Parasitic Wasps Essay, Research Paper

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 mosquitoes. 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 1950’s and 1960’s, 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 protozoan, 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. 1.Sporozoites in salivary gland.

2.Oцcysts

in stomach wall. 3.Male and female gametocytes. 4.Liver phase. 5.Release of

merozoites from liver. 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 1500’s and 1600’s. Physicians diagnose malaria by identifying

Plasmodia in a patient’s 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 impregnated 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. Recommended Daily Allowances 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 today’s

world, where stress and poor lifestyle habits may tax the body’s nutritional

resources. Scientific data suggest that the consumption of many nutrients above

the RDAs may prevent or combat many common illnesses. Nutrient RDA Sources

Vitamin A 10,000 IU Vitamin B1 (Thiamine) 1.5 mg Vitamin B2 (Riboflavin) 1.7 mg

Vitamin B3 (Niacin) 20 mg Vitamin B6 (Pyridoxine) 2 mg Vitamin C 60 mg citrus

fruits, strawberries, tomatoes, cantaloupe, broccoli, asparagus, peppers,

spinach, potatoes Vitamin D 400 IU Vitamin E 30 IU vegetable oils (soy, corn,

olive, cottonseed, safflower, and sunflower), nuts, sunflower seeds, wheat germ.

Beta Carotene 15-50 mg dark green, yellow, and orange vegetables including

spinach, collard greens, broccoli, carrots, peppers, and sweet potatoes; yellow

fruits such as apricots and peaches. Folic Acid 0.2 mg Iron 15 mg Zinc 15 mg (IU

= international units; mg = milligrams) Micronutrients 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. Vitamin E Neither the American

Heart Association nor professional medical societies endorse vitamin E

supplements, though, mainly because most of the published research is

observational. To date, there have only been two controlled clinical trials

evaluating vitamin E. There is some evidence that vitamin E (a-tocopherol) plays

a role in the development of malaria infection. The malaria parasite is

sensitive to oxidant stress and antioxidant agents such as Vitamin E may

potentiate the infection in vivo (Skinner-Adams, T, et al 1998). Addition of

vitamin E to cultures in vivo has been found to improve the growth of Plasmodium

falciparum in old, normal red blood cells. In addition vitamin E deficient mice

are resistant to Plasmodium Yoelii infection, while low serum vitamin E levels

in humans with falciparum malaria are associated with a relatively short

parasite clearance time. Vitamin E like any other antioxidant vitamins also

behave as a pro-oxidant under certain conditions and may therefore paradoxically

inhibit the growth and development of malaria parasites at high blood

concentrations. In a study results showed that vitamin E has limited ability to

influence the growth of P. falciparum in vivo at medium concentrations, which

span and exceed those present in normal blood serum (Skinner-Adams, T, et al

1998). Some inhibitory activity was seen at concentrations equivalent to the

upper limit of normal human plasma concentrations. Subphysiological vitamin E

concentrations may, through increasing oxidant stress and perhaps membrane

effects which impair merozoite invasion, inhibit the development of P.

falciparum in humans. At supraphsiological concentrations, vitamin E behaves as

a pro-oxidant and inhibition is seen. As malaria infection is associated with

depressed serum vitamin E concentrations in humans, the maintenance of

relatively high oxidant stress environment should aid in the treatment of

malaria. Although treatment with vitamin E may have an unpredictable effect on

parasite burden, reflecting factors such as dose, pre-treatment plasma

concentrations, and liver stores. Due to this, supplementation with vitamin E

may not be appropriate in the acute phase of the illness. Vitamin A

(Beta-carotene, Retinol) Beta-carotene is a previtamin-A compound found in

plants. The body converts beta-carotene to vitamin-A. Vitamin A can be found in

fresh apricots, asparagus, broccoli, cantaloupe, carrots, endive, kale, leaf

lettuce, liver, mustard greens, pumpkin, spinach, squash, winter, sweet potatoes

and watermelon. Vitamin A has many beneficial uses it; 1) Aids in treatment of

many eye disorders, including prevention of night blindness and formation of

visual purple in the eye; 2) Promotes bone growth, teeth development,

reproduction; 3) Helps form and maintain healthy skin, hair, mucous membranes;

4) Builds body’s resistance to respiratory infections; 5) Helps treat acne,

impetigo, boils, carbuncles, open ulcers when applied externally. It is thought

that the vitamin helps in shorting the duration of illnesses and helps in

fighting infection. Vitamin A deficiencies may also lead to diarrhoea a malaria

related diseases. Clinical vitamin A deficiency in children, although still of

public health significance in many countries, currently are rare in the United

States and other industrially developed countries. Whereas clinical vitamin A

deficiency is becoming less common in less industrialised countries, subclinical

deficiency, also termed marginal vitamin A status, is still prevalent. In this

regard, the incidence of mortality among pre-school children in many less

industrialised countries is reduced by approximately 30% when vitamin A

supplements are provided. Each year, vitamin A deficiency contributes to the

deaths of between 2 and 3 million children, to approximately 500,000 cases of

permanent blindness, and to increased morbidity for many adults, especially

among pregnant women. Vitamin A deficiency in children is common in countries

where rice is a primary food staple. With support from The Micronutrient

Initiative, PATH completed a feasibility study on the introduction of vitamin

A-fortified Ultra Rice in the rural province of East Nusa Tenggara Timur in

Indonesia. The project was implemented by PATH, several local national

government officers (NGOs), and Bon Dente Nutrition, a private company involved

in the development of food products and fortificants. The trial verified the

stability of vitamin A under field conditions, validated a mixing procedure for

small rice millers, demonstrated consumer acceptability of the product, and

confirmed the feasibility of selling vitamin A-fortified rice in local outlets.

Furthermore, the trial attracted national, provincial, and local government

interest in fortification of rice. Malaria Morbidity in Young Children Vitamin A

is often deficient in individuals living in malaria endemic areas, is essential

for normal immune function, and several studies show it could play a part in

potentiating resistance to malaria. Studies have shown that vitamin A deficient

rats and mice are more susceptible to malaria than normal animals, and this

susceptibility is readily reversed by vitamin A supplementation. Also, a genetic

locus, which includes cellular retinol-binding protein, influences malaria

mortality and parasitemia in mice. In vitro, addition of free retinol to

P.falciparum cultures reduced parasite replication in one study but not in

another (Shankar A H, et al 1999). In humans there has been evidence for the

role of protective vitamin A but it has not been proven. Although cross

sectional studies with children and adults have shown that low plasma vitamin A

concentrations are associated with increased blood parasite counts. However

increased parasite counts can trigger an acute phase response, which transiently

depresses the circulating vitamin A concentration. The number of episodes of

falciparum malaria among children in Papua New Guinea was 30% lower in children

that received vitamin A supplementation than in those who received a placebo. At

a cost of US $0.03 per supplement and US $0.25 per delivery, vitamin A ranks at

supplementation ranks among the more cost effective non-pharmacological

interventions for malaria. The mechanism by which vitamin A affects morbidity

due to P. falciparum remain unknown. Also the beneficial effects of vitamin A

are less evident in children younger than 1 year (Shankar A H, et al 1999).

Nutrient status influences immune function and resistance to disease. It is also

thought that other nutrients such as zinc and thiamine may also reduce malaria

morbidity. Cost, safety, and potential efficiency of targeted nutritional

supplementation suggest that a rational approach to development of such

interventions for malaria would be useful. These could be integrated with other

controls such as treated bednets, chemoprophylaxis, future detection and rapid

detection and treatment. Vitamin A supplementation may be an effective,

inexpensive, and programmatically way of controlling P. falciparum malaria.

Fortification Vitamin A deficiency is a serious public health problem in

Guatemala, affecting an estimated 22% of all children under five (Phillips, M,

et al, 1996). There is considerable international evidence that rectifying

vitamin A deficiencies offers important health benefits and at relatively low

cost, making such programs highly cost effective. Though in the case of

Guatemala some approaches may be more efficient than others (Phillips, M, et al,

1996). There are three main strategies for combating vitamin A deficiency

world-wide. These strategies are food fortification, capsule distribution and

diet modification. Guatemala has examples of each of these three strategies in

operation. The sugar fortification programme, initiated in 1987-88, established

by law that all sugar that is processed and marketed for direct household

consumption in the country should contain 15 mg of vitamin A per gram of sugar.

A level originally designed to meet 100% of the vitamin A requirements given

average sugar consumption per day for young children. This national

fortification program has been complemented by geographically targeted

interventions in areas where localised deficiencies where detected. These

include the distributing vitamin A capsules and promoting the production and

consumption of vitamin A rich foods in areas which had high prevalence of

vitamin A deficiency (Phillips, M, et al, 1996). In contrast to the capsule and

food production/education programs, fortification reaches individuals regardless

of their need for vitamin A and unlike the capsule program is not specifically

targeted at women and children. The low cost of distributing the fortificant

through sugar compensates for the fact that quite a substantial amount of the

vitamin A reaches consumers who do not need it. The only time when fortification

looked lees attractive was in the 1989 program, when very low fortificant levels

where detected in sugar samples despite adequate amounts of vitamin A being

imported. The cost effectiveness of the capsule and food production/education

programs has been high as the areas where they are implemented are often

dispersed rural areas meaning transportation costs are high. Although the

capsule method seems to be more effective when considering high risk groups

(Phillips, M, et al, 1996). Also a suitable vehicle for fortification must be

considered if it is to be implemented. The food should be one which is consumed

in a fairly homogeneous fashion by the targeted group, one which it is

technically and economically feasible to fortify and one which will be

culturally acceptable after fortification. With a very small budget it would

probably be more worthwhile to invest in a focussed capsule distribution or

perhaps a food production/education program in a high deficiency area rather

than in fortification, whose effects would be highly diluted. Where universal

coverage is not possible, it may be necessary to assess the relative efficiency

of targeting interventions at different geographical areas (West, K, P, et al

1984). Vitamin C (Ascorbic Acid) Vitamin C is responsible for a number of

benefits; it promotes healthy capillaries, gums, teeth, aids iron absorption,

treats anaemia, especially for iron-deficiency anaemia, increases iron

absorption from intestines, contributes to haemoglobin and red-blood-cell

production in bone marrow, blocks production of nitrosamines. Pregnancy requires

vitamin-C supplements because of demands made by bone development, teeth and

connective-tissue formation of fetus. Breast-feeding requires vitamin-C

supplementation to support rapid growth of child. Anaemia as we know is a major

public health problem. As in many developing countries, the most vulnerable

population groups are pregnant and lactating women and pre-school and school-age

children. School-age children are highly vulnerable to iron deficiency because

there iron requirements for growth often exceed the dietary iron supply. Several

strategies have been proposed to overcome this problem including the use of iron

supplements. This approach is effective but its usefulness is often limited by

low compliance. Food fortification with iron is generally considered the most

effective way to increase iron intake and can be achieved by fortifying a

dietary staple such as cereal flour or by fortifying widely consumed foodstuffs

such as sugar and salt. This strategy supplies everyone in the population with

iron supplements including people who do not need it like adult men and

postmenopausal women. The preferred approach to target children would be to

fortify a speciality food for that age group. One possibility would be to

fortify a chocolate-flavoured milk drink with iron as was done in a recent study

(Davidson, L, et al 1998). These chocolate drinks as well as milk contain

inhibitors of iron absorption. A way around this is to add vitamin C (ascorbic

acid) as is done in industrially produced foods. The study showed the effect of

added ascorbic acid on iron absorption from the chocolate flavoured drink was

clear. The geometric mean iron absorption increased from 5.4% to 7.7% when the

ascorbic acid content was doubled, from 25 to 50 mg. The enhancing effect of

ascorbic acid on iron absorption is believed to be due to its ability to reduce

ferric iron to ferrous iron, which binds less strongly with polyphenols and

phytic acid (found in the test meal) to form insoluble complexes (Fairweather-Tait,

S, and Hurrel, R F, 1996). Iron Erythrocytic 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 malaria 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 chelators have shown antimalarial

activity in vitro and in vivo. One of these may prove to be more clinically

useful than DFO. Anaemia is said to be one of the malaria related diseases, it

affects 30% of the world’s population. It is an important health problem because

it may increase maternal morbidity and decrease physical work capacity owing to

reduction in O2 delivery to tissues (World Health Organisation 1975).

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