Babesiosis is an infection spread by ticks and caused by Babesia parasites, which are tiny organisms (protozoa) that enter and destroy red blood cells. Many infected people do not develop symptoms. When symptoms do appear, they often resemble the flu and may include fever, chills, sweating, headache, body aches, and tiredness. Severe illness can cause the rapid breakdown of red blood cells (hemolytic anemia), yellowing of the skin and eyes (jaundice), dark urine, a low number of platelets (which help with blood clotting), and serious complications such as kidney failure, breathing problems, or the formation of blood clots.
In the United States, babesiosis has become more common in recent years. Between 2011 and 2019, the Centers for Disease Control and Prevention (CDC) recorded 16,456 cases across 37 states, with more than 98% occurring in ten states in the Northeast and upper Midwest. Some states saw sharp increases; for example, Vermont experienced a more than 1,600% rise in reported cases during that period. In 2020, the CDC reported 1,827 cases, with nearly all coming from these same high-risk states.
The species most often responsible for human infection in the U.S. is Babesia microti, which naturally infects small mammals such as the white-footed mouse. Humans usually become infected through the bite of an infected blacklegged tick (Ixodes scapularis), the same tick that spreads Lyme disease. Although less common, babesiosis can also be transmitted through blood transfusions, organ transplants, or from an infected mother to her baby during pregnancy.
Certain groups are at higher risk for severe disease. These include older adults, the median age of reported U.S. cases is about 65 years, people with weakened immune systems, and individuals without a functioning spleen. Co-infections with other tick-borne diseases are also a concern; studies suggest that about 42% of infected individuals may also have another tick-borne infection, such as Lyme disease.
Environmental changes appear to be contributing to the spread of babesiosis. The ticks that carry Babesia are expanding into new regions, and factors such as warmer temperatures and changes in land use may be helping them spread.
Prevention focuses on reducing the risk of tick bites. Recommended measures include using insect repellents, wearing protective clothing, checking the body (and pets) regularly for ticks, and reducing tick habitats by keeping grass short and removing leaf litter.
Treatment depends on the severity of illness. Mild cases may clear on their own, but moderate to severe cases usually require medication. Standard treatments include combinations such as azithromycin with atovaquone or, for more serious infections, quinine with clindamycin.
History of Babesiosis
Babesiosis was first recognized in the late 19th century as a disease affecting animals before its significance in human health was understood. In 1888, the Romanian bacteriologist Victor Babeș described intraerythrocytic parasites—organisms living inside red blood cells—in cattle suffering from febrile illness and hemoglobinuria (the presence of hemoglobin in urine). These organisms were later classified as protozoa of the genus Babesia, marking one of the earliest documented discoveries of a tick-borne pathogen. Throughout the early 20th century, babesiosis remained primarily associated with veterinary medicine, especially as a major cause of “Texas cattle fever,” a disease that had severe economic consequences for the livestock industry in North America. The identification of ticks as vectors for the parasite played a crucial role in shaping early research on tick-borne diseases.
Human babesiosis was not recognized until several decades later. The first well-documented human case was reported in 1957 in Croatia (then Yugoslavia), involving a splenectomized farmer who developed severe illness caused by Babesia divergens. The absence of a spleen, a key organ for filtering parasites from the blood, helped researchers understand the role of host immunity in disease severity. By the late 1960s and early 1970s, additional cases emerged in the United States, most notably on Nantucket Island, Massachusetts, leading to the colloquial name “Nantucket fever.” As diagnostic methods improved, it became clear that babesiosis was more widespread than initially believed, particularly in regions where blacklegged tick populations were expanding.
Over the following decades, the geographic range of human babesiosis grew significantly, especially in the northeastern and upper midwestern United States. This expansion coincided with ecological changes such as suburbanization, reforestation, increased deer populations, and climate-related shifts that supported the spread of Ixodes ticks.
Babesia Species
Multiple species of Babesia are capable of causing disease in humans, and each species is associated with distinct geographic regions, tick vectors, and clinical characteristics. In the United States, the most common cause of human babesiosis is Babesia microti. This species circulates primarily among small mammals such as the white-footed mouse and is transmitted by the blacklegged tick (Ixodes scapularis), which also spreads Lyme disease and anaplasmosis. B. microti infections range from asymptomatic to severe, and co-infection with other tick-borne pathogens is common due to shared vectors.
In Europe, Babesia divergens is the predominant species affecting humans. This species is typically transmitted by Ixodes ricinus, the European counterpart to Ixodes scapularis. B. divergens infections tend to be more severe and progress rapidly, particularly in individuals who are asplenic (without a spleen) or immunocompromised. Historically, most cases have been linked to cattle reservoirs, although wildlife hosts also contribute to transmission.
Two additional species, Babesia duncani and Babesia venatorum, have been recognized more recently. B. duncani is found mainly in the western United States, though its ecology and reservoir hosts are less well understood. It has been associated with severe and sometimes fatal infections. B. venatorum, originally identified in Europe and parts of Asia, has been reported in both immunocompetent and immunocompromised patients and is also transmitted by Ixodes ricinus.
The clinical severity, treatment response, and epidemiology of babesiosis vary depending on the species involved. For example, B. microti infections often respond well to combination therapies such as azithromycin with atovaquone, whereas B. divergens infections may require more aggressive treatment due to rapid disease progression.
Transmission of Babesiosis
Babesiosis is mainly transmitted through specific routes involving blood contact or exposure to infected vectors.
Tick-Borne Transmission
The most common and epidemiologically significant mode of transmission is through the bite of infected Ixodes ticks. In the United States, the blacklegged tick (Ixodes scapularis) is the primary vector for Babesia microti, the species responsible for most human infections. In Europe and parts of Asia, Ixodes ricinus and Ixodes persulcatus transmit Babesia divergens and Babesia venatorum. These ticks function as both vectors and hosts: they acquire the parasites while feeding on infected reservoir animals, typically small mammals such as the white-footed mouse—and later transmit them to humans during subsequent blood meals.
Transmission occurs during the tick’s prolonged feeding process, which may last 36–48 hours or longer. During this time, the parasites migrate from the tick’s midgut to its salivary glands and are injected into the human bloodstream through saliva. The probability of infection increases markedly the longer the tick remains attached, making early detection and removal one of the most effective personal preventive strategies.
Geographically, tick-borne transmission is most common in areas with dense tick populations and abundant reservoir hosts. This includes much of the northeastern and upper midwestern United States, where cases have sharply increased over the past two decades. Environmental factors such as reforestation, suburban expansion into wildlife habitats, rising deer populations, and climate-related shifts that extend the tick activity season, have contributed to the expanding risk.
Blood Transfusion Risks
Babesiosis is also a recognized transfusion-transmitted infection, a route of spread that is particularly concerning because infected individuals often have asymptomatic or mild infections and may not know they are carrying the parasite. Babesia species can survive for extended periods in refrigerated blood products, making contaminated donations a potential source of infection.
This mode of transmission poses heightened risks for certain groups, including immunocompromised patients, individuals without a functioning spleen, the elderly, and those requiring frequent transfusions such as patients with sickle cell disease or malignancies. Transfusion-transmitted babesiosis has been associated with severe and sometimes fatal outcomes due to the sudden introduction of large numbers of parasites into the recipient’s bloodstream.
To address this risk, many blood banks in endemic regions have implemented nucleic acid testing (NAT), which screens donated blood for Babesia DNA. These screening programs have significantly reduced, but not eliminated, transfusion-related cases.
Congenital Transmission
Congenital transmission, though rare, occurs when Babesia parasites are passed from an infected mother to her fetus during pregnancy or delivery. Documented cases have shown that newborns can present with symptoms such as jaundice, anemia, fever, and poor feeding due to the destruction of red blood cells shortly after birth. Because maternal infections may be asymptomatic, congenital cases can be difficult to anticipate and diagnose.
The mechanisms behind congenital transmission are not fully understood but may involve direct transfer of parasitized red blood cells across the placenta. Infants born through this pathway typically require prompt diagnosis and treatment due to their immature immune systems and increased vulnerability to severe disease.
Signs and Symptoms
When symptoms do occur, they typically begin 1 to 4 weeks after the bite of an infected tick, although the incubation period may be shorter (as little as one week) in transfusion-related infections because parasites are introduced directly into the bloodstream. The most common symptoms are nonspecific and flu-like.
Early manifestations often include fever, chills, fatigue, muscle aches (myalgia), sweating, headache, and a general sense of illness or malaise. These symptoms reflect the destruction of red blood cells as the parasite replicates within them, as well as the inflammatory response triggered by parasite antigens. Fever may be intermittent or continuous and can reach high temperatures. Fatigue tends to be profound and may persist for weeks even after acute symptoms resolve.
Gastrointestinal symptoms, although less specific, are also reported. These may include nausea, loss of appetite, abdominal discomfort, and occasionally vomiting. Some patients develop a dry cough or mild respiratory symptoms, which can be mistaken for viral infections or early pneumonia. Because these symptoms overlap with many other conditions, including Lyme disease, malaria, influenza, and viral syndromes, clinical suspicion often depends on a history of tick exposure.
Laboratory findings often show hemolytic anemia, hemolytic anemia, a condition in which red blood cells are destroyed faster than they can be produced. This often results in low hemoglobin levels, elevated indirect bilirubin, increased lactate dehydrogenase (LDH), and reduced haptoglobin, all of which indicate active hemolysis. Patients may exhibit jaundice (yellowing of the skin and eyes) and dark urine, both consequences of the breakdown of hemoglobin. Additional abnormalities may include thrombocytopenia (low platelet count).
Because symptoms are nonspecific and laboratory findings mimic other infections that destroy red blood cells, diagnosis may be overlooked, especially outside endemic areas. Co-infection with other tick-borne pathogens such as Borrelia burgdorferi (Lyme disease) and Anaplasma phagocytophilum can further complicate the clinical picture, leading to more severe or atypical presentations.
Severe Complications
Severe babesiosis occurs more frequently in certain high-risk groups, including older adults, immunocompromised individuals, people without a functioning spleen, and patients with underlying chronic diseases such as cancer, HIV/AIDS, or cardiovascular conditions. In these populations, parasite levels in the blood may rise rapidly, resulting in extensive red blood cell destruction and widespread inflammation.
One of the most serious complications is acute respiratory distress syndrome (ARDS), a condition in which fluid accumulates in the lungs, making breathing difficult and requiring intensive medical support. Another major complication is disseminated intravascular coagulation (DIC), a life-threatening disorder characterized by widespread activation of the clotting system, leading to both excessive clotting and severe bleeding.
Multi-organ involvement is common in advanced cases. Patients may develop acute kidney failure, caused either by reduced blood flow, hemoglobin toxicity from severe hemolysis, or microvascular clots. Congestive heart failure may occur due to increased cardiac workload and reduced oxygen-carrying capacity of the blood. In some cases, patients experience hepatic dysfunction, severe metabolic imbalances, or shock. Profound anemia can necessitate repeated blood transfusions, particularly in those with high levels of parasitemia (the percentage of infected red blood cells). Mortality is highest among immunocompromised and elderly individuals, especially those with delayed diagnosis or treatment.
Asymptomatic Cases
A significant proportion of individuals infected with Babesia, particularly Babesia microti, remain completely asymptomatic. These silent infections can persist for weeks, months, or even more than a year, depending on the person’s immune status. Although these carriers experience no clinical symptoms, they may still harbor viable parasites in their bloodstream.
Asymptomatic infections are especially important from a public health perspective because they can lead to transfusion-transmitted babesiosis. Blood donors are often unaware that they are infected, and standard blood processing does not eliminate the parasite. Many asymptomatic carriers are identified only during blood donor screening, epidemiological investigations, or when they later develop symptoms due to immunosuppression.
While most asymptomatic individuals never progress to severe disease, illness may occur if the immune system weakens, for example, through chemotherapy, splenectomy, organ transplantation, or advanced age. Such reactivation or progression underscores the importance of monitoring high-risk individuals who are known to be infected.
Diagnosis of Babesiosis
Laboratory diagnosis focuses on direct detection of Babesia organisms in the bloodstream and indirect tests that identify the host immune response or parasite genetic material.
A complete diagnostic workup typically begins with a full blood count, peripheral blood smears, and biochemical tests. Many patients exhibit hemolytic anemia, thrombocytopenia, and elevated liver enzymes, findings that raise suspicion for a hemolytic process or systemic infection. Because babesiosis can be easily mistaken for other tick-borne diseases, clinicians often perform a combined panel that includes tests for Borrelia burgdorferi (Lyme disease) and Anaplasma phagocytophilum, particularly in regions where co-infections are common.
Timing is crucial: parasitemia may be intermittent or present at low levels, especially in individuals with partial immunity or chronic infection. Therefore, repeated sampling may be required if clinical suspicion remains high despite an initially negative test.
Microscopy and Blood Smears
The microscopic examination of stained blood smears remains the cornerstone, or “gold standard”, for diagnosing babesiosis. Thin blood smears stained with Giemsa or Wright stain allow direct visualization of the parasites within red blood cells.
Babesia trophozoites typically appear as:
- Ring forms resembling those seen in Plasmodium infections (malaria), which can lead to misdiagnosis without careful evaluation.
- Pear-shaped or amoeboid forms depending on the species and stage.
- The pathognomonic Maltese cross formation, a tetrad of merozoites dividing within an erythrocyte, highly specific, though not always present.
Quantification of parasitemia is a key step. Severe disease often correlates with higher parasite loads (e.g., >4% parasitemia), although even low-level infections can cause significant pathology in asplenic or immunocompromised patients.
However, microscopy has important limitations. Its sensitivity decreases substantially when parasitemia is <0.1%, a common scenario in mild, chronic, or post-treatment cases. Therefore, a negative smear must never be used to confidently rule out babesiosis. Experienced microscopists are also essential, as misidentification may occur when differentiating Babesia from Plasmodium or artifact structures.
Serology and Molecular Techniques
Indirect immunofluorescence assay (IFA) is the most widely used serologic method. It detects host antibodies directed against specific Babesia species. High IgM or IgG titers, often ≥1:256—suggest recent or active infection, although titers may remain elevated for months after clinical recovery.
Serologic testing is particularly useful in:
- Chronic or low-grade infections
- Blood donors being screened for transfusion safety
- Identifying species that are difficult to visualize microscopically
However, it cannot reliably distinguish between current and past infection, and antibody responses may be blunted in immunocompromised individuals.
PCR has revolutionized the diagnosis of babesiosis by enabling high-sensitivity detection of Babesia DNA, even when parasitemia is extremely low. PCR is invaluable in:
- Confirming infection when smears are negative
- Differentiating Babesia species (e.g., B. microti, B. duncani, B. divergens)
- Monitoring treatment response
- Screening blood supplies for transfusion-transmitted babesiosis
PCR assays are now widely used by reference laboratories and blood banks due to their superior sensitivity and specificity.
Treatment Options
The therapeutic approach varies significantly based on the patient’s immune status, degree of parasitemia, presence of co-infections, and the extent of organ involvement.
Antiparasitic Medications
Pharmacologic therapy is the cornerstone of babesiosis treatment, aimed at eliminating intraerythrocytic Babesia parasites and resolving hemolysis. Two major combination regimens are used:
1. Atovaquone–Azithromycin (First-line Therapy)
The preferred regimen for most patients is the combination of atovaquone and azithromycin. This choice is supported by strong clinical evidence demonstrating its favorable safety profile and high efficacy in mild-to-moderate disease.
- Atovaquone interferes with mitochondrial electron transport in the parasite, inhibiting nucleic acid and ATP synthesis.
- Azithromycin suppresses protein synthesis by binding to the 50S ribosomal subunit, providing synergistic parasiticidal activity.
This regimen is typically administered for 7–10 days, although treatment may be extended in patients with persistent symptoms or low-level parasitemia. Drug absorption improves when atovaquone is taken with fatty meals, an important counseling point for patients.
2. Clindamycin–Quinine (Alternative or Severe Cases)
The combination of clindamycin and quinine is generally reserved for:
- Severe babesiosis
- Patients intolerant to first-line therapy
- Cases with rapidly rising parasitemia or organ dysfunction
However, this regimen is associated with higher toxicity, with quinine often causing tinnitus, hearing disturbances, gastrointestinal upset, hypoglycemia, and cardiac conduction abnormalities. Clindamycin adds the risk of gastrointestinal intolerance and, rarely, Clostridioides difficile infection.
Supportive Care
Patients commonly experience fever, chills, and malaise; thus supportive care includes:
- Antipyretics to manage fever
- Adequate hydration, often intravenous in moderate-to-severe cases, to mitigate renal stress and support hemodynamic stability
- Rest and avoidance of strenuous activity to reduce metabolic demands during active hemolysis
These measures are especially important early in the disease, when fever and intravascular hemolysis peak.
- Routine monitoring involves checking:
- Hemoglobin and hematocrit levels
- Platelet counts
- Bilirubin and LDH levels (reflecting hemolysis)
- Renal and hepatic function
Patients with significant anemia may require packed red blood cell transfusions. Electrolyte abnormalities and acidosis should be addressed promptly to prevent further complications.
Because Babesia microti is frequently transmitted alongside Borrelia burgdorferi (Lyme disease) or Anaplasma phagocytophilum, patients may require additional antimicrobial therapy targeting these co-infections. Failure to treat coexisting infections may prolong symptoms and complicate recovery.
Treatment of Severe Cases
Severe babesiosis is a medical emergency requiring aggressive therapy, typically in a hospital setting or intensive care unit. Severe disease is characterized by:
- Parasitemia ≥10%
- Severe hemolytic anemia
- Acute respiratory distress syndrome (ARDS)
- Kidney failure
- Liver dysfunction
- Hemodynamic instability
- Disseminated intravascular coagulation (DIC)
IV clindamycin combined with oral or IV quinine is the regimen of choice in severe disease. These medications achieve rapid parasite clearance, which is essential in preventing irreversible organ damage.
One of the defining interventions for severe babesiosis is exchange transfusion, where a portion of the patient’s infected erythrocytes is replaced with parasite-free donor red blood cells. This procedure is indicated when:
- Parasitemia is extremely high (often ≥10%)
- Severe hemolysis is present
- The patient displays signs of end-organ dysfunction
Exchange transfusion rapidly lowers parasite burden, improves oxygen-carrying capacity, and reduces circulating inflammatory mediators.
Prevention Strategies
Tick avoidance remains the most effective and widely recommended method for preventing babesiosis. Because Babesia microti is transmitted when an infected tick feeds for an extended period, typically 36–48 hours, reducing tick contact and ensuring rapid tick removal significantly lowers the risk of infection.
Individuals in wooded, brushy, or grassy environments should adopt several protective behaviors:
- Wear long sleeves and long pants, preferably light-colored to make ticks easier to spot. Tucking pants into socks can help prevent ticks from reaching the skin.
- Use permethrin-treated clothing, which can kill ticks on contact. Permethrin remains active through multiple washes and is recommended by public health agencies for people living or working in endemic areas.
- Apply EPA-registered insect repellents to exposed skin. Repellents containing DEET, picaridin, IR3535, or oil of lemon eucalyptus (OLE) have proven efficacy against ticks.
- Perform full-body tick checks immediately after returning indoors. Ticks often attach in hidden areas such as the scalp, behind the knees, the waistline, and the armpits.
- Shower within two hours of coming indoors, which can help remove unattached ticks and reduce the risk of infection.
- Prompt removal of attached ticks using fine-tipped tweezers minimizes the likelihood of transmission because Babesia requires prolonged feeding to be transmitted.
Ticks thrive in areas with dense vegetation and moisture. Modifying the environment around homes reduces tick habitat:
- Keep grass short, prune shrubs, and remove leaf litter, wood piles, and overgrown brush where ticks and their rodent hosts hide.
- Create gravel or woodchip barriers between lawns and wooded areas to reduce tick migration into frequently used spaces.
- Use tick-targeted pesticide treatments or tick tubes (that target rodents carrying ticks) in high-risk properties when recommended by pest control professionals.
- Treat pets with veterinarian-approved tick prevention products. Pets can bring ticks into the home even if they do not develop babesiosis themselves.
Blood Donation Screening
Babesiosis can spread through blood transfusions. Blood establishments have implemented nucleic acid testing (NAT) to detect Babesia DNA in donated blood. This method reduces the risk of transfusion-transmitted babesiosis.
Donors in endemic areas are screened more rigorously. Some blood banks defer donations from individuals with recent tick exposure.
Patients receiving blood transfusions, especially those immunocompromised or elderly, should be monitored for babesiosis symptoms.
Potential Complications
Babesiosis can lead to serious health issues, especially in individuals with weakened immune systems or pre-existing conditions. The infection primarily affects red blood cells and vital organs, causing significant physiological stress.
Hemolytic Anemia
Babesia parasites invade and destroy red blood cells, leading to hemolytic anemia. This results in a decrease in red blood cell count, reducing oxygen delivery to tissues. Symptoms include fatigue, paleness, shortness of breath, and rapid heart rate.
Laboratory tests often show elevated levels of lactate dehydrogenase (LDH) and bilirubin, markers of red blood cell breakdown. Severe anemia may require blood transfusions. In some cases, hemolysis triggers jaundice due to bilirubin accumulation.
Patients with underlying hemoglobin disorders or compromised immune systems are at greater risk. Persistent hemolysis can cause complications such as dark urine and an enlarged spleen.
Organ Dysfunction
Severe babesiosis can extend beyond hematologic complications and affect multiple organ systems. Systemic inflammation, reduced tissue oxygenation, and deposition of hemolytic debris collectively contribute to organ failure. Several organs are particularly vulnerable:
Kidneys
Acute kidney injury (AKI) is a recognized complication and occurs through several mechanisms. Free hemoglobin released from lysed red blood cells can accumulate in the renal tubules, causing obstruction and oxidative damage. Reduced renal perfusion—secondary to anemia, intravascular volume depletion, or sepsis—further compounds injury. Clinically, kidney involvement manifests as decreased urine output, rising creatinine levels, electrolyte imbalances, and fluid retention. In severe cases, renal replacement therapy (dialysis) may be required.
Liver
The liver is often affected due to its role in processing bilirubin and filtering damaged blood cells. Elevated liver enzymes (AST, ALT, ALP) are common, signaling hepatocellular stress. Hyperbilirubinemia, both direct and indirect, contributes to jaundice and may indicate impaired hepatic clearance. In high parasitemia states, hepatic dysfunction may progress rapidly, especially among individuals with pre-existing liver disease or those receiving immunosuppressive therapy.
Lungs
Respiratory complications, although less common, represent some of the most severe outcomes. Acute respiratory distress syndrome (ARDS) can develop in the setting of overwhelming inflammation, capillary leak, and diffuse alveolar damage. Patients may experience shortness of breath, hypoxia, and diffuse pulmonary infiltrates on imaging. ARDS requires immediate critical care management, often including mechanical ventilation.
Sepsis and Septic Shock
In fulminant cases, babesiosis can trigger a systemic inflammatory response resembling bacterial sepsis. Massive hemolysis, immune dysregulation, and tissue hypoxia collectively drive cytokine release and widespread inflammation. This can result in hypotension, altered mental status, coagulopathy, and multi-organ failure. Septic shock requires aggressive fluid resuscitation, vasopressors, and close monitoring in an intensive care setting.
Splenic Complications
The spleen plays a key role in filtering parasitized erythrocytes. As parasitemia increases, the spleen becomes increasingly congested and enlarged. Splenomegaly is common, and in rare cases, splenic rupture may occur due to increased vascular fragility and pressure. Rupture presents with acute abdominal pain, internal bleeding, and hemodynamic instability, requiring surgical intervention.
Patients without a functioning spleen (asplenia) are at particularly high risk of severe babesiosis. Without splenic filtration, parasitemia can rise dramatically, leading to overwhelming infection and increased mortality.
Cardiovascular Complications
Cardiac involvement may occur in severe disease due to prolonged hypoxia, anemia-induced strain, and systemic inflammation. Patients may develop arrhythmias, myocarditis, or heart failure, especially if underlying cardiac disease exists. Tachycardia is a common compensatory response to anemia, but persistent demand on the heart can exacerbate existing cardiovascular conditions.
Babesiosis in Animals
Babesiosis affects several animal species, primarily transmitted through tick bites.
Canine Babesiosis
Canine babesiosis is caused mainly by Babesia canis and Babesia gibsoni. These protozoan parasites invade red blood cells, leading to hemolytic anemia.
Symptoms include pale mucous membranes, jaundice, fever, and weakness.
Dogs exposed to ticks in endemic areas are at risk. Treatment commonly involves antiprotozoal drugs such as imidocarb dipropionate or atovaquone combined with azithromycin.
Other Animal Hosts
Babesiosis also affects cattle, horses, and wild animals. In cattle, Babesia bovis and Babesia bigemina cause bovine babesiosis, often called “Texas cattle fever.”
Affected animals show high fever, anemia, and reduced milk production. Economic losses in livestock due to babesiosis are significant.
Equine babesiosis, caused by Babesia caballi and Theileria equi, leads to fever, anemia, and swelling. Wild animals like deer can serve as reservoirs.
Control relies on tick management and preventive measures like acaricides to reduce transmission.