Babesia microti

1. Babesia microti
By Raz S. Abdulla
2
nd
stage
Bio dep.
2010-2011

2. Outline…
•Taxonomy
•Babesiosis
•Morphology
•Geographic Distribution
•Hosts
•Life Cycle
•Pathogenesis/Clinical Signs & Symptoms
•Diagnosis
•Treatment
•References

3. Taxonomy
•Kingdom: Protista
•Phylum: Apicomplexa
•Class: Aconidasida
•Order: Piroplasmida
•Family: Babesiidae
•Babesia microti

4. Babesiosis
•Prior to 1969 Babesia infections were rare
and limited to B. divergens (a cattle
parasite) and some others species that
were parasitic in rodents.
•It was only seen in splenectomized patients
who had disabled immune systems as a
result of the splenectomy.
•1969, Nantucket Island, Mass: 1
st
human
Babesia infection in a non-splenectomized
patient.
•Hundreds of cases have been reported
since.

5. Morphology
•Easily misdiagnosed as
Plasmodium in areas high in
Malaria prevalence due to its
“ring shape”
•Variation in shape and size
•Do not produce pigment
Intraerythrocytic Babesia microti

6. Geographic Distribution
•Worldwide
–Europe: B. divergens, most common
–United States: B. microti, most common in
NE and MW portions
•WA-1 strain recently found on west coast
* May not be as prevalent in malaria-endemic
countries*

7. Hosts
•Definitive host: Humans or Deer tick
•Vector: Ixodes scapularis (Deer tick)
•Intermediate host: White-footed
mouse and other rodents and Deer
–When the deer or mouse pop. increases,
the tick pop. does too.

8. Life Cycle
1.Babesia infected tick introduces sporozoites into
the mouse host.
3.Sporozoites enter erythrocytes and undergo
asexual reproduction (budding).
5.In the blood, parasites undergo male and female
differentiation (micro- and macrogametes are
formed).
7.The deer tick (definitive host) takes a blood meal
ingesting gametes, which can now undergo
fertilization within the gut, 5. resulting in
sporozoite formation. Spread to salivary glands.

9. Life Cycle Cont’d…
6. During a blood meal, the tick infects the human
host. Inoculation occurs by a tick larva, nymph
or adult.
3.Sporozoites invade erythrocytes and a
trophozoite differentiates, replicating asexually
by budding: responsible for the
clinical manifestations. This
forms 2-4 merozoites which
eventually reinvade other RBCs.
•Humans are for all practical purposes “dead-
end” hosts, because subsequent transmission
after the tick feeds on a human is unlikely.
Human to human transmission is well
recognized to occur through blood transfusions.
Babesia can be transmitted in utero.

11. Pathogenesis
(Signs & Symptoms)
•1-4 weeks (can last several weeks): fever,
chills, headache, nausea, vomiting, and/or
muscle aches (myalgia), hemolytic anemia,
jaundice and splenomegaly.
•May be mild in otherwise healthy people
•May be asymptomatic
•Severe form of Babesiosis may be life-
threatening if untreated (usually people who
have been splenectomized, the elderly, or
who have impaired immune systems).

12. Diagnosis
•Microscopic examination: thick and thin blood
smears stained with Giesma
•Antibody detection: detects even low levels of
parasitic invasion
–Indirect fluorescent antibody test (IFA) detects
antibodies (IgM & IgG) of patients with B. microti
infection
–Recommended only if low levels of parasitemia or
blood smear is inconclusive
•Diagnosis can be derived from molecular
techniques, such as PCR
–Valuable in investigations of new Babesia species

13. Treatment
•Clindamycin*: antibiotic with little or no
side effects
•Quinine or Atovaquone*: antiparasitic
•Azithromycin*: antibiotic, some side
effects
•Clindamycin combined with Quinine is
treatment of choice
*FDA approved, but considered investigational

14. http://search.vadlo.com/b/trk?
uid=e1f97e9edb7582e5&sn=1586
21799&ip=95.159.83.217&lgkKy=
babesia+microti+ppt&rn=1&http://
course1.winona.edu/kbates/Parasi
tology/Babesia%20microti.ppt
ReferenceS