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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.
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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