Some More About Malaria

Being a part of my last article, here are more facts about Malaria that I promised to bring on light. Some erythrocytic parasites differentiate into sexual forms known as gametocytes. After infected blood is ingested by a female mosquito, exflagellation of the male gametocyte is followed by fertilization of the female gametocyte in the insect gut. The resulting zygote, which develops as an oocyst in the gut wall, eventually gives rise to sporozoites, which invade the salivary gland of the mosquito. The insect then can infect a human host by taking a blood meal.

Symptomatic malaria is typified by high spiking fevers that may have a periodic pattern (see above), chills, headache, myalgias, malaise, and gastrointestinal symptoms. In addition, each Plasmodium species causes a distinct illness: (1) P. falciparum is the most dangerous. By invading erythrocytes of any age, sequestering in the vasculature, and producing endotoxin-like products, this species can cause an overwhelming parasitemia, hypoglycaemia, and shock with multiorgan failure. Delay in treatment may lead to death.

If treated early, the infection usually responds within 48 hours. If treatment is inadequate, recrudescence of infection may result. (2) P. vivax infection has a low mortality rate in untreated adults and is characterized by relapses caused by the reactivation of latent tissue forms. (3) P. ovale causes a malarial infection with a periodicity and relapses similar to those of P. vivax, but it is milder. (4) P. malariae causes a generally indolent infection that is common in localized areas of the tropics. Clinical attacks may occur years or decades after infection.
Antimalarials can be categorized by the stage of the parasite that they affect and by their intended use for either prophylaxis or treatment. The various stages of the malaria life cycle that occur in humans differ from one another not only in their morphology and metabolism but also in their drug sensitivity. For this reason, the classification of antimalarials drugs is best done in the context of the life cycle.

The tabulated spectrum of activity leads to several generalizations. The first relates to prophylaxis: Since none of the drugs kills sporozoites, it is not truly possible to prevent infection but only to prevent the development of symptomatic malaria caused by the asexual erythrocytic forms. The second relates to treatment of an established infection: None of the antimalarials is effective against all liver and red cell stages of the life cycle that may coexist in the same patient. Complete cure therefore may require more than one drug.

The patterns of clinically useful activity fall into three general classes. Class I agents are not reliable against primary or latent liver stages or against P. falciparum gametocytes. Their action is directed against the asexual erythrocytic forms. These drugs will treat, or prevent, clinically symptomatic malaria. When used prophylactically, the class I drugs must be taken for several weeks after exposure until parasites complete the liver phase and become susceptible to therapy. The spectrum is somewhat expanded for the class II agents, which target not only the asexual erythrocytic forms but also the primary liver stages of P. falciparum. This additional activity shortens to several days the required period for post exposure prophylaxis. Finally, primaquine is unique in its spectrum of activity, which includes reliable efficacy against primary and latent liver stages as well as gametocytes. Primaquine has no place in the treatment of symptomatic malaria but rather is used most commonly to eradicate the hypnozoites of P. vivax and P. ovale, which are responsible for relapsing infections.

Aside from their antiparasitic activity, the utility of antimalarials for prophylaxis or therapy is dictated by their pharmacokinetics and safety. Thus, quinine and primaquine, which have short half-lives and common toxicities, generally are reserved for treatment of established infection and not used for prophylaxis in a healthy traveller. In contrast, chloroquine is relatively safe and has a one-week half-life that is convenient for prophylactic dosing (in those few areas still reporting chloroquine-sensitive malaria).

Older classifications of the antimalarials are defined extensively in the 10th edition of this book. Briefly, causal prophylactics act on the initial hepatic stages, drugs for terminal prophylaxis and radical cure target hypnozoites, and agents for suppressive prophylaxis or cure target the asexual red cell forms.

By: Ammarah Khan

    

3 Responses to “Some More About Malaria”

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