Lyme disease is an infection caused by the bacterium Borrelia burgdorferi, transmitted to humans through the bite of an infected blacklegged tick. This infection can affect various body systems, leading to a wide range of symptoms. Anemia is a medical condition characterized by a deficiency of healthy red blood cells or a reduced concentration of hemoglobin, diminishing the blood’s capacity to carry oxygen. The systemic impact of Borrelia infection can disrupt the body’s normal processes, leading to the development of anemia as a complication.
The Confirmed Link Between Lyme and Anemia
Lyme disease can directly or indirectly lead to the development of anemia, particularly in cases of persistent infection. The most frequent form observed in patients with chronic inflammatory conditions like Lyme is known as Anemia of Chronic Disease (ACD), also called Anemia of Inflammation. This type of anemia is typically mild to moderate and develops from the body’s altered iron handling in response to the infection, not a simple lack of dietary iron.
A different type of anemia can also occur due to co-infections transmitted by the same tick bite. For example, babesiosis is caused by a parasite, Babesia microti, which directly invades and destroys red blood cells, leading to hemolytic anemia. When Lyme disease is the primary trigger, the resulting anemia is a complication of the immune response rather than a direct attack on red blood cells by the Borrelia bacteria itself.
Biological Pathways Leading to Anemia
The primary mechanism linking Borrelia burgdorferi infection to anemia involves the systemic inflammatory response it provokes, which is the hallmark of Anemia of Chronic Disease. When the immune system detects the persistent bacterial presence, it releases inflammatory signaling molecules known as cytokines, such as interleukin-6 (IL-6). These cytokines act as messengers that stimulate the liver to increase the production and release of a peptide hormone called hepcidin.
Hepcidin is the master regulator of iron balance in the body, and its elevated levels are the direct cause of functional iron deficiency in ACD. The hormone works by binding to a protein called ferroportin, which is the only known cellular exporter of iron. Ferroportin is found on the surface of cells that store and recycle iron, specifically macrophages and cells lining the gut.
When hepcidin binds to ferroportin, it causes the iron exporter to be internalized and degraded. This action effectively locks iron inside the storage cells, preventing its release into the bloodstream. Iron absorbed from the diet and iron recycled from old red blood cells are thus sequestered within the body’s stores, making it unavailable to the bone marrow for new red blood cell production. The result is a state of hypoferremia, or low iron in the circulating blood, even though the total iron stores in the body may be normal or high. This defense mechanism impairs the host’s ability to generate new hemoglobin.
Identifying Anemia in Lyme Patients
Diagnosing anemia in a patient with Lyme disease requires a thorough laboratory investigation to determine the specific type. A complete blood count (CBC) is the foundational test, which reveals the number of red blood cells and the amount of hemoglobin, confirming the presence of anemia. In ACD, the red blood cells are typically described as normocytic (normal size) or sometimes microcytic (small size).
Differential Diagnosis and Testing
The next step is a differential diagnosis, which involves a panel of iron studies to distinguish ACD from a simple iron deficiency anemia. In true iron deficiency, both serum ferritin (the iron storage protein) and serum iron levels are low. However, in ACD, the persistent inflammation causes ferritin levels to be normal or even elevated because iron is trapped in storage cells. Conversely, serum iron and total iron-binding capacity (TIBC) are often low because iron is not being released into circulation. Inflammatory markers, such as C-reactive protein (CRP), are also assessed, as elevated levels help confirm the systemic inflammation driving the ACD. If hemolytic anemia is suspected, a blood smear is necessary to check for the presence of parasites, such as Babesia, which would indicate a co-infection.
Treatment Approaches for Lyme-Related Anemia
The management of Lyme-related anemia focuses on resolving the underlying cause, which is the Borrelia infection and the resulting systemic inflammation. Antibiotic therapy, tailored to the stage and manifestation of the Lyme disease, is the primary course of action. As the antibiotics clear the infection, the inflammatory cytokine production decreases, which subsequently lowers the hepcidin levels.
With hepcidin levels normalized, stored iron can be released back into the bloodstream, allowing the bone marrow to resume normal red blood cell production, thereby resolving the Anemia of Chronic Disease. Iron supplementation is generally avoided in ACD because the body’s iron stores are already adequate. Providing extra iron can be ineffective and potentially risky, as free iron may be utilized by the bacteria. Iron is only supplemented if laboratory tests confirm a coexisting true iron deficiency anemia.