example For Students

Parasitic wasps Essay Malaria is one of the most prevalent and dangerous diseases known to man. It has existed for centuries and affects a myriad of people in the tropical region. Even today, with our newly discovered treatments for many of the tropical diseases, over 10% of the people that are infected with malaria each year and do not receive proper treatment die. In Africa alone, over 1 million children die each year because of malaria and new cases are reported frequently. Malaria is very dangerous and harmful to man. However, the protozoan that causes malaria has existed since man came into being. Fossils of mosquitoes that are 30 million years old contain the vector for malaria. After written history, many civilisations have known about malaria. The Greek physician Hippocrates described the symptoms of malaria in the 5th Century BC The name malaria is derived from the Italian words, mal and aria, meaning bad air, because people of earlier times believed that the disease was caused by polluted air near swaps and wetlands in Europe. The scientific identification of malaria was not found until 1880. The French army physician, Charles Laveran, while stationed in Algeria, noticed strange shapes of red blood cells in certain patients and identified the disease scientifically and linked to a certain protozoan. Although the disease had been identified, it was not until 1897, when British army physician, Ronald Ross studied birds and discovered that the malarial protozoan was transmitted through mosquito es. Soon after, two Italian scientists noted that mosquitoes spread malaria to humans as well. Many attempts have been made to try to eradicate the disease. As early as 7 AD, in Rome, swamps were drained to try to prevent the bad air from reaching nearby cities. Recently, in the 1950s and 1960s, about 25 years after the development of DDT, the United Nations World Health Organisation tried to wipe out the disease through the use of DDT. Although, the number of cases was reduces in many areas, they started again. Scientists today believe that malaria can never be eradicated due to the fact that the protozoan can manipulate easily and become resistant to a drug that is overused. The mosquitoes that spread malaria are also becoming resistant to insecticides. Malaria can be treated on an individual basis and treatments and medicines can be used. To understand these treatments however, one must understand what happens to a malarial protozoan. The disease, malaria, is cause by the protozo an, Plasmodium, which lives in tropical regions all around the world. There are only four species of this protozoan that cause malaria in humans, Plasmodium ovale, Plasmodium vivax, Plasmodium malariae, and Plasmodium falciparum. These protozoans are spread from infected to healthy people through the bite of the Anopheles mosquito, blood transfusions, or through hypodermic injections. This makes malaria one of the most easily communicable diseases in the world. These enter red cells where both sexual and asexual cycles continue. Malaria is spread only through the females of the 60 different types of the Anopheles mosquito, as the males do not feed on blood. The symptoms of this disease are many, however a physician must be consulted to avoid risk to a person. To treat malaria, many drugs are used today. Forms of these drugs date back to the 1500s and 1600s. Physicians diagnose malaria by identifying Plasmodia in a patients body. Once identified, malaria can be treated with chloroquine and primaquine. Since some forms of Plasmodia falciparum have become resistant to these, quinine, mefloquine, or halofautrine are used. Almost all of the cases of malaria can be treated if done in the proper way. However, to suffer the pain and illness of malaria, people can use many preventive measures. All swampy areas must be avoided as well as tropical water that may be contaminated or local food. People should just protect themselves from mosquitoes and risk of infection will be tremendously lowered. This can be done by im pregnated bednets. These involve surrounding the bed with a curtain that is sprayed with certain compounds. These are normally pyrethroids or organophosphates, which create an effective barrier between the mosquito and its blood meal. Alternative barrier methods are insect repellents. These are certain chemicals that that when applied to the skin as a spray or lotion is quite effective at deterring the mosquito from landing on a person in order to feed. Other methods of controlling malaria are the use of insecticides and vaccines. Insecticides are chemicals such as pyrethrum, which are sprayed within persons living quarters. This was thought to kill the female mosquito preventing it from spreading malaria and laying further eggs as long as it had no means from escaping the room before spraying. Vaccines work by stimulating antibody production to destroy a foreign organism in the body. As the foreign organism has the same surface antigens as the pathogenic organism, the antibody that the body produces to destroy the antigenic material in the vaccination will be equally as effective against the pathogenic organism. The lymphocytes that produce the antibody will remain in the blood stream. When the pathogenic organism enters the body the lymphocytes will be triggered to produce the antibody in order to destroy the invading organism. At the moment this is where a lot of malaria research is centred in trying to produce a malaria vaccine. Man evolved as a hunter-gatherer, with populations of low densities compared with other primates. At these low densities man would not have been the preferred host of many parasites, but would have experienced malaria as a zoonosis. It is postulated that the development of agriculture around 10,000 to 7000 years ago resulted in man made changes in nutrition, the environment and population density. These changes are so recent in genetic terms that the species has not adapted. The success of our species, expressed as population expansion, has been at the cost of widespread disease, of which malaria related diseases are common manifestations. The burden is heaviest on pregnant women and children under five years old. Over 8 million of the 13 million under-five deaths in the world each year can be put down to diarrhoea, pneumonia, malaria, and vaccine-preventable diseases. But this simple way of classifying hides the fact that death is not usually an event with one cause but a process with many causes. In particular, it is the conspiracy between malnutrition and infection, which pulls many people into the downward spiral of an early death and poor growth in children. Now, a new study has attempted to quantify the role of malnutrition in child deaths. Using data from 53 developing countries, researchers from Cornell University have concluded that over half of those 13 million child deaths each year are associated with malnutrition. Further, they show that more than three-quarters of all these malnutrition-assisted deaths are linked not to severe malnutrition but to mild and moderate forms. This suggests that nutrition programmes focusing only on the severely malnourished will have far less impact than programmes to improve nutrition among the much larger number of mildly and moderately malnourished children. As discussed in the 1994 edition of The Progress of Nations, low-cost methods of reducing all forms of malnutrition are available and have been shown to work. And action on both fronts to improve nutrition and to protect against disease could save many more lives (and be far more cost-effective) than action on either front alone. Malnutrition receives few banner headlines, like the AIDS crisis does. There is no excuse for starvation, with technology and science making food as plentiful as it is. Yet famine and malnutrition are not the same thing. Many of these children may be getting food. But what are missing are the nutrients they need to grow into healthy and productive adults. A report by UNICEF indicates that at least 100 million young children and several million pregnant women have damaged immune systems not because of HIV or AIDS, but because of malnutrition It is thought that malaria can be prevented and risk of infection lowered with varies nutritional aspects. These include minerals such as Iron, zinc and Vitamins A, C, D, E, antioxidants, fatty acids and carbohydrates. Over the years, as the control of diseases such as malaria has improved, the significance of malnutrition has emerged more clearly. There is a need to understand its cause to ensure secure foundations for schemes of prevention, and thus preventing disease. Nutrition and many tropical infections such as malaria interact, not just because of extensive geographical overlap between areas where malaria occur or nutrient deficiencies are common. The clinical and public health implications and the range of such interactions are becoming increasingly appreciated. It is evident that in many countries malnutrition is responsible for the high mortality in children along with disease. It is with children and pregnant women particularly that most of the research with nutrition and malaria has been done. Malaria is truly a grave problem and could affect any ignorant person. However, if a person takes certain precautions and does not get involved with insects, they might just be safe from being one of the 300,000,000 people who are infected each year, or even worse, one of the 1,500,000 people that die of malaria annually. Most people are familiar with the Recommended Daily Allowances (RDA) for vitamins and minerals that have been established by the Food and Nutrition Board of the National Research Council. The RDA is defined as the level of intake of an essential nutrient that is judged to be adequate to meet the known needs of healthy people. At these levels, in other words, people should not develop the deficiency illness associated with a lack of that nutrient. The RDA does not apply to people with special nutritional needs, nor does it suggest that these are the optimal dietary levels for these nutrients for normal people. We now know that mild to moderate deficiency of basic nutrients, while not causing the classic deficiency illnesses, may contribute to a host of other illnesses, especially in todays world, where stress and poor lifestyle habits may tax the bodys nutritional resources. Scientific data suggest that the consumption of many nutrients above the RDAs may prevent or combat many common illnesses. Vitamin C60 mgcitrus fruits, strawberries, tomatoes, cantaloupe, broccoli, asparagus, peppers, spinach, potatoesVitamin E30 IUvegetable oils (soy, corn, olive, cottonseed, safflower, and sunflower), nuts, sunflower seeds, wheat germ. Beta Carotene15-50 mgdark green, yellow, and orange vegetables including spinach, collard greens, broccoli, carrots, peppers, and sweet potatoes; yellow fruits such as apricots and peaches. (IU = international units; mg = milligrams)Investigations into interactions between nutrient status and infectious disease are seriously complicated by the difficulties of assessing status of many nutrients during the acute phase response to infection. Many nutrients are acute phase reactants for example, plasma retinol, zinc and iron and the degree of transferrin saturation all decrease, and plasma copper and ferritin and erythrocyte protoporphyrin increase, in response to infection or trauma (Filteau, S M, and Tomkins, A M, 1994). There is an urgent need for research into nutritional assessment of infected individuals and populations since these are frequently the people whose nutritional status is of most concern. The consistent alterations of micronutrient metabolism suggests that these may have advantages in the fight against infection, the alterations in iron metabolism have been suggested as a means of pathogen replication (Thurnham, 1990). The redistribution of zinc to liver and bone marrow after infection of inflammatory cytokines may serve to support acute phase protein synthesis and haematopoesis. Patients with chronic inflammatory conditions have increased concentrations of zinc in mononuclear leukocytes, which may indicate that cells of the immune system are also favoured for zinc during inflammatory responses. The potential benefits of retinol fluxes during infection have not been explored. Although it is clear that a decreased plasma concentration of a nutrient during infection may be a beneficial adaptation rather than a harmful deficiency (Filteau, S M, and Tomkins, A M, 1994). The problems of assessing nutrient status during infection have made it difficult to determine whether infections decrease status itself over the long term. Several factors could contribute to impaired status, including decreased appetite, decreased absorption due to diarrhoea, or increased requirement for nutrients for immune functions or tissue repair. Internet Hackers EssayErythrocytic malaria parasites live in the blood which is rich in haemoglobin, a ready source of nutrients, but also a potential source of toxic forms of iron. In acquiring nutrients the parasites take up large quantities of haemoglobin. In this process, globin is hydrolysed to free amino acids and haem is converted to haemozoin. Globin hydrolysis is presumed to provide the bulk of amino acids for parasite protein synthesis, and haem processing is thought to both detoxify haem molecules and provide necessary parasite iron. The processes of haemoglobin catabolism and iron utilisation are targets for a number of compounds with antimalarial activity. Erythrocytic parasites require iron for the synthesis of iron containing proteins such as ribonucleotide reductase, superoxide dismutase and cytochromes and for de novo haem biosynthesis. The source of free iron for malaria parasites is not known. Three possible sources are serum iron, free erythrocytic iron and haemoglobin. There are some reports of iron uptake from serum by parasitised erythrocytes, supporting a serum source for parasite iron. This backs-up the observations that iron deficient individuals are partially protected against malaria infection. Although studies showing a lack of transferin receptors on parasitised erythrocytes, argues against a serum source for parasite iron (Peto, T E A, Thompson, J L, 1986). Observations show that cell-impermeant, serum depleting, iron chelators have no antimalarial activity in culture. A report showed that the antimalarial effects of iron chelators in mice are independent of host iron status and a study showed that the course of malar ia in children is unaffected by iron supplementation (Peto, T E A, Thompson, J L, 1986). Arguing against free erythrocytic iron as the source of parasite iron are observations that iron chelators inserted into the erythrocyte cytoplasm are non toxic to cultured parasites. Considering this, the large amount of haemoglobin that is degraded by erythrocytic parasites, and the observation that small amounts of iron are released from haem after incubation at the pH of the food vacuole, it is logical that haemoglobin is the principal source of parasite iron (Rosenthal P J and Meshnick, S R, 1996). Although this has never been tested. The best studied antimalarial iron chelator is deferoxamine (desferrioxamine B, DFO). Its antimalarial activity has been demonstrated in vitro, in animals and patients with both moderate and severe P. falciparum infections. The entry of DFO into the parasite is essential for antimalarial activity. DFO treatment of patients with cerebral malaria had a much greater effect on coma recovery time than on parasite clearance time, suggesting that iron chelation may have an effect on the disease process beyond its anti parasitic effect (Rosenthal, P J, 1996). This suggests that it may be possible that iron deposition in tissue may be partially responsible for severe malaria. Indeed, haemozoin deposition in the brain was significantly higher in mice with cerebral malaria like illness than in mice with ordinary malaria. Although DFO has shown promising activity, it is unlikely to be of practical use as it is expensive and must be administrated by continuous infusion. A number of other iron che lators have shown antimalarial activity in vitro and in vivo. 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