Antimalarial medication
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Antimalarial medications or simply antimalarials are a type of
Specifically, antimalarial drugs may be used to treat malaria in three categories of individuals, (i) those with suspected or confirmed infection, (ii) those visiting a malaria-endemic regions who have no immunity, to prevent infection via malaria prophylaxis, and (iii) or in broader groups of individuals, in routine but intermittent preventative treatment in regions where malaria is endemic via intermittent preventive therapy.[not verified in body] Practice in treating cases of malaria is most often based on the concept of combination therapy[verification needed] (e.g., using agents such as artemether and lumefantrine against chloroquine-resistant Plasmodium falciparum infection[verification needed][4]), since this offers advantages including reduced risk of treatment failure, reduced risk of developed resistance, as well as the possibility of reduced side-effects.[not verified in body] Prompt parasitological confirmation by microscopy, or alternatively by rapid diagnostic tests, is recommended in all patients suspected of malaria before treatment is started.[5][page needed] Treatment solely on the basis of clinical suspicion is considered when a parasitological diagnosis is not possible.[5][page needed]
Anti-malaria aid campaigns have a globally positive impact for health outcomes and beyond.[6]
Medications
It is practical to consider antimalarials by chemical structure since this is associated with important properties of each drug, such as mechanism of action.[citation needed]
This section needs additional citations for verification. (March 2020) |
The treatment regimen of quinine is complex and is determined largely by the parasite's level of resistance and the reason for drug therapy (i.e. acute treatment or prophylaxis). The
Use of quinine is characterised by a frequently experienced syndrome called
Chloroquine
Chloroquine was, until recently, the most widely used anti-malarial. It was the original prototype from which most methods of treatment are derived. It is also the least expensive, best tested and safest of all available drugs. The emergence of drug-resistant parasitic strains is rapidly decreasing its effectiveness; however, it is still the first-line drug of choice in most sub-Saharan African countries. It is now suggested that it is used in combination with other antimalarial drugs to extend its effective usage. Popular drugs based on chloroquine phosphate (also called nivaquine) are Chloroquine FNA, Resochin and Dawaquin.
Chloroquine is a
Children and adults should receive 25 mg of chloroquine per kg given over three days. A
Hydroxychloroquine
Hydroxychloroquine was derived in the 1950s by adding a hydroxy group to existing Chloroquine, making it more tolerable than Chloroquine by itself.[8][9][10]
Amodiaquine
The drug should be given in doses between 25 mg/kg and 35 mg/kg over three days in a similar method to that used in chloroquine administration. Adverse reactions are generally similar in severity and type to that seen in chloroquine treatment.
Pyrimethamine
Pyrimethamine is used in the treatment of uncomplicated malaria. It is particularly useful in cases of chloroquine-resistant P. falciparum strains when combined with sulfadoxine.[12] It acts by inhibiting dihydrofolate reductase in the parasite thus preventing the biosynthesis of purines and pyrimidines, thereby halting the processes of DNA replication, cell division and reproduction. It acts primarily on the schizonts during the erythrocytic phase, and nowadays is only used in concert with a sulfonamide[12]
Proguanil
Sulfonamides
Sulfonamides are not recommended for chemoprophylaxis because of rare but severe skin reactions experienced. However it is used frequently for clinical episodes of the disease.
Mefloquine
This section needs additional citations for verification. (March 2020) |
The major commercial manufacturer of mefloquine-based malaria treatment is Roche Pharmaceuticals, which markets the drug under the trade name "
A dose of 15–25 mg/kg is recommended, depending on the prevalence of mefloquine resistance. The increased dosage is associated with a much greater level of intolerance, most noticeably in young children; with the drug inducing vomiting and
Mefloquine can only be taken for a period up to six months due to side effects. After this, other drugs (such as those based on paludrine/nivaquine) again need to be taken.[14][medical citation needed]
Atovaquone
Primaquine
This section needs additional citations for verification. (March 2020) |
Primaquine is a highly active 8-aminoquinolone that is effective against P. falcipraum gametocytes but also acts on merozoites in the bloodstream and on hypnozoites, the dormant hepatic forms of P. vivax and P. ovale.[15] It is the only known drug to cure both relapsing malaria infections and acute cases. The mechanism of action is not fully understood but it is thought to block oxidative metabolism in Plasmodia. It can also be combined with methylene blue.[16]
For the prevention of relapse in P. vivax and P. ovale 0.15 mg/kg should be given for 14 days. As a gametocytocidal drug in P. falciparum infections a single dose of 0.75 mg/kg repeated seven days later is sufficient. This treatment method is only used in conjunction with another effective blood schizonticidal drug. There are few significant side effects although it has been shown that primaquine may cause
Artemisinin and derivatives
This section needs additional citations for verification. (March 2020) |
- drug fever have been reported by a small number of patients.[citation needed] Some cardiac changes were reported during a clinical trial, notably non specific ST changes and a first degree atrioventricular block (these disappeared when the patients recovered from the malarial fever).[citation needed]
- Artemether is a methyl ether derivative of dihydroartemesinin. It is similar to artemesinin in mode of action but demonstrates a reduced ability as a hypnozoiticidal compound, instead acting more significantly to decrease gametocyte carriage. Similar restrictions are in place, as with artemesinin, to prevent the development of resistance, therefore it is only used in combination therapy for severe acute cases of drug-resistant P. falciparum. It should be administered in a 7-day course with 4 mg/kg given per day for three days, followed by 1.6 mg/kg for three days. Side effects of the drug are few but include potential neurotoxicity developing if high doses are given.[citation needed]
- Artesunate is a hemisuccinate derivative of the active metabolite dihydroartemisin. Currently[when?] it is the most frequently used of all the artemesinin-type drugs. Its only effect is mediated through a reduction in the gametocyte transmission. It is used in combination therapy and is effective in cases of uncomplicated P. falciparum. The dosage recommended by the WHO is a five or seven day course (depending on the predicted adherence level) of 4 mg/kg for three days (usually given in combination with mefloquine) followed by 2 mg/kg for the remaining two or four days. In large studies carried out on over 10,000 patients in Thailand no adverse effects have been shown.[citation needed]
- Dihydroartemisinin is the active metabolite to which artemesinin is reduced. It is the most effective artemesinin compound and the least stable. It has a strong blood schizonticidal action and reduces gametocyte transmission. It is used for therapeutic treatment of cases of resistant and uncomplicated P. falciparum. 4 mg/kg doses are recommended on the first day of therapy followed by 2 mg/kg for six days. As with artesunate, no side effects to treatment have thus far been recorded.[citation needed]
- ethyl ether derivative of dihydroartemisinin. It is used in combination therapy for cases of uncomplicated resistant P. falciparum. The recommended dosage is 150 mg/kg per day for three days given by IM injections. With the exception of a small number of cases demonstrating neurotoxicity following parenteral administration no side effects have been recorded.[citation needed]
Halofantrine
A dose of 8 mg/kg of halofantrine is advised to be given in three doses at six-hour intervals for the duration of the clinical episode. It is not recommended for children under 10 kg despite data supporting the use and demonstrating that it is well tolerated. The most frequently experienced side-effects include nausea, abdominal pain, diarrhea, and itch. Severe
Lumefantrine
Lumefantrine is a relative of halofantrine that is used in some combination antimalarial regimens.[20]
Doxycycline
Probably one of the more prevalent antimalarial drugs prescribed, due to its relative effectiveness and cheapness,
When treating acute cases and given in combination with quinine; 100 mg of doxycycline should be given per day for seven days. In prophylactic therapy, 100 mg (adult dose) of doxycycline should be given every day during exposure to malaria.
The most commonly experienced side effects are permanent enamel hypoplasia (although this is only relevant during the period of tooth development during the first decade of life), transient depression of bone growth, gastrointestinal disturbances and some increased levels of photosensitivity. Due to its effect of bone and tooth growth it is not used in children under 8, pregnant or lactating women and those with a known hepatic dysfunction.
Tetracycline is only used in combination for the treatment of acute cases of P. falciparum infections. This is due to its slow onset. Unlike doxycycline it is not used in chemoprophylaxis. For tetracycline, 250 mg is the recommended adult dosage (it should not be used in children) for five or seven days depending on the level of adherence and compliance expected. Oesophageal ulceration, gastrointestinal upset and interferences with the process of ossification and depression of bone growth are known to occur. The majority of side effects associated with doxycycline are also experienced.
Clindamycin
Clindamycin is a derivative of lincomycin, with a slow action against blood schizonticides. It is only used in combination with quinine in the treatment of acute cases of resistant P. falciparum infections and not as a prophylactic. Being more toxic than the other antibiotic alternatives, it is used only in cases where the Tetracyclines are contraindicated (for example in children).
Clindamycin should be given in conjunction with quinine as a 300 mg dose (in adults) four times a day for five days. The only side effects recorded in patients taking clindamycin are nausea, vomiting and abdominal pains and cramps. However these can be alleviated by consuming large quantities of water and food when taking the drug.
Resistance
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Anti-malarial drug resistance has been defined as: "the ability of a parasite to survive and/or multiply despite the administration and absorption of a drug given in doses equal to or higher than those usually recommended but within tolerance of the subject. The drug in question must gain access to the parasite or the infected red blood cell for the duration of the time necessary for its normal action."[21] Resistance to antimalarial drugs is common.[22]
In most instances this refers to parasites that remain following on from an observed treatment; thus, it excludes all cases where anti-malarial prophylaxis has failed.[
Drug resistant parasites are often used to explain malaria treatment failure. However, they are two potentially very different clinical scenarios. The failure to clear parasitemia and recover from an acute clinical episode when a suitable treatment has been given is anti-malarial resistance in its true form. Drug resistance may lead to treatment failure, but treatment failure is not necessarily caused by drug resistance despite assisting with its development. A multitude of factors can be involved in the processes including problems with non-compliance and adherence, poor drug quality, interactions with other pharmaceuticals, poor absorption, misdiagnosis and incorrect doses being given. The majority of these factors also contribute to the development of drug resistance.
The generation of resistance can be complicated and varies between Plasmodium species. It is generally accepted to be initiated primarily through a
The first type of resistance to be acknowledged was to chloroquine in Thailand in 1957. The biological mechanism behind this resistance was subsequently discovered to be related to the development of an efflux mechanism that expels chloroquine from the parasite before the level required to effectively inhibit the process of haem polymerization (that is necessary to prevent buildup of the toxic byproducts formed by haemoglobin digestion). This theory has been supported by evidence showing that resistance can be effectively reversed on the addition of substances which halt the efflux. The resistance of other quinolone anti-malarials such as amodiaquine, mefloquine, halofantrine and quinine are thought to have occurred by similar mechanisms.
Plasmodium have developed resistance against antifolate combination drugs, the most commonly used being sulfadoxine and pyrimethamine. Two gene mutations are thought to be responsible, allowing synergistic blockages of two enzymes involved in folate synthesis. Regional variations of specific mutations give differing levels of resistance.
Atovaquone is recommended to be used only in combination with another anti-malarial compound as the selection of resistant parasites occurs very quickly when used in mono-therapy. Resistance is thought to originate from a single-point mutation in the gene coding for cytochrome-b.
Spread of resistance
There is no single factor that confers the greatest degree of influence on the spread of drug resistance, but a number of plausible causes associated with an increase have been acknowledged. These include aspects of economics, human behaviour, pharmacokinetics, and the biology of
The most influential causes are examined below:
- The biological influences are based on the parasites ability to survive the presence of an anti-malarial thus enabling the persistence of resistance and the potential for further transmission despite treatment. In normal circumstances any parasites that persist after treatment are destroyed by the host's immune system, therefore any factors that act to reduce the elimination of parasites could facilitate the development of resistance. This attempts to explain the poorer response associated with immunocompromisedindividuals, pregnant women and young children.
- There has been evidence to suggest that certain parasite-vector combinations can alternatively enhance or inhibit the transmission of resistant parasites, causing 'pocket-like' areas of resistance.
- The use of anti-malarials developed from similar basic chemical compounds can increase the rate of resistance development, for example cross-resistance to chloroquine and amodiaquine, two 4-aminoquinolones and mefloquine conferring resistance to quinine and halofantrine. This phenomenon may reduce the usefulness of newly developed therapies prior to large-scale usage.
- The resistance to anti-malarials may be increased by a process found in some species of Plasmodium, where a degree of phenotypic plasticity was exhibited, allowing the rapid development of resistance to a new drug, even if the drug has not been previously experienced.
- The pharmacokinetics of the chosen anti-malarial are key; the decision of choosing a long half-life over a drug that is metabolised quickly is complex and still remains unclear. Drugs with shorter half-life's require more frequent administration to maintain the correct plasma concentrations, therefore potentially presenting more problems if levels of adherence and compliance are unreliable, but longer-lasting drugs can increase the development of resistance due to prolonged periods of low drug concentration.
- The pharmacokinetics of anti-malarials is important when using combination therapy. Mismatched drug combinations, for example having an 'unprotected' period where one drug dominates can seriously increase the likelihood of selection for resistant parasites.
- Ecologically there is a linkage between the level of transmission and the development of resistance, however at present this still remains unclear.
- The treatment regime prescribed can have a substantial influence on the development of resistance. This can involve the drug intake, combination and interactions as well as the drug's pharmacokinetic and dynamic properties.
Prevention
The prevention of anti-malarial drug resistance is of enormous public health importance. It can be assumed that no therapy currently[when?] under development or to be developed in the foreseeable future will be totally protective against malaria. In accordance with this, there is the possibility of resistance developing to any given therapy that is developed. This is a serious concern, as the rate at which new drugs are produced by no means matches the rate of the development of resistance. In addition, the most newly developed therapeutics tend to be the most expensive and are required in the largest quantities by some of the poorest areas of the world. Therefore, it is apparent that the degree to which malaria can be controlled depends on the careful use of the existing drugs to limit, insofar as it is possible, any further development of resistance.
Provisions essential to this process include the delivery of fast primary care where staff are well trained and supported with the necessary supplies for efficient treatment. This in itself is inadequate in large areas where malaria is endemic thus presenting an initial problem. One method proposed that aims to avoid the fundamental lack in certain countries' health care infrastructure is the privatisation of some areas, thus enabling drugs to be purchased on the open market from sources that are not officially related to the health care industry. Although this is now gaining some support there are many problems related to limited access and improper drug use, which could potentially increase the rate of resistance development to an even greater extent.
There are two general approaches to preventing the spread of resistance: preventing malaria infections, and preventing the transmission of resistant parasites.
Preventing malaria infections developing has a substantial effect on the potential rate of development of resistance, by directly reducing the number of cases of malaria thus decreasing the need for anti-malarial therapy. Preventing the transmission of resistant parasites limits the risk of resistant malarial infections becoming endemic and can be controlled by a variety of non-medical methods including
A hope for future of anti-malarial therapy is the development of an effective malaria vaccine. This could have enormous public health benefits, providing a cost-effective and easily applicable approach to preventing not only the onset of malaria but the transmission of gametocytes, thus reducing the risk of resistance developing. Anti-malarial therapy also could be diversified by combining a potentially effective vaccine with current[when?] chemotherapy, thereby reducing the chance of vaccine resistance developing.
Combination therapy
The problem of the development of malaria resistance must be weighed against the essential goal of anti-malarial care; that is to reduce
The combinations of drugs currently[when?] prescribed can be divided into two categories: non-artemesinin-based combinations and artemesinin based combinations. It is also important to distinguish fixed-dose combination therapies (in which two or more drugs are co-formulated into a single tablet) from combinations achieved by taking two separate antimalarials.
Non-artemisinin based combinations
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Components | Description | Dose |
---|---|---|
Sulfadoxine-pyrimethamine (SP) (Fansidar) | This fixed-dose combination has been used for many years, causes few adverse effects, is cheap and effective in a single dose, thus decreasing problems associated with adherence and compliance. In technical terms Fansidar is not generally considered a true combination therapy since the components do not possess independent curative activity.[5][page needed] Fansidar should no longer be used alone for treatment of falciparum malaria. | 25 mg/kg of sulfadoxine and 1.25 mg/kg of pyrimethamine. |
SP plus chloroquine | High levels of resistance to one or both components means this combination is effective in few locations and it is not recommended by the World Health Organization (WHO).[5][page needed] | Chloroquine 25 mg/kg over three days with a single dose of SP as described above. |
SP plus amodiaquine | This combination has been shown to produce a faster rate of clinical recovery than SP and chloroquine, but is clearly inferior to artemisinin-based combinations (ACTs) for the treatment of malaria.[5][page needed] | 10 mg/kg of Amodiaquine per day for three days with a single standard dose of SP. |
SP plus mefloquine (Fansimef) | This single dose pill offered obvious advantages of convenience over more complex regimes but it has not been recommended for use for many years owing to widespread resistance to the components. | |
Quinine plus tetracycline/doxycycline | This combination retains a high cure rate in many areas. Problems with this regime include the relatively complicated drug regimen, where quinine must be taken every eight hours for seven days. Additionally, there are significant side effects with quinine ('cinchonism') and tetracyclines are contraindicated in children and pregnant women (these groups should use clindamycin instead). With the advent of artemisinin-combination therapies, quinine-based treatment is less popular than previously. | Quinine 10 mg/kg doses every eight hours and tetracycline in 4 mg/kg doses every six hours for seven days. |
Artemisinin-based combination therapies should be used in preference to amodiaquine plus sulfadoxine-pyrimethamine for the treatment of uncomplicated P. falciparum malaria.[5][page needed]
Artemisinin-based combination therapies (ACTs)
Artemesinin has a very different mode of action than conventional anti-malarials (see information above), which makes it particularly useful in the treatment of resistant infections. However, to prevent the development of resistance to this drug it is only recommended in combination with another non-artemesinin based therapy. It produces a very rapid reduction in the parasite biomass with an associated reduction in clinical symptoms and is known to cause a reduction in the transmission of gametocytes thus decreasing the potential for the spread of resistant alleles. At present there is no known resistance to Artemesinin (though some resistant strains may be emerging)[24] and very few reported side-effects to drug usage, however this data is limited.
Components | Description | Dose |
---|---|---|
Artesunate and ASAQ )
|
This combination has been tested and proved to be efficacious in many areas where amodiaquine retains some efficacy. A potential disadvantage is a suggested link with neutropenia. It's recommended by the WHO for uncomplicated falciparum malaria.[5][page needed] | Dosage is as a fixed-dose combination ( ASAQ ) recommended as 4 mg/kg of Artesunate and 10 mg/kg of Amodiaquine per day for three days.
|
Artesunate and mefloquine (Artequin or ASMQ) | This has been used as an efficacious first-line treatment regimen in areas of Thailand for many years. Mefloquine is known to cause vomiting in children and induces some neuropsychiatric and cardiotoxic effects. These adverse reactions seem to be reduced when the drug is combined with artesunate, it is suggested that this is due to a delayed onset of action of mefloquine. This is not considered a viable option to be introduced in Africa due to the long half-life of mefloquine, which potentially could exert a high selection pressure on parasites. It's recommended by the WHO for uncomplicated falciparum malaria.[5][page needed] | The standard dose required is 4 mg/kg per day of Artesunate plus 25 mg/kg of Mefloquine as a split dose of 15 mg/kg on day two and 10 mg/kg on day three. |
Artemether and Coartem Riamet, Faverid, Amatem, Lonart or AL)
|
This combination has been extensively tested in 16 clinical trials, proving effective in children under five and has been shown to be better tolerated than artesunate plus mefloquine combinations. There are no serious side effects documented but the drug is not recommended in pregnant or lactating women due to limited safety testing in these groups. This is the most viable option for widespread use and is available in fixed-dose formulas thus increasing compliance and adherence. It's recommended by the WHO for uncomplicated falciparum malaria.[5][page needed] | |
Artesunate and sulfadoxine/pyrimethamine (Ariplus or Amalar plus) | This is a well tolerated combination but the overall level of efficacy still depends on the level of resistance to sulfadoxine and pyrimethamine thus limiting is usage. It is recommended by the WHO for uncomplicated falciparum malaria.[5][page needed] | It is recommended in doses of 4 mg/kg of Artesunate per day for three days and a single dose of 25 mg/kg of SP. |
Dihydroartemisinin-piperaquine (Duo-Cotecxin, or Artekin) | Has been studied mainly in China, Vietnam and other countries in SEAsia. The drug has been shown to be highly efficacious (greater than 90%). It's recommended by the WHO for uncomplicated falciparum malaria.[5][page needed] | |
Artesinin/piperaguine/primaquine (Fast Elimination of Malaria through Source Eradication (FEMSE)) | This protocol involves three doses of Artequick, spaced a month apart. The first dose is accompanied by one of primaquine. An experimental program in the Comoros islands employed the protocol. At the outset, more than 90% of the inhabitants of some villages had malaria. On one island the number of cases fell by 95%. In 2012, on the second island, the number of cases fell by 97%.[25] | |
Pyronaridine and artesunate (Pyramax) | Pyramax developed by Shin Poong Pharmaceutical and Medicines for Malaria Venture (MMV). This is a first fixed-dose artemisinin-based combination therapy to be granted a positive scientific opinion for efficacy, safety and quality from European Medicines Agency (EMA) under Article 58 for the treatment of P. falciparum and P. vivax in adults and children over 20 kg based on five multi-centre phase III trials conducted in Africa and South-East Asia. Pyramax has been shown to be highly efficacious (greater than 97%) in both species and only ACT approved by stringent regulatory authority for treatment of both P. falciparum and P vivax by now. |
Other combinations
Several other anti-malarial combinations have been used or are in development. For example, Chlorproguanil-dapsone and artesunate appeared efficacious in trials from the late 90s and 2000s, but the problem of haemolysis in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency is likely to prevent widespread use.[26]
By type of malaria
Antimalarial drugs and combinations may also be sorted according to the type of malaria in which they are used.
Falciparum malaria
Artemisinin-based combination therapies (ACTs) are the recommended antimalarial treatments for uncomplicated malaria caused by
In severe falciparum malaria, it is recommended that rapid clinical assessment and confirmation of the diagnosis is made, followed by administration of full doses of parenteral antimalarial treatment without delay with whichever effective antimalarial is first available.
- an ACT
- artesunate plus clindamycin or doxycycline;
- quinine plus clindamycin or doxycycline.
Vivax malaria
Malaria in poultry
No medications are approved in the United States for treatment of malaria in poultry.[27]
See also
- antiplasmodialproperties
- Malaria prophylaxis
- Medicines for Malaria Venture (MMV)– a not-for-profit organization which is managing the largest–ever portfolio of over 50 antimalarial projects in collaboration with over 100 pharmaceutical, academic, and endemic-country partners in 38 countries.
- Amazon Malaria Initiative – a regional USAID project in 11 countries in the Latin America and the Caribbean region.
- RAVREDA – a regional network of national malaria control programs that conduct antimalarial drug efficacy surveillance and other activities to address malaria.
- Project 523
References
- ^ PMID 29802605.
- ISBN 978-1-4557-0737-9.
- ^ "Updating the WHO G6PD classification of variants and the International Classification of Diseases" (PDF). www.who.int. 2019. Retrieved 2020-03-24.
- ^ Prevention, CDC-Centers for Disease Control and (2023-06-28). "CDC - Malaria - Diagnosis & Treatment (United States) - Treatment (U.S.) - Guidelines for Clinicians (Part 1)". www.cdc.gov. Retrieved 2023-09-12.
- ^ ISBN 978-92-4-154912-7.
- .
- ^ Sparkes, Roland. Article, www.belmonthistory.org.uk [1] Archived 2022-08-06 at the Wayback Machine, retrieved 2010-01-05[full citation needed]
- ^ "Fact check: Hydroxychloroquine is not the same as quinine and can't be made at home". Reuters. 31 May 2020.
- ^ "New preparation of hydroxychloroquine".
- ^ "Preparation method of hydroxychloroquine sulfate".
- ^ ISBN 978-0-08-055232-3, retrieved 2023-08-04
- ^ a b "Pyrimethamine". go.drugbank.com. Retrieved 2023-08-04.
- ^ a b "Proguanil". go.drugbank.com. Retrieved 2023-08-04.
- ISBN 978-90-389-2055-9.
- S2CID 206250162.
- PMID 29422384.
- ^ "Rectal artemisinins rapidly eliminate malarial parasites". EurekAlert!. 2008-03-27. Archived from the original on 3 April 2008. Retrieved 2008-03-28.
- ^ "The History of Traditional Chinese Medicine". Archived from the original on 25 December 2007. Retrieved 2007-12-19.
- ^ "Using Artemisia annua L. tea to fight malaria" (PDF). November 13, 2008. Archived from the original (PDF) on 2008-11-13.
- PMID 9449273.
- ISBN 9783709113264.
- PMID 15085184.
- PMID 26998432.
- PMID 19138391.
- ^ "Malaria eradication: Cure all?". The Economist. 2014-01-25. Retrieved 2014-02-16.
- PMID 19690618.
- ^ Wettere, Arnaud J. Van (2020-02-25). "Plasmodium Infection in Poultry - Poultry". Merck Veterinary Manual. Retrieved 2022-07-21.
Further reading
- World Health Organization (2015). Guidelines for the treatment of malaria (Third ed.). ISBN 978-92-4-154912-7.
- World Health Organization (2012). Management of severe malaria: a practical handbook (Third ed.). ISBN 978-92-4-154852-6.
External links
- Medicines for Malaria Venture (MMV) [MMV] " MMV Science " – for information on the largest–ever portfolio of over 50 antimalarial projects, working in collaboration with over 100 pharmaceutical, academic, and endemic-country partners in 38 countries.
- The Worldwide Antimalarial Resistance Network (WWARN) is a global collaboration generating quality-assured, timely information to track the emergence and spread of antimalarial resistance — critical information for ensuring that anyone infected with malaria receives safe and effective treatment.
- 2007 guidelines are available from the UK Health Protection Agency Archived 2013-09-28 at the Wayback Machine website as a PDF file and includes detailed country-specific information for UK travelers.
- The World Health Organization provides country-specific advice on malaria prevention. HPA and WHO advice are broadly in line with each other (although there are some differences).
- The Centers for Disease Control and Prevention website hosts constantly updated country-specific information on malaria. The advice on this website is less detailed, is very cautious and may not be appropriate for all areas within a given country. This is the preferred site for travelers from the US.