Many species of the genus Streptococcus cause hemolysis. Streptococcal bacteria species are classified according to their hemolytic properties. Note that these hemolytic properties are not necessarily present in vivo.
Beta-hemolytic species, including S. pyogenes and S. agalactiae, completely rupture the red blood cells (visible as a halo in culture).
Gamma-hemolytic, or non-hemolytic, species do not cause hemolysis and rarely cause illness.
The genus Enterococcus includes lactic acid bacteria formerly classified as gamma-hemolytic Group D in the genus streptococcus (see above), including E. faecilis (S. faecalis), E. faecium (S. faecium), E. durans (S. durans), and E. avium (S. avium).
Staphylococcus is another Gram-positive cocci. S. aureus, the most common cause of "staph" infections, is frequently hemolytic on blood agar.
Because the feeding process of the Plasmodium parasites damages red blood cells, malaria is sometimes called "parasitic hemolysis" in medical literature.
Hemolytic disease of the newborn is an autoimmune disease resulting from the mother's antibodies crossing the placenta to the fetus. This most often occurs when the mother has previously been exposed to blood antigens present on the fetus but foreign to her, through either a blood transfusion or a previous pregnancy.
Because in vivo hemolysis destroys red blood cells, in uncontrolled, chronic or severe cases it can lead to hemolytic anemia.
Paroxysmal nocturnal hemoglobinuria (PNH), sometimes referred to as Marchiafava-Micheli syndrome, is a rare, acquired, potentially life-threatening disease of the blood characterized by complement-induced intravascular hemolytic anemia.
Extrinsic hemolysis is caused by the red blood cell's environment:
Intravascular hemolysis may occur when red blood cells are targeted by autoantibodies, leading to complement fixation, or by damage by parasites such as Babesia. Additionally, thrombotic microangiopathy (TMA) can result in hemolysis of red blood cells. TMA is frequently observed in aHUS patients where clots form in the small vessels of the kidney resulting in damaged red blood cells as they attempt to pass through the restricted vessels.
If extravascular hemolysis is extensive, hemosiderin can be deposited in the spleen, bone marrow, kidney, liver, and other organs, resulting in hemosiderosis.
Outside the body
Hemolysis of blood samples. Red blood cells without (left and middle) and with (right) hemolysis. If as little as 0.5% of the red blood cells are hemolyzed, the released hemoglobin will cause the serum or plasma to appear pale red or cherry red in color. Note that the hemolyzed sample appears clearer, because there are significantly fewer cells to scatter light.
In vitro hemolysis can be caused by improper technique during collection of blood specimens, by the effects of mechanical processing of blood, or by bacterial action in cultured blood specimens.
From specimen collection
Most causes of in vitro hemolysis are related to specimen collection. Difficult collections, unsecure line connections, contamination, and incorrect needle size, as well as improper tube mixing and incorrectly filled tubes are all frequent causes of hemolysis. Excessive suction can cause the red blood cells to be smashed on their way through the hypodermic needle owing to turbulence and physical forces. Such hemolysis is more likely to occur when a patient's veins are difficult to find or when they collapse when blood is removed by a syringe or a modern vacuum tube. Experience and proper technique are key for any phlebotomist, nurse or doctor to prevent hemolysis.
In vitro hemolysis during specimen collection can cause inaccurate laboratory test results by contaminating the surrounding plasma with the contents of hemolyzed red blood cells. For example, the concentration of potassium inside red blood cells is much higher than in the plasma and so an elevated potassium level is usually found in biochemistry tests of hemolyzed blood.
After the blood collection process, in vitro hemolysis can still occur in a sample due to external factors, such as prolonged storage, incorrect storage conditions and excessive physical forces by dropping or vigorously mixing the tube.
From mechanical blood processing during surgery
In some surgical procedures (especially some heart operations) where substantial blood loss is expected, machinery is used for intraoperative blood salvage. A centrifuge process takes blood from the patient, washes the red blood cells with normal saline, and returns them to the patient's blood circulation. Hemolysis may occur if the centrifuge rotates too quickly (generally greater than 500 rpm)--essentially this is hemolysis occurring outside of the body. Unfortunately, increased hemolysis occurs with massive amounts of sudden blood loss, because the process of returning a patient's cells must be done at a correspondingly higher speed to prevent hypotension, pH imbalance, and a number of other hemodynamic and blood level factors. Modeling of fluid flows to predict the likelihood of red cell membrane rupture in response to stress is an active area of research.
From bacteria culture
Hemolysis from streptococcus. Examples of the blood culture patterns created by (from left) alpha-, beta- and gamma-hemolytic streptococci.
Visualizing the physical appearance of hemolysis in cultured blood samples may be used as a tool to determine the species of various Gram-positive bacteria infections (e.g., Streptococcus).
Red blood cells (erythrocytes) have a short lifespan (approximately 120 days), and old (senescent) cells are constantly removed and replaced with new ones via erythropoiesis. This breakdown/replacement process is called erythrocyte turnover. In this sense, erythrolysis or hemolysis is a normal process that happens continually. However, these terms are usually used to indicate that the lysis is pathological.
Complications may also arise from the increased workload for the kidney as it secretes erythropoietin to stimulate the bone marrow to produce more reticulocytes (red blood cell precursors) to compensate for the loss of red blood cells due to hemolysis.
^ abReiter, Christopher D.; Wang, Xunde; Tanus-Santos, Jose E.; Hogg, Neil; Cannon, Richard O.; Schechter, Alan N.; Gladwin, Mark T. (2002-11-11). "Cell-free hemoglobin limits nitric oxide bioavailability in sickle-cell disease". Nature Medicine. Springer Nature. 8 (12): 1383-1389. doi:10.1038/nm1202-799. ISSN1078-8956. PMID12426562. S2CID19878520.
^Rother, Russell P.; Bell, Leonard; Hillmen, Peter; Gladwin, Mark T. (2005-04-06). "The Clinical Sequelae of Intravascular Hemolysis and Extracellular Plasma Hemoglobin". JAMA. 293 (13): 1653-1662. doi:10.1001/jama.293.13.1653. ISSN0098-7484. PMID15811985. The systemic removal of nitric oxide has been shown to contribute to clinical morbidities, including severe esophageal spasm and dysphagia, abdominal pain, erectile dysfunction, and thrombosis.16,17,23-26 In addition, systemic release of hemoglobin is associated with pulmonary and systemic hypertension,17,20,53-55 decreased organ perfusion, and increased mortality.53-58 Plasma hemoglobin and its breakdown product heme can also directly activate endothelial cells and further promote inflammation and coagulation.27