Monday, 24 June 2013

CREATED BY : RAGIL BAGUS T
ENGLISH DIPLOMA PROGRAM
JENDERAL SOEDIRMAN UNIVERSITY


MALARIA

 Malaria is a mosquito-borne infectious disease of humans and other animals caused by protists (a type of microorganism) of the genus Plasmodium. It begins with a bite from an infected female Anopheles mosquito, which introduces the protists through saliva into the circulatory system. In the blood, the protists travel to the liver to mature and reproduce. Malaria causes symptoms that typically include fever and headache, which in severe cases can progress to coma or death. The disease is widespread in tropical and subtropical regions in a broad band around the equator, including much of Sub-Saharan Africa, Asia, and the Americas.
Five species of Plasmodium can infect and be transmitted by humans. The vast majority of deaths are caused by P. falciparum and P. vivax, while P. ovale, and P. malariae cause a generally milder form of malaria that is rarely fatal. The zoonotic species P. knowlesi, prevalent in Southeast Asia, causes malaria in macaques but can also cause severe infections in humans. Malaria is prevalent in tropical and subtropical regions because rainfall, warm temperatures, and stagnant waters provide habitats ideal for mosquito larvae. Disease transmission can be reduced by preventing mosquito bites by distribution of mosquito nets and insect repellents, or with mosquito-control measures such as spraying insecticides and draining standing water.
Malaria is typically diagnosed by the microscopic examination of blood using blood films, or with antigen-based rapid diagnostic tests. Modern techniques that use the polymerase chain reaction to detect the parasite's DNA have also been developed, but these are not widely used in malaria-endemic areas due to their cost and complexity. The World Health Organization has estimated that in 2010, there were 219 million documented cases of malaria. That year, between 660,000 and 1.2 million people died from the disease,[1] many of whom were children in Africa. The actual number of deaths is not known with certainty, as accurate data is unavailable in many rural areas, and many cases are undocumented. Malaria is commonly associated with poverty and may also be a major hindrance to economic development.
Despite a need, no effective vaccine currently exists, although efforts to develop one are ongoing. Several medications are available to prevent malaria in travellers to malaria-endemic countries (prophylaxis). A variety of antimalarial medications are available. Severe malaria is treated with intravenous or intramuscular quinine or, since the mid-2000s, the artemisinin derivative artesunate, which is superior to quinine in both children and adults and is given in combination with a second anti-malarial such as mefloquine. Resistance has developed to several antimalarial drugs; for example, chloroquine-resistant P. falciparum has spread to most malarial areas, and emerging resistance to artemisinin has become a problem in some parts of Southeast Asia.
 


The signs and symptoms of malaria typically begin 8–25 days following infection;[2] however, symptoms may occur later in those who have taken antimalarial medications as prevention.[3] Initial manifestations of the disease—common to all malaria species—are similar to flu-like symptoms,[4] and can resemble other conditions such as septicemia, gastroenteritis, and viral diseases.[3] The presentation may include headache, fever, shivering, joint pain, vomiting, hemolytic anemia, jaundice, hemoglobin in the urine, retinal damage,[5] and convulsions.
The classic symptom of malaria is paroxysm—a cyclical occurrence of sudden coldness followed by rigor and then fever and sweating, occurring every two days (tertian fever) in P. vivax and P. ovale infections, and every three days (quartan fever) for P. malariae. P. falciparum infection can cause recurrent fever every 36–48 hours or a less pronounced and almost continuous fever.[6]
Severe malaria is usually caused by P. falciparum (often referred to as falciparum malaria). Symptoms of falciparium malaria arise 9–30 days after infection.[4] Individuals with cerebral malaria frequently exhibit neurological symptoms, including abnormal posturing, nystagmus, conjugate gaze palsy (failure of the eyes to turn together in the same direction), opisthotonus, seizures, or coma.[4]
Complications
There are several serious complications of malaria. Among these is the development of respiratory distress, which occurs in up to 25% of adults and 40% of children with severe P. falciparum malaria. Possible causes include respiratory compensation of metabolic acidosis, noncardiogenic pulmonary oedema, concomitant pneumonia, and severe anaemia. Acute respiratory distress syndrome (ARDS) may develop in 5–25% in adults and up to 29% of pregnant women but it is rare in young children.[7] Coinfection of HIV with malaria increases mortality.[8] Renal failure is a feature of blackwater fever, where hemoglobin from lysed red blood cells leaks into the urine.[4]
Infection with P. falciparum may result in cerebral malaria, a form of severe malaria that involves encephalopathy. It is associated with retinal whitening, which may be a useful clinical sign in distinguishing malaria from other causes of fever.[9] Splenomegaly, severe headache, hepatomegaly (enlarged liver), hypoglycemia, and hemoglobinuria with renal failure may occur.[4]
Malaria in pregnant women is an important cause of stillbirths, infant mortality and low birth weight,[10] particularly in P. falciparum infection, but also with P. vivax.[11]


Cause
Malaria parasites belong to the genus Plasmodium (phylum Apicomplexa). In humans, malaria is caused by P. falciparum, P. malariae, P. ovale, P. vivax and P. knowlesi.[12][13] Among those infected, P. falciparum is the most common species identified (~75%) followed by P. vivax (~20%).[3] Although P. falciparum traditionally accounts for the majority of deaths,[14] recent evidence suggests that P. vivax malaria is associated with potentially life-threatening conditions about as often as with a diagnosis of P. falciparum infection.[15] P. vivax proportionally is more common outside of Africa.[16] There have been documented human infections with several species of Plasmodium from higher apes; however, with the exception of P. knowlesi—a zoonotic species that causes malaria in macaques[13]—these are mostly of limited public health importance.[17]





The life cycle of malaria parasites: A mosquito causes infection by taking a blood meal. First, sporozoites enter the bloodstream, and migrate to the liver. They infect liver cells, where they multiply into merozoites, rupture the liver cells, and return to the bloodstream. Then, the merozoites infect red blood cells, where they develop into ring forms, trophozoites and schizonts that in turn produce further merozoites. Sexual forms are also produced, which, if taken up by a mosquito, will infect the insect and continue the life cycle.
In the life cycle of Plasmodium, a female Anopheles mosquito (the definitive host) transmits a motile infective form (called the sporozoite) to a vertebrate host such as a human (the secondary host), thus acting as a transmission vector. A sporozoite travels through the blood vessels to liver cells (hepatocytes), where it reproduces asexually (tissue schizogony), producing thousands of merozoites. These infect new red blood cells and initiate a series of asexual multiplication cycles (blood schizogony) that produce 8 to 24 new infective merozoites, at which point the cells burst and the infective cycle begins anew.[18] Other merozoites develop into immature gametes, or gametocytes. When a fertilised mosquito bites an infected person, gametocytes are taken up with the blood and mature in the mosquito gut. The male and female gametocytes fuse and form zygotes (ookinetes), which develop into new sporozoites. The sporozoites migrate to the insect's salivary glands, ready to infect a new vertebrate host. The sporozoites are injected into the skin, alongside saliva, when the mosquito takes a subsequent blood meal.[19]
Only female mosquitoes feed on blood; male mosquitoes feed on plant nectar, and thus do not transmit the disease. The females of the Anopheles genus of mosquito prefer to feed at night. They usually start searching for a meal at dusk, and will continue throughout the night until taking a meal.[20] Malaria parasites can also be transmitted by blood transfusions, although this is rare.[21]


Recurrent malaria
Symptoms of malaria can reappear (recur) after varying symptom-free periods. Depending upon the cause, recurrence can be classified as either recrudescence, relapse, or reinfection. Recrudescence is when symptoms return after a symptom-free period. It is caused by parasites surviving in the blood as a result of inadequate or ineffective treatment.[22] Relapse is when symptoms reappear after the parasites have been eliminated from blood but persist as dormant hypnozoites in liver cells. Relapse commonly occurs between 8–24 weeks and is commonly seen with P. vivax and P. ovale infections.[3] P. vivax malaria cases in temperate areas often involve overwintering by hypnozoites, with relapses beginning the year after the mosquito bite.[23] Reinfection means the parasite that caused the past infection was eliminated from the body but a new parasite was introduced. Reinfection cannot readily be distinguished from recrudescence, although recurrence of infection within two weeks of treatment for the initial infection is typically attributed to treatment failure.[24]


Pathophysiology


Malaria infection develops via two phases: one that involves the liver (exoerythrocytic phase), and one that involves red blood cells, or erythrocytes (erythrocytic phase). When an infected mosquito pierces a person's skin to take a blood meal, sporozoites in the mosquito's saliva enter the bloodstream and migrate to the liver where they infect hepatocytes, multiplying asexually and asymptomatically for a period of 8–30 days.[25]
After a potential dormant period in the liver, these organisms differentiate to yield thousands of merozoites, which, following rupture of their host cells, escape into the blood and infect red blood cells to begin the erythrocytic stage of the life cycle.[25] The parasite escapes from the liver undetected by wrapping itself in the cell membrane of the infected host liver cell.[26]
Within the red blood cells, the parasites multiply further, again asexually, periodically breaking out of their host cells to invade fresh red blood cells. Several such amplification cycles occur. Thus, classical descriptions of waves of fever arise from simultaneous waves of merozoites escaping and infecting red blood cells.[25]
Some P. vivax sporozoites do not immediately develop into exoerythrocytic-phase merozoites, but instead produce hypnozoites that remain dormant for periods ranging from several months (7–10 months is typical) to several years. After a period of dormancy, they reactivate and produce merozoites. Hypnozoites are responsible for long incubation and late relapses in P. vivax infections,[23] although their existence in P. ovale is uncertain.[27]
The parasite is relatively protected from attack by the body's immune system because for most of its human life cycle it resides within the liver and blood cells and is relatively invisible to immune surveillance. However, circulating infected blood cells are destroyed in the spleen. To avoid this fate, the P. falciparum parasite displays adhesive proteins on the surface of the infected blood cells, causing the blood cells to stick to the walls of small blood vessels, thereby sequestering the parasite from passage through the general circulation and the spleen.[28] The blockage of the microvasculature causes symptoms such as in placental malaria.[29] Sequestered red blood cells can breach the blood–brain barrier and cause cerebral malaria.[30]
Although the red blood cell surface adhesive proteins (called PfEMP1, for P. falciparum erythrocyte membrane protein 1) are exposed to the immune system, they do not serve as good immune targets because of their extreme diversity; there are at least 60 variations of the protein within a single parasite and even more variants within whole parasite populations. The parasite switches through a broad repertoire of PfEMP1 surface proteins, thereby avoiding detection by protective antibodies.[31]


Genetic resistance
Main article: Genetic resistance to malaria
Due to the high levels of mortality and morbidity caused by malaria—especially the P. falciparum species—it has placed the greatest selective pressure on the human genome in recent history. Several genetic factors provide some resistance to it including sickle cell trait, thalassaemia traits, glucose-6-phosphate dehydrogenase deficiency, and the absence of Duffy antigens on red blood cells.[32][33]
The impact of sickle cell trait on malaria immunity is of particular interest. Sickle cell trait causes a defect in the hemoglobin molecule in the blood. Instead of retaining the biconcave shape of a normal red blood cell, the modified hemoglobin S molecule causes the cell to sickle or distort into a curved shape. Due to the sickle shape, the molecule is not as effective in taking or releasing oxygen. Infection causes red cells to sickle more, and so they are removed from circulation sooner. This reduces the frequency with which malaria parasites complete their life cycle in the cell. Individuals who are homozygous (with two copies of the abnormal hemoglobin beta allele) have sickle-cell anaemia, while those who are heterozygous (with one abnormal allele and one normal allele) experience resistance to malaria. Although the shorter life expectancy for those with the homozygous condition seems to be unfavourable to the trait's survival, the trait is preserved because of the benefits provided by the heterozygous form.[33][34]

Liver dysfunction
Liver dysfunction as a result of malaria is rare and is usually a result of a coexisting liver condition such as viral hepatitis or chronic liver disease. The syndrome is sometimes called malarial hepatitis, although inflammation of the liver (hepatitis) does not actually occur. While traditionally considered a rare occurrence, malarial hepatopathy has seen an increase, particularly in Southeast Asia and India. Liver compromise in people with malaria correlates with a greater likelihood of complications and death.[35]




Diagnosis

Approximately 30% of people will no longer have a fever upon arriving to a health care facility. Owing to the non-specific nature of the presentation, diagnosis of malaria in non-endemic areas requires a high degree of suspicion, which might be elicited by any of the following: recent travel history, enlarged spleen, fever without localizing signs, low platelets, and hyperbilirubinemia combined with a normal peripheral blood leukocyte count.[3]
Malaria is usually confirmed by the microscopic examination of blood films or by antigen-based rapid diagnostic tests (RDT).[36][37] Microscopy is the most commonly used method to detect the malarial parasite—about 165 million blood films were examined for malaria in 2010.[38] Despite its widespread usage, diagnosis by microscopy suffers from two main drawbacks: many settings (especially rural) are not equipped to perform the test, and the accuracy of the results depends on both the skill of the person examining the blood film and the levels of the parasite in the blood. The sensitivity of blood films ranges from 75–90% in optimum conditions, to as low as 50%. Commercially available RDTs are often more accurate than blood films at predicting the presence of malaria parasites, but they are widely variable in diagnostic sensitivity and specificity depending on manufacturer, and are unable to tell how many parasites are present.[38]
In regions where laboratory tests are readily available, malaria should be suspected, and tested for, in any unwell patient who has been in an area where malaria is endemic. In areas that cannot afford laboratory diagnostic tests, it has become routine to use only a history of subjective fever as the indication to treat for malaria—a presumptive approach exemplified by the common teaching "fever equals malaria unless proven otherwise". A drawback of this practice is overdiagnosis of malaria and mismanagement of non-malarial fever, which wastes limited resources, erodes confidence in the health care system, and contributes to drug resistance.[39] Although polymerase chain reaction-based tests have been developed, these are not widely implemented in malaria-endemic regions as of 2012, due to their complexity.[3]
Classification
Malaria is classified into either "severe" or "uncomplicated" by the World Health Organization (WHO).[3] It is deemed severe when any of the following criteria are present, otherwise it is considered uncomplicated.[40]
Cerebral malaria is defined as a severe P. falciparum-malaria presenting with neurological symptoms, including coma (with a Glasgow coma scale less than 11, or a Blantyre coma scale greater than 3), or with a coma that lasts longer than 30 minutes after a seizure.[41]


Prevention



Methods used to prevent malaria include medications, mosquito elimination and the prevention of bites. The presence of malaria in an area requires a combination of high human population density, high mosquito population density and high rates of transmission from humans to mosquitoes and from mosquitoes to humans. If any of these is lowered sufficiently, the parasite will eventually disappear from that area, as happened in North America, Europe and much of the Middle East. However, unless the parasite is eliminated from the whole world, it could become re-established if conditions revert to a combination that favours the parasite's reproduction.[42]
Many researchers argue that prevention of malaria may be more cost-effective than treatment of the disease in the long run, but the capital costs required are out of reach of many of the world's poorest people. There is a wide disparity in the costs of control (i.e. maintenance of low endemicity) and elimination programs between countries. For example, in China—whose government in 2010 announced a strategy to pursue malaria elimination in the Chinese provinces—the required investment is a small proportion of public expenditure on health. In contrast, a similar program in Tanzania would cost an estimated one-fifth of the public health budget.[43]


Vector control refers to preventative methods used to decrease malaria and morbidity and mortality by reducing the levels of transmission. For individual protection, the most effective chemical insect repellents to reduce human-mosquito contact are those based on DEET and picaridin.[44] Insecticide-treated mosquito nets (ITNs) and indoor residual spraying (IRS) have been shown to be highly effective vector control interventions in preventing malaria morbidity and mortality among children in malaria-endemic settings.[45][46] IRS is the practice of spraying insecticides on the interior walls of homes in malaria-affected areas. After feeding, many mosquito species rest on a nearby surface while digesting the bloodmeal, so if the walls of dwellings have been coated with insecticides, the resting mosquitoes can be killed before they can bite another victim and transfer the malaria parasite.[47] As of 2006, the World Health Organization advises the use of 12 insecticides in IRS operations, including DDT and the pyrethroids cyfluthrin and deltamethrin.[48] This public health use of small amounts of DDT is permitted under the Stockholm Convention on Persistent Organic Pollutants (POPs), which prohibits the agricultural use of DDT.[49]
One problem with all forms of IRS is insecticide resistance via evolution. Mosquitoes affected by IRS tend to rest and live indoors, and due to the irritation caused by spraying, their descendants tend to rest and live outdoors, meaning that they are less affected by the IRS, which greatly reduces its effectiveness as a defense mechanism.[50]



Mosquito nets help keep mosquitoes away from people and significantly reduce infection rates and transmission of malaria. Nets are not a perfect barrier and are often treated with an insecticide designed to kill the mosquito before it has time to find a way past the net. Insecticide-treated nets are estimated to be twice as effective as untreated nets and offer greater than 70% protection compared with no net.[51] Between 2000 and 2008, the use of ITNs saved the lives of an estimated 250,000 infants in Sub-Saharan Africa.[52] Although ITNs prevent malaria, only about 13% of households in Sub-Saharan countries own them.[53] A recommended practice for usage is to hang a large "bed net" above the center of a bed to drape over it completely with the edges tucked in. Pyrethroid-treated nets and long-lasting insecticide-treated nets offer the best personal protection, and are most effective when used from dusk to dawn.[54]


Other methods                                    
Community participation and health education strategies promoting awareness of malaria and the importance of control measures have been successfully used to reduce the incidence of malaria in some areas of the developing world.[55] Recognizing the disease in the early stages can stop the disease from becoming fatal. Education can also inform people to cover over areas of stagnant, still water, such as water tanks that are ideal breeding grounds for the parasite and mosquito, thus cutting down the risk of the transmission between people. This is generally used in urban areas where there are large centers of population in a confined space and transmission would be most likely in these areas.[56] Intermittent preventive therapy is another intervention that has been used successfully to control malaria in pregnant women and infants,[57] and in preschool children where transmission is seasonal.[58]



Medications
Main article: Malaria prophylaxis
Several drugs, most of which are used for treatment of malaria, can be taken to prevent contracting the disease during travel to endemic areas. Chloroquine may be used where the parasite is still sensitive.[59] Because of the prevalence of drug-resistant Plasmodium, one of three medications—mefloquine (Lariam), doxycycline (available generically), or the combination of atovaquone and proguanil hydrochloride (Malarone)—is frequently needed.[59] Doxycycline and the atovaquone and proguanil combination are the best tolerated; mefloquine is associated with death, suicide, and higher rates of neurological and psychiatric symptoms.[59]
The prophylactic effect does not begin immediately upon starting the drugs, so people temporarily visiting malaria-endemic areas usually begin taking the drugs one to two weeks before arriving and should continue taking them for four weeks after leaving (with the exception of atovaquone proguanil that only needs to be started two days prior and continued for seven days afterwards).[60] Use of prophylactic drugs is seldom practical for full-time residents of malaria-endemic areas, and their use is usually restricted to short-term visitors and travellers to malarial regions. This is due to the cost of purchasing the drugs, negative adverse effects from long-term use, and because some effective anti-malarial drugs are difficult to obtain outside of wealthy nations.[61] The use of prophylactic drugs where malaria-bearing mosquitoes are present may encourage the development of partial immunity.[62]


Treatment
Further information: Antimalarial medication
The treatment of malaria depends on the severity of the disease. Uncomplicated malaria may be treated with oral medications. The most effective strategy for P. falciparum infection is the use of artemisinins in combination with other antimalarials (known as artemisinin-combination therapy, or ACT), which reduces the ability of the parasite to develop resistance to any single drug component.[63] These additional antimalarials include amodiaquine, lumefantrine, mefloquine or sulfadoxine/pyrimethamine.[64] Another recommended combination is dihydroartemisinin and piperaquine.[65][66] ACT is about 90% effective when used to treat uncomplicated malaria.[52] To treat malaria during pregnancy, the WHO recommends the use of quinine plus clindamycin early in the pregnancy (1st trimester), and ACT in later stages (2nd and 3rd trimesters).[67] In the 2000s (decade), malaria with partial resistance to artemisins emerged in Southeast Asia.[68][69]
Severe malaria requires the parenteral administration of antimalarial drugs. Until the mid-2000s the most used treatment for severe malaria was quinine, but artesunate has been shown to be superior to quinine in both children and adults.[70] Treatment of severe malaria also involves supportive measures that are optimally performed in a critical care unit, including management of high fevers (hyperpyrexia) and the subsequent seizures that may result from it, and monitoring for respiratory depression, hypoglycemia, and hypokalemia.[14] Infection with P. vivax, P. ovale or P. malariae is usually treated on an outpatient basis (while a person is at home). Treatment of P. vivax requires both treatment of blood stages (with chloroquine or ACT) as well as clearance of liver forms with primaquine.[71]


Disability-adjusted life year for malaria per 100,000 inhabitants in 2004
   no data
   <10
  0–100
  100–500
   500–1000
   1000–1500
  1500–2000
   2000–2500
  2500–2750
   2750–3000
   3000–3250
   3250–3500
   ≥3500
When properly treated, people with malaria can usually expect a complete recovery.[72] However, severe malaria can progress extremely rapidly and cause death within hours or days.[73] In the most severe cases of the disease, fatality rates can reach 20%, even with intensive care and treatment.[3] Over the longer term, developmental impairments have been documented in children who have suffered episodes of severe malaria.[74] Chronic infection without severe disease can occur, a form of acquired immunity where the immune system is also less responsive to Salmonella and the Epstein–Barr virus.[75]
Malaria causes widespread anemia during a period of rapid brain development, and also direct brain damage. This neurologic damage results from cerebral malaria to which children are more vulnerable.[74] Some survivors of cerebral malaria have an increased risk of neurological and cognitive deficits, behavioural disorders, and epilepsy.[76] Malaria prophylaxis was shown to improve cognitive function and school performance in clinical trials when compared to placebo groups.[74]



The WHO estimates that in 2010 there were 219 million cases of malaria resulting in 660,000 deaths,[78] equivalent to roughly 2000 deaths every day.[3] Using a different set of predictive models to estimate mortality, a 2012 study determined the number of documented and undocumented deaths in 2010 to be 1.24 million.[79] The majority of cases (65%) occur in children under 15 years old.[79] About 125 million pregnant women are at risk of infection each year; in Sub-Saharan Africa, maternal malaria is associated with up to 200,000 estimated infant deaths yearly.here are about 10,000 malaria cases per year in Western Europe, and 1300–1500 in the United States. About 900 people died from the disease in Europe between 1993 and 2003. Both the global incidence of disease and resulting mortality have declined in recent years. According to the WHO, deaths attributable to malaria in 2010 were reduced by over a third from a 2000 estimate of 985,000, largely due to the widespread use of insecticide-treated nets and artemisinin-based combination therapies.
Malaria is presently endemic in a broad band around the equator, in areas of the Americas, many parts of Asia, and much of Africa; in Sub-Saharan Africa, 85–90% of malaria fatalities occur. An estimate for 2009 reported that countries with the highest death rate per 100,000 of population were Ivory Coast with 86.15, Angola (56.93) and Burkina Faso (50.66). An estimate for 2010 said the deadliest countries per population were Burkina Faso, Mozambique and Mali.The Malaria Atlas Project aims to map global endemic levels of malaria, providing a means with which to determine the global spatial limits of the disease and to assess disease burden.[82][83] This effort led to the publication of a map of P. falciparum endemicity in 2010. As of 2010, about 100 countries have endemic malaria. Every year, 125 million international travellers visit these countries, and more than 30,000 contract the disease.
The geographic distribution of malaria within large regions is complex, and malaria-afflicted and malaria-free areas are often found close to each other. Malaria is prevalent in tropical and subtropical regions because of rainfall, consistent high temperatures and high humidity, along with stagnant waters in which mosquito larvae readily mature, providing them with the environment they need for continuous breeding. In drier areas, outbreaks of malaria have been predicted with reasonable accuracy by mapping rainfall.Malaria is more common in rural areas than in cities. For example, several cities in the Greater Mekong Subregion of Southeast Asia are essentially malaria-free, but the disease is prevalent in many rural regions, including along international borders and forest fringes. In contrast, malaria in Africa is present in both rural and urban areas, though the risk is lower in the larger cities.



Conclusion : 
            
Malaria is a dangerous disease, it can strike anyone who has a place to stay dirty, we have to keep our families from danger is, in many ways I have explained above. start now, start living healthy and clean in order to avoid the disease. with diligent exercise, and clean up the places that become mosquito breeding.

References :

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