Blood and bone marrow changes in malaria

ContextMany US clinicians and laboratory personnel are unfamiliar with the diagnosis and treatment of malaria.ObjectivesTo examine the evidence base for management of uncomplicated and severe malaria and to provide clinicians with practical recommendations for the diagnosis and treatment of malaria in the United States.Evidence AcquisitionSystematic MEDLINE search from 1966 to 2006 using the search term malaria (with the subheadings congenital, diagnosis, drug therapy, epidemiology, and therapy). Additional references were obtained from searching the bibliographies of pertinent articles and by reviewing articles suggested by experts in the treatment of malaria in North America.Evidence SynthesisImportant measures to reduce morbidity and mortality from malaria in the United States include the following: obtaining a travel history, considering malaria in the differential diagnosis of fever based on the travel history, and prompt and accurate diagnosis and treatment. Chloroquine remains the treatment of choice for Plasmodium falciparum acquired in areas without chloroquine-resistant strains. In areas with chloroquine resistance, a combination of atovaquone and proguanil or quinine plus tetracycline or doxycycline or clindamycin are the best treatment options. Chloroquine remains the treatment of choice for all other malaria species, with the exception of P vivax acquired in Indonesia or Papua New Guinea, in which case atovaquone-proguanil is best, with mefloquine or quinine plus tetracycline or doxycycline as alternatives. Quinidine is currently the recommended treatment for severe malaria in the United States because the artemisinins are not yet available. Severe malaria occurs when a patient with asexual malaria parasitemia, and no other confirmed cause of symptoms, has 1 or more designated clinical or laboratory findings. The only adjunctive measure recommended in severe malaria is exchange transfusion.ConclusionsMalaria remains a diagnostic and treatment challenge for US clinicians as increasing numbers of persons travel to and emigrate from malarious areas. A strong evidence base exists to help clinicians rapidly initiate appropriate therapy and minimize the major mortality and morbidity burdens caused by this disease.

https://jamanetwork.com/journals/jama/articlepdf/207162/jcr70004_2264_2277.pdf

Treatment of Malaria in the United States: A Systematic Review

Malaria remains a highly prevalent disease in more than 90 countries and accounts for at least 1 million deaths every year. Plasmodium falciparum infection is often associated with a procoagulant t...

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Blood Coagulation, Inflammation, and Malaria

Different parameters of fibrinolytic systems like t-PA, PAI, D-dimer, and inhibitors of blood coagulation, i.e., protein C (PC), protein S(PS), and antithrombin III (AT-III), have been studied in cases of acute malaria due to Plasmodium falciparum and plasmodium vivax infection, and these patients were followed up. It was observed that the plasma PAI-1 was very high in cases of P. falciparum malaria infection as compared to normal controls and P. vivax infection. The changes in complicated cases of P. falciparum were remarkable as compared to uncomplicated ones. The PC, PS, and AT-III levels were also low in P. falciparum, particularly so in complicated cases, and were normal in P. vivax infection. The factor VIII R:Ag levels were invariably high in acute malaria. On follow-up of some of these cases the values came back to normal after the antiparasite treatment. The monocyte procoagulant activity was found to be significantly higher in P. falciparum infection as compared to that of P. vivax infection. All these findings therefore contribute towards the production of a hypercoagulable state in P. falciparum infection and partly explain the complications of P. falciparum infection like cerebral malaria.

Fibrinolysis, inhibitors of blood coagulation, and monocyte derived coagulant activity in acute malaria.

Platelet counts were investigated in 26 patients withP. falciparum malaria and 39 patients withP. vivax malaria before and after treatment. Before schizontocidal treatment 22 of 26 (85%) patients withP. falciparum malaria and 30 of 39 (72%) patients withP. vivax malaria had depressed platelet counts below 150,000/Μl blood. There was a correlation between low platelet counts and high counts of malarial plasmodia (parasitized red blood cells) inP. falciparum andP. vivax infections (p < 0.001). Platelet survival, studied by malonaldehyde formation in three patients during the period of decreasing parasitaemia, revealed a shortened life span to 2–3 days in comparison to 7–10 days in normal controls. In all patients platelet counts rose to threefold the initial values within 5 days after clearance of parasites.

Robert J. Dostalek

Papers

Blood coagulation studies in Plasmodium falciparum malaria.