Patient receiving an intravenous treatment representing transfusion-related Babesia risk in people with sickle cell disease
Lyme Science Blog
Sep 02

Can Babesiosis Be More Dangerous in People With Sickle Cell Disease?

2
Visited 1939 Times, 3 Visits today

Can Babesiosis Be More Dangerous in People With Sickle Cell Disease?

Babesiosis and sickle cell disease both affect red blood cells
Hemolysis can become more complicated when the conditions overlap
Frequent transfusions create an additional route of Babesia exposure

Can babesiosis be more dangerous in people with sickle cell disease? Potentially. People with sickle cell disease may face several added concerns when they develop babesiosis, including underlying anemia, ongoing red blood cell destruction, impaired splenic function, and exposure to repeated blood transfusions.

A 2026 review examined the relationship between sickle cell disease and several parasitic infections, including Babesia. The evidence reveals an interesting paradox: sickle-shaped red blood cells may make it more difficult for Babesia to reproduce normally, yet patients with sickle cell disease may still be vulnerable to important complications when infection occurs.1

This distinction matters because a lower parasite burden does not necessarily eliminate the clinical concerns created when two conditions capable of affecting red blood cells occur together.

Why babesiosis and sickle cell disease can be a difficult combination

Babesia parasites infect red blood cells. The infection can cause fever, chills, sweats, fatigue, headache, muscle aches, and other symptoms of babesiosis. In more serious cases, destruction of infected and uninfected red blood cells can contribute to hemolytic anemia and other complications.

Sickle cell disease also involves abnormal red blood cells and chronic hemolysis. Red blood cells containing sickle hemoglobin can become rigid and distorted, have a shortened lifespan, and be removed from circulation more rapidly than normal red blood cells.

When babesiosis occurs in someone who already has sickle cell disease, the effects on red blood cells can therefore overlap. The 2026 review cautioned that babesiosis may exacerbate anemia and hemolysis in these patients.1

Can sickle-shaped red blood cells make it harder for Babesia to grow?

Surprisingly, laboratory and animal research suggests that sickle cell red blood cells may create a less favorable environment for Babesia replication.

In laboratory experiments discussed in the 2026 review, Babesia divergens was able to invade red blood cells containing normal hemoglobin, sickle cell trait, and sickle cell disease. However, parasites developing inside sickle cell disease red blood cells showed abnormal development, impaired release from infected cells, and a reduced ability to establish infection in new red blood cells.1

A mouse model produced a similar observation. Mice with sickle cell disease developed approximately four- to five-fold lower parasitemia than mice with normal hemoglobin or sickle cell trait despite having comparable immune responses.1

Researchers have proposed several possible explanations, including increased oxidative stress, altered red blood cell membranes, shortened red blood cell survival, and increased clearance of abnormal cells by the spleen.1

These findings are intriguing, but they should not be interpreted as evidence that sickle cell disease protects patients from clinically important babesiosis. Much of this evidence comes from laboratory and animal research rather than large clinical studies in people with sickle cell disease.

Lower parasitemia may not tell the entire story

Parasitemia describes the percentage of red blood cells infected with Babesia. It is an important measurement when evaluating babesiosis, particularly in seriously ill patients.

However, the interaction between parasite burden and illness severity can be more complicated in someone who already has a disorder affecting red blood cells.

Babesiosis can cause destruction not only of infected red blood cells but also of uninfected cells. A patient with sickle cell disease may already have chronic anemia and accelerated red blood cell destruction before becoming infected.1

Therefore, even if sickle cell red blood cells limit parasite replication to some degree, the additional hemolysis associated with babesiosis may still be clinically important.

The available research does not establish that patients with sickle cell disease will necessarily become severely ill at low parasitemia. Rather, it shows why clinicians should consider the patient’s underlying hematologic condition alongside the parasite count.

The spleen is another important consideration

The spleen plays an important role in removing abnormal and parasite-infected red blood cells from circulation.

People with sickle cell disease can progressively lose normal splenic function because repeated sickling and vascular injury damage the spleen. This is known as functional asplenia.

Loss of normal splenic function is particularly relevant to babesiosis because patients without adequate splenic function are recognized as being at increased risk for severe disease.

This creates another reason why the laboratory observation that sickle cell red blood cells may inhibit Babesia replication should not be interpreted as proof that patients with sickle cell disease are protected from serious babesiosis.

Blood transfusions create another Babesia risk

Most people associate babesiosis with the bite of an infected blacklegged tick. But unlike Lyme disease, Babesia can also be transmitted through blood transfusion.

This route is particularly relevant for people with sickle cell disease because some patients require frequent red blood cell transfusions or chronic red cell exchange therapy.

The 2026 review identified several reported cases of transfusion-associated babesiosis in patients with sickle cell disease and highlighted transfusion exposure as an important concern in this population.1

A particularly instructive case was reported by Costa and colleagues in 2023. A 30-year-old man with sickle cell disease had received chronic automated red cell exchange therapy since childhood.2

He developed fever, neck pain, and sensitivity to light approximately two months after a red cell exchange. After meningitis was excluded, he returned with persistent fever, chills, headache, fatigue, and loss of appetite.2

A blood smear eventually revealed intraerythrocytic organisms with less than 0.5% parasitemia. Testing confirmed Babesia microti infection.2

He had received 65 units of red blood cells

The patient did not report outdoor activities or other risk factors suggesting that he had acquired babesiosis from a tick bite.

Investigators instead examined his transfusion history.

During the six months before his illness, he had received 65 red blood cell units from 54 donors. Fifty-eight of those units had undergone Babesia nucleic acid testing before transfusion, but seven had not.2

Investigators ultimately identified an asymptomatic donor associated with one of the unscreened units who had antibodies to Babesia microti. The case was considered transfusion-transmitted babesiosis.2

The patient was treated with atovaquone and azithromycin, and his symptoms resolved.2

The case illustrates why unexplained fever, fatigue, worsening anemia, or other compatible symptoms in a frequently transfused patient should not automatically be attributed to sickle cell disease or a transfusion reaction.

Why transfusion-transmitted babesiosis can be difficult to recognize

Babesia infection following a transfusion may not be immediately obvious.

Patients with sickle cell disease may already experience anemia, pain, fatigue, hemolysis, and complications related to transfusion. Some of these findings can overlap with manifestations of babesiosis.

The 2026 review noted that reported cases have sometimes presented diagnostic challenges because babesiosis can resemble complications such as delayed hemolytic transfusion reactions.1

In addition, an infected blood donor may have no symptoms. Babesia can persist in the blood of an apparently healthy person, allowing infection to be transmitted without the donor knowing that he or she is infected.

Blood donor screening has substantially reduced this risk, but transfusion-transmitted babesiosis has not been completely eliminated. The 2023 case illustrates how blood collected under different screening circumstances can still create vulnerabilities for patients requiring specialized and repeated transfusions.2

For a broader discussion of this issue, see Babesia and the blood supply.

What symptoms might raise concern for babesiosis?

Babesiosis can produce symptoms including fever, chills, sweats, fatigue, headache, muscle aches, and loss of appetite. Laboratory abnormalities may include anemia, thrombocytopenia, and evidence of hemolysis.

In a person with sickle cell disease, these findings may be harder to interpret because some can overlap with the underlying disorder or its complications.

A history of tick exposure is useful when present, but its absence does not exclude babesiosis. This is particularly important in a patient who has received blood transfusions.

Clinicians may need to consider the patient’s symptoms, transfusion history, exposure history, blood counts, markers of hemolysis, peripheral blood smear, and appropriate Babesia testing rather than relying on any single finding.

What does the 2026 review tell us?

The most important message from the 2026 review may be that the relationship between sickle cell disease and babesiosis is more complicated than simply asking whether sickle cells are protective or harmful.1

Laboratory and animal evidence suggests that the altered red blood cell environment in sickle cell disease can interfere with Babesia replication. At the same time, patients may have chronic hemolysis, anemia, impaired splenic function, and substantial transfusion exposure.

Human evidence remains limited. The authors noted that specific studies examining Babesia seroprevalence among patients with sickle cell disease are lacking despite the increased transfusion exposure in this population.1

More clinical research is needed to determine how these competing biological factors influence parasite burden, symptoms, disease severity, and treatment outcomes in people with sickle cell disease.

Frequently Asked Questions

Does sickle cell disease protect against babesiosis?

It has not been shown to protect patients from clinically important babesiosis. Laboratory and animal studies suggest that sickle cell red blood cells may interfere with Babesia replication, but people with sickle cell disease may simultaneously have other risk factors for complications, including anemia, hemolysis, impaired splenic function, and repeated transfusions.

Can Babesia be transmitted through a blood transfusion?

Yes. Babesia infects red blood cells and can be transmitted through transfused blood. Blood donor screening has reduced this risk, but transfusion-transmitted babesiosis can still occur.

Why are blood transfusions particularly relevant in sickle cell disease?

Some people with sickle cell disease require repeated red blood cell transfusions or chronic red cell exchange therapy. Repeated exposure to donor blood creates additional opportunities for transfusion-transmitted infection, although the absolute risk has been reduced substantially by blood donor screening.

Can someone with sickle cell disease have babesiosis with low parasitemia?

Yes. Reported cases include patients with relatively low measured parasitemia. Parasite burden is clinically important, but it should be interpreted together with symptoms, anemia, hemolysis, splenic function, underlying disease, and other clinical findings.

Should unexplained fever after a transfusion raise concern for Babesia?

Babesiosis is one of several possible explanations for unexplained fever after transfusion. It may deserve consideration when compatible symptoms, hemolysis, epidemiologic exposure, or repeated transfusions are present. Other infectious and noninfectious transfusion complications must also be considered.

Clinical Takeaway

The relationship between babesiosis and sickle cell disease is complex. Experimental research suggests that sickle cell red blood cells may restrict Babesia replication, but that potential biological effect does not eliminate the clinical risks associated with infection.

Patients with sickle cell disease may already have anemia, chronic hemolysis, impaired splenic function, and repeated exposure to blood transfusions. These factors can complicate both the presentation and recognition of babesiosis.

Human evidence remains limited, and more research is needed before conclusions can be drawn about whether sickle cell disease consistently changes the severity of babesiosis.

For patients with sickle cell disease, unexplained fever, worsening anemia, or hemolysis deserves careful evaluation for babesiosis when tick exposure or transfusion exposure makes the infection clinically plausible.

Related Articles

These articles provide additional information about Babesia symptoms, treatment, and red blood cell complications:

Babesiosis Treatment: My Go-To Clinical Tips
Babesia Anemia: Can Babesiosis Destroy Red Blood Cells?
Babesia Treatment Duration: When Is 7–10 Days Not Enough?

References

  1. Bhosale CR, Morcos ZL, Escudero A, Neupane R, Kahook Z, Miranda G, Deehan E, Gregg RK, Potter AK. More than malaria: Exploring Babesia, Leishmania and Trypanosoma in sickle cell disease. Current Research in Parasitology & Vector-Borne Diseases. 2026;9:100396.
  2. Costa V, Mercure-Corriveau N, Gourneau J, Tobian AAR, Jones JM, Lauriello A, Lanzkron S, Crowe EP, Bloch EM. Transfusion-transmitted babesiosis in a patient with sickle cell disease undergoing chronic red cell exchange. Transfusion. 2023;63(3):652-655.

Dr. Daniel Cameron, MD, MPH
Lyme disease clinician with over 30 years of experience and past president of ILADS.

SymptomsTestingCoinfectionsRecoveryPediatricPrevention

Related Posts

Leave a Comment

Your email address will not be published. Required fields are marked *