Long-term, individual-based field studies, the application of genetic techniques, and phylogenetic reconstructions have led to substantial advances in our understanding of the diversity and evolution of mammalian breeding systems and their consequences. These studies show how differences in ecology, life histories, and phylogeny affect the distributions of breeding females and breeding males; how the distributions of both sexes affect the evolution of breeding systems and the composition and kinship structure of social groups; how differences in breeding systems and the social environment that individuals encounter affect the selection pressures operating on both sexes and the evolution of their behavior, physiology, and morphology; and how these differences affect the demography and dynamics of populations and their responses to variation in density, climate, and human impact.
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Increasing drug resistance in Plasmodium falciparum and a resurgence of malaria in tropical areas have effected a change in treatment of malaria in the last two decades. Symptoms of malaria are fever, chills, headache, and malaise. The prognosis worsens as the parasite counts, counts of mature parasites, and counts of neutrophils containing pigment increase. Treatment depends on severity, age of patient, degree of background immunity, likely pattern of susceptibility to antimalarial drugs, and the cost and availability of drugs. Chloroquine should be used for P. vivax, P. malariae, and P. ovale. P. vivax has shown high resistance to chloroquine in Oceania, however. Primaquine may be needed to treat P. vivax and P. ovale to rid the body of hypnozoites that survive in the liver. Chloroquine can treat P. falciparum infections acquired in North Africa, Central America north of the Panama Canal, Haiti, or the Middle East but not in most of Africa and some parts of Asia and South America. In areas of low grade resistance to chloroquine, amodiaquine can be used to effectively treat falciparum malaria. A combination of sulfadoxine-pyrimethamine is responsive to falciparum infections with high grade resistance to chloroquine. Mefloquine, halofantrine, or quinine with tetracycline can be used to treat multidrug-resistant P. falciparum. Derivatives of artemisinin obtained from qinghao or sweet wormwood developed as pharmaceuticals in China are the most rapidly acting of all antimalarial drugs. Children tend to tolerate antimalarial drugs well. Children who weigh less than 15 kg should not be given mefloquine. Health workers should not prescribe primaquine to pregnant women or newborns due to the risk of hemolysis. Chloroquine, sulfadoxine-pyrimethamine, quinine, and quinidine can be safely given in therapeutic doses throughout pregnancy. Clinical manifestations of severe malaria are hypoglycemia, convulsions, severe anemia, acute renal failure, jaundice, pulmonary edema, cerebral malaria, shock, and acidosis. Health workers should be prepared to treat these symptoms accordingly.
In 1932, when Knowles and Das Gupta [ 1 ] succeeded in transmitting to humans the monkey malaria they had discovered, it appeared that a new agent for malaria therapy had been discovered. Since the Nobel Prize-winning research of Julius WagnerJauregg, malaria therapy had become widely used for the treatment of general paralysis of the insane (neurosyphilis), one of the main reasons for admission to psychiatric institutions. But it soon became apparent that this infection could rapidly become uncontrollable, and after several fatalities, its use was largely discontinued in favor of the less virulent human parasite Plasmodium vivax. Malaria parasites are generally rather choosy, both about their mammalian, avian, or reptilian hosts and their respective mosquito vectors. Transmission of Plasmodium knowlesiy for malaria therapy, from human to human was by blood passage. So initially, it was uncertain whether natural infection could take place and, thus, whether this could be a zoonosis. In 1960, Eyles et al. [2] demonstrated the first experimental mosquito transmission of a
Background to the debate In a 2007 article in PLoS Medicine [10], Holger J. Schünemann and colleagues described a new process used by the World Health Organization for rapidly developing clinical management guidelines in emergency situations. These situations include outbreaks of emerging infectious diseases. The authors discussed how they developed such a "rapid advice" guideline for the pharmacological management of avian influenza A (H5N1) virus infection. The guideline recommends giving the antiviral drug oseltamivir at a dose of 75 mg twice daily for five days. In this Debate, Nicholas White argues that such dosing is inadequate, Robert Webster and Elena Govorkova say that combination antiviral therapy should be used, and Tim Uyeki reminds us that clinical care of patients with H5N1 entails much more than antiviral treatment. These issues may also apply to therapy of patients hospitalized with severe disease due to novel swine-origin influenza A (H1N1) virus infection.
For an infection affecting approximately 5% of the World's population at any time, and killing between one and two million children each year, there are remarkably few drugs available for the treatment of falciparum malaria. Traditionally, antimalarial drug research has been stimulated by wars in tropical malarious areas involving economically-powerful temperate-climate powers. Armies fighting in the tropics lose more soldiers to malaria than bullets (Melville, 1911). The Second World War and the conflict in Vietnam brought us most of the drugs available today. The list is small, and the parasite has not been idle: Plasmodium falciparum has now developed resistance to all of our available drugs. The situation is particularly bad in South-East Asia.
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No abstract is provided for this article.
