BABESIOSI

By
Roderick D. Balce,
RMT
BABESIOSIS
I. Introduction
A. History
B. Epidemiology
C. Overview
II. Description of the Organism
A. Taxonomy
B. Morphology
C. Life Cycle
D. Comparison Between Babesia
and Plasmodium
III. Pathogenesis
A. Vector
B. Modes of transmission
C. Mechanisms of Injury
IV. Pathobiology
A. Clinical features
B. Infection in
Immunocompromised Host
C. Immunology
V.Laboratory Diagnosis
VI. Clinical Management
VII. Prevention and Control
VIII. Recent Updates
 I. INTRODUCTION
A. Brief History
1888 – Victor Babes discovered
microorganisms in the erythrocytes
of cattle.
1893 – Smith and Kilbourne
established Pyrosoma as the first
identified arthropod-born protozoan.
1957 – Skrabalo and Deanovic
described the first confirmed human
case of babesiosis caused by B.
B. Epidemiology
 Most cases of babesiosis have
been reported from the USA
usually caused by B. microti
 In Europe, 84% of cases have
occurred in splenectomized
individuals
 In Nigeria and Mozambique, over
half of the persons tested were
seropositive for Babesia
 Several cases were also reported
in Asia and South Africa
C. Overview
Babesiosis is a malaria-like,
hemoparasitic infection caused by the
protozoan genus Babesia.
Causative agent: B. microti and related
organisms
Infective Stage: Sporozoite
Mode of Transmission: Skin inoculation
Vector: Ticks (Ixodes spp.)
Reservoirs: Rodent, cattle, deer
Diagnostic Procedures: Thick & Thin
Blood Smear,
Serological tests, PCR
II. CAUSATIVE AGENT
A. Taxonomy
Kingdom Protista

Phylum Apicomplexa

Class Sporozea Class Aconoidasida

Subclass Coccidia Subclass Piroplasmia

Suborder Suborder Eimeriina Order Piroplasmidora

Hemosporiina

Isospora, Cyclospora, Babesia

Plasmodium Cryptosporidium,
Sarcocystis,
Toxoplasma
C. Life Cycle
B. Morphology
 piriform, round or oval depending
upon the species
 resembles P. falciparum but has
several distinguishing features:
pleomorphic, can be vacuolated, and
does not produce pigment
 tetrad form is a diagnostic feature

(A and B) B. microti ring forms, about 1.5–

2.5 nm in diameter (Giemsa-stained).
(C ) Tetrads, about 1–2.5 nm in diameter.
(D) Rings; (E) Pyriforms; (F) Band
forms
(G) B. microti rings ; (H) Plasmodium vivax young
ring;
(I) Plasmodium falciparum multiple parasites;
Maurer’s dots can be seen.
 Babesia sp. in a thin blood smear
stained with Giemsa.  Note the
tetrads, a dividing form
pathognomonic for Babesia, in both
images.
 D. Comparison Between
Babesia and P. falciparum
Babesia spp. P. falciparum
Ring forms Larger, usually pear- Smaller, no central
shaped, can contain a vacuole, applique or
central vacuole, tetrad acole forms diagnostic
Schizonts and forms diagnostic
Absent Present
gametocytes
Hemozoin Absent Present
pigment
Asexual Budding (forming Schizogony (forming
division tetrads of trophozoites) schizonts and
Vector Ticks (Ixodes dammini merozoites)
Mosquito (Anopheles
or scapularis) minimus flavirostris)
Life cycle Asynchronous Undergoes exo-
erythrocytic cycle erythrocytic and
synchronous
erythrocytic
schizogony
III. PATHOGENESIS
A. The Tick Vector
 3 developmental forms exist – larva,
nymph, and adult
 blood meal is required to progress to
the next developmental stage

 all 3 forms may feed on humans but

the nymph is the main vector of
babesiosis
Ixodes dammini
B. Modes of Transmission
 Skin inoculation or tick bite
 Co-transmission with B.
burgdorferi
 Blood transfusion – Babesia can
survive for 21-35 days under
standard blood storage
conditions; 60 cases have been
documented in 2006
 Transplacental – 2 cases have
documented on humans
C. Mechanisms of Injury
 Hemolysis and resultant anemia –
due to humoral mechanisms
resulting from the production of
anti-erythrocyte membrane
antibodies
 Cytoadherence of erythrocytes
within the vasculature – due to a
cryofibrinogen complex present
in the plasma of patients
 Release of harmful mediators –
due to the production and release
 IV. PATHOBIOLOGY
A. Clinical Features
Symptoms: fever, malaise, fatigue,
anorexia, rigors, headache,
myalgia, arthralgia, nausea,
vomiting, abdominal pain,
photophobia, conjunctivitis, sore
throat, and cough
Physical Findings: splenomegaly,
hepatomegaly, skin changes,
jaundice
Laboratory Findings: hemoglobinuria,
decreased haptoglobin, increased
reticulocyte count,
thrombocytopenia, high ESR, (+)
direct Coomb’s test, proteinuria,
increased BUN and creatinine,
increased bilirubin, ALP, AST,
ALT, and LD
 Disease is more fatal in
splenectomized individuals.
 American cases are less severe than
European ones.
 B. Infection in
Immunocompromised Host
 HIV infection predisposes to severe
babesiosis which can be prolonged
and chronic.
 Patients show high parasitemia and
may develop CNS involvement or
complications such as CHF, RDS,
and renal failure.
 Relapse of symptoms is possible.
V. LABORATORY
DIAGNOSIS
Thick and Thin Blood Smear
Serologic Tests
Indirect Immunofluorescent Test
ELISA
Xenodiagnosis
Invitro culture
Polymerase Chain Reaction
(PCR)
 Direct diagnostic method for detection:
(A) Photomicrograph of positive Babesia-
IFAT, 400
(B) Display detail 1000, oil (zoomed)
(C) Negative IFAT control.
Babesia spp.-specific PCR designed for amplification
of a highly specific region of the 18S rRNA gene
(Armstrong et al., 1998).
P – positive control, N – negative, control, S –
patient sample, I – inhibition control, M – 123-bp
marker.
VI. CLINICAL
MANAGEMENT
A. Antiparasitic Treatment
Quinine 650 mg p.o. 3 times daily
Clindamycin 600 mg p.o., i.v. 3
times daily
Azithromycin 500 mg/1st day,
250 mg therafter p.o. once
daily
Atovaquone 750 mg p.o. twice
daily
Doxycycline 200 mg p.o. once
daily
 VII. PREVENTION AND
CONTROL
Avoidance of exposure to the
tick vector
Application of insect
repellents such as DEET or
permethrin
Discouraging blood donors
from endemic areas
Babesiosis: Recent
insights into an
ancient disease

K.-P. Hunfeld, A. Hildebrandt, J.S.

Gray

International Journal for

Parasitology 38 (2008)
1219–1237
 New Developments in the
Phylogeny of B. microti and B.
microti-like organisms
Molecular analysis of 18S rRNA
and β-tubulin gene fragments of
parasites resulted in the
identification of three separate
clades
As a consequence B. microti,
long regarded as a single
species, is now regarded as a
genetically diverse species
 New tools for a more rapid
molecular diagnosis of Babesia
spp. infection
Development of sensitive and
specific multiplex PCR assays that
can yield results within one day
and can detect as few as three
parasites in 100 uL blood
Use of a single diagnostic test
covering agents such as Babesia
spp., Borrelia spp., Anaplasma
spp., and Rickettsia spp.
 Shared features in
the pathobiology of
babesiosis and
malaria
Peter J. Krause1, Johanna Daily,
Sam R. Telford, Edouard Vannier,
Paul Lantos
and Andrew Spielman

TRENDS in Parasitology
The clinical manifestations of
malaria and babesiosis are
similar.
Most cases of babesiosis and
malaria consist of a mild to
moderate illness characterized
by fever, sweats, chills,
headache, myalgia, back and
abdominal pain, nausea,
vomiting, diarrhea and pallor.
They differ in the periodicity of
They share similar pathology in
the brain, lung, kidney and other
organs.
Erythrocyte cytoadherence and
sequestration generally are found
in the cerebral vasculature of
patients dying of cerebral malaria.
Several studies of Babesia cerebral
disease have demonstrated
extensive erythrocyte
cytoadherence and sequestration
in the brains of infected animals.
Pulmonary complications are
often observed in adults
experiencing severe malaria.
Likewise, pulmonary disease is
the most common complication in
people experiencing severe
babesial infection with up to 20%
of patients suffering from non-
cardiac pulmonary edema.
Studies point to the central role
of cytokines, and especially TNF,
in babesia and malaria
Renal impairment is a common
complication of P. falciparum and
babesial infections. Renal failure has
been reported in 5% of severe B.
microti human infection and even
more frequently in patients
experiencing severe B. duncani
infection.
On autopsy of patients dying of
malaria, several distinct pathologic
patterns are noted in the kidneys,
with erythrocyte sequestration
contributing to the pathology.
Studies in animals infected with