Peripheral gangrene in an 18-month-old boy with<i>Plasmodium vivax</i>malaria

Raghunandan, J; Rajeshwari, K; Dubey, Arbind; Singh, Taru

doi:10.1179/2046905512y.0000000006

Cited by 8 publications

(5 citation statements)

References 16 publications

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“…In falciparum malaria, peripheral parasitemia underestimates the total parasite biomass due to sequestration of parasitized RBCs within endothelium-lined microvasculature. While P. vivax is not thought to sequester in the endothelium-lined microvasculature to the same degree as P. falciparum , limited histopathological reports show intact P. vivax -infected RBCs in the bone marrow [38] , [39] , [40] , [41] , [42] , [43] and spleen [44] , [45] , organs containing circulatory compartments that are not endothelium-lined. The spleen is a lymphoid organ whose primary role is to clear abnormal erythrocytes from the circulation, and hence plays a fundamental role in removing parasitized RBCs, especially in falciparum malaria where RBC deformability is markedly decreased.…”

Section: Discussionmentioning

confidence: 99%

Parasite Biomass-Related Inflammation, Endothelial Activation, Microvascular Dysfunction and Disease Severity in Vivax Malaria

et al. 2015

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Plasmodium vivax can cause severe malaria, however its pathogenesis is poorly understood. In contrast to P. falciparum, circulating vivax parasitemia is low, with minimal apparent sequestration in endothelium-lined microvasculature, and pathogenesis thought unrelated to parasite biomass. However, the relationships between vivax disease-severity and total parasite biomass, endothelial autocrine activation and microvascular dysfunction are unknown. We measured circulating parasitemia and markers of total parasite biomass (plasma parasite lactate dehydrogenase [pLDH] and PvLDH) in adults with severe (n = 9) and non-severe (n = 53) vivax malaria, and examined relationships with disease-severity, endothelial activation, and microvascular function. Healthy controls and adults with non-severe and severe falciparum malaria were enrolled for comparison. Median peripheral parasitemia, PvLDH and pLDH were 2.4-fold, 3.7-fold and 6.9-fold higher in severe compared to non-severe vivax malaria (p = 0.02, p = 0.02 and p = 0.015, respectively), suggesting that, as in falciparum malaria, peripheral P. vivax parasitemia underestimates total parasite biomass, particularly in severe disease. P. vivax schizonts were under-represented in peripheral blood. Severe vivax malaria was associated with increased angiopoietin-2 and impaired microvascular reactivity. Peripheral vivax parasitemia correlated with endothelial activation (angiopoietin-2, von-Willebrand-Factor [VWF], E-selectin), whereas markers of total vivax biomass correlated only with systemic inflammation (IL-6, IL-10). Activity of the VWF-cleaving-protease, ADAMTS13, was deficient in proportion to endothelial activation, IL-6, thrombocytopenia and vivax disease-severity, and associated with impaired microvascular reactivity in severe disease. Impaired microvascular reactivity correlated with lactate in severe vivax malaria. Findings suggest that tissue accumulation of P. vivax may occur, with the hidden biomass greatest in severe disease and capable of mediating systemic inflammatory pathology. The lack of association between total parasite biomass and endothelial activation is consistent with accumulation in parts of the circulation devoid of endothelium. Endothelial activation, associated with circulating parasites, and systemic inflammation may contribute to pathology in vivax malaria, with microvascular dysfunction likely contributing to impaired tissue perfusion.

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Section: Discussionmentioning

confidence: 99%

Parasite Biomass-Related Inflammation, Endothelial Activation, Microvascular Dysfunction and Disease Severity in Vivax Malaria

et al. 2015

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“…) and peripheral gangrene (Raghunandan et al . ). Acalculous cholecystitis has been described in both adults and children (Curley et al .…”

Section: Section 13: Severe Vivax Malariamentioning

confidence: 97%

Severe Malaria

2014

Tropical Med Int Health

459

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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“…Causes of SLE peripheral gangrene are unknown and multifactorial, and the underlying mechanism is complex and diverse, though can be summarized as follows: (1) vasculitis and infectious disorders that could cause vasculitis, (2) rheumatological disorders, (3) mechanical and obstructive disorder, (4) premature atherosclerosis, (5) vasospasm, (6) overlap syndrome, and (7) hypercoagulabilitythrombosis related to antiphospholipid (APL) antibodies or embolus originating from the heart secondary to Libmansack endocarditis, all of which may contribute to the development of gangrene [12,[15][16][17][18][19][20][21][22].…”

Section: Discussionmentioning

confidence: 99%

Systemic Lupus Erythematosus with Multiple Autoimmune Disease Presented with Extensive Peripheral Gangrene

Alzughayyar

Zalloum

Elqadi

et al. 2020

Case Reports in Rheumatology

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Systemic lupus erythematosus (SLE) is an autoimmune disease and can be associated with other autoimmune diseases. SLE usually presents with skin change and rarely presents with gangrene. SLE gangrene usually involves the digits of upper extremities. We report the first case of SLE associated with an extremely rare constellation of neuromyelitis Optica (NMO) and diabetes mellitus type 1, presented with a rare form of the SLE gangrene which involves bilateral lower extremities up to midlegs, a case that has not yet been reported in the literature. Although SLE gangrene may respond to immunosuppressants, it has a high risk of complications that can end up with amputations.

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Peripheral gangrene in an 18-month-old boy withPlasmodium vivaxmalaria

Cited by 8 publications

References 16 publications

Parasite Biomass-Related Inflammation, Endothelial Activation, Microvascular Dysfunction and Disease Severity in Vivax Malaria

Parasite Biomass-Related Inflammation, Endothelial Activation, Microvascular Dysfunction and Disease Severity in Vivax Malaria

Severe Malaria

Systemic Lupus Erythematosus with Multiple Autoimmune Disease Presented with Extensive Peripheral Gangrene

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