Combating malaria with house design, temp and net

Check this document in the use of house design to combat Malaria:

http://www.rollbackmalaria.org/files/files/working-groups/VCWG/housing%20and%20malaria/Jakob%20Knudsen.pdf

temp malaria PItemp malaria

Malaria is a mosquito-borne infectious disease affecting humans and other animals caused by parasitic protozoans(a group of single-celled microorganisms) belonging to the Plasmodium type.[2] Malaria causes symptoms that typically include feverfeeling tiredvomiting, and headaches. In severe cases it can cause yellow skinseizurescoma, or death.[1] Symptoms usually begin ten to fifteen days after being bitten. If not properly treated, people may have recurrences of the disease months later.[2] In those who have recently survived an infection, reinfection usually causes milder symptoms. This partial resistance disappears over months to years if the person has no continuing exposure to malaria.[1]

The disease is most commonly transmitted by an infected female Anopheles mosquito. The mosquito bite introduces the parasites from the mosquito’s saliva into a person’s blood.[2] The parasites travel to the liver where they mature and reproduce. Five species of Plasmodium can infect and be spread by humans.[1] Most deaths are caused by P. falciparum because P. vivaxP. ovale, and P. malariae generally cause a milder form of malaria.[2][1]The species P. knowlesi rarely causes disease in humans.[2] Malaria is typically diagnosed by the microscopic examination of blood using blood films, or with antigen-based rapid diagnostic tests.[1] Methods that use the polymerase chain reaction to detect the parasite’s DNA have been developed, but are not widely used in areas where malaria is common due to their cost and complexity.[5]

The risk of disease can be reduced by preventing mosquito bites through the use of mosquito nets and insect repellents, or with mosquito control measures such as spraying insecticides and draining standing water.[1] Several medications are available to prevent malaria in travellers to areas where the disease is common. Occasional doses of the combination medication sulfadoxine/pyrimethamine are recommended in infants and after the first trimesterof pregnancy in areas with high rates of malaria. Despite a need, no effective vaccine exists, although efforts to develop one are ongoing.[2] The recommended treatment for malaria is a combination of antimalarial medicationsthat includes an artemisinin.[2][1] The second medication may be either mefloquinelumefantrine, or sulfadoxine/pyrimethamine.[6] Quinine along with doxycycline may be used if an artemisinin is not available.[6] It is recommended that in areas where the disease is common, malaria is confirmed if possible before treatment is started due to concerns of increasing drug resistance. Resistance among the parasites has developed to several antimalarial medications; for example, chloroquine-resistant P. falciparum has spread to most malarial areas, and resistance to artemisinin has become a problem in some parts of Southeast Asia.[2]

The disease is widespread in the tropical and subtropical regions that exist in a broad band around the equator.[1]This includes much of Sub-Saharan AfricaAsia, and Latin America.[2] In 2015, there were 296 million cases of malaria worldwide resulting in an estimated 731,000 deaths.[3][4] Approximately 90% of both cases and deaths occurred in Africa.[7] Rates of disease have decreased from 2000 to 2015 by 37%,[7] but increased from 2014 during which there were 198 million cases.[8] Malaria is commonly associated with poverty and has a major negative effect on economic development.[9][10] In Africa, it is estimated to result in losses of US$12 billion a year due to increased healthcare costs, lost ability to work, and negative effects on tourism.[11]

File:Malaria.webm

Video explanation

Signs and symptoms

Main symptoms of malaria[12]

The signs and symptoms of malaria typically begin 8–25 days following infection;[12] however, symptoms may occur later in those who have taken antimalarial medications as prevention.[5] Initial manifestations of the disease—common to all malaria species—are similar to flu-like symptoms,[13] and can resemble other conditions such as sepsisgastroenteritis, and viral diseases.[5] The presentation may include headachefevershiveringjoint painvomitinghemolytic anemiajaundicehemoglobin in the urineretinal damage, and convulsions.[14]

The classic symptom of malaria is paroxysm—a cyclical occurrence of sudden coldness followed by shivering 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. malariaeP. falciparum infection can cause recurrent fever every 36–48 hours, or a less pronounced and almost continuous fever.[15]

Severe malaria is usually caused by P. falciparum (often referred to as falciparum malaria). Symptoms of falciparum malaria arise 9–30 days after infection.[13] Individuals with cerebral malaria frequently exhibit neurological symptoms, including abnormal posturingnystagmusconjugate gaze palsy (failure of the eyes to turn together in the same direction), opisthotonusseizures, or coma.[13]

Complications

Malaria has several serious complications. 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. Although rare in young children with severe malaria, acute respiratory distress syndrome occurs in 5–25% of adults and up to 29% of pregnant women.[16] Coinfection of HIV with malaria increases mortality.[17] Renal failure is a feature of blackwater fever, where hemoglobin from lysed red blood cells leaks into the urine.[13]

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.[18] Enlarged spleenenlarged liver or both of these, severe headache, low blood sugar, and hemoglobin in the urine with renal failure may occur.[13] Complications may include spontaneous bleeding, coagulopathy, and shock.[19]

Malaria in pregnant women is an important cause of stillbirthsinfant mortalityabortion and low birth weight,[20] particularly in P. falciparum infection, but also with P. vivax.[21]

Cause

Malaria parasites belong to the genus Plasmodium (phylum Apicomplexa). In humans, malaria is caused by P. falciparumP. malariaeP. ovaleP. vivax and P. knowlesi.[22][23] Among those infected, P. falciparum is the most common species identified (~75%) followed by P. vivax (~20%).[5] Although P. falciparum traditionally accounts for the majority of deaths,[24] 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.[25] P. vivax proportionally is more common outside Africa.[26] There have been documented human infections with several species of Plasmodium from higher apes; however, except for P. knowlesi—a zoonotic species that causes malaria in macaques[23]—these are mostly of limited public health importance.[27]

Global warming is likely to affect malaria transmission, but the severity and geographic distribution of such effects is uncertain.[28][29]

Life cycle

The life cycle of malaria parasites. A mosquito causes an infection by a bite. 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. 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.[30]

Other merozoites develop into immature gametocytes, which are the precursors of male and female gametes. When a fertilized 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 an ookinete—a fertilized, motile zygote. Ookinetes develop into new sporozoites that migrate to the insect’s salivary glands, ready to infect a new vertebrate host. The sporozoites are injected into the skin, in the saliva, when the mosquito takes a subsequent blood meal.[31]

Only female mosquitoes feed on blood; male mosquitoes feed on plant nectar and 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.[32] Malaria parasites can also be transmitted by blood transfusions, although this is rare.[33]

Recurrent malaria

Symptoms of malaria can recur after varying symptom-free periods. Depending upon the cause, recurrence can be classified as either recrudescencerelapse, 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.[34] 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.[5] P. vivax malaria cases in temperate areas often involve overwintering by hypnozoites, with relapses beginning the year after the mosquito bite.[35] 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.[36] People may develop some immunity when exposed to frequent infections.[37]

Pathophysiology

Micrograph of a placenta from a stillbirth due to maternal malaria. H&E stain. Red blood cells are anuclear; blue/black staining in bright red structures (red blood cells) indicate foreign nuclei from the parasites.

Electron micrograph of a Plasmodium falciparum-infected red blood cell (center), illustrating adhesion protein “knobs”

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.[38]

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.[38]The parasite escapes from the liver undetected by wrapping itself in the cell membrane of the infected host liver cell.[39]

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.[38]

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,[35] although their existence in P. ovale is uncertain.[40]

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.[41] The blockage of the microvasculature causes symptoms such as in placental malaria.[42] Sequestered red blood cells can breach the blood–brain barrier and cause cerebral malaria.[43]

Genetic resistance

According to a 2005 review, due to the high levels of mortality and morbidity caused by malaria—especially the P. falciparumspecies—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 traitthalassaemia traits, glucose-6-phosphate dehydrogenase deficiency, and the absence of Duffy antigens on red blood cells.[44][45]

The impact of sickle cell trait on malaria immunity illustrates some evolutionary trade-offs that have occurred because of endemic malaria. Sickle cell trait causes a change in the hemoglobin molecule in the blood. Normally, red blood cells have a very flexible, biconcave shape that allows them to move through narrow capillaries; however, when the modified hemoglobin S molecules are exposed to low amounts of oxygen, or crowd together due to dehydration, they can stick together forming strands that cause the cell to sickle or distort into a curved shape. In these strands the molecule is not as effective in taking or releasing oxygen, and the cell is not flexible enough to circulate freely. In the early stages of malaria, the parasite can cause infected red cells to sickle, 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 without severe anemia. Although the shorter life expectancy for those with the homozygous condition would tend to disfavor the trait’s survival, the trait is preserved in malaria-prone regions because of the benefits provided by the heterozygous form.[45][46]

Liver dysfunction

Liver dysfunction as a result of malaria is uncommon and usually only occurs in those with another liver condition such as viral hepatitis or chronic liver disease. The syndrome is sometimes called malarial hepatitis.[47] While it has been 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.[47]

Diagnosis

The blood film is the gold standardfor malaria diagnosis.

Ring-forms and gametocytes of Plasmodium falciparum in human blood

Owing to the non-specific nature of the presentation of symptoms, 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, low number of platelets in the blood, and higher-than-normal levels of bilirubin in the blood combined with a normal level of white blood cells.[5]Reports in 2016 and 2017 from countries were malaria is common suggest high levels of over diagnosis due to insufficient or inaccurate laboratory testing.[48][49][50]

Malaria is usually confirmed by the microscopic examination of blood films or by antigen-based rapid diagnostic tests(RDT).[51][52] In some areas, RDTs need to be able to distinguish whether the malaria symptoms are caused by Plasmodium falciparum or by other species of parasites since treatment strategies could differ for non-P. falciparum infections.[53]Microscopy is the most commonly used method to detect the malarial parasite—about 165 million blood films were examined for malaria in 2010.[54] 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.[54]

In regions where laboratory tests are readily available, malaria should be suspected, and tested for, in any unwell person who has been in an area where malaria is endemic. In areas that cannot afford laboratory diagnostic tests, it has become common to use only a history of fever as the indication to treat for malaria—thus 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.[55] Although polymerase chain reaction-based tests have been developed, they are not widely used in areas where malaria is common as of 2012, due to their complexity.[5]

Classification

Malaria is classified into either “severe” or “uncomplicated” by the World Health Organization (WHO).[5] It is deemed severe when any of the following criteria are present, otherwise it is considered uncomplicated.[56]

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.[57]

Various types of malaria have been called by the names below:[58]

Name Pathogen Notes
algid malaria Plasmodium falciparum severe malaria affecting the cardiovascular system and causing chills and circulatory shock
bilious malaria Plasmodium falciparum severe malaria affecting the liver and causing vomiting and jaundice
cerebral malaria Plasmodium falciparum severe malaria affecting the cerebrum
congenital malaria various plasmodia plasmodium introduced from the mother via the fetal circulation
falciparum malaria, Plasmodium falciparummalaria, pernicious malaria Plasmodium falciparum
ovale malaria, Plasmodium ovale malaria Plasmodium ovale
quartan malaria, malariae malaria, Plasmodium malariae malaria Plasmodium malariae paroxysms every fourth day (quartan), counting the day of occurrence as the first day
quotidian malaria Plasmodium falciparumPlasmodium vivax paroxysms daily (quotidian)
tertian malaria Plasmodium falciparumPlasmodium ovalePlasmodium vivax paroxysms every third day (tertian), counting the day of occurrence as the first
transfusion malaria various plasmodia plasmodium introduced by blood transfusionneedle sharing, or needlestick injury
vivax malaria, Plasmodium vivax malaria Plasmodium vivax

Prevention

An Anopheles stephensi mosquito shortly after obtaining blood from a human (the droplet of blood is expelled as a surplus). This mosquito is a vector of malaria, and mosquito control is an effective way of reducing its incidence.

Methods used to prevent malaria include medications, mosquito elimination and the prevention of bites. There is no vaccine for malaria. The presence of malaria in an area requires a combination of high human population density, high anopheles 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 parts 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 favors the parasite’s reproduction. Furthermore, the cost per person of eliminating anopheles mosquitoes rises with decreasing population density, making it economically unfeasible in some areas.[59]

Prevention of malaria may be more cost-effective than treatment of the disease in the long run, but the initial costs required are out of reach of many of the world’s poorest people. There is a wide difference 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.[60]

In areas where malaria is common, children under five years old often have anemia which is sometimes due to malaria. Giving children with anemia in these areas preventive antimalarial medication improves red blood cell levels slightly but did not affect the risk of death or need for hospitalization.[61]

Mosquito control

Man spraying kerosene oil in standing water, Panama Canal Zone1912

Vector control refers to methods used to decrease malaria by reducing the levels of transmission by mosquitoes. For individual protection, the most effective insect repellents are based on DEET or picaridin.[62] Insecticide-treated mosquito nets (ITNs) and indoor residual spraying (IRS) have been shown to be highly effective in preventing malaria among children in areas where malaria is common.[63][64] Prompt treatment of confirmed cases with artemisinin-based combination therapies (ACTs) may also reduce transmission.[65]

Walls where indoor residual spraying of DDT has been applied. The mosquitoes remain on the wall until they fall down dead on the floor.

A mosquito net in use.

Mosquito nets help keep mosquitoes away from people and 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.[66] Between 2000 and 2008, the use of ITNs saved the lives of an estimated 250,000 infants in Sub-Saharan Africa.[67] About 13% of households in Sub-Saharan countries owned ITNs in 2007[68]and 31% of African households were estimated to own at least one ITN in 2008. In 2000, 1.7 million (1.8%) African children living in areas of the world where malaria is common were protected by an ITN. That number increased to 20.3 million (18.5%) African children using ITNs in 2007, leaving 89.6 million children unprotected[69] and to 68% African children using mosquito nets in 2015.[70] Most nets are impregnated with pyrethroids, a class of insecticides with low toxicity. They are most effective when used from dusk to dawn.[71] It is recommended to hang a large “bed net” above the center of a bed and either tuck the edges under the mattress or make sure it is large enough such that it touches the ground.[72]

Indoor residual spraying is the spraying of insecticides on the walls inside a home. After feeding, many mosquitoes rest on a nearby surface while digesting the bloodmeal, so if the walls of houses have been coated with insecticides, the resting mosquitoes can be killed before they can bite another person and transfer the malaria parasite.[73] As of 2006, the World Health Organization recommends 12 insecticides in IRS operations, including DDT and the pyrethroids cyfluthrin and deltamethrin.[74] This public health use of small amounts of DDT is permitted under the Stockholm Convention, which prohibits its agricultural use.[75] One problem with all forms of IRS is insecticide resistance. 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.[76]

There are a number of other methods to reduce mosquito bites and slow the spread of malaria. Efforts to decrease mosquito larva by decreasing the availability of open water in which they develop or by adding substances to decrease their development is effective in some locations.[77] Electronic mosquito repellent devices which make very high-frequency sounds that are supposed to keep female mosquitoes away, do not have supporting evidence.[78]

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.[79] Recognizing the disease in the early stages can prevent 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.[80] Intermittent preventive therapy is another intervention that has been used successfully to control malaria in pregnant women and infants,[81] and in preschool children where transmission is seasonal.[82]

Medications

There are a number of drugs that can help prevent or interrupt malaria in travelers to places where infection is common. Many of these drugs are also used in treatment. Chloroquine may be used where chloroquine-resistant parasites are not common.[83] In places where Plasmodium is resistant to one or more medications, three medications—mefloquine (Lariam), doxycycline (available generically), or the combination of atovaquone and proguanil hydrochloride (Malarone)—are frequently used when prophylaxis is needed.[83] Doxycycline and the atovaquone plus proguanil combination are the best tolerated; mefloquine is associated with death, suicide, and neurological and psychiatric symptoms.[83]

The protective effect does not begin immediately, and people visiting areas where malaria exists usually start taking the drugs one to two weeks before arriving and continue taking them for four weeks after leaving (except for atovaquone/proguanil, which only needs to be started two days before and continued for seven days afterward).[84] The use of preventative drugs is often not practical for those who live in areas where malaria exists, and their use is usually only in pregnant women and short-term visitors. This is due to the cost of the drugs, side effects from long-term use, and the difficulty in obtaining anti-malarial drugs outside of wealthy nations.[85]During pregnancy, medication to prevent malaria has been found to improve the weight of the baby at birth and decrease the risk of anemia in the mother.[86] The use of preventative drugs where malaria-bearing mosquitoes are present may encourage the development of partial resistance.[87]

Treatment

Advertisement entitled "The Mosquito Danger". Includes 6 panel cartoon: #1 breadwinner has malaria, family starving; #2 wife selling ornaments; #3 doctor administers quinine; #4 patient recovers; #5 doctor indicating that quinine can be obtained from post office if needed again; #6 man who refused quinine, dead on stretcher.

An advertisement for quinine as a malaria treatment from 1927.

Malaria is treated with antimalarial medications; the ones used depends on the type and severity of the disease. While medications against fever are commonly used, their effects on outcomes are not clear.[88]

Simple or uncomplicated malaria may be treated with oral medications. The most effective treatment for P. falciparum infection is the use of artemisinins in combination with other antimalarials (known as artemisinin-combination therapy, or ACT), which decreases resistance to any single drug component.[89] These additional antimalarials include: amodiaquinelumefantrine, mefloquine or sulfadoxine/pyrimethamine.[90] Another recommended combination is dihydroartemisinin and piperaquine.[91][92]ACT is about 90% effective when used to treat uncomplicated malaria.[67] 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).[93] In the 2000s (decade), malaria with partial resistance to artemisins emerged in Southeast Asia.[94][95] Infection with P. vivaxP. ovale or P. malariae usually do not require hospitalization. Treatment of P. vivax requires both treatment of blood stages (with chloroquine or ACT) and clearance of liver forms with primaquine.[96] Treatment with tafenoquine prevents relapses after confirmed P. vivax malaria.[97]

Severe and complicated malaria are almost always caused by infection with P. falciparum. The other species usually cause only febrile disease.[98] Severe and complicated malaria are medical emergencies since mortality rates are high (10% to 50%).[99] Cerebral malaria is the form of severe and complicated malaria with the worst neurological symptoms.[100]Recommended treatment for severe malaria is the intravenous use of antimalarial drugs. For severe malaria, parenteralartesunate was superior to quinine in both children and adults.[101] In another systematic review, artemisinin derivatives (artemether and arteether) were as efficacious as quinine in the treatment of cerebral malaria in children.[102] Treatment of severe malaria involves supportive measures that are best done in a critical care unit. This includes the management of high fevers and the seizures that may result from it. It also includes monitoring for poor breathing effort, low blood sugar, and low blood potassium.[24]

Resistance

Drug resistance poses a growing problem in 21st-century malaria treatment.[103] Resistance is now common against all classes of antimalarial drugs apart from artemisinins. Treatment of resistant strains became increasingly dependent on this class of drugs. The cost of artemisinins limits their use in the developing world.[104]Malaria strains found on the Cambodia–Thailand border are resistant to combination therapies that include artemisinins, and may, therefore, be untreatable.[105]Exposure of the parasite population to artemisinin monotherapies in subtherapeutic doses for over 30 years and the availability of substandard artemisinins likely drove the selection of the resistant phenotype.[106] Resistance to artemisinin has been detected in Cambodia, Myanmar, Thailand, and Vietnam,[107] and there has been emerging resistance in Laos.[108][109]

Prognosis

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.[110] However, severe malaria can progress extremely rapidly and cause death within hours or days.[111] In the most severe cases of the disease, fatality rates can reach 20%, even with intensive care and treatment.[5] Over the longer term, developmental impairments have been documented in children who have suffered episodes of severe malaria.[112] Chronicinfection without severe disease can occur in an immune-deficiency syndrome associated with a decreased responsiveness to Salmonella bacteria and the Epstein–Barr virus.[113]

During childhood, malaria causes anemia during a period of rapid brain development, and also direct brain damage resulting from cerebral malaria.[112] Some survivors of cerebral malaria have an increased risk of neurological and cognitive deficits, behavioural disorders, and epilepsy.[114] Malaria prophylaxis was shown to improve cognitive function and school performance in clinical trials when compared to placebo groups.[112]

Epidemiology

Distribution of malaria in the world:[115]♦ Elevated occurrence of chloroquine- or multi-resistant malaria
♦ Occurrence of chloroquine-resistant malaria
♦ No Plasmodium falciparum or chloroquine-resistance
♦ No malaria

Deaths due to malaria per million persons in 2012

  0–0
  1–2
  3–54
  55–325
  326–679
  680–949
  950–1,358

The WHO estimates that in 2015 there were 214 million new cases of malaria resulting in 438,000 deaths.[116] Others have estimated the number of cases at between 350 and 550 million for falciparum malaria[117] The majority of cases (65%) occur in children under 15 years old.[118] 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.[20] There are about 10,000 malaria cases per year in Western Europe, and 1300–1500 in the United States.[16] About 900 people died from the disease in Europe between 1993 and 2003.[62] Both the global incidence of disease and resulting mortality have declined in recent years. According to the WHO and UNICEF, deaths attributable to malaria in 2015 were reduced by 60%[70] from a 2000 estimate of 985,000, largely due to the widespread use of insecticide-treated nets and artemisinin-based combination therapies.[67] In 2012, there were 207 million cases of malaria. That year, the disease is estimated to have killed between 473,000 and 789,000 people, many of whom were children in Africa.[2] Efforts at decreasing the disease in Africa since the turn of millennium have been partially effective, with rates of the disease dropping by an estimated forty percent on the continent.[119]

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.[120] An estimate for 2009 reported that countries with the highest death rate per 100,000 of population were Ivory Coast (86.15), Angola (56.93) and Burkina Faso (50.66).[121] A 2010 estimate indicated the deadliest countries per population were Burkina Faso, Mozambique and Mali.[118] 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.[122][123] This effort led to the publication of a map of P. falciparum endemicity in 2010.[124] As of 2010, about 100 countries have endemic malaria.[125][126] Every year, 125 million international travellers visit these countries, and more than 30,000 contract the disease.[62]

The geographic distribution of malaria within large regions is complex, and malaria-afflicted and malaria-free areas are often found close to each other.[127] 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.[128] In drier areas, outbreaks of malaria have been predicted with reasonable accuracy by mapping rainfall.[129] 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.[130] In contrast, malaria in Africa is present in both rural and urban areas, though the risk is lower in the larger cities.[131]

History

Ancient malaria oocysts preserved in Dominican amber

Although the parasite responsible for P. falciparum malaria has been in existence for 50,000–100,000 years, the population size of the parasite did not increase until about 10,000 years ago, concurrently with advances in agriculture[132] and the development of human settlements. Close relatives of the human malaria parasites remain common in chimpanzees. Some evidence suggests that the P. falciparum malaria may have originated in gorillas.[133]

References to the unique periodic fevers of malaria are found throughout recorded history.[134] Hippocrates described periodic fevers, labelling them tertian, quartan, subtertian and quotidian.[135] The Roman Columella associated the disease with insects from swamps.[135] Malaria may have contributed to the decline of the Roman Empire,[136] and was so pervasive in Rome that it was known as the “Roman fever“.[137] Several regions in ancient Rome were considered at-risk for the disease because of the favourable conditions present for malaria vectors. This included areas such as southern Italy, the island of Sardinia, the Pontine Marshes, the lower regions of coastal Etruria and the city of Rome along the Tiber River. The presence of stagnant water in these places was preferred by mosquitoes for breeding grounds. Irrigated gardens, swamp-like grounds, runoff from agriculture, and drainage problems from road construction led to the increase of standing water.[138]

Additional educational resources

Willcox ML, Bodeker G, Rasoanaivo P. Traditional medicinal plants and malaria. Boca Raton: CRC, 2004—book contains detailed systematic reviews and guidelines for further studies in malaria control

The Research Initiative on Traditional Antimalarial Methods (www.who.int/tdr/publications/publications/ritam.htm)—features a report of the inaugural meeting of RITAM

World Health Organization Essential Drugs and Medicine Policy (www.who.int/medicines/organization/trm/orgtrmmain.shtml)—details WHO Traditional Medicine Strategy 2002-5

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