Bite cells are irregularly shaped red blood cells identified during a microscopic examination of a blood sample. Their appearance signals damage from oxidative stress, which leads to the premature destruction of red cells, known as hemolysis. Their presence acts as an important diagnostic clue, pointing toward underlying conditions that compromise the cell’s natural defenses against damaging oxygen molecules. Recognizing this cell shape helps doctors narrow down the cause of red blood cell loss and guide further testing.
Identifying Bite Cells
A bite cell, also known as a degmacyte, has a distinctive membrane defect. Under a high-power microscope during a peripheral blood smear analysis, the cell appears to have a semi-circular piece removed from its edge, much like a bite taken out of an apple. This characteristic indentation can vary in size, and a single cell may display multiple “bites.”
The cell’s remaining structure is often smaller and denser than a normal red blood cell due to the loss of a membrane portion. While they are sometimes confused with other fragmented red cells, the smooth, semi-circular nature of the defect distinguishes the bite cell.
The Mechanism of Bite Cell Formation
Bite cell formation begins with an increase in oxidative stress within the cell’s chemical environment. Red blood cells rely on protective enzymes to neutralize harmful reactive oxygen species and prevent damage. When this defense system is overwhelmed or impaired, the cell’s internal structures are exposed to chemical attack.
This oxidative damage primarily targets hemoglobin, the protein responsible for carrying oxygen. The damaged hemoglobin molecules begin to denature, forming rigid aggregates known as Heinz bodies. These Heinz bodies adhere to the inner surface of the red blood cell membrane, making the cell less flexible.
The spleen, the body’s primary blood filter, plays the final mechanical role in bite cell creation. As the red blood cell attempts to squeeze through the narrow channels of the splenic tissue, resident immune cells, called splenic macrophages, detect the rigid Heinz bodies. The macrophages then physically “pit” or remove the denatured hemoglobin from the cell. This selective removal process results in the macrophage taking a chunk of the cell membrane along with the Heinz body, leaving the cell with the characteristic semi-circular defect.
Health Conditions Linked to Bite Cells
The presence of bite cells in a peripheral blood smear indicates oxidative hemolysis, necessitating further testing to identify the underlying cause. The most common genetic condition associated with this finding is Glucose-6-Phosphate Dehydrogenase (G6PD) deficiency. G6PD is an enzyme responsible for protecting red blood cells from oxidative damage, and a deficiency leaves the cells highly vulnerable to stress.
In G6PD deficiency, bite cell formation is often triggered by an external factor. Common triggers include acute infections, which generate oxidative stress as part of the immune response. Certain medications are also triggers, such as antimalarial drugs like primaquine, and sulfa-containing antibiotics, which act as potent oxidative agents.
Another trigger for hemolysis in G6PD-deficient patients is the consumption of fava beans, a reaction known as favism. The compounds in the beans increase oxidative stress, leading to the rapid formation of Heinz bodies and the appearance of bite cells. Exposure to high doses of certain oxidative drugs, like dapsone, can also induce bite cell formation even in individuals without a G6PD deficiency. This observation prompts clinicians to investigate for conditions like G6PD deficiency or to review the patient’s recent exposure to medications, toxins, or foods. Identifying and removing the oxidative trigger is often the first step in managing the condition.