Lyme disease, caused by the bacterium Borrelia burgdorferi and transmitted by infected ticks, is a complex infectious process. When an infection becomes persistent, the body’s sustained immune response can interfere with normal physiological processes. One consequence of this chronic inflammatory state is the development of anemia, characterized by a reduced number of healthy red blood cells or a decrease in hemoglobin.
The Direct Link Between Lyme Disease and Anemia
Lyme disease can lead to anemia through two primary pathways. The most common link is chronic inflammation triggered by the Borrelia bacteria, resulting in Anemia of Chronic Disease (ACD), or Anemia of Inflammation. This is a secondary effect where the body’s defense mechanisms disrupt iron utilization and red blood cell production.
The second cause of anemia, often more severe, involves a tick-borne co-infection. The same tick that transmits Borrelia burgdorferi can also transmit the parasitic organism Babesia microti. This co-infection, known as babesiosis, directly invades and destroys red blood cells, causing hemolytic anemia. While true iron-deficiency anemia can sometimes coexist, ACD resulting from the persistent inflammatory state is the typical hematological finding in Lyme disease.
Biological Mechanisms Driving Anemia
The development of Anemia of Chronic Disease (ACD) is driven by persistent immune activation characteristic of chronic infection. This sustained inflammation involves the release of pro-inflammatory cytokines, particularly Interleukin-6 (IL-6), which plays a central role in altering the body’s iron metabolism.
IL-6 acts on the liver, stimulating the production of hepcidin, the master regulator of systemic iron balance. Increased hepcidin levels reduce the iron available for red blood cell production in two key ways.
First, hepcidin causes the degradation of ferroportin, a protein that transports iron out of storage cells like macrophages and liver cells. This action effectively traps iron within these storage sites, preventing its release into the bloodstream. Second, elevated hepcidin also inhibits the absorption of dietary iron in the gut.
The result is a state of “functional iron deficiency,” where the body has sufficient iron stores, but that iron is inaccessible to the bone marrow for making new red blood cells.
Beyond iron sequestration, the inflammatory environment also directly suppresses the bone marrow’s ability to produce red blood cells, a process called erythropoiesis. Cytokines inhibit the production and function of erythropoietin, the hormone that signals the bone marrow to create red blood cells. The combination of iron withholding and direct bone marrow suppression results in the characteristic mild-to-moderate anemia seen in chronic infectious diseases.
Diagnostic Approach to Anemia in Lyme Patients
Diagnosing anemia requires careful interpretation of blood tests to distinguish ACD from true iron-deficiency anemia (IDA). A complete blood count (CBC) confirms anemia and typically shows red blood cells that are normocytic (normal size) or mildly microcytic (small) in ACD. This contrasts with the distinctly microcytic cells often seen in IDA.
The iron panel provides the clearest differentiation between the two conditions. In ACD, serum iron and Total Iron-Binding Capacity (TIBC) are low because iron is actively sequestered. Ferritin, a protein used to store iron, is usually normal or elevated because it functions as an acute-phase reactant, increasing during inflammation.
This pattern—low serum iron despite normal or high ferritin—is the hallmark of ACD, indicating iron is trapped in storage. Conversely, true IDA is characterized by low serum iron, high TIBC, and low ferritin. Healthcare providers also rely on inflammatory markers, such as Erythrocyte Sedimentation Rate (ESR) or C-Reactive Protein (CRP), to confirm the systemic inflammation driving ACD.
Managing Anemia Related to Lyme Infection
The most effective strategy for managing Anemia of Chronic Disease is treating the underlying inflammatory cause, which means treating the Lyme infection itself. When the Borrelia bacteria are eradicated, the chronic immune response subsides, leading to a decrease in inflammatory cytokines and hepcidin levels. This allows iron metabolism to normalize, and the bone marrow can resume efficient red blood cell production.
Traditional iron supplements are generally ineffective for ACD and can be counterproductive. Since the body is withholding iron from the bloodstream, oral iron simply adds to sequestered stores and may contribute to oxidative stress without resolving the anemia. Iron supplementation is reserved only for cases where a coexisting true iron deficiency is confirmed by diagnostic testing.
For patients experiencing severe symptoms, symptomatic treatments may be considered. These options include the use of Erythropoiesis-Stimulating Agents (ESAs), which help overcome the cytokine-mediated suppression of the bone marrow. Blood transfusions are typically reserved for individuals with critically low hemoglobin levels or acute symptoms requiring rapid correction.