Babesiosis BMJ

Babesiosis
Straight to the point of care
Last updated: Sep 08, 2021

Table of Contents
Overview 3
Summary 3
Definition 3
Theory 4
Epidemiology 4
Aetiology 4
Pathophysiology 5
Classification 5
Case history 6
Diagnosis 8
Approach 8
History and exam 10
Risk factors 11
Investigations 13
Differentials 16
Criteria 17
Management 18
Approach 18
Treatment algorithm overview 20
Treatment algorithm 22
Emerging 28
Primary prevention 28
Secondary prevention 28
Patient discussions 29
Follow up 30
Monitoring 30
Complications 31
Prognosis 32
Guidelines 33
Diagnostic guidelines 33
Treatment guidelines 33
Online resources 34
References 35
Images 40
Disclaimer 42
Babesiosis Overview
Summary
Babesiosis is transmitted to humans through the blood meal of Ixodes ticks, the same vector as for Lyme
disease and human granulocytic anaplasmosis.
OVERVIEW
Peak transmission occurs from May to September in upper midwestern and northeastern US. The disease is
rare in other countries.
Transfusion-related transmission is emerging as an important secondary mode of transmission; therefore,

transmission can occur anywhere and at any time of year.
Usually asymptomatic or presents as a mild viral-type illness in young and healthy people. May cause more
serious disease or be fatal in asplenic or immunocompromised patients and in older people.
Diagnosis is made by visualisation of parasites on a peripheral blood smear or by molecular testing.
Management depends on the severity of disease and includes observation and monitoring, antimicrobials,
and/or exchange transfusion.
Definition
Babesiosis is a tick-borne zoonotic disease typically characterised by fever, haemolysis, and
haemoglobinuria. It is most frequently caused by the intra-erythrocytic parasite Babesia microti , commonly
transmitted through the bite of Ixodes ticks (deer ticks).[1]
This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Sep 08, 2021.
BMJ Best Practice topics are regularly updated and the most recent version of the topics
3
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Babesiosis Theory
Epidemiology
Babesiosis has been a nationally notifiable condition in the US since 2011, although it may not be a
reportable condition in every state. In 2019, 2420 cases were reported, with the majority reported from
THEORY
states in the northeastern and upper midwestern US (i.e., Connecticut, Massachusetts, Minnesota, New
Jersey, New York, Rhode Island, and Maine).[9] Peak transmission occurs from May to September in upper
midwestern and northeastern US.[6]
In the US, most cases of babesiosis are caused by Babesia microti .[1] However, babesiosis due to species
other than B microti (such as B duncani /MO-1) has been reported in northern California, Washington
State, Kentucky, and Missouri in the US, and in Canada.[4] [CDC: Babesiosis - national surveillance] (http://
www.cdc.gov/parasites/babesiosis/surveillance.html)
Babesiosis is rare in Europe, occurring mostly in splenectomised patients in France and the UK, and is most
frequently due to B divergens .[8] A case of babesiosis was reported in the UK in 2020.[10] Babesiosis is
also rare in other countries. Infection with B venatorum has been reported in East Asia.[11]
Aetiology
In the US, most cases of babesiosis are caused by Babesia microti . Less commonly, other Babesia types
( B duncani in the US; B divergens in Europe; and B venatorum in Europe and East Asia) may also
cause babesiosis.[11] Clinical infections are more common in asplenic patients, those with concurrent Lyme
disease or human granulocytic anaplasmosis, patients with immunosuppression (either due to HIV infection
or drug induced), or older patients.
Infection may result due to:
• Tick bite: in the great majority of patients infection is transmitted through the bite of Ixodes ticks.
[Centers for Disease Control and Prevention: tick ID] (https://www.cdc.gov/ticks/tickbornediseases/
tickID.html) The vast majority of cases in the US occur in people who live in or have travelled to
areas endemic for babesiosis, including coastal regions of the northeastern US and the northern
midwest.[12] [6] Residents of endemic areas can have seroprevalence rates as high as 10%.[13]
Approximately one third of patients with evidence of babesiosis recall a preceding tick bite.[5] Thus, a
history of preceding tick bite is helpful, but a history of no known preceding tick bite should not be used
to rule out disease. Attached ticks should be removed promptly, as the risk of infection increases with
the amount of time the tick remains attached.
• Blood transfusion: infection has also been transmitted through blood transfusion, an uncommon
but emerging route of disease transmission. The US Food and Drug Administration recommends
regional testing for Babesia in blood donor samples.[14] The risk of transmission through transfusion
in endemic areas has been estimated to be 0.17% per unit of packed cells.[15] Over 70 cases of
transfusion-associated disease transmission have been reported over the past 30 years in the US,
with most of the cases occurring in the past 10 years. Many of the donors and recipients were not
residents of areas endemic for babesiosis, but donors had travelled to areas of endemicity in the
weeks or months preceding donation.[16] Most donors are asymptomatic at the time of donation, and
it is common for a single donor or donation to infect multiple patients.[17] This highlights the important
impact of prolonged asymptomatic parasitaemia in many infected people.[18] [19]
• Vertical transmission: congenital infection has been reported, with data suggesting that transplacental
infection can occur.[20]
4 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Sep 08, 2021.
Babesiosis Theory
Pathophysiology
Babesia parasites are deposited into the dermis of humans who are bitten by an Ixodes tick during the
last hours of tick feeding, which may last for 48 to 72 hours or more. These parasites invade RBCs and
THEORY
reproduce asexually inside the cells. The incubation period for development of symptoms ranges from 5 to
30 days, but may be as long as 63 days in blood transfusion cases.[21] Haemolysis occurs when parasites
burst from erythrocytes and through erythrophagocytosis by macrophages.[8] [22] It is not clear whether
sequestration of infected RBCs plays a part in pathophysiology, as it does in malaria.
Clearance of parasites is likely to depend on both the innate and adaptive branches of the immune system.
B microti infection in mice depleted of T cells leads to higher parasitaemia than in those with intact immune
systems.[23] Additionally, studies in mice indicate that CD4+ T cells are critical for control and elimination of
Babesia organisms. The production of the cytokine interferon (IFN)-gamma, which is associated with CD4+
T-cell activation (Th-1 cells), is key to a successful immune response. Babesia -immune mice depleted
of the IFN-gamma gene became highly susceptible to re-challenge with B microti , indicating that IFN-
gamma is important for protective immunity.[24] Additionally, killed, fixed B microti parasites given to mice
with a glucan adjuvant (which stimulates granulocyte and macrophage production) controlled parasitaemia
significantly more than killed, fixed parasites given alone.[25] Macrophages and natural killer cells play a
role in control of parasitaemia and survival in infections with the WA-1 strain, but their role with B microti in
humans is not well understood.[26]
Classification
Aetiological classification
Babesia microti
• The most common species causing disease in the US, endemic in coastal regions of the northeast
and the lakes region of the upper midwest, transmitted by the deer tick. Isolated cases of human
babesiosis caused by B microti -like parasites have been reported in Germany, Japan, and Taiwan
and uncharacterised babesias have also been detected in patients from South Africa, Brazil, India, and
Egypt.[2]
B divergens
• The most common species causing disease in Europe, but only 40 to 50 cases have been reported
overall.
• A related though quite distinct babesia, B venatorum (EU1), was incriminated in similar, though
generally milder cases in Austria, Italy, and Germany.[3]
• In the US, B divergens -like parasites (i.e., MO-1) have caused acute disease in 3 asplenic patients.
B duncani (CA-5, WA-1, CA-1)[4]
• Other species of Babesia found to cause sporadic cases in California, Washington State, Missouri,
and Kentucky.
5
Babesiosis Theory
Case history
Case history #1
THEORY
A 35-year-old woman living in coastal Connecticut finds a tick attached behind her knee in August. Her
primary care provider removes the tick, notes it to be an engorged Ixodes scapularis nymph, and gives
her 1 dose of doxycycline for prophylaxis of Lyme disease. Two weeks later, the woman develops gradual
onset of malaise and fatigue, followed by fever. She visits her primary care provider again, who orders an
FBC, liver profile, and serology for antibodies to Borrelia burgdorferi and Anaplasma phagocytophilum
and obtains a Giemsa-stained thin blood smear. The blood smear reveals small, intra-erythrocytic
ring forms consistent with Babesia microti . The patient receives a 7-day course of azithromycin and
atovaquone, with complete resolution of symptoms. Antibodies to Borrelia burgdorferi and Anaplasma
phagocytophilum are not detected.
Case history #2
A 65-year-old man living in Nantucket, Massachusetts and receiving rituximab for lymphoma presents
to the emergency department of his local hospital with 2 days of fever and shaking chills. He is noted to
have severe anaemia, proteinuria, and haemoglobinuria. The patient is admitted to hospital, and broad-
spectrum antibiotics are started for presumed bacterial infection. Soon after admission, he develops
respiratory failure, requiring mechanical ventilation. A blood smear obtained on day 2 reveals intra-
erythrocytic ring forms with parasitaemia of 20%. The patient has not travelled away from Nantucket in
several years. Treatment for babesiosis with intravenous clindamycin and oral quinine is initiated, and
the patient also receives exchange transfusions. Parasitaemia decreases and the patient no longer
needs mechanical ventilation by day 4. He is discharged home after 14 days, but his outpatient course is
complicated by relapsing parasitaemia requiring additional courses of anti-babesial treatment.
Other presentations
Most infections of Babesia microti in young healthy people are subclinical or mild and are likely often to
go undiagnosed. Because unengorged Ixodes scapularis nymphs are quite small (2 mm), most patients
do not recall receiving a tick bite.
Clinical infections are more common in asplenic patients, those with concurrent Lyme disease, patients
with immunosuppression (either due to HIV infection or drug induced), or older patients. Symptoms
appear 1 to 4 weeks after the tick bite, with a gradual onset of malaise, fatigue, myalgias, arthralgias,
shaking, and chills.[5] A sustained or intermittent fever may develop within 1 week of symptom onset.
Less frequent symptoms include anorexia, vomiting, cough, abdominal pain, photophobia, conjunctival
injection, and a sore throat.[6]
Manifestations such as haemolytic anaemia or thrombocytopenia may be severe or life threatening,

and disease can rarely also be fatal. Complications include acute respiratory failure, disseminated
intravascular coagulation, congestive heart failure, coma, renal failure, and splenic rupture or infarct.[6] [7]
Infection with Babesia divergens , which is more commonly found in Europe, occurs mostly in asplenic
patients, and is always fulminant and haemolytic.[8] Infections with rarer species, such as Babesia
duncani , MO-1 and CA-1, also tend to be fulminant.[4]
Babesiosis Theory
THEORY
7
Babesiosis Diagnosis
Approach
Diagnosis of babesiosis is based on epidemiological, clinical, and laboratory information. Diagnostic criteria
include the presence of viral infection-like symptoms and identification of babesial parasites in blood by
smear evaluation, or by polymerase chain reaction (PCR) amplification of babesial DNA.
Babesiosis is a nationally notifiable disease in some countries and should be reported to local authorities.
History
Disease occurs mainly in those who live in or travel to endemic areas, or who have received a blood
transfusion containing the parasite within the previous 9 weeks.[29] Peak transmission occurs from May
to September in upper midwestern and northeastern US; however, transfusion-related transmission can
occur anywhere and at any time of year.[6] The disease is rare in other countries. Because unengorged
Ixodes scapularis nymphs are quite small (2 mm), most patients do not always recall receiving a tick bite.
Most infections of Babesia microti in young healthy people are subclinical or mild and are likely to
often go undiagnosed. A full history should be taken to include recognised conditions (e.g., asplenia/
previous splenectomy, malignancy, and HIV infection), as clinical infections are more common in asplenic
patients, those with concurrent Lyme disease, patients with immunosuppression (either due to HIV or
drug induced), or older patients. Symptoms may appear 1 to 4 weeks after the tick bite, with a gradual
onset of malaise, fatigue, myalgias, sweats, arthralgias, shaking, and chills.[5] A sustained or intermittent
fever may develop within 1 week of symptom onset.
Less frequent symptoms include anorexia, vomiting, cough, abdominal pain, photophobia, conjunctival
injection, and a sore throat. Manifestations such as haemolytic anaemia or thrombocytopenia may be
severe or life-threatening, and disease can (rarely) also be fatal.[6]
Infection with B divergens , which is more commonly found in Europe, occurs mostly in asplenic patients
and is always fulminant and haemolytic.[8] Infections with rarer species such as B duncani , MO-1, and
CA-1 also tend to be fulminant.[4]
DIAGNOSIS
Physical examination
Physical examination findings are non-specific and may include fever, splenomegaly, hepatomegaly, or
jaundice.[6] Pyrexia is one of the most common findings on physical examination. Petechiae, splinter
haemorrhages, or ecchymoses are infrequently found and, if present, indicate disseminated intravascular
coagulation.
Investigations
Because the clinical findings are non-specific, laboratory testing is required to confirm the diagnosis.
Those who require testing include:
• Any patient with influenza-like symptoms who reports a history of a tick bite and who lives in or has
travelled to an endemic area over the previous 5 weeks. Endemic areas include coastal areas of
the northeastern US and the lakes region of the upper midwest.
• Persistent influenza-like symptoms in a patient with no history of tick bite residing in an endemic
area, as two-thirds of those diagnosed with babesiosis report no history of a tick bite.
• Patients who have received a recent blood transfusion and have viral illness-type symptoms and/or
laboratory evidence of haemolysis.
• Patients with evidence of Lyme disease who do not respond adequately to antibiotic treatment for
Lyme disease (persistence of high fever after >48 hours of appropriate antibiotics, persistence of
viral illness-type symptoms after resolution of erythema migrans with antibiotics).
Initial laboratory investigations include:[6]
• FBC: may reveal decreased haematocrit (due to haemolytic anaemia), leukopaenia, or

thrombocytopaenia.
• LFTs: transaminases may be elevated.
• Serum creatinine and urea: may be elevated in severe cases.
• Urinalysis may reveal the presence of dark urine with urobilinogen and conjugated bilirubin
indicating haemolysis.
The Infectious Diseases Society of America (IDSA) recommends peripheral blood smear examination or
PCR for diagnostic confirmation of acute babesiosis, rather than antibody testing.[29]
Peripheral blood smear
• Light-microscopic identification of the parasite on Giemsa- or Wright-stained thin blood smears is

recommended for diagnostic confirmation.[6] [29]
• Manual review of blood smears should be requested explicitly. Multiple smears should be
examined, as only a few RBCs may be infected during the initial stages of infection.[6]
• Babesia may be confused with malarial parasites on blood smear (both appear as intraerythrocytic
rings). Therefore, additional laboratory testing may be considered to confirm the diagnosis and
identify the specific babesial pathogen.[6] Babesiosis and malaria have no geographic overlap, so
the epidemiologic history of the patient is extremely important.
• B microti may form tetrads (Maltese cross) within RBC.
Molecular testing
• PCR amplification of blood for babesial DNA is another diagnostic confirmation option, when
available.[6] [29]
DIAGNOSIS
• PCR may be considered in patients with intraerythrocytic ring-like structures on blood smear, to
differentiate from malaria, and for patients with negative smears for whom clinical suspicion is
high.[30] [31]
Serological testing
• Serological testing can provide supportive evidence for the diagnosis, but does not reliably
distinguish between active and prior infection.[6]
• A single positive antibody test is not sufficient to establish a diagnosis as Babesia antibodies can
persist in the blood for a year or more following apparent clearance of infection (with or without
treatment). Therefore, in patients who have a positive antibody test only, IDSA recommends
confirmation with peripheral blood smear or PCR before treatment is considered.[29]
ELISA and/or immunofluorescence assay for Lyme disease should be included in the differential
diagnosis of any patient who develops fever or clinical illness after tick bite. It is transmitted through the
bite of the deer tick (Ixodes scapularis ), the same vector as for B microti .
PCR and/or immunofluorescence assay or buffy coat smear for human granulocytic anaplasmosis should
be included in the differential diagnosis of any patient who develops fever or clinical illness after tick bite.
It is transmitted through the bite of the deer tick (I scapularis) , the same vector as for B microti.
9
Follow-up laboratory testing
Once started on treatment, patients with moderate to severe disease should have the haematocrit
and peripheral blood smear monitored daily or every other day until parasitaemia falls below 5% of
erythrocytes parasitised.[32] Quantitative PCR can be used to monitor B microti parasitaemia, even at
submicroscopic levels, during and after treatment.[30] [31]
Testing for Borrelia burgdorferi (Lyme disease) antibodies and Anaplasma phagocytophilum (HGA or
ehrlichiosis) co-infection in patients with severe or persistent symptoms despite receipt of appropriate anti-
babesial therapy should be considered.
Additionally, testing for HIV infection and for other causes of immunodeficiency (such as malignancy or
asplenia) should be considered in patients with severe or prolonged disease.[33]
History and exam

Key diagnostic factors
presence of risk factors (common)
• Key risk factors include travel to or residence in areas endemic for babesiosis, exposure to Ixodes
scapularis ticks, and immunosuppression or asplenia.
Other diagnostic factors

constitutional symptoms (common)
• Fatigue, fever, chills, myalgias, arthralgias, headache, anorexia, nausea, vomiting, and abdominal pain
have all been reported with varying frequency during babesiosis infection.
• Not all patients are symptomatic or febrile.
pyrexia (common)
DIAGNOSIS
• A sustained or intermittent fever may develop within 1 week of symptom onset.

• One of the most common findings on physical examination.
jaundice (uncommon)
• May be found on physical examination.
hepatosplenomegaly (uncommon)
• May be found on physical examination.
petechiae, splinter haemorrhages, or ecchymoses (uncommon)

• Infrequently found on physical examination and indicate disseminated intravascular coagulation.
dark urine (uncommon)

• Infrequently found on physical examination and may indicate haemolysis.
conjunctival injection (uncommon)

• Occurs infrequently.
cough (uncommon)
sore throat (uncommon)

photophobia (uncommon)
Risk factors
Strong
residence in or travel to an endemic region
• The vast majority of cases occur in people who live in or have travelled to areas endemic for
babesiosis in the US. Disease is spread through the bite of Ixodes ticks, which have a specific
geographic distribution.
• Endemic areas include coastal regions of the northeastern US and the northern midwest.[6] [12]
• Residents of endemic areas can have seroprevalence rates as high as 10%.[13]
exposure to Ixodes scapularis ticks

• I scapularis deer ticks transmit Babesia microti , as well as Borrelia burgdorferi and Anaplasma
phagocytophilum .
• Risk of disease transmission increases with duration of tick attachment, so prompt removal of ticks
may help prevent spread of disease.
• Approximately one third of patients with evidence of babesiosis recall a preceding tick bite.[5] Thus, a
history of preceding tick bite is helpful, but a history of no known preceding tick bite should not be used
to rule out disease.
DIAGNOSIS
asplenia
• People who have had surgical removal of their spleen or who have a non-functional spleen are at
higher risk for clinical infections and severe or persistent disease.
• Three of 9 (33%) patients who died after transfusion-related babesiosis, and 11 of 34 (32%) patients
admitted to hospital with severe babesiosis, had previous splenectomy.[5] [16] Another study found
that 10 of 14 case patients (71%) with relapsing or persistent disease were asplenic.[27]
immunosuppression
• Clinical infections are more common in patients with immunosuppression (either due to HIV or drug
induced).
• Immunosuppression also increases the risk of severe or persistent disease. Immunosuppressed
patients are more likely to experience complications, with higher peak parasitaemia, higher number of
babesiosis-related hospital admissions, and higher rates of fatalities.[27]
• In one study of immunosuppressed patients, 57% had B-cell lymphoma and had received rituximab
alone or with high-dose corticosteroids or further chemotherapy; 10 of the 14 patients were asplenic;
and 1 patient had HIV infection and met the case definition for AIDS with a CD4+ cell count <200.[27]
11
• Additionally, a case of severe disease in a patient receiving a tumour necrosis factor (TNF)-alpha
inhibitor for rheumatoid arthritis has been reported.[28]
Weak
blood transfusion
• The risk of transmission through transfusion in endemic areas has been estimated to be 0.17% per
unit of packed cells.[15] The US Food and Drug Administration recommends regional testing for
Babesia in blood donor samples.[14] Over 70 cases of transfusion-associated disease transmission
have been reported over the past 30 years in the US, most occurring in the past 10 years. Many
of the donors and recipients were not residents of areas endemic for babesiosis, but donors had
travelled to areas of endemicity in the weeks or months preceding donation.[16] Most donors are
asymptomatic at the time of donation, and it is common for a single donor or donation to infect multiple
patients.[17] This highlights the important impact of prolonged asymptomatic parasitaemia in many
infected people.[18] [19]
age >50 years

• Although all age groups appear to be equally affected, clinical infections are more common in older
patients. Most cases of severe disease also occur in those >50 years of age, although severe cases
have also been reported in very young patients.
Lyme disease
• Clinical infections are more common in patients with concurrent Lyme disease. This is transmitted
through the bite of the deer tick ( Ixodes scapularis ), the same vector as for Babesia microti .
human granulocytic anaplasmosis

• Clinical infections are more common in patients with concurrent human granulocytic anaplasmosis
disease. This is transmitted through the bite of the deer tick ( Ixodes scapularis ), the same vector as
for Babesia microti .
maternal infection during pregnancy

DIAGNOSIS
• Congenital infection has been reported, with data suggesting that transplacental infection can
occur.[20]
Investigations
1st test to order
Test Result
peripheral blood smear (Giemsa or Wright stained) presence of ring-like
structures within RBCs
• Order in all patients with suspected disease for diagnostic
confirmation.[6] [29]
• Manual review of blood smears should be requested explicitly.
Multiple smears should be examined, as only a few RBCs may be
infected during the initial stages of infection.[6]
• Babesia may be confused with malarial parasites on blood smear
(both appear as intraerythrocytic rings). Therefore, additional
laboratory testing may be considered to confirm the diagnosis and
identify the specific babesial pathogen.[6] Babesiosis and malaria
have no geographical overlap, so the epidemiological history of the
patient is extremely important.
• Test sensitivity depends on both the quality of the smear preparation
and the training of the person interpreting the smear.
DIAGNOSIS
Thin blood smear, Babesia microti , with ring forms
From the collection of Sarah Hochman, Albert
Einstein College of Medicine; used with permission
13
Test Result
Photomicrograph revealing the presence of what were determined

to be numbers of intraerythrocytic Babesia sp. ring-form parasites
CDC/ Dr Mae Melvin
polymerase chain reaction for babesial DNA presence of Babesia

microti DNA
• An alternative diagnostic confirmation option in patients with
suspected babesiosis, when available.[6] [29]
• May be considered in patients with detectable ring-like structures on
thin blood smear, to help differentiate from malaria, or for patients
with no detectable ring forms on smear for whom clinical suspicion is
high.[30] [31]
FBC variable; leukopaenia
with low haematocrit;
• Leukopaenia is common.
thrombocytopaenia
• Decreased haematocrit may be due to haemolytic anaemia.[6]
serum creatinine and urea variable; may be elevated
DIAGNOSIS
• May be elevated in severe cases.[6]

LFTs variable; transaminases
may be elevated
• Usually shows mildly to moderately elevated transaminases.[6]
urinalysis variable; trace to
moderate protein,
• Presence of dark urine, with urobilinogen and conjugated bilirubin,
urobilinogen and
may indicate haemolysis.
conjugated bilirubin may
be found
ELISA and/or immunofluorescence assay for Lyme disease variable; typically

negative; positive result
• Excludes Lyme disease as the principal diagnosis.
may indicate co-infection
• Lyme disease should be included in the differential diagnosis of any
patient who develops fever or clinical illness after tick bite.
• Patients with confirmed babesiosis who remain symptomatic despite
appropriate anti-babesial therapy should also be tested for Lyme
disease, as co-infection can occur and can worsen symptoms of
babesiosis.
• Specimens negative for Lyme disease by a sensitive ELISA or
immunofluorescence assay need not be tested further.
Test Result
polymerase chain reaction and/or immunofluorescence assay or variable; typically
buffy coat smear for human granulocytic anaplasmosis negative; positive result
may indicate co-infection
• Excludes human granulocytic anaplasmosis (HGA) as the principal
diagnosis.
• HGA should be included in the differential diagnosis of any patient
who develops fever or clinical illness after tick bite.
• Patients with confirmed babesiosis who remain symptomatic despite
appropriate anti-babesial therapy should be tested for HGA, as co-
infection can occur and can worsen symptoms of babesiosis.
• Anaplasma phagocytophilum may be detected as granulocytic
inclusions on thin blood smear as well.
Other tests to consider
Test Result
indirect immunofluorescence antibody assay for Babesia positive
microti
• Can provide supportive evidence for the diagnosis, but does not
reliably distinguish between active and prior infection.[6] The
Infectious Diseases Society of America (IDSA) recommends
peripheral blood smear examination or PCR for diagnostic
confirmation of acute babesiosis, rather than antibody testing.[29]
• A single positive antibody test is not sufficient to establish a diagnosis
as Babesia antibodies can persist in the blood for a year or more
following apparent clearance of infection (with or without treatment).
Therefore, in patients who have a positive antibody test only, IDSA
recommends confirmation with peripheral blood smear or PCR before
treatment is considered.[29]
• May be performed on acute and convalescent (4-6 weeks) serum
samples, although many will have detectable antibodies at acute
presentation. An IgG titer ≥1:1024 or the presence of IgM indicates
active or recent infection. A four-fold increase in IgG between acute
DIAGNOSIS
and convalescent serum confirms the diagnosis.[29]
• ELISA and immunoblot tests are also available but have limited use
for diagnosis.[29]
IgG/IgM immunoblot for Lyme disease presence of bands
signifying antibody to
• Only for patients with positive ELISA for Lyme disease.
Borrelia burgdorferi
HIV serology variable

• Confirms or excludes HIV infection in patients with severe or
prolonged disease. Results should be interpreted with caution as a
case of false-positive HIV serology has been reported in a patient
with active babesiosis.[33]
15
Differentials
Condition Differentiating signs / Differentiating tests

symptoms
Lyme disease • Lyme disease ( Borrelia • ELISA or
burgdorferi ) is transmitted immunofluorescence
through the bite of the deer for Borrelia burgdorferi
tick ( Ixodes scapularis ), the antibodies.
same vector as for Babesia • Diagnosis of Lyme disease
microti . does not exclude diagnosis
• Signs and symptoms may be of babesiosis, as co-infection
similar. can occur.
• Early Lyme disease may
manifest with a characteristic
'bull's-eye' rash (erythema
migrans). Erythema migrans
is not seen in babesiosis.
Human granulocytic • Caused by Anaplasma • Giemsa-stained thin blood

anaplasmosis phagocytophilum . smear may show the intra-
• Spreads through the bite of granulocytic inclusions
the Ixodes deer tick, the characteristic of human
same vector as for Babesia granulocytic anaplasmosis
microti and Lyme disease. (HGA).
• May present acutely, with • Acute and convalescent
fever, chills, and headache, phase indirect fluorescent
as opposed to the more assay may reveal antibodies
gradual onset of babesiosis. against A phagocytophilum .
However, it may also present • Diagnosis of HGA does
as a mild, self-limiting illness. not exclude diagnosis of
babesiosis, as co-infection
can occur.
Rock y Mountain spot ted • Signs and symptoms may be • Immunofluorescence or

DIAGNOSIS
fever similar. Luminex assay demonstrate

• Both are tick-borne RMSF antibodies (usually
infections, and both may confirmed on convalescent
cause fever, myalgias, serum).
thrombocytopenia, and
anaemia.
• Rocky Mountain
spotted fever (RMSF)
frequently presents with a
maculopapular or petechial
rash, whereas a rash is rare
in babesiosis.
Tularaemia • Transmitted via ticks, flies, • Francisella tularensis can

and other arthropod vectors. be isolated by blood culture
• Causes fever and anorexia with buffered charcoal and
similar to babesiosis. It can yeast extract or media
also cause septicaemia and supplemented with cysteine.
death, even in people with
intact immune systems.
Condition Differentiating signs / Differentiating tests

symptoms
• Unlike babesiosis,
it frequently causes
suppurative lymphadenitis.
Malaria infection • Signs and symptoms may be • Giemsa- or Wright-stained

similar. However, geographic thin blood smear: both
distribution of malaria and Babesia microti and
babesiosis is different, and Plasmodium falciparum form
the cyclic nature of malaria multiple intra-erythrocytic
fever is absent in babesiosis. rings, but P falciparum
• If a patient has travelled to forms extra-erythrocytic
or resides in coastal areas of gametocytes, whereas B
the northeastern US or the microti does not. B microti
lakes region of the midwest, may also form tetrads
babesiosis is more likely. (Maltese cross) within RBCs.
If the patient has travelled
to sub-Saharan Africa or
tropical regions, malaria is
more likely.
Infectious mononucleosis • Signs and symptoms • FBC may reveal an atypical

may be similar, although leukocytosis, as opposed to
splenomegaly is more leukopenia observed with
prevalent. babesiosis.
• Symptomatic infection often • Heterophile antibody test
affects young, otherwise is positive for Epstein-Barr
healthy people, whereas virus.
babesiosis is commonly
symptomatic in older or
immunocompromised
people.
Cytomegalovirus • Signs and symptoms may be • FBC may reveal an atypical

infection similar. leukocytosis, whereas
DIAGNOSIS
• Lymphadenopathy babesiosis may present with
is commonly seen in leukopenia.
cytomegalovirus (CMV) and • Polymerase chain reaction of
not in babesiosis. blood or body fluids for CMV
DNA confirms infection.
Criteria
A case definition is available from the Centers for Disease Control and Prevention (CDC):
[CDC: babesiosis (Babesia spp.) 2011 case definition] (https://wwwn.cdc.gov/nndss/conditions/babesiosis/

case-definition/2011)
17
Babesiosis Management
Approach
Management options in patients with a confirmed diagnosis include observation and monitoring, oral or
parenteral antimicrobials, and/or exchange transfusion depending on disease severity. The goal of treatment
is to reduce symptoms of disease and to eliminate parasitaemia while preventing complications of disease.
Current treatment recommendations presented here are for Babesia microti.
Asymptomatic patients
Observation is sufficient in asymptomatic patients. Antimicrobial therapy is not required unless parasites
are seen on thin blood smear for more than 1 month. Monitoring parasitemia using polymerase chain
reaction (PCR) testing is not indicated in asymptomatic immunocompetent hosts.[29]
Symptomatic patients: mild to moderate disease

These patients are generally immunocompetent, experience mild to moderate symptoms, have a
parasitaemia <4%, and are ambulatory and do not require hospital admission.[29]
Azithromycin plus atovaquone is the preferred first-line treatment option as it is clinically effective and
well-tolerated. Azithromycin slightly increases the risk of pyloric stenosis in infants <6 weeks of age, and
so should be used with caution in this group.[6] [29]
Clindamycin plus quinine is an alternative option. This combination is less preferred as it is frequently
associated with adverse effects such as tinnitus, vertigo, and gastrointestinal upset. However, it may
be considered when azithromycin plus atovaquone is not tolerated or is unavailable. Clindamycin
plus quinine is preferred when parasitaemia and symptoms have failed to abate following initiation of
atovaquone plus azithromycin.[6] [29]
The treatment course is 7 to 10 days. Clinical improvement generally occurs within a few days of starting
treatment. Fever and parasites on blood smear usually clear within a week. Monitoring parasitaemia
using peripheral blood smears is recommended during treatment of the acute illness; however, testing is
not recommended once symptoms have resolved. Fatigue and low-grade parasitaemia may persist for
weeks or months after treatment. Further monitoring and treatment are rarely needed in these patients as
relapse rarely occurs.[6] [29]
Monitoring parasitaemia during treatment of acute illness using peripheral blood smears is recommended;
however, testing is not recommended once symptoms have resolved.[29]
Symptomatic patients: acute severe disease

Patients should be admitted to hospital and treated with a combination of either:
• Intravenous azithromycin plus oral atovaquone; or

• Intravenous clindamycin plus oral quinine.
The Infectious Diseases Society of America (IDSA) recommends azithromycin plus atovaquone as the
preferred first-line treatment option as it is clinically effective and well-tolerated. Azithromycin slightly
MANAGEMENT
increases the risk of pyloric stenosis in infants <6 weeks of age, and so should be used with caution
in this group. Clindamycin plus quinine is preferred when parasitaemia and symptoms have failed to
abate following initiation of atovaquone plus azithromycin. It is also the preferred option in children as
there is a lack of evidence for the use of azithromycin plus atovaquone in children. Some experts may
use intravenous quinidine in place of oral quinine; however, quinidine is no longer available in some
countries.[29]
The Centers for Disease Control and Prevention recommends intravenous clindamycin plus oral
quinine as the preferred option in severely ill patients (parasitaemia levels ≥10% and/or organ-system
dysfunction).[6] [29]
Worsening of symptoms or increasing parasitaemia despite azithromycin plus atovaquone followed by

clindamycin plus quinine should prompt consideration of an alternative antimicrobial regimen.[29] Consult
an infectious diseases specialist for guidance on an appropriate regimen.
Treatment with the intravenous antibiotic should continue until symptoms abate, before the patient is
switched to all oral therapy. The treatment course is typically 7 to 10 days in total.[29] Longer duration
of therapy may be required in patients with very high parasitaemia or in those with severe or persistent
symptoms, although no controlled studies have evaluated prolonged therapy. The treatment duration may
also need to be extended to at least 6 weeks in patients who are immunocompromised.[29] [32]
Aggressive supportive care (e.g., vasopressor therapy, mechanical ventilation, dialysis) may be required
in some patients.[6] Cases of infection with B divergens and B divergens -like species (such as MO-1)
are medical emergencies and should be treated as such. Consultation with a critical care and infectious
disease specialist is recommended.
Exchange transfusion using red blood cells rapidly decreases parasitaemia by replacing parasitised with
non-parasitised erythrocytes. It may be considered for patients with high-grade parasitaemia (>10%) or
those who have any one or more of the following: severe haemolytic anaemia and/or severe pulmonary,
renal, or hepatic compromise. In cases of life-threatening babesiosis, the potential benefits of exchange
transfusion likely outweigh potential risks. Adverse effects include transfusion reactions, worsening of
thrombocytopaenia, and complications associated with venous access devices. Consultation with a
transfusion services physician or haematologist in conjunction with an infectious diseases specialist
is recommended.[29] Trials of systematic comparisons between antimicrobial therapy alone and
antimicrobial therapy plus exchange transfusion have not been published.
Close clinical and laboratory follow-up, including FBC, renal and hepatic function, and peripheral blood
smear is essential to ensure clinical improvement, reduction in parasitaemia, and improvement in other
laboratory abnormalities, such as anaemia or renal dysfunction. In immunocompromised patients who
experience severe disease, peripheral blood smear should be monitored at least daily until parasitaemia
is <4%. After this, blood smears should be obtained at least weekly until no parasites are detected.
PCR testing should be considered if blood smears have become negative but symptoms persist. There
is no standardised approach to monitoring highly immunocompromised patients but close clinical and
laboratory follow-up are important.[29] Patients may have persistent low levels of parasitaemia for months
after completing treatment.
Patients with persistent symptoms or with especially severe disease despite appropriate therapy may
have co-infection with Borrelia burgdorferi or Anaplasma phagocytophilum , or both. Those found to be
co-infected should be treated appropriately. An underlying immunodeficiency should also be excluded in
MANAGEMENT
patients with severe or prolonged disease despite appropriate therapy. Consultation with an infectious
disease specialist is recommended.
19
Recurrent or refractory disease
Recurrent or prolonged parasitaemia is more frequently seen in immunocompromised people, especially
in patients with HIV.[1]
Peripheral blood smears and/or PCR should be performed if symptoms recur.[29]
Re-treatment with anti-babesial therapy, tailored to the severity of recurrent disease, may be required
if parasites are seen on blood smear or if babesial DNA is detected by PCR more than 3 months after
initial treatment, regardless of symptoms.[32] Consultation with an infectious disease specialist is
recommended.
Alternative antibiotic options used for refractory disease in immunocompromised patients include:[29]
• Atovaquone plus azithromycin plus clindamycin

• Atovaquone plus clindamycin
• Atovaquone/proguanil plus azithromycin
• Atovaquone plus azithromycin plus clindamycin plus quinine.
However, these regimens have limited evidence of efficacy
Clinical resistance to therapy has been documented in some severely immunocompromised patients who
required multiple courses of therapy.[34] In these cases, prolonged therapy has been required for cure.
Treatment algorithm overview

Please note that formulations/routes and doses may differ between drug names and brands, drug
formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer
Acute ( summary )
asymptomatic documented infection
1st observation
mild to moderate disease
1st oral antimicrobial therapy
acute#severe disease
1st oral and parenteral antimicrobial therapy
adjunct supportive care and monitoring
adjunct exchange transfusion
adjunct treatment of co-infection

MANAGEMENT
Ongoing ( summary )
recurrent or refractory disease
1st specialist referral and re-treatment
MANAGEMENT
21
Treatment algorithm
Please note that formulations/routes and doses may differ between drug names and brands, drug
formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer
MANAGEMENT
Acute
asymptomatic documented infection
1st observation
» Antimicrobial therapy is not required unless

parasites are seen on thin blood smear for more
than 1 month. Monitoring parasitaemia using
polymerase chain reaction (PCR) testing is not
indicated in asymptomatic immunocompetent
hosts.[29]
mild to moderate disease
1st oral antimicrobial therapy

Primary options
» azithromycin: children: 10 mg/kg orally

once daily (maximum 500 mg/dose) on the
first day, followed by 5 mg/kg once daily
(maximum 250 mg/dose); adults: 500 mg
orally on the first day, followed by 250 mg
orally once daily
-and-
» atovaquone: children: 20 mg/kg orally twice
daily, maximum 750 mg/dose; adults: 750 mg
orally twice daily
Secondary options
» clindamycin: children: 7-10 mg/kg orally

three to four times daily, maximum 600 mg/
dose; adults: 600 mg orally three times daily
-and-
» quinine sulfate: children: 8 mg/kg orally
three times daily, maximum 650 mg/dose;
adults: 650 mg orally three times daily
» Patients are generally immunocompetent,

experience mild to moderate symptoms, have a
parasitaemia <4%, and are ambulatory and do
not require hospital admission.[29]
» Azithromycin plus atovaquone is the preferred

first-line treatment option as it is clinically
effective and well-tolerated. Azithromycin slightly
increases the risk of pyloric stenosis in infants
<6 weeks of age, and so should be used with
caution in this group.[6] [29]
» Clindamycin plus quinine is an alternative

option. This combination is less preferred as it
is frequently associated with adverse effects
MANAGEMENT
such as tinnitus, vertigo, and gastrointestinal

upset. However, it may be considered when
azithromycin plus atovaquone is not tolerated
or is unavailable. Clindamycin plus quinine is
preferred when parasitaemia and symptoms
23
Acute
have failed to abate following initiation of
atovaquone plus azithromycin.[6] [29]
» Treatment course is 7 to 10 days. Clinical

improvement generally occurs within a few
days of starting treatment. Fever and parasites
on blood smear usually clear within a week.
Monitoring parasitaemia using peripheral blood
smears is recommended during treatment
of the acute illness; however, testing is not
recommended once symptoms have resolved.
Fatigue and low-grade parasitaemia may persist
for weeks or months after treatment. Further
monitoring and treatment are rarely needed in
these patients as relapse rarely occurs.[6] [29]
acute#severe disease
1st oral and parenteral antimicrobial therapy

Primary options
» azithromycin: children: 10 mg/kg

intravenously every 24 hours until symptoms
abate, followed by 5-10 mg/kg orally once
daily, maximum 500 mg/day; adults: 500 mg
intravenously every 24 hours until symptoms
abate, followed by 250-500 mg orally once
daily
A high dose of oral azithromycin (500–
1000 mg) should be considered in
immunocompromised patients.
-and-
» atovaquone: children: 20 mg/kg orally twice
daily, maximum 750 mg/dose; adults: 750 mg
orally twice daily
Secondary options
» clindamycin: children: 7-10 mg/kg

intravenously every 6-8 hours until symptoms
abate, followed by 7-10 mg/kg orally three
to four times daily, maximum 600 mg/dose;
adults: 600 mg intravenously every 6 hours
until symptoms abate, followed by 600 mg
orally three times daily
-and-
» quinine sulfate: children: 8 mg/kg orally
three times daily, maximum 650 mg/dose;
adults: 650 mg orally three times daily
» Patients should be admitted to hospital

and treated with a combination of either
MANAGEMENT
intravenous azithromycin plus oral atovaquone;

or intravenous clindamycin plus oral quinine.
» The Infectious Diseases Society of America

(IDSA) recommends azithromycin plus
atovaquone as the preferred first-line treatment
Acute
option as it is clinically effective and well-
tolerated. Azithromycin slightly increases the
risk of pyloric stenosis in infants <6 weeks of
age, and so should be used with caution in this
group. Clindamycin plus quinine is preferred
when parasitaemia and symptoms have failed
to abate following initiation of atovaquone plus
azithromycin. It is also the preferred option in
children as there is a lack of evidence for the
use of azithromycin plus atovaquone in children.
Some experts may use intravenous quinidine in
place of oral quinine; however, quinidine is no
longer available in some countries.[29]
» The Centers for Disease Control and

Prevention recommends intravenous clindamycin
plus oral quinine as the preferred option in
severely ill patients (parasitaemia levels ≥10%
and/or organ-system dysfunction).[6] [29]
» Worsening of symptoms or increasing

parasitaemia despite azithromycin plus
atovaquone followed by clindamycin plus
quinine should prompt consideration of an
alternative antimicrobial regimen.[29] Consult an
infectious diseases specialist for guidance on an
appropriate regimen.
» Treatment with the intravenous antibiotic

should continue until symptoms abate, before
the patient is switched to all oral therapy. The
treatment course is typically 7 to 10 days in
total.[29] Longer duration of therapy may be
required in patients with very high parasitaemia
or in those with severe or persistent symptoms,
although no controlled studies have evaluated
prolonged therapy. The treatment duration may
also need to be extended to at least 6 weeks in
patients who are immunocompromised.[32] [29]
adjunct supportive care and monitoring
Treatment recommended for SOME patients in
selected patient group
» Aggressive supportive care (e.g., vasopressor
therapy, mechanical ventilation, dialysis) may
be required in some patients. Cases of infection
with B divergens and B divergens -like species
(such as MO-1) are medical emergencies and
should be treated as such. Consultation with a
critical care and infectious disease specialist is
recommended.[6]
MANAGEMENT
» Close clinical and laboratory follow-up,

including FBC, renal and hepatic function,
and peripheral blood smear is essential to
ensure clinical improvement, reduction in
parasitaemia, and improvement in other
25
Acute
laboratory abnormalities, such as anaemia
or renal dysfunction. In immunocompromised
patients who experience severe disease,
peripheral blood smear should be monitored
at least daily until parasitaemia is <4%. After
this, blood smears should be obtained at
least weekly until no parasites are detected.
PCR testing should be considered if blood
smears have become negative but symptoms
persist. There is no standardised approach to
monitoring highly immunocompromised patients
but close clinical and laboratory follow-up are
important.[29]Patients may have persistent
low levels of parasitaemia for months after
completing treatment.
»
adjunct exchange transfusion
» Exchange transfusion using red blood cells
rapidly decreases parasitaemia by replacing
parasitised with non-parasitised erythrocytes.
It may be considered for patients with high-
grade parasitaemia (>10%) or those who
have any one or more of the following: severe
haemolytic anaemia and/or severe pulmonary,
renal, or hepatic compromise. In cases of life-
threatening babesiosis, the potential benefits of
exchange transfusion likely outweigh potential
risks. Adverse effects include transfusion
reactions, worsening of thrombocytopaenia, and
complications associated with venous access
devices. Consultation with a transfusion services
physician or haematologist in conjunction
with an infectious diseases specialist is
recommended.[29]
» Trials of systematic comparisons between

antimicrobial therapy alone and antimicrobial
therapy plus exchange transfusion have not
been published.
adjunct treatment of co-infection
» Patients with persistent symptoms or with
especially severe disease despite appropriate
therapy may have co-infection with B burgdorferi
MANAGEMENT
or A phagocytophilum , or both. Those found to

be co-infected should be treated appropriately.
Consultation with an infectious disease specialist
is recommended.
Ongoing
recurrent or refractory disease
1st specialist referral and re-treatment
» Recurrent or prolonged parasitaemia is more

frequently seen in immunocompromised people,
especially in patients with HIV.[1]
» Re-treatment with anti-babesial therapy,

tailored to severity of recurrent disease, may be
required if parasites are seen on blood smear
or if babesial DNA is detected by polymerase
chain reaction >3 months after initial treatment,
regardless of symptoms.[32]
» Clinical resistance to therapy has

been documented in some severely
immunocompromised patients who required
multiple courses of therapy.[34]In these cases
prolonged therapy has been required for cure.
» Consultation with an infectious disease

specialist is recommended.
MANAGEMENT
27
Emerging
Pentamidine plus trimethoprim/sulfamethoxa zole
This combination is moderately effective in improving symptoms and clearing parasitaemia in Babesia
divergens infection, but adverse reactions to intravenous pentamidine limit its use. Furthermore,
pentamidine's effect is too slow for its use against B divergens -like parasites.[35]
A zithromycin plus quinine

This combination was used successfully in 2 Taiwanese patients who had not improved after clindamycin
plus quinine. Both patients were cleared of parasitaemia with a course of azithromycin plus quinine.[36] [37]
Clindamycin plus dox ycycline plus a zithromycin

Use of this combination has been published as a case report.[38] An immunocompromised patient with HIV
infection presented with prolonged (for months) fever of unknown origin, and was subsequently found to have
babesiosis. The infection did not respond to clindamycin plus quinine, although treatment was complicated
by addition of antiretrovirals and episodic treatment interruptions. The infection was later controlled, but not
cured, with clindamycin, doxycycline, and high-dose azithromycin.
Atovaquone/proguanil
Use of atorvaquone/proguanil has been published as a case report of a patient with AIDS who failed to
respond to azithromycin plus atovaquone or clindamycin plus quinine, but who then responded to a 5-
drug regimen of atovaquone/proguanil, azithromycin, clindamycin, and quinine for 3 weeks, followed by
atovaquone/proguanil alone for 60 days.[39]
Primary prevention
No prophylactic treatment is available for high-risk patient groups.
If possible, areas endemic for Ixodes scapularis (deer tick) should be avoided between May and September,
especially tick-infested areas.[1] If exposure to ticks is unavoidable, exposed skin should be covered with
light-coloured clothes, and skin and clothes should be frequently inspected visually to identify ticks prior
to attachment. Application of tick and insect repellents that contain DEET to skin and clothes provides
additional protection, as does applying permethrin to clothes.[1] Tick feeding may last for 48 to 72 hours or
more. Attached ticks should be removed promptly, as the risk of infection increases with the amount of time
the tick remains attached.
Secondary prevention
Babesiosis is a nationally notifiable disease in some countries and should be reported to local authorities.
As with primary prevention, preventative measures are limited to avoidance of exposure to deer ticks ( Ixodes
scapularis ) in areas endemic for disease, and to applying insect repellent containing DEET when in wooded
areas.
As babesiosis is not usually transmitted from person to person, no screening or prophylaxis is required for
contacts of infected patients. However, there is a risk of transmission from blood donors with the advent of
MANAGEMENT
transfusion-related cases.[19] Consequently, there has been discussion in the scientific community regarding
the need for routine screening of blood donors for babesiosis.[41] The US Food and Drug Administration
(FDA) has approved nucleic acid and arrayed fluorescent immunoassay tests for use as donor screening
tests on whole blood, blood components, and living organ and tissue donors. The FDA recommends regional
testing for Babesia in blood donor samples using nucleic acid tests.[14]
Patient discussions
Patients should be instructed to complete the entire course of medication and to inform their healthcare
provider if symptoms of fever, myalgias, or fatigue worsen or fail to resolve. They should be told to refrain
from donating blood until advised that it is safe to do so.
Patients should be advised to avoid exposure to ticks or tick-infested areas to prevent re-infection.
[CDC: babesiosis] (https://www.cdc.gov/parasites/babesiosis/index.html)
[National Organization for Rare Disorders (NORD): babesiosis] (https://rarediseases.org/rare-diseases/

babesiosis)
MANAGEMENT
29
Babesiosis Follow up
Monitoring
Monitoring
FOLLOW UP
For patients with asymptomatic infection with positive babesial smears or positive polymerase chain
reaction (PCR) for babesial DNA, smears and/or PCR should be repeated and treatment should be
considered if parasitaemia persists for more than 1 month.[29]
In immunocompetent patients, monitoring parasitaemia during treatment of acute illness using peripheral
blood smears is recommended. However, testing is not recommended once symptoms have resolved.[29]
In immunocompromised patients, close clinical and laboratory follow-up, including FBC, renal and
hepatic function, and peripheral blood smear is essential to ensure clinical improvement, reduction in
parasitaemia, and improvement in other laboratory abnormalities, such as anaemia or renal dysfunction.
In immunocompromised patients who experience severe disease, peripheral blood smears should
be monitored at least daily until parasitaemia is <4%. After this, blood smears should be obtained
at least weekly until no parasites are detected. PCR testing should be considered if blood smears
have become negative but symptoms persist. There is no standardised approach to monitoring highly
immunocompromised patients but close clinical and laboratory follow-up are important.[29] Patients may
have persistent low levels of parasitaemia for months after completing treatment.
Complications
Complications Timeframe Likelihood
FOLLOW UP
acute respiratory failure short term low
Rare complication of severe infection, frequently due to adult respiratory distress syndrome. More
frequently seen with parasitaemia >10% and in older or immunocompromised patients.
disseminated intravascular coagulation short term low
Rare complication of severe infection, seen with parasitaemia >10% and in older or immunocompromised
patients.
congestive heart failure short term low
Rare complication of severe infection, seen in the setting of severe anaemia from haemolysis. Often
occurs in patients with underlying cardiac dysfunction or known coronary artery disease.
coma short term low
Rare complication of severe infection, seen in the setting of multi-organ failure in older or
immunocompromised patients with parasitaemia >10%.
acute renal failure short term low
Rare complication of severe infection, although varying degrees of renal dysfunction with severe disease
are more frequently seen.
treatment-related tinnitus or vertigo variable medium
Frequently seen in patients receiving clindamycin and quinine, often necessitating dose reduction.
Symptoms may persist for months after treatment is completed.
recurrent parasitaemia variable low
Most frequently seen in immunocompromised patients, especially those with HIV infection, and in patients
with severe disease.
Rare complication of mild or moderate disease in young, healthy patients.
autoimmune haemolytic anaemia variable low
Sporadic cases of post-babesiosis warm-antibody autoimmune haemolytic anaemia have been reported in
asplenic patients. Immunosuppressant treatment may be required.[40]
splenic complications variable low
31
Complications Timeframe Likelihood

Splenic complications are rare and include splenomegaly, splenic rupture, and splenic infarct. Unlike other
severe complications, these complications often occur in younger and immunocompetent patients, and
FOLLOW UP
they do not correlate with parasitaemia level.[7]
Prognosis
The majority of cases that are diagnosed and treated resolve without complication. In such cases,
prognosis is excellent. However, patients with confirmed infection should refrain from donating blood until
documentation of parasite clearance.
Additionally, many cases of babesiosis are asymptomatic or subclinical and go undiagnosed. These cases
resolve without specific antimicrobial treatment, although parasitaemia may persist for months.
Age <50 years and immunocompetent

In these patients the vast majority of infections are mild and respond quickly to antimicrobial therapy.
Complications are rare. A few cases of severe disease in young, healthy patients have been reported.
Age >50 years and/or immunosuppressed

Severe disease with complications such as persistent or relapsing parasitaemia, disseminated intravascular
coagulation, or renal failure is more common in this patient group. Three of 9 (33%) patients who died after
transfusion-related babesiosis and 11 of 34 (32%) patients admitted to hospital with severe babesiosis
had previous splenectomy.[5] [16] Another study found that 10 of 14 case patients (71%) with relapsing
or persistent disease were asplenic.[27] Immunosuppressed patients often require prolonged courses of
antimicrobial therapy and may require multiple courses for recurrent parasitaemia. In immunocompromised
patients, higher doses of azithromycin may be used.[29] Close follow-up after hospital discharge is
recommended.
Babesiosis Guidelines
Diagnostic guidelines
North America
2020 Guideline on diagnosis and management of babesiosis (ht tps://

academic.oup.com/cid/article/72/2/e49/6012666)
Published by: Infectious Diseases Society of America (IDSA) Last published: 2020
Tick borne diseases of the United States: a reference manual for health care
providers (ht tps://www.cdc.gov/ticks/tickbornediseases/index.html)
Published by: Centers for Disease Control and Prevention Last published: 2018
Treatment guidelines
GUIDELINES
North America
2020 guideline on diagnosis and management of Babesiosis (ht tps://

academic.oup.com/cid/article/72/2/e49/6012666)
Published by: Infectious Diseases Society of America (IDSA) Last published: 2020
Tick borne diseases of the United States: a reference manual for health care
providers (ht tps://www.cdc.gov/ticks/tickbornediseases/index.html)
Published by: Centers for Disease Control and Prevention Last published: 2018
33
Babesiosis Online resources
Online resources
1. CDC: Babesiosis - national surveillance (http://www.cdc.gov/parasites/babesiosis/surveillance.html)
(external link)
2. Centers for Disease Control and Prevention: tick ID (https://www.cdc.gov/ticks/tickbornediseases/

tickID.html) (external link)
3. CDC: babesiosis (Babesia spp.) 2011 case definition (https://wwwn.cdc.gov/nndss/conditions/

babesiosis/case-definition/2011) (external link)
4. CDC: babesiosis (https://www.cdc.gov/parasites/babesiosis/index.html) (external link)
5. National Organization for Rare Disorders (NORD): babesiosis (https://rarediseases.org/rare-diseases/

babesiosis) (external link)
ONLINE RESOURCES
Babesiosis References
Key articles
• Vannier E, Krause PJ. Human babesiosis. N Engl J Med. 2012;366:2397-2407. Abstract (http://
REFERENCES
www.ncbi.nlm.nih.gov/pubmed/22716978?tool=bestpractice.bmj.com)
• Centers for Disease Control and Prevention. Tickborne diseases of the United States: a reference
manual for health care providers, fifth edition. Jun 2018 [internet publication]. Full text (https://
www.cdc.gov/lyme/resources/tickbornediseases.pdf)
• Krause PJ, Auwaerter PG, Bannuru RR, et al. Clinical practice guidelines by the Infectious Diseases
Society of America (IDSA): 2020 guideline on diagnosis and management of Babesiosis. Clin Infect
Dis. 2021 Jan 27;72(2):e49-e64. Full text (https://www.doi.org/10.1093/cid/ciaa1216) Abstract (http://
• Sanchez E, Vannier E, Wormser GP, et al. Diagnosis, treatment, and prevention of Lyme disease,
human granulocytic anaplasmosis, and babesiosis: a review. JAMA. 2016;315:1767-77. Abstract
(http://www.ncbi.nlm.nih.gov/pubmed/27115378?tool=bestpractice.bmj.com)
References
1. Vannier E, Krause PJ. Human babesiosis. N Engl J Med. 2012;366:2397-2407. Abstract (http://
2. Hunfeld KP, Hildebrandt A, Gray JS. Babesiosis: recent insights into an ancient disease. Int
J Parasitol. 2008;38:1219-1237. Abstract (http://www.ncbi.nlm.nih.gov/pubmed/18440005?
tool=bestpractice.bmj.com)
3. Häselbarth K, Tenter AM, Brade V, et al. First case of human babesiosis in Germany - clinical
presentation and molecular characterisation of the pathogen. Int J Med Microbiol. 2007;297:197-204.
Abstract (http://www.ncbi.nlm.nih.gov/pubmed/17350888?tool=bestpractice.bmj.com)
4. Conrad PA, Kjemtrup AM, Carreno RA, et al. Description of Babesia duncani n.sp.
(Apicomplexa: Babesiidae) from humans and its differentiation from other piroplasms. Int
J Parasitol. 2006;36:779-789. Abstract (http://www.ncbi.nlm.nih.gov/pubmed/16725142?
5. Hatcher JC, Greenberg PD, Antique J, et al. Severe babesiosis in Long Island: review of
34 cases and their complications. Clin Infect Dis. 2001;32:1117-1125. Full text (http://
cid.oxfordjournals.org/content/32/8/1117.full) Abstract (http://www.ncbi.nlm.nih.gov/
pubmed/11283800?tool=bestpractice.bmj.com)
6. Centers for Disease Control and Prevention. Tickborne diseases of the United States: a reference
manual for health care providers, fifth edition. Jun 2018 [internet publication]. Full text (https://
www.cdc.gov/lyme/resources/tickbornediseases.pdf)
35
7. Dumic I, Madrid C, Rueda Prada L, et al. Splenic complications of Babesia microti infection in
humans: a systematic review. Can J Infect Dis Med Microbiol. 2020;2020:6934149. Full text (https://
www.doi.org/10.1155/2020/6934149) Abstract (http://www.ncbi.nlm.nih.gov/pubmed/32566058?
REFERENCES
8. Gelfand JA, Vannier E. Babesia species. In: Mandell GL, Bennett JE, Dolin R, eds. Mandell, Douglas
and Bennett's principles and practice of infectious disease. 6th ed. Philadelphia, PA: Elsevier;
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9. Centers for Disease Control and Prevention. National notifiable diseases surveillance system, 2019
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27. Krause PJ, Gewurz BE, Hill D, et al. Persistent and relapsing babesiosis in immunocompromised
patients. Clin Infect Dis. 2008;46:370-376. Full text (http://cid.oxfordjournals.org/content/46/3/370.full)
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39
Babesiosis Images
Images
IMAGES
Figure 1: Thin blood smear, Babesia microti , with ring forms

From the collection of Sarah Hochman, Albert Einstein College of Medicine; used with permission
Babesiosis Images
IMAGES
Figure 2: Photomicrograph revealing the presence of what were determined to be numbers of
intraerythrocytic Babesia sp. ring-form parasites
CDC/ Dr Mae Melvin
41
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Contributors:
// Authors:
Sarah Hochman, MD
Assistant Professor
Department of Medicine, Division of Infectious Diseases and Immunology, New York University School of
Medicine, New York, NY
DISCLOSURES: SH declares that she has no competing interests.
Louis Weiss, MD, MPH

Professor of Medicine
Division of Infectious Diseases, Professor of Pathology, Division of Parasitology and Tropical Medicine,
Albert Einstein College of Medicine, Bronx, NY
DISCLOSURES: LW has received grant funding from the National Institute of Allergy and Infectious
Diseases. He is also the author of references cited in this topic.
// Peer Reviewers:
Jeremy Gray, BSc, MSc, PhD

Professor
Department of Environmental Resource Management, University College Dublin, Belfield, Dublin, Republic
of Ireland
DISCLOSURES: JG declares that he has no competing interests.
Sam Telford III, ScD

Associate Professor of Biomedical Sciences
Division of Infectious Diseases, Cummings School of Veterinary Medicine, Tufts University, Boston, MA
DISCLOSURES: ST has active research funding from the NIH. ST is an author or co-author of numerous
primary publications on the biology of babesiosis, as well as reviews that have been referenced in this topic.
Raymond J. Dat twyler, MD

Professor of Medicine and Microbiology/Immunology
Chief of Allergy, Immunology and Rheumatology, New York Medical College, Valhalla, NY
DISCLOSURES: RJD declares that he has no competing interests.

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Babesiosis

Straight to the point of care

Last updated: Sep 08, 2021

Transfusion-related transmission is emerging as an important secondary mode of transmission; therefore,

Diagnosis is made by visualisation of parasites on a peripheral blood smear or by molecular testing.

Infection may result due to:

Manifestations such as haemolytic anaemia or thrombocytopenia may be severe or life threatening,

• FBC: may reveal decreased haematocrit (due to haemolytic anaemia), leukopaenia, or

Peripheral blood smear

• Light-microscopic identification of the parasite on Giemsa- or Wright-stained thin blood smears is

History and exam

Other diagnostic factors

• A sustained or intermittent fever may develop within 1 week of symptom onset.

petechiae, splinter haemorrhages, or ecchymoses (uncommon)

dark urine (uncommon)

conjunctival injection (uncommon)

sore throat (uncommon)

exposure to Ixodes scapularis ticks

age >50 years

human granulocytic anaplasmosis

maternal infection during pregnancy

Photomicrograph revealing the presence of what were determined

polymerase chain reaction for babesial DNA presence of Babesia

• May be elevated in severe cases.[6]

ELISA and/or immunofluorescence assay for Lyme disease variable; typically

Other tests to consider

HIV serology variable

Condition Differentiating signs / Differentiating tests

Human granulocytic • Caused by Anaplasma • Giemsa-stained thin blood

Rock y Mountain spot ted • Signs and symptoms may be • Immunofluorescence or

fever similar. Luminex assay demonstrate

Tularaemia • Transmitted via ticks, flies, • Francisella tularensis can

Condition Differentiating signs / Differentiating tests

Malaria infection • Signs and symptoms may be • Giemsa- or Wright-stained

Infectious mononucleosis • Signs and symptoms • FBC may reveal an atypical

Cytomegalovirus • Signs and symptoms may be • FBC may reveal an atypical

[CDC: babesiosis (Babesia spp.) 2011 case definition] (https://wwwn.cdc.gov/nndss/conditions/babesiosis/

Symptomatic patients: mild to moderate disease

Symptomatic patients: acute severe disease

• Intravenous azithromycin plus oral atovaquone; or

Worsening of symptoms or increasing parasitaemia despite azithromycin plus atovaquone followed by

Peripheral blood smears and/or PCR should be performed if symptoms recur.[29]

• Atovaquone plus azithromycin plus clindamycin

Treatment algorithm overview

mild to moderate disease

1st oral antimicrobial therapy

1st oral and parenteral antimicrobial therapy

adjunct supportive care and monitoring

adjunct exchange transfusion

adjunct treatment of co-infection

1st specialist referral and re-treatment

» Antimicrobial therapy is not required unless

1st oral antimicrobial therapy

» azithromycin: children: 10 mg/kg orally

» clindamycin: children: 7-10 mg/kg orally

» Patients are generally immunocompetent,

» Azithromycin plus atovaquone is the preferred

» Clindamycin plus quinine is an alternative

such as tinnitus, vertigo, and gastrointestinal

» Treatment course is 7 to 10 days. Clinical

1st oral and parenteral antimicrobial therapy

» azithromycin: children: 10 mg/kg

» clindamycin: children: 7-10 mg/kg