Malaria anemia

Lactic acidosis and hypoglycemia (with falciparum malaria) Anemia Splenomegaly P. falciparum Infections... 

Plasmodium vivax, responsible for the most prevalent form of malaria (benign tertian), has an incubation period of 8—27 days (14 average). A variety seen in northern and northeastern Europe has an incubation period as long as 8—10 months. The disease can cause splenic mpture and anemia. Relapses (renewed manifestations of erythrocytic infection) can occur with this type of malaria. Overall, P. vivax is stiU susceptible to chloroquine however, resistant strains have been reported from Papua New Guinea and parts of Indonesia. Plasmodium malariae the cause of quartan malaria, has an incubation period of 15—30 days and its asexual cycle is 72 hours. This mildest form of malaria can cause nephritis in addition to the usual symptoms. It is a nonrelapsing type of malaria but the ted blood ceU infection can last for many years. No resistance to chloroquine by this plasmodium has been reported. Plasmodium ovale responsible for ovale tertian malaria, has an incubation period of 9—17 days (15 average). Relapses can occur in people infected with this plasmodium. No chloroquine resistance has been reported for this parasite. 

P. falciparum malaria is a life-threatening emergency. Complications include hypoglycemia, acute renal failure, pulmonary edema, severe anemia (high parasitism), thrombocytopenia, heart failure, cerebral congestion, seizures, coma, and adult respiratory distress syndrome. 

Figure 8.5 Monitoring the in vivo time course of P. yoleii malaria infection in mice inoculated with live parasites at day 0.15 (Upper trace) Parasite count obtained by microscopy of blood smear, folded with anemia model from the literature (para-sites/vol) = (parasites/RBC) x (RBC/vol). (Lower trace) Integrated LDMS heme signal from 300 shots across three consecutive sample wells each sample (30 pil) is processed following protocol C, and examined on a commercial LD TOF instrument. Infection is more easily and more rapidly discerned both at earlier and later times by LDMS, compared to the traditional optical microscopy examination.

It now appears certain that destruction of malaria parasites in vivo depends in part, if not wholly, upon the presence of humoral antibodies, and this must explain the success achieved with the passive transfer experiments. The exact role of the T and B lymphocytes in immunity in malaria infection in man still needs clarification. In rats the ability to resist P. berghei infection seems to be thymus dependent, and higher parasitemias were encountered in the thymectomized rats, which also developed severe anemia (B6). 

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 hemolysis are the principal causes of the enlarged spleen and liver these effects often result in anemia, leukopenia, thrombocytopenia, and hyperbilirubinemia. The cyclical nature of the acute attacks (48 hours for... 

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-... 

Although dapsone (Avlosulfon) was once used in the treatment and prophylaxis of chloroquine-resistant P. falciparum malaria, the toxicities associated with its administration (e.g., agranulocytosis, methemoglobinemia, hemolytic anemia) have severely reduced its use. 

Malaria. An infectious disease endemic in parts of Africa, Asia, Turkey, the West Indies, Central and South America, and Oceania, caused by protozoa of the genus Plasmodium, and usually transmitted by the bites of infected anopheline mosquitoes. It is characterized by prostration associated with paroxysms of high fever, shaking chills, sweating, anemia, and splenomegaly, which may lead to death. 

I Contraindications Hypersensitivity to pyrimethamine, megaloblastic anemia due to folate deficiency, monotherapy for freafmenf of acufe malaria. 

Deficiency of the first enzyme of the pentose phosphate pathway, glucose 6-phosphate dehydrogenase, is widespread.11 Its geographical distribution suggests that, like the sickle-cell trait, it confers some resistance to malaria. A partial deficiency of 6-phosphogluconolactonase (Eq. 17-12, step b) has also been detected within a family and may have contributed to the observed hemolytic anemia.1... 

However, the mechanism of the malaria protection is complex (64). It probably involves a sufficient survival time of particularly the malaria-infected heterozygous infant girls to allow them to develop immunological defences against malaria. This could mean that after puberty, their better state of health might render them more fertile than their less protected sisters. Since the occurrence of G-6-PD deficiency, of sickle cell anemia,... 

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