Anaemia and malaria

Abstract

Malaria is a major cause of anaemia in tropical areas. Malaria infection causes haemolysis of infected and uninfected erythrocytes and bone marrow dyserythropoiesis which compromises rapid recovery from anaemia. In areas of high malaria transmission malaria nearly all infants and young children, and many older children and adults have a reduced haemoglobin concentration as a result. In these areas severe life-threatening malarial anaemia requiring blood transfusion in young children is a major cause of hospital admission, particularly during the rainy season months when malaria transmission is highest. In severe malaria, the mortality rises steeply below an admission haemoglobin of 3 g/dL, but it also increases with higher haemoglobin concentrations approaching the normal range. In the management of severe malaria transfusion thresholds remain uncertain. Prevention of malaria by vector control, deployment of insecticide-treated bed nets, prompt and accurate diagnosis of illness and appropriate use of effective anti-malarial drugs substantially reduces the burden of anaemia in tropical countries.

Micronutrient levels and their effect on the prognosis of visceral leishmaniasis treatment; a prospective cohort study.

“…Malaria co-infection decreases the serum iron level of visceral leishmaniasis patients by 12.69 mcg/dl, the iodine level by 3.78 mcg/l, the serum vitamin A level by 4.8 mcg/dl and the serum vitamin D level by 0.61 ng/ml. This nding was supported by other research results [53][54][55]. This is due to the multiple effects of malaria on serum micronutrient levels like ingestion of the nutrients by the parasites, decreases the intake from the host, increases the execration of the nutrients through vomiting, perspiration, etc [56][57][58].…”

Sickle cell disease and malaria: decreased exposure and asplenia can modulate the risk from Plasmodium falciparum

“…Malaria infection may be fatal in any person: however, the risk of fatality is influenced by several genetic and acquired factors. Among the former, SCD is one of the foremost: it increases greatly the mortality from malaria infection; probably in large part because the P. falciparum-induced destruction of both parasitized and non-parasitized erythrocytes will precipitate a severe exacerbation of the already existing chronic anaemia [16,17]. This is in striking contrast to the well known significant protection enjoyed by haemoglobin S heterozygotes (sickle cell trait) against P. falciparum malaria [7], and the triumph of good over evil: protection by the sickle gene against malaria [18].…”

Malaria-induced remodelling of the bone marrow microenvironment mediates loss of haematopoietic stem cell function

“…berghei infection was chosen as our model as it is a natural rodent infection that includes the skin and livers stages and reproduces several features of human malaria. Malaria is a widespread and severe infection and its effects on HSCs are still poorly understood beyond reports of increased morbidity and infection susceptibility in survivors (Orf & Cunnington, 2015;White, 2018).…”

“…Plasmodium infects and destroys red blood cells, and multiple studies have investigated its impact on erythropoiesis (Dörmer et al, 1983;Maggio-Price, Brookoff & Weiss, 1985;Wickramasinghe et al, 1989;Boehm et al, 2018). It is generally accepted that malaria survivors have compromised haematopoietic and immune function in the short-and long-term (Orf & Cunnington, 2015;White, 2018), and recent studies have begun to link this to alteration in cells of myeloid lineages (Orf & Cunnington, 2015;Mamedov et al, 2018). It is likely that these effects can be traced back to changes in the earliest stages of haematopoiesis, including the HSC compartment.…”