Babesiosis is caused by parasites of the genus Babesia that infect red blood cells. It is transmitted through the bites of infected ticks. Symptoms can range from mild to severe illness including fever, chills, sweats, headache, body aches, loss of appetite, nausea, or fatigue. Diagnosis involves examining blood smears for the characteristic ring-shaped parasites or detecting antibodies through serologic tests. Treatment involves antibiotic combinations like atovaquone-azithromycin or clindamycin-quinine. Prevention focuses on avoiding tick bites through proper clothing, repellents, and tick checks.

1. Babesiosis

2.  Introduction
 History
 Classification
 Structure
 Lifecycle
 Epidemiology
 Pathogenesis
 Clinical features
 Diagnosis
 Treatment
 Animal models
 Prevention

3. Introduction
• Infection due to parasites belonging to genus Babesia
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•
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•
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•
B. microti
B. divergens
B. duncani
WA-1
MO-1
KO -1
EU-1
• Obligate intracellular: RBCs
• Requires both a competent vertebrate and nonvertebrate
host to maintain transmission cycles
• Transmitted by ixodid ticks to their vertebrate hosts

4. History
Theobald Smith (July 31, 1859 – December 10, 1934) Along with
Kilbourne Discovered arthropod borne transmission in 1893
Cattle Febrile heamturia : Bloodied waters of
Egypt

5. History
 1957- 1st human case- Yugoslavian farmer
 1968- 1st recognized in California (USA)
 1976- Ixodes dammini identified as vector for B.
microti
 1993- 1st description of WA-1
 1996- 1st description of MO-1

6. Classification
 Taxonomic Classification
 phylum Apicomplexa (also called Sporozoa),
 class Aconoidasida (Piroplasmea)
 order Piroplasmida
 families Babesiidae and Theileriidae;

absence of a preerythrocytic cycle in Babesia and the absence
of transovarial transmission in Theileria.

7. • Initially, Babesia species identified - morphological
parameters of the intraerythrocytic forms
(i.e., trophozoites)
• This analysis, along with host specificity, has provided
> 100 species of Babesia
• 7 spp. affect humans

8. Large(2.5-5µm)
Transovarial
Small (1.0–2.5µm)
Transstadial
Babesiosis, HOMER et.al. CMR, July 2000, p. 451–469

9. Structure

10. Lifecycle
Reservoir
White tailed deer
For all except
B. meri
ornithodorrus

11. Epidemiology
WA-1
B. microti 300
cases
 Temperate climates
B. divergens

12. Epidemiology
 Frequency of B. microti & WA-1 in US > reported cases

because self- limiting & mild in humans
 Mortality in USA – 5%
 Survey in California – 16% prevalence WA-1
 Survey of Blood donors - 3-8% prevalence B. microti
 Human cases of B. microti reported
Coastal areas of southern New England
 Eastern Long Island
 Minnesota
 Winsconsin

 WA-1 – throughout pacific coasts
Babesiosis, HOMER et.al. CMR, July 2000, p. 451–469

13. Contd..
 Sporadic cases – Europe (France & British Isles),
Africa, Asia
• Cattle Babesia (B. divergens, B. microti)
 83% Babesiosis in Europe - B. divergens
 Mortality rate – 42% Europe
 Few cases reported – China, Taiwan, Egypt, S. Africa,
Mexico
 Transfusion- acquired Babesia several cases in USA,
but none in Europe & elsewhere

14. India
 Single case report
 51 year old patient from Madhya Pradesh
 History
 Working nursing home in gwalior
 Fever, vomiting, headache, arthralgia
 No h/o tick bite or visit to endemic area
 No other family member
 No h/o splenectomy or blood transfusion
IJMM 2005;23:267-9

15.  O/E
 Liver and spleen palpable
 Scleral icterus, passed dark coloured urine
 Investigations
 WBC count 1,900/cumm
 Platelet count 55,000/cumm
 LDH raised

16.  Peripheral blood smear – ring forms varied greatly
confused P. Falciparum
 Antimalarial treatment – no response
 Smear reviewed – pear shaped, tetrad - babesiosis
suspected
 HRP II – negative
 Quinine + clindamycin – Pt. afebrile within 2 days

17. Pathogenesis
Env
Host
Agent

18.  Modification and rupture of RBCs

Replication neoAg`s d/t membrane alteration

Docking sites for IgG and complement
 phagocytosis in spleen  Anemia
 Lack of periodicity: Asynchronous replication
 More severe manifestations in immunosuppresed and
elderly

20. • establishment stage antibodies (IgG) play a role in
preventing erythrocyte infection by binding the free
sporozoites.
• progression stage organisms invade erythrocyte
– innate immune system control growth rate of the merozoites
– NK cells and macrophages - soluble factors: IFN-g by NK
cells and TNF-a, nitric oxide (NO), and ROSs by macrophages
(Mf).
• resolution stage decrease in parasite numbers -
intracellular degeneration inside the erythrocyte, as
evidenced by the appearance of crisis forms.

21. Clinical features
• Disease manifestations asexual reproductive stage
• Predisposing factors +/• Mild to severe illness
– Generalized weakness
– Fever
– Gastrointestinal symptoms (anorexia, nausea, abdominal
–
–
–
–
–
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pain, vomiting, diarrhea, etc.)
Headache
Myalgia
Weight loss
Arthralgia
Respiratory symptoms (cough, shortness of breath, etc.)
Dark urine

22. Clinical examination
 Hepatomegaly and splenomegaly
 Hemolytic anemia - lasts from several days to few
months occur in clinically severe cases, most
commonly in asplenic or elderly

23.  Pulmonary manifestations - rare in babesiosis, but
non-cardiogenic pulmonary edema (NCPE) is the most
frequent manifestation
 not related
 degree of parasitemia
 splenic function and its onset may be early or late
 16 reported cases - reviewing the literature on the
pulmonary complications

24. Common Complications
 Acute respiratory distress syndrome
 Anemia requiring transfusion
 Congestive heart failure
 Disseminated intravascular coagulation
 Hypotension/shock
 Myocardial infarction
 Renal failure

25. HUMAN COINFECTION
• Coinfection with B. microti & other tick-borne
pathogens, particularly B. burgdorferi (Lymes disease)
•
serosurveys - 13% of Lyme disease patients in babesia-endemic
areas are coinfected with B. microti
• B. microti is transmitted by the same Ixodes tick that
perpetuates the agents of
Lyme disease
• human granulocytic ehrlichiosis
• novel Bartonella species
•
• P. leucopus is also the vertebrate reservoir for at least
three of the known pathogens

27. • Patients coinfected with B. microti and B. burgdorferi
experience
•
•
more severe symptoms, resulting in fatality in rare cases
persistence of postinfectious fatigue.
• B. burgdorferi DNA persisted for prolonged periods
• B. microti - no significant effect on the duration of
parasitemia

28. Blood
transfusion
Splenectomy
Tick bite
Travel
history
Clinical
presentation
Diagnosis
Age

29.  A positive Coombs test in combination with hemolytic
anemia & elevated procalcitonin levels is highly
suspicious of babesiosis
 Laboratory tests
 examination of stained blood smears
 serologic evaluation with indirect (immuno) fluorescent
antibody tests (IFATs)
 PCR

30.  Examination of thin blood
smears
 most frequently used technique
 Wright’s or Giemsa stain
 simple rings (annular),
 pear-shaped (pyriform),
 Maltese cross (tetrad form)
 High parasitemia present during
acute infections

varying from 5 to 80% of
erythrocytes

31. • Duration of detectable parasitemia on blood smears
varies
•
3 weeks to 12 weeks with the longest duration of smear
positivity being 7 months for a splenectomized patient
• Quantitative buffy coat system (QBC) – Merozoites
stained with acridine orange
•
•
Simple & rapid
Showed 100% correlation with blood smear exam.
(Mattia et al, 1993)

32.  Distinguishing features differentiate the two
organisms.
 Babesial organisms usually form tetrads ("Maltese
cross"),
 Do not have hemozoin pigments within the affected red
blood cells
 Have extracellular merozoites

33. Serodiagnosis
 IFATs - B. microti infections, chronic infections
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Hamster-derived B. microti Ag
Distinguish between B. microti, WA-1, B. divergens
Specific and sensitive
Diagnostic titers above 1:64
Higher cutoff titers (1:128 to 1:256) greater diagnostic
specificity
IgM and IgG
Problematic in HIV, splenectomy
Time consuming & labor intensive

34. IFAT
 Antibody titers can remain elevated for as long as 13
months to 6 years after infection
 Although persistence of antibody does not necessarily
reflect a measurable infection, levels of IgG antibody
decline less rapidly in persistently infected patients

35. ELISA
 ELISA – Recombinant antigen - 4 antigens used




rBMN1-2
rBMN1-15
rBMN1-17
rMN-10
- 27/40
- 27/40
- 27/40
- 27/40
 Showed high sensitivity & specificity
 Soluble whole parasite antigen (B. divergens)
Loades et al, 2000

36. Problem associated with
serological tests
•
Relationship between antibody titers, the presence of
parasites, and the state of protective immunity is not clear
•
Antibodies may persist for long periods after the disease has
cleared
•
Overestimate of disease prevalence
•
Antibody titers may be observed in the absence of protective
immunity

37. PCR assay
• Based on universal primer amplification of a fragment
of the small subunit rRNA gene
• Highly conserved among babesias
• Heterologous between Babesia spp. and other
intraerythrocytic protozoal parasites as well as within
the genus Babesia itself
• Distinguishes readily between B. divergens, B.
microti, and Plasmodium spp., it provides a valuable
adjunctive

38.  Advantages over IFA testing.
 Less time consuming
 conducted by generalist technicians
 more readily be standardized
 sensitivity and specificity comparable to those of
conventional IFAs

39. MASP(microaerophilous stationary
phase) culture technique

Quantities of parasite nucleic acid needed for defining
phylogenetic relationships of these species,

Methods for detection of the parasite in otherwise
asymptomatic individuals

Producing parasite antigens

Attenuated strains of Babesia - immunization.

40. Laboratory diagnosis
• B. microti immunoblot kits
• Animal Inoculation
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2-4 weeks
Sensitive (300 org./ml blood)
Time consuming, expensive

41. Animal models
 Rats
 BALB/ c mice
 Splenectomized calves
 Gerbils

42. Treatment

43.  Imidocarb and the combination of oxomemazine and
phenamidine were most effective in vitro
 Imidocarb, although not licensed for human use, most
effective agent for treating B. divergens infections in
cattle
 other pharmacologic interventions -
chloroquine, tetracycline, primaquine, sulfadiazine, an
d pyrimethamine

44. Prevention
• Avoidance of or minimization of exposure to tick•
•
•
•
infested areas
Ase of tick repellents before entering a tick-infested
area thorough examination of skin after exposure.
Ticks found before attachment -removed, and
Ticks found after attachment removed within 24 h
limit the possibility of transmission
Application of pesticide to host nests and on the coats
of reservoir hosts can interrupt transmission

45. Vaccines
 Live vaccines

living parasites cattle
 Recombinant vaccines
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
B. bovis & B. bigemina vaccine cattle
Soluble parasite antigen (SPA)
No effective B. microti vaccine
 Human vaccines – Expt. Stage
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
MRA gene (Maltase cross form-related antigen)
37 kDa glycoprotein (Bd37)

46. Summary
 Emerging disease
 Common in the Americas
 Can be confused with plasmodium falciparum
infection
 Diagnosis requires high index of suspicion
 Treatment involves use of At or Az or Clin + Quin

47. Thank you