Spleen Rupture in a Case of Untreated Plasmodium vivax Infection

Siqueira, André Machado; Magalhães, Belisa Maria Lopes; Melo, Gisely Cardoso de; Ferrer, M. Carmen Olivé; Castillo, Paola; Martín-Jaular, Lorena; Fernández-Becerra, Carmen; Ordi, Jaume; Martinez, Antonio; Lacerda, Marcus Vinícius Guimarães; Portillo, Hernando A. del

doi:10.1371/journal.pntd.0001934

Cited by 58 publications

(54 citation statements)

References 26 publications

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“…Viable asexual trophozoites of P. vivax in infected reticulocytes (or erythroblasts) have indeed been observed in the bone marrow (95,(166)(167)(168)(169)(170)(171) and spleen (172). In one case, a subpatent parasitemia confirmed by PCR contrasted with a ruptured spleen very heavily laden with P. vivax-infected reticulocytes (175). Rupture or infarct of the spleen is a relatively rare and seriously threatening complication of vivax malaria (173), and this seems to reflect a natural affinity for hemopoietic tissues by P. vivax parasites.…”

Section: A Plausible and Testable Hypothesis On Pathogenesismentioning

confidence: 94%

Evidence and Implications of Mortality Associated with Acute Plasmodium vivax Malaria

2013

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SUMMARYVivax malaria threatens patients despite relatively low-grade parasitemias in peripheral blood. The tenet of death as a rare outcome, derived from antiquated and flawed clinical classifications, disregarded key clinical evidence, including (i) high rates of mortality in neurosyphilis patients treated with vivax malaria; (ii) significant mortality from zones of endemicity; and (iii) the physiological threat inherent in repeated, very severe paroxysms in any patient, healthy or otherwise. The very well-documented course of this infection, with the exception of parasitemia, carries all of the attributes of “perniciousness” historically linked to falciparum malaria, including severe disease and fatal outcomes. A systematic analysis of the parasite biomass in severely ill patients that includes blood, marrow, and spleen may ultimately explain this historic misunderstanding. Regardless of how this parasite is pernicious, recent data demonstrate that the infection comes with a significant burden of morbidity and associated mortality. The extraordinary burden of malaria is not heavily weighted upon any single continent by a single species of parasite—it is a complex problem for the entire endemic world, and both species are of fundamental importance. Humanity must rally substantial resources, intellect, and energy to counter this daunting but profound threat.

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Section: A Plausible and Testable Hypothesis On Pathogenesismentioning

confidence: 94%

Evidence and Implications of Mortality Associated with Acute Plasmodium vivax Malaria

2013

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“…It has been hypothesised that total parasite biomass in uncomplicated and severe malaria may be higher than that represented by peripheral parasitaemia due to accumulation of parasitised red cells in organs such as the spleen (Machado Siqueira et al . ; Baird ); however, this requires further investigation.…”

Section: Pathogenesis Of Disease In Vivax Malariamentioning

confidence: 98%

“…The administration of an artemisinin derivate by the rectal route as pre‐referral treatment has been found feasible and acceptable at the community level (Machado Siqueira et al . ; Baird ).…”

Section: Section 11: Antimalarial Drug Treatment Of Severe Malariamentioning

confidence: 99%

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Severe Malaria

2014

Tropical Med Int Health

465

354

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Fever and diarrhea developed in a 34-year-old Swiss man two weeks after his return from Madagascar. Before his visit he had not taken any prophylactic antimalarial drugs. Despite self-treatment with ciprofloxacin and metronidazole, he remained febrile. He also reported hematuria and dark urine. On admission, his temperature was 39.2°C and his vital signs and mental status were normal. The abdomen was tender, and the spleen was palpable 15 cm below the costal margin. The hemoglobin level was 12.4 g per deciliter, the hematocrit was 35 percent, the white-cell count was 8500 per cubic millimeter, and the platelet count was 15,000 per cubic millimeter. The creatinine level was 2.6 mg per deciliter (234 µmol per liter), the lactate dehydrogenase level was 1920 U per liter (normal, 187 to 443), and the bilirubin level was 11.5 mg per deciliter (197 µmol per liter); the results of other liver-function tests were in the normal range. Examination of blood smears showed severe infestation with Plasmodium falciparum, with 70 to 80 percent of red cells containing up to five parasites (small ring forms) per cell (long arrow in Panel A). Other features of P. falciparum that were present included chromatin dots (arrowheads in Panel A) and appliqué forms (short arrow in Panels A and B; Wright's stain, ¬1000). About 70 percent of the neutrophils contained hemozoin (shown in a band form [long arrows] in Panel B). The patient was treated with intravenous quinine sulfate and exchange transfusions, with dramatic improvement. The degree of parasitemia fell to 65 percent after the first exchange transfusion and to 8 percent after the second. The patient's course was complicated by acute renal failure, the acute respiratory distress syndrome, and spontaneous rupture of the spleen, necessitating continuous hemofiltration, mechanical ventilation, and laparotomy with splenectomy. Despite these complications , the patient was able to return home within three months and was well at the last follow-up visit.

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“…25,44 Recently, in an untreated ruptured spleen that was infected with P. vivax, a diffuse hypercellularity in red pulp that presented with many P. vivax-iRBCs in the cords, massive proliferating plasma cells, and striking intra-sinusoidal histiocytosis were observed by immunohistopathological analysis. 45 These findings suggest that intrasplenic structural changes by excessive hyperplastic growth can cause blood flow obstruction, contributing to local splenic hypoxia in P. vivax infection. However, whether sequestration and cytoadhesion of P. vivax-iRBCs in sinusoids are important in pathogenesis remains unclear.…”

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confidence: 88%

Malaria-Induced Splenic Infarction

Hwang

Lee

2014

The American Society of Tropical Medicine and Hygiene

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Abstract. Splenic infarction is a rare complication of malaria. We report two recent cases of splenic infarction after Plasmodium vivax infection. No systematic review of malaria-induced splenic infarction was available, therefore we conducted a systematic review of the English, French, and Spanish literature in PubMed and KoreaMed for reports of malaria-associated splenic infarction from 1960 to 2012. Of the 40 cases collected on splenic infarction by Plasmodium species, 23 involved P. vivax, 11 Plasmodium falciparum, one Plasmodium ovale, and five a mixed infection of P. vivax and P. falciparum. Of the 40 cases, 2 (5.0%) involved splenectomy and 5 (12.5%) were accompanied by splenic rupture. The median time from symptom onset to diagnosis was 8.5 days (range, 3-90 days). Improved findings after treatment were observed in 8 (88.9%) of 9 patients with splenic infarction on follow-up by computed tomography or ultrasonography. All patients survived after treatment with the exception of one patient with cerebral malaria. Clinicians should consider the possibility of splenic infarction when malaria-infected patients have left upper quadrant pain.

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Spleen Rupture in a Case of Untreated Plasmodium vivax Infection

Cited by 58 publications

References 26 publications

Evidence and Implications of Mortality Associated with Acute Plasmodium vivax Malaria

Evidence and Implications of Mortality Associated with Acute Plasmodium vivax Malaria

Severe Malaria

Malaria-Induced Splenic Infarction

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