Life Cycle of the Malarial Parasite

The malarial parasite is a single-cell protozoan (plas-modium).Although more than 100 species of plasmodia have been identified, only four are capable of infecting humans (Plasmodium malariae, P. ovale, P. vivax, and P. falciparum); the rest attack a variety of animal hosts. P. falciparum and P. vivax malaria are the two most common forms.

P. vivax malaria is the most prevalent type of infection and is characterized by periodic acute attacks of chills and fever, profuse sweating, enlarged spleen and liver, anemia, abdominal pain, headaches, and lethargy. Hyperactivity of the reticuloendothelial system and he-molysis are the principal causes of the enlarged spleen and liver; these effects often result in anemia, leuko-penia, thrombocytopenia, and hyperbilirubinemia. The cyclical nature of the acute attacks (48 hours for

P. vivax, P. ovale, and P. falciparum) is characteristic of malaria and reflects the relatively synchronous passage of the parasites from one red blood cell stage in their life cycle to another. If P. vivax malaria is not treated, the symptoms may subside for several weeks or months and then recur. These relapses are due to a latent liver form of the parasite (see the following section), which is not present in P. falciparum strains. Although the fatality rate of P. vivax malaria is low, it is an exhausting infection and renders the patient more susceptible to other diseases.

Unchecked P. falciparum malaria is the most serious and most lethal form of the disease. It is responsible for 90% of the deaths from malaria. The parasitemia achieved can be quite high and will be associated with an increased incidence of serious complications (e.g., hemolytic anemia, encephalopathy). P. falciparum malaria produces all of the symptoms listed for P. vivax malaria and in addition can cause renal failure and pulmonary and cerebral edema. The tissue anoxia occurring in P. falciparum infections results from the unique sequestering of infected erythrocytes deep in the capil laries during the last three-fourths of the intraerythro-cytic cycle.

Members of the genus Plasmodium have a complex life cycle (Fig. 53.1). A sexual stage occurs within the Anopheles mosquito, while asexual stages take place in the host. Malaria is actually transmitted from one human to another through the insect vector. Initially, a female mosquito is infected by biting a human with the disease whose blood contains male and female gamete forms of the parasite. Fertilization takes place in the mosquito gut, and after differentiation and multiplication, the mature sporozoite forms migrate to the insect's salivary glands. At the mosquito's next feeding, the sporozoites are injected into the bloodstream of another human to begin the asexual stages. After a relatively brief residence (less than an hour) in the systemic circulation, the sporozoites invade liver parenchymal cells, where they divide and develop asexually into multinucleated schizonts. These are the primary exo-erythrocytic tissue forms of the parasite. When this primary stage of development is completed (6-12 days), the schizonts will rupture, releasing merozoites into the

Anopheles mosquito (sexual stage)

Bloodstream

Latent

EFFECTIVE DRUG: Primaquine

Bloodstream

P. vivax P. ovale P. malariae P. falciparum

P. vivax P. ovale P. malariae P. falciparum

Exoerythrocytic liver state—asymptomatic

Latent

EFFECTIVE DRUG: Primaquine

Sexual forms

EFFECTIVE DRUGS:

Pyrimethamine Primaquine

Sexual forms

Parasites in erythrocyte

Intraerythrocytic schizogony—symptomatic, cyclical

EFFECTIVE DRUGS:

Chloroquine Amodiaquine Pyrimethamine Trimethoprim

EFFECTIVE DRUGS:

Chloroquine Amodiaquine Pyrimethamine Trimethoprim

Dapsone

Quinoline methanol Phenanthrene methanol

Parasites in erythrocyte

Intraerythrocytic schizogony—symptomatic, cyclical

Sulfadiazine

Quinine

Quinacrine

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