Malaria in American Soldiers

Martelo, Orlando J.

doi:10.1001/archinte.1969.00300140029007

Cited by 30 publications

(18 citation statements)

References 21 publications

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“…8,9 Since then, reports of primaquine resistance or primaquine failure have become fairly common from areas such as Papua New Guinea, Southeast Asia, India, and Colombia. [3][4][5][6][7][10][11][12] These five cases originating in Ethiopia support other reports suggesting that the incidence of P. vivax malaria in east Africa, and its failure to respond to standard doses of primaquine in this area, may actually be higher than suspected. 1,2 Relapses despite primaquine treatment may reflect changes in primaquine response among formerly susceptible strains, or geographic spread of strains that have long been known to be refractory.…”

supporting

confidence: 71%

Short report: a consideration of primaquine dose adjustment for radical cure of Plasmodium vivax malaria.

Schwartz¹,

Regev‐Yochay²,

Kurnik³

2000

The American Journal of Tropical Medicine and Hygiene

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Abstract. Relapse of Plasmodium vivax malaria following standard primaquine dosing has been reported from many areas, and more recently from sub-Saharan Africa. In this report we describe eight episodes (in five patients) of treatment failure in non-immune Israeli travelers returning from Ethiopia. Retrospective calculation of the primaquine dose per kilogram of body weight for 23 treatment courses showed a lower total dose per kilogram in heavier patients. The mean calculated dose (95% CI) in the eight failed treatments was 2.5 Ϯ 0.3 mg/kg compared with 4.4 Ϯ 0.5 mg/kg in the 15 successful treatment courses. Weight-adjusted dosing regimens may prevent inadvertent subtherapeutic drug failure, and thus apparent primaquine failure. In these cases, no relapses were observed in those who received Ͼ 3.5 mg/kg. Consideration should be given to adjusting the dose of primaquine according to body weight. For those infected by strains from Ethiopia a dose Ͼ 3.5 mg/kg is preferable.Although Plasmodium vivax accounts for less than 10% of the malaria cases in Africa, there has been an increase in recent accounts of infection among travelers to these regions, such as Israelis returning from Ethiopia 1 and U.S. military returning from Somalia. 2

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confidence: 71%

Short report: a consideration of primaquine dose adjustment for radical cure of Plasmodium vivax malaria.

Schwartz¹,

Regev‐Yochay²,

Kurnik³

2000

The American Journal of Tropical Medicine and Hygiene

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“…Profound thrombocytopenia is a well-recognized complication of falciparum malaria but has been less well described in vivax malaria. Of 173 cases of malaria in U.S. soldiers reported by Martelo et al [2] in 1969, 93% had P. vivax but only 15% had thrombocytopenia with no documentation of the lowest platelet count. In Horstmann's series [3], the lowest count in 39 cases of vivax malaria was 44x10 9 /L.…”

Section: Discussionmentioning

confidence: 96%

Plasmodium vivax malaria presenting with severe thrombocytopenia

et al. 2002

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Plasmodium falciparum and Plasmodium vivax malaria are endemic infections in India and are commonly associated with mild hematological abnormalities. Severe thrombocytopenia is common in isolated falciparum and mixed falciparum/vivax malaria, but is very rare in isolated P.vivax infection. We hereby report a case of severe thrombocytopenia (platelet count of 8x10 9 /L) in a case of vivax malaria. This is only the second case ever reported in the literature of such profound thrombocytopenia in a case of isolated P.vivax malaria. Key Words: Plasmodium vivax, malaria, severe thrombocytopenia. Malaria is common in most parts of India and is usually caused by P. falciparum and P. vivax. Though mild thrombocytopenia is common in both falciparum and vivax malaria, severe thrombocytopenia is reported especially in P. falciparum malaria and is very rare in isolated P. vivax infection. Both non-immunological as well as immunological destruction of platelets have been implicated in causing thrombocytopenia in such cases but the mechanisms involved are still not completely clear. Case ReportA 43-year-old male, resident of eastern India, arrived at the hospital emergency room with complaints of high grade, intermittent fever associated with chills and rigors during seven days. He also had a two-day history of mild spontaneous bleeding from the gums. There was no history of bleeding from any other site and no past or family history suggestive of bleeding diathesis. There was no history of any drug ingestion. On examination, the patient was febrile with a temperature of 40 o C. He had slight pallor and the liver and spleen were palpable 2 cm and 3 cm below the costal margin, respectively. There were no purpuric spots and the tourniquet test was negative.Routine blood investigations revealed 7.5 g/dL hemoglobin and a WBC count of 6.3x10 9 /L, with 54% neutrophils, 39% lymphocytes, 4% eosinophils and 3% monocytes. The platelet count was 8x10 9 /L. The peripheral blood smear showed numerous gametocytes of P. vivax in a background of marked thrombocytopenia. The 'OptiMAL® Rapid Malaria Dipstick Test' (DiaMed AG,Switzerland) for P. falciparum was negative but was positive for P. vivax. The bleeding time was prolonged to 9 minutes while the clotting time was 3 minutes, with a prothrombin time of 14 seconds (control 13 seconds) and activated partial thromboplastin time of 40 seconds (control 36 seconds). Glucose-6-phosphate dehydrogenase levels were normal and disseminated intravascular coagulation (DIC) was ruled out by normal levels of fibrinogen degradation products (FDP). Total serum bilirubin was 1.4 mg/dL with normal serum transaminase levels. Dengue serology (IgG and IgM) and Elisa for HIV were nonreactive. The patient was treated with antimalarials (quinine sulphate 10 mg/kg thrice daily) for 7 days and was given 6 units of platelet transfusions

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“…These include anaemia and thrombocytopenia in addition to neutrophilia, monocy tosis, eosinopenia, plasmacytosis and lymphocytosis (Facer and Jenkins, 1989), with atypical lymphocytes (Kueh and Yeo, 1982). Peripheral blood neutropenia has also been reported in some (Dale and Wolff, 1973) but not other (Martello et al, 1969) Phagocytosis of pigment and of parasites by monocytes/macrophages, and less frequently by neutrophils has been observed in the peripheral blood of patients with malaria (Vernes, 1980).…”

Section: Introductionmentioning

confidence: 99%

Falciparum malaria in naturally infected human patients: IV-Ultrastructural changes in peripheral white blood cells

El-Shoura

1993

Ann. Parasitol. Hum. Comp.

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Ultrastructure of white blood cells (WBC) were studied in peri pheral venous blood from Saudi patients with acute falciparum malaria (AFM) and compared with their counterparts in same patients 2 weeks after chloroquine treatment and full recovery. A counting system was incorporated to determine the rate of abnormal to normal cell type in plastic thick sections during the course of the disease. Neutrophilia, monocytosis, eosinopenia and lymphocytosis were associated with various ultrastructural abnor malities including: (1) Knobby phagocytic polymorphnuclear neu trophils (PMN) and promyelocytes, and PMN with highly vacuo lated cytoplasm. (2) Irregularly outlined electron-dense nuclei in non-functional monocytes. (3) Unusual distribution of nuclear chro matin in resting B-lymphocytes, while others possess highly vacuo lated cytoplasm and knobby surfaces. (4) Absence of granules in granular lymphocytes containing the known diagnostic paratubular crystalline arrays. (5) Plasmablasts containing electron-dense gra nules and swollen mitochondria. These abnormalities were sug gested to be due to the high level o f parasitaemia producing some toxic soluble products. They may also be attributed to alteration of bone marrow macrophages as a sequence of their interaction with soluble parasite products or their phagocytic parasitized red cells and debris released during the rupture of schizonts. This study showed that the number of abnormal WBC increases in patients with high level of parasitaemia; plasmablasts have the lowest rate o f abnormalities, while monocytes have the highest; old patients present with lower degree of parasitaemia than young patients due to a less mature immune system; and the AFM may have independent effects on the structure of human WBC. Résumé : Paludisme à P. falciparum. IV-Altérations ultrastructurales des globules blancs périphériques.L 'ultrastructure des globules blancs est étudiée dans le sang vei neux périphérique chez des malades d 'Arabie Saoudite atteints de paludisme aigu à falciparum. Elle est comparée à celle des glo bules blancs chez les mêmes malades deux semaines après traite ment à la chloroquine et guérison totale.Des comptages ont été réalisés sur coupes semi-fines pour déter miner le pourcentage d'anomalies cellulaires pendant le cours de la maladie. Neutrophilie, monocytose, éosinopénie et lymphocy tose étaient associées à diverses anomalies ultrastructurales : 1) protubérances de l'enveloppe évoquant des knobs chez les promyélocytes, parfois associées à un cytoplasme très vacuolisé chez les polynucléaires neutrophiles ; 2) contour nucléaire irrégu lièrement dense chez les monocytes non fonctionnels ; 3) distribution anormale de la chromatine nucléaire dans certains lymphocytes B au repos, tandis que d 'autres ont un cytoplasme vacuolisé et une surface rugueuse ; 4) absence de granules chez les lymphocytes gra nuleux contenant les structures cristallines paratubulaires ; 5) granules denses et mitochondries gonflées dans les plasmoblastes.Cette étude montre que, le nombre de glo...

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Malaria in American Soldiers

Cited by 30 publications

References 21 publications

Short report: a consideration of primaquine dose adjustment for radical cure of Plasmodium vivax malaria.

Short report: a consideration of primaquine dose adjustment for radical cure of Plasmodium vivax malaria.

Plasmodium vivax malaria presenting with severe thrombocytopenia

Falciparum malaria in naturally infected human patients: IV-Ultrastructural changes in peripheral white blood cells

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