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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

At present, in countries of tropical Africa, chemotherapy is the main and often the only operationally, administratively, and financially feasible method of malaria control. This applies particularly in rural areas. This article reviews experience with chemotherapy in Africa since the late 1940s with mepacrine, proguanil, pyrimethamine, chloroquine, amodiaquine, and sulfones and sulfonamides in combination with dihydrofolate reductase inhibitors. Chloroquine has proved to be the most effective compound and it is the drug of choice as long as malarial parasites remain susceptible to it. Because of reports from East Africa of strains of Plasmodium falciparum resistant to 4-aminoquinolines, it is essential that national and regional policies be developed for the rational use of antimalarials.In most of the countries, the scope of activities is still limited to the administration of antimalarial drugs to sick persons through a limited network of health institutions. In some countries, however, attempts have been made to extend the coverage of drug administration by involving voluntary collaborators or through the provision of suppressive treatment to vulnerable groups of the population (such as infants, young children, pregnant women, nursing mothers, and schoolchildren) but the efficacy of such methods depends on the degree of involvement of voluntary collaborators, primary health workers, and communities.
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PMID:Use of drugs for malaria control in tropical Africa. 31 34

Chloroquine resistance has arisen in both human and murine forms of malaria. CR Plasmodium berghei in mice does not produce the malaria pigment which is characteristic of the CS form. Determinations of carbon monoxide production (i.e., host heme catabolism) by individual mice revealed that those infected with CS P. berghei produce only one fourth as much carbon monoxide as do CR infected mice at all levels of infection. These observations confirm the idea that malaria pigment is composed of precipitated host cell hemoglobin and suggest that drug resistance is accompanied by a basic alteration in parasite-mediated hemoglobin catabolism.
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PMID:Host heme catabolism in drug-sensitive and drug-resistant malaria. 33 45

Physicians should be prepared to provide prophylactic medications for travelers to malarious areas and to treat patients with malaria. Chloroquine hydrochloride is the suppressive agent of choice for treatment of mild infections due to all species of malaria except for those due to chloroquine-resistant strains of Plasmodium falciparum. For treatment of severe infections with P falciparum and for treatment of all infections due to chloroquine-resistant strains of P falciparum quinine is the suppressive agent of choice. Chloroquine is also the prophylactic agent of choice for most travelers. To prevent infection with P vivax or P ovale, primaquine must also be given. A RBC glucose-6-phosphate dehydrogenase level should be obtained before administration of primaquine. For prophylaxis of chloroquine-resistant strains of P falciparum, no completely satisfactory regime is presently available in the United States.
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PMID:Carl Jung. 35 49

Physicians should be prepared to provide prophylactic medications for travelers to malarious areas and to treat patients with malaria. Chloroquine hydrochloride is the suppressive agent of choice for treatment of mild infections due to all species of malaria except for those due to chloroquine-resistant strains of Plasmodium falciparum. For treatment of severe infections with P falficparum, quinine is the suppressive agent of choice. Chloroquine is also the prophylactic agent of choice for most travelers. To prevent infection with P vivax or P ovale, primaquine must also be given. A RBC glucose-6-phosphate dehydrogenase level should be obtained before administration of primaquine. For prophylaxis of chloroquine-resistant strains of P falciparum, no completely satisfactory regimen is presently available in the United States.
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PMID:Therapy and prophylaxis of malaria. 35 50

The process of mefloquine accumulation was studied in mouse erythrocytes infected with either Plasmodium berghei CS (chloroquine susceptible) or P. berghei CR (chloroquine resistant). In both cases, mefloquine was accumulated by a saturable process with an apparent dissociation constant of 2.5 x 10(-6) M and an apparent maximal capacity of 700 mumol per kg of erythrocyte pellet; uninfected mouse erythrocytes accumulated more than half as much mefloquine as infected erythrocytes. The process of accumulation was not stimulated by providing glucose as a substrate, and it was not inhibited in infected erythrocytes by azide, iodoacetate, or incubation at 2 degrees C. Although mefloquine was accumulated more effectively than chloroquine by uninfected erythrocytes and by erythrocytes infected with P. berghei CR, competition between chloroquine and mefloquine was observed, raising the possibility that the same process of accumulation serves both drugs. Chloroquine competitively inhibits mefloquine accumulation, with an apparent inhibitor constant of 1.7 x 10(-3) M, and mefloquine competitively inhibits chloroquine accumulation, with an apparent inhibitor constant of 2 x 10(-6) M. The same process of accumulation and the same group of receptors could serve both drugs if mefloquine has greater access than chloroquine to the receptors. Regardless of whether the same process serves both drugs, undiminished accumulation by erythrocytes infected with P. berghei CR provides an explanation for the superiority of mefloquine in treating chloroquine-resistant malaria.
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PMID:Chloroquine resistance in malaria: accessibility of drug receptors to mefloquine. 37 44

The effect of pyrimethamine and the combination of pyrimethamine-sulfadoxine (Fansidar) upon the termination of the acute attack of vivax malaria was studied in Thailand. Pyrimethamine was found to be ineffective, providing clearance of parasitaemia in only two of six patients by the end of seven days following treatment. The combination, administered in a two-tablet single dose (sulfadoxine 1 gm, pyrimethamine 50 mg) eliminated parasitaemia in only six of ten patients within seven days. Three tablets (sulfadoxine 1 . 5 gm, pyrimethamine 75 mg) given to 11 patients, provided clearance of parasitaemia in all within seven days; however, mean parasite and fever clearance times in this group were prolonged at 90 and 50 hours respectively. Chloroquine remains the drug of choice for the termination of the acute attack of vivax malaria. Subsequent primaquine is necessary for the prevention of relapse.
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PMID:Treatment of vivax malaria with sulfadoxine-pyrimethamine and with pyrimethamine alone. 37 85

A review of chloroquine and sulfa-antifol combination treated falciparum malaria patients revealed a high incidence of chloroquine-resistance, wither R1 or R2, in patients infected in Southeast Asia or Oceania. In addition, more than one tenth of the patients infected in Laos or Thailand were resistant to sulfa-antifol combinations. Chloroquine-resistant cases were sensitive to sulfa-antifol combinations. On the other hand, while all patients treated in Tokyo who had been infected in Africa or Sri Lanka were sensitive to chloroquine, a field study suggested the presence of chloroquine-resistant P. falciparum in the area near Kaduna, Nigeria. One patient infected in Nigeria showed partial resistance to the MP (sulfamonomethoxine-pyrimethamine) combination, and another patient infected in the Central African Empire showed resistance to the MP combination, increasing from R1 to R3 within a short period. The incidence of resistance to sulfa-antifol combination therapy was high in the West African tropical region. The continent, county and area of infection should be taken in consideration when selecting antimalarial drug(s) for the treatment and suppression of falciparum malaria.
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PMID:Chemotherapy of falciparum malaria: regional differences in responsiveness to treatment. 39 91

Chloroquine is considered essentially nontoxic when used for the chemosuppression of malaria, but gastrointestinal upsets, headache, blurring of vision, pruritus, and uritcaria may occur during chloroquine therapy. Recently, Bhargava et al. and Eronini and Eronini have reported the extrapyramidal syndrome (EPS) following chloroquine therapy in adults. The clinical manifestations included upward rolling of the eyeballs, retraction of neck and back, trismus with marked difficulty in speech, and coarse tremors. Observations of 4 instances of EPS in children following chloroquine therapy for malaria are reported. A 2-1/2 year old girl was admitted to the All India Institute of Medical Sciences Hospital with a 4 day history of intermittent high grade pyrexia with chills and rigors. Following treatment with oral chloroquine in the recommended therapeutic dosage, the fever responded, but the child became drowsy and developed paroxysms of involuntary movements of the tongue, torticollis, torsion dystonia of the limbs, and parosysms of tonic muscular spasms. She completely recovered spontaneously within 48 hours. The 2nd case was that of a 12-year old female brought to the hospital with a 15-day history of intermittent high grade fever with chills and rigors. The patient was started on chloroquine sulfate in the recommended therapeutic dose. After an interval of 4 days she developed coarse tremors of the hands, upward rolling of the eyeballs, episodic deviation of the angle of the mouth towards the left, and trismus. These symptoms disappeared spontaneously within 8 hours. A 6-year old girl, the 3rd case, developed episodes of opisthotonous, upward rolling of the eyeballs, protrusions of the tongue, intermittent writhing movements of the upper limbs, and drowsiness following the ingestion of 6 tablets of chloroquine sulfate for suspected diagnosis of malaria. She spontaneously recovered from EPS over a period of about 48 hours. The 4th case, a 7-year old boy, gave a history of high grade fever with chills and rigors of 1 day's duration. He developed drowsiness, tonic spasms of the neck, upward rolling of the eyeballs, and writhing contortions of all limbs about 2 hours following intravenous administration of 100 mg of chloroquine. 8 hours later an additional 100 mg chloroquine was given intravenously for the mistaken diagnosis of cerebral malaria. On examination the child was drowsy, had generalized stiffness, torticollis, and trismus. He recovered gradually over a 48-hour period without any specific therapy. The exact mechanism of production of EPS remains uncertain.
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PMID:Extrapyramidal syndrome following chloroquine therapy. 45 22

In cases of severe malaria chloroquine phosphate is frequently given--diluted or undiluted--by the intravenous route. It is known that cardiac arrhythmias and hypotension may complicate such therapy, but cardiac arrest is not a well recognised hazard. In this report we describe such a tragic complication, and advocate that undiluted chloroquine should not be administered intravenously in severely ill patients since such patients usually have associated electrolyte disturbances which may render the heart vulnerable to toxic drugs. Chloroquine may be given diluted in normal saline infused over several hours with a close watch over the blood pressure.
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PMID:Cardiac arrest after intravenous chloroquine injection. 45 5

Imported malaria has been increasing in the United States. Locally acquired cases are reported in drug addicts. Extended incubation periods can be misleading. Pyrexia is the most common manifestation, but it may not follow a regular pattern. A high index of suspicion and examination of peripheral blood smears establish the diagnosis. Chloroquine and primaquine are the drugs of choice for uncomplicated malaria; quinine sulfate is preferred in the treatment of chloroquine-resistant malaria. Malarial prophylaxis should include travelers' education and chemoprophylactic agents such as chloroquine, chloroguanide, pyrimethamine and amodiaquine.
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PMID:Malaria--a red alert. 46 29


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