Scanning electron micrograph of human red blood cells (ca. 6–8 μm in diameter)
Glucose-6-phosphate dehydrogenase
Malaria parasite connecting to a red blood cell
There is an immense size variation in vertebrate red blood cells, as well as a correlation between cell and nucleus size. Mammalian red blood cells, which do not contain nuclei, are considerably smaller than those of most other vertebrates.
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Main symptoms of malaria
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The life cycle of malaria parasites. Sporozoites are introduced by a mosquito bite. They migrate to the liver, where they multiply into thousands of merozoites. The merozoites infect red blood cells and replicate, infecting more and more red blood cells. Some parasites form gametocytes, which are taken up by a mosquito, continuing the life cycle.
Typical mammalian red blood cells: (a) seen from surface; (b) in profile, forming rouleaux; (c) rendered spherical by water; (d) rendered crenate (shrunken and spiky) by salt. (c) and (d) do not normally occur in the body. The last two shapes are due to water being transported into, and out of, the cells, by osmosis.
Micrograph of a placenta from a stillbirth due to maternal malaria. H&E stain. Red blood cells are anuclear; blue/black staining in bright red structures (red blood cells) indicate foreign nuclei from the parasites.
Scanning electron micrograph of blood cells. From left to right: human red blood cell, thrombocyte (platelet), leukocyte.
Electron micrograph of a Plasmodium falciparum-infected red blood cell (center), illustrating adhesion protein "knobs"
Two drops of blood are shown with a bright red oxygenated drop on the left and a deoxygenated drop on the right.
The blood film is the gold standard for malaria diagnosis.
Animation of a typical human red blood cell cycle in the circulatory system. This animation occurs at a faster rate (~20 seconds of the average 60-second cycle) and shows the red blood cell deforming as it enters capillaries, as well as the bars changing color as the cell alternates in states of oxygenation along the circulatory system.
Ring-forms and gametocytes of Plasmodium falciparum in human blood
The most common red blood cell membrane lipids, schematically disposed as they are distributed on the bilayer. Relative abundances are not at scale.
An Anopheles stephensi mosquito shortly after obtaining blood from a human (the droplet of blood is expelled as a surplus). This mosquito is a vector of malaria, and mosquito control is an effective way of reducing its incidence.
Red blood cell membrane proteins separated by SDS-PAGE and silverstained
Man spraying kerosene oil in standing water, Panama Canal Zone, 1912
Red blood cell membrane major proteins
Walls where indoor residual spraying of DDT has been applied. The mosquitoes remain on the wall until they fall down dead on the floor.
Affected by Sickle-cell disease, red blood cells alter shape and threaten to damage internal organs.
A mosquito net in use.
Effect of osmotic pressure on blood cells
An advertisement for quinine as a malaria treatment from 1927.
Micrographs of the effects of osmotic pressure
Deaths due to malaria per million persons in 2012
Variations of red blood cell shape, overall termed poikilocytosis.
Past and current malaria prevalence in 2009
Ancient malaria oocysts preserved in Dominican amber
British doctor Ronald Ross received the Nobel Prize for Physiology or Medicine in 1902 for his work on malaria.
Chinese medical researcher Tu Youyou received the Nobel Prize for Physiology or Medicine in 2015 for her work on the antimalarial drug artemisinin.
Artemisia annua, source of the antimalarial drug artemisinin
U.S. Marines with malaria in a field hospital on Guadalcanal, October 1942
Members of the Malaria Commission of the League of Nations collecting larvae on the Danube delta, 1929
1962 Pakistani postage stamp promoting malaria eradication program
Malaria clinic in Tanzania
Child with malaria in Ethiopia
World War II poster
Disability-adjusted life year for malaria per 100,000 inhabitants in 2004
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<10
0–100
100–500
500–1000
1000–1500
1500–2000
2000–2500
2500–2750
2750–3000
3000–3250
3250–3500
≥3500

Most people who develop symptoms are male, due to the X-linked pattern of inheritance, but female carriers can be affected due to unfavorable lyonization or skewed X-inactivation, where random inactivation of an X-chromosome in certain cells creates a population of G6PD-deficient red blood cells coexisting with unaffected red blood cells.

- Glucose-6-phosphate dehydrogenase deficiency

In the blood, the merozoites rapidly invade individual red blood cells, replicating over 24–72 hours to form 16–32 new merozoites.

- Malaria

Lipid rafts that have been implicated in cell signaling events in nonerythroid cells have been shown in erythroid cells to mediate β2-adregenic receptor signaling and increase cAMP levels, and thus regulating entry of malarial parasites into normal red cells.

- Red blood cell

Several genetic factors provide some resistance to it including sickle cell trait, thalassaemia traits, glucose-6-phosphate dehydrogenase deficiency, and the absence of Duffy antigens on red blood cells.

- Malaria

A side effect of this disease is that it confers protection against malaria, in particular the form of malaria caused by Plasmodium falciparum, the most deadly form of malaria.

- Glucose-6-phosphate dehydrogenase deficiency

Furthermore, the pentose phosphate pathway plays an important role in red blood cells; see glucose-6-phosphate dehydrogenase deficiency for more information.

- Red blood cell
Scanning electron micrograph of human red blood cells (ca. 6–8 μm in diameter)

3 related topics with Alpha

Overall

Blood smear showing iron-deficiency anemia, with small, pale red blood cells.

Anemia

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Blood smear showing iron-deficiency anemia, with small, pale red blood cells.
Main symptoms that may appear in anemia
The hand of a person with severe anemia (on the left, with ring) compared to one without (on the right)
Figure shows normal red blood cells flowing freely in a blood vessel. The inset image shows a cross-section of a normal red blood cell with normal hemoglobin.
Peripheral blood smear microscopy of a patient with iron-deficiency anemia
A Giemsa-stained blood film from a person with iron-deficiency anemia. This person also had hemoglobin Kenya.

Anemia or anaemia (British English) is a blood disorder in which the blood has a reduced ability to carry oxygen due to a lower than normal number of red blood cells, or a reduction in the amount of hemoglobin.

Causes of increased breakdown include genetic disorders such as sickle cell anemia, infections such as malaria, and certain autoimmune diseases.

Glucose-6-phosphate dehydrogenase deficiency and glutathione synthetase deficiency, causing increased oxidative stress

Figure shows normal red blood cells flowing freely in a blood vessel. The inset image shows a cross-section of a normal red blood cell with normal hemoglobin.

Hemolytic anemia

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Figure shows normal red blood cells flowing freely in a blood vessel. The inset image shows a cross-section of a normal red blood cell with normal hemoglobin.

Hemolytic anemia is a form of anemia due to hemolysis, the abnormal breakdown of red blood cells (RBCs), either in the blood vessels (intravascular hemolysis) or elsewhere in the human body (extravascular).

Defective red cell metabolism (as in glucose-6-phosphate dehydrogenase deficiency and pyruvate kinase deficiency).

Acquired hemolytic anemia is also encountered in burns and as a result of certain infections (e.g. malaria).

Figure (A) shows normal red blood cells flowing freely through a blood vessel. The inset shows a cross-section of a normal red blood cell with normal haemoglobin. Figure (B) shows abnormal, sickled red blood cells sticking at the branching point in a blood vessel. The inset image shows a cross-section of a sickle cell with long polymerized sickle haemoglobin (HbS) strands stretching and distorting the cell shape to look like a crescent moon.

Sickle cell disease

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Group of blood disorders typically inherited from a person's parents.

Group of blood disorders typically inherited from a person's parents.

Figure (A) shows normal red blood cells flowing freely through a blood vessel. The inset shows a cross-section of a normal red blood cell with normal haemoglobin. Figure (B) shows abnormal, sickled red blood cells sticking at the branching point in a blood vessel. The inset image shows a cross-section of a sickle cell with long polymerized sickle haemoglobin (HbS) strands stretching and distorting the cell shape to look like a crescent moon.
Sickle cell anaemia
Sickle cells in human blood - both normal red blood cells and sickle-shaped cells are present.
Normal blood cells next to a sickle blood cell, coloured scanning electron microscope image
Sickle cell disease is inherited in an autosomal recessive pattern.
Distribution of the sickle cell trait, shown in pink and purple
Historical distribution of malaria (no longer endemic in Europe), shown in green
Modern distribution of malaria
Base-pair substitution that causes sickle cell anemia
HBB gene (responsible for sickle cell anaemia) is located on the short (p) arm of chromosome 11 at position 15.5.
Scanning electron micrograph showing a mixture of red blood cells, some with round normal morphology, some with mild sickling showing elongation and bending
Possible advantage of being heterozygous for sickle cell anemia disease (A) vs. normal blood cell response (B) when infected with malaria
Percentage of newborns screened for sickle cell disease within Metropolitan France from 2006 to 2018
Percentage of newborns screened regionally and overall for sickle cell disease in Metropolitan France in 2018

It results in an abnormality in the oxygen-carrying protein haemoglobin found in red blood cells.

In 1954, the protective effect against malaria of sickle cell trait was described.

This is particularly common in people with coexistent G6PD deficiency.