Destruction of RBCs occurs commonly in the course of many infectious diseases. Those diseases with the most profound effect on RBCs will be reviewed here.

Transmitted by mosquitoes, malaria is the world's most common cause of hemolytic anemia. RBC hemolysis results from direct parasitization of the RBCs. Hemolysis also results from direct parasitization of RBCs in babesiosis, which is transmitted by ticks or blood transfusions. Infection with Bartonella is also associated with direct parasitization of RBCs and resultant hemolysis.

Hemophilus influenzae type B infection can produce hemolysis by altering the RBC surface. The capsular polysaccharide of the bacterium binds to the RBC surface and then antibodies destroy the bacterium as well as the RBC. Those with H. influenzae meningitis have the greatest potential to develop severe hemolysis.

Clostridium perfringens (welchii) infection can result in severe hemolysis by direct lysis of red blood cells. The organism releases enzymes that acutely degrade the phospholipids of the RBC membrane bilayer and the proteins in the structural membrane. This infection is seen most commonly in patients with acute cholecystitis, after surgery involving the biliary tree, after abortions, and in uterine infections. Clinically, the patient may have acute hemodynamic collapse and profound intravascular hemolysis. Clostridium septicemia has a mortality rate over 50 percent.

Mycoplasma pneumoniae and infectious mononucleosis are associated with cold agglutin disease, as described earlier.

Many viral infections can be accompanied by hemolytic anemia, including measles, cytomegalovirus, varicella, herpes simplex, coxsackie, and human immunodeficiency virus.

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