Free research paper example on Malaria:
In humans Malaria is caused by one of four different protozoan parasites; Plasmodium vivax, P. faliparum, P. malaria, and P. ovale (Grimes, Grimes, & Hamelink, 1991). Humans can become infected by these protozoa mainly by way of vector; specifically the female Anopheles mosquito or by transfusion of infected blood or needle sharing with an infected person (Taber’s Cyclopedic Medical Dictionary, 1997).
It has been mentioned in ancient Sanskrit and Chinese documents. The disease is thought to have been brought to North America in the 16th and 17th centuries via African slaves and European colonists (Turkington, 1998). Currently malaria is mostly isolated to Sub-Saharan Africa, India, Southern Asia, and Central and South America therefore predisposing travelers and the indigenous people in these locations to this disease (McConell, 2002).
The malaria life cycle involves two hosts. The first cycle begins when the mosquito ingests microgametocytes (male) and macro gametocytes (female) from an infected human during a blood meal. These undergo development into a zygote within the mosquito, which is known as the sporogonic cycle. This zygote moves into the mid-gut of the mosquito maturing into an oocyst which then ruptures releasing sporozoites. These sporozoites make their way to the salivary glands of the mosquito and are transferred into a human host when the mosquito bites (Center for Disease Control).
Once the Anopheles mosquito has bitten a human the sporozoites travel through the blood stream and infect liver cells. The pre-erythrocytic schizogony stage begins when the sporozoites enter the parenchymal cells in the liver and multiply. In twelve days there will be many thousand young parasites known as merozoites in one liver cell. The liver cell then ruptures and releases these merozoites into the blood stream where they enter the red blood cells. Inside the red blood cells they undergo rapid asexual multiplication. This action destroys the erythrocytes and releases more merozoites into the blood stream to infect additional erythrocytes (RPH Laboratory Medicine). It is in this erythrocytic stage that the clinical manifestations of the disease become evident (CDC).
The clinical presentation of the disease depends on the infecting species, level of parasitemia, and the immune status of the host. Depending on these criteria malaria can become rapidly fatal within as little as 24 hours. The common clinical presentation of the disease includes: fever, chills, headache, mayalgias, arthralgias, weakness, vomiting, and diarrhea. These are commonly mistaken for flu like illness. The P. vivax and P. ovale parasites can persist in the liver in a dormant state for weeks or even years and then cause relapses (CDC). Antibodies are produced during an infection but they do not protect against future exposure or contraction of the disease (Turkington & Ashby, 1998).
Symptoms can progress rapidly into more sever complications. Complications such as: anemia, disseminated intravascular coagulation, acute renal failure, pulmonary edema, liver failure, fluid, electrolyte and acid-base disturbances may develop due to the breakdown of microcirculation in the capillaries of the internal organs through uninhibited parasitic multiplication and pathological changes of the red blood cells (World Health Organization, 2003). Cerebral malaria is often a complication arising in adults infected with malaria. It may result in future acute psychiatric complications such as schizophrenic and manic syndromes, depression and anxiety disorders (Aloa, Yolles, & Armenta, 2000). Approximately 300 million people worldwide are affected by malaria and between 1 and 1.5 million people die from it every year (WHO, 2003). The psychological impact on an individual diagnosed with malaria would be great due to the high mortality rate. The fear of dying from the disease would be wide spread among those in close proximity of anyone diagnosed due to the way the disease is spread, by vector.
Confirming diagnosis is made by laboratory examination of the patient’s blood. Examining blood smears is the standard for diagnosis. Thick blood smears reveal the concentration of parasites and thin smears reveal the parasite type (RPH Laboratory Medicine).
Another method of detection is Becton-Dickinson’s Quantitative Buffy Coat (QBC II) method in which blood is stained with Acridine Orange and then centrifuged. The DNA can then be viewed by ultraviolet light. This method is not always successful in distinguishing between the different parasites (RPH Laboratory Medicine).
For travelers entering a high-risk geographical area it is strongly recommended that they start prophylactic antimalarial drugs one week prior to leaving and four weeks after returning. Travelers should also keep in mind that these drugs are not 100% effective and other preventative measures as listed above should be taken (Turkington, 1998). The choice of antimalarial drug depends on which type of parasite the individual is most likely to encounter. If P. falciparum is the parasite, a second consideration is whether or not it is chloroquine sensitive or resistant, as drug treatment will differ (McConnell, 2002). Malarone is a prophylactic drug, which works by preventing folic acid from changing into its active form, therefore disabling the parasites to further form DNA and RNA. The antibiotic Doxycycline, inhibits bacterial growth by decreasing protein synthesis which is a necessary component of DNA and RNA (Lehne, 2001). These are only two of many antimalarial drugs to choose from, others include: Lariam, Aralen and Plaquenil(McConnell, 2002).
Drugs used in the prophylactic treatment of malaria are also used as the main course of treatment for infected persons (Taber’s Cyclopedic Medical Dictionary). Malaria is effectively treated in its early stages with oral antimalarial medications. In severe cases hospitalization, I.V. fluids, medications, RBC transfusions, kidney dialysis and assisted breathing by ventilator may be necessary (Turkington, 1998).
The relationship between the global environment and malaria is frightening. We are in essence contributing to the spread of the disease everyday in way of global warming. The more fossil fuels we use in the well-developed countries, the warmer our climate becomes, the more ideal the climate is for mosquitoes to breed. We are also contributing to the spread of the disease by way of fast and convenient air travel. We are able to travel from one corner of the globe to another in a matter of days, which in some instances is less time than it takes to notice the first signs of malaria. Although air travel is convenient, it is also a way spreading the disease and the drug resistant strains of the disease, to uninfected areas. Because of the ability the parasite has to attain resistance to antimalarial drugs in a short period of time, one would think that the pharmaceutical companies would be spending more money to find an improved antimalarial. Alas, malaria is a disease of the poor.
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