Review
Canine babesiosis in Europe:
how many diseases?
Vesna Matijatko1, Marin Torti1 and Theo P. Schetters2
1
University of Zagreb, Faculty of Veterinary Medicine, Clinic for Internal Diseases, Heinzelova 55, 10000 Zagreb, Croatia
2
Merck Sharp & Dohme Animal Health, PO Box 31, 5830 AA Boxmeer, The Netherlands
Babesiosis, recognized since ancient times as an impor-
tant disease of livestock and more recently as an
emerging disease in dogs worldwide, is caused by
intraerythrocytic protozoa of the genus Babesia and
is transmitted by ticks. The pathophysiology of canine
babesiosis has been extensively studied but many ques-
tions remain unanswered, especially regarding the di-
versity of disease manifestations in different European
countries. Continued investigation of the similarities
and differences in host–parasite interplay in canine ba-
besiosis in different European countries should lead to a
better understanding of the disease process, potentially
leading to better prediction of disease outcome and the
development of new treatment modalities. From the
European point of view it is important to conduct these
studies on Babesia canis.
Canine babesiosis: a riddle yet to be solved
In recent years, more and more cases of babesiosis in dogs
have been reported in Europe, and it appears that canine
babesiosis is an emerging infectious disease. The parasite
is transmitted by ticks, and migration of ticks to hitherto
uninfested geographical areas could explain the increasing
incidence of clinical cases in Europe. The clinical presen-
tation of canine babesiosis is diverse and ranges from
transient anorexia to a complex syndrome in which multi-
ple organ systems are affected. Several factors play a role
in the development and outcome of the infection; these
include the abundance of the tick vector, the percentage of
ticks that are infected, and the Babesia species involved.
This review presents an update on canine babesiosis with a
focus on the clinical disease as manifested in Europe.
Babesia species that infect dogs
Canine babesiosis is caused by apicomplexan parasites
that are classified either as large (5  2.5 mm) or small
Babesia (2  1.5 mm) [1]. Large Babesia canis was divided
into three different species, namely Babesia canis, Babesia
rossi and Babesia vogeli [2]. Recently, a new large babesian
species, Babesia sp. (Coco) was discovered [3,4]. B. canis, B.
vogeli and B. rossi, previously considered to be subspecies
of B. canis, are identical morphologically but show great
variations in geographic distribution, vector specificity,
genetic characteristics and the clinical signs they induce
in dogs, and are therefore now widely considered to be
Corresponding author: Matijatko, V. (vesna.matijatko@vef.hr).
1471-4922/$ – see front matter ß 2011 Elsevier Ltd. All rights reserved. doi:10.1016/j.pt.2011.11.003 Trends in Parasitology, March 2012, Vol. 28, No. 3
separate species [5,6]. Different species of large and small
Babesia are shown in Table 1.
Babesia parasites are naturally transmitted only by
ticks, and in the case of canine babesiosis there is a very
strong association between the Babesia species that is
transmitted and the tick species (reviewed in [7]). As a
consequence, the prevalence of babesiosis is dependent on
the presence of the tick vector in the environment (Table 2).
Canine babesiosis in Europe
In Europe the predominant cause of canine babesiosis is B.
canis, and clinical cases have been reported from Austria [8],
Croatia [9,10], France [11], Germany [12], Hungary [13],
Italy [14], the Netherlands [15], Poland [16], Portugal [17],
Slovenia [18], Spain [19], Switzerland [20], and recently
Norway [21]. The disease can be clinically classified into
uncomplicated and complicated forms. Uncomplicated ba-
besiosis has been suggested to be a consequence of anemia
resulting from hemolysis [22], whereas complicated canine
babesiosis may be a consequence of the development of
systemic inflammatory response syndrome (SIRS) and mul-
tiple organ dysfunction syndrome (MODS), both of which are
cytokine-mediated phenomena [22,23]. Clinical signs of
uncomplicated babesiosis include pale mucous membranes,
fever, anorexia, depression, splenomegaly, hypotension and
water hammer pulse [24–27]. Clinical manifestations of the
complicated form of babesiosis depend on the particular
complications that develop. In Europe, a higher mortality
rate is noted in countries that have reported complications
that are strikingly similar to those of the South African form
of babesiosis [28], namely MODS, cerebral babesiosis, shock,
rhabdomyolysis, acute renal failure (ARF), acute respirato-
ry distress syndrome (ARDS), acute liver dysfunction and
acute pancreatitis (AP). The highest mortality rate is noted
in Hungary where MODS is reported in 16% of cases,
hepatopathy in 24%, AP in 6%, ARF in 30%, disseminated
intravascular coagulation (DIC) in 17%, immune-mediated
hemolytic anemia (IMHA) in 8%, ARDS in 6%, and cerebral
babesiosis in 3% [29]. In Croatia the most common compli-
cation was MODS (10%) [30]. It is interesting to note that
within MODS the most common complication was ARF,
followed by hepatopathy, ARDS and cerebral babesiosis
[31,32]. In a study of B. canis infection in Croatia, a consid-
erable number of dogs with hypotensive shock were
observed [32]. In contrast to these findings, B. canis infection
in other European countries has only low mortality. For
example, in Poland the mortality rate is 3.9% and the most
commonly reported complication is ARF [26], whereas in
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Review Trends in Parasitology March 2012, Vol. 28, No. 3

Table 1. Groups of canine Babesia species
Group Species
Large Babesia Babesia canis
Babesia rossi
Babesia vogeli
Babesia sp. (Coco)
Small Babesia Babesia gibsoni
Babesia conradae
Babesia microti-like (Theileria annae)
Spain and Italy the most common complication noted in B.
canis-infected dogs is DIC [33,34]. In those countries MODS
has not been reported, and the mortality rate is significantly
lower. Indeed, it seems that in Spain the infection with
newly discovered small Babesia species results in a more
severe disease (mortality rate 22%) that is associated with
ARF [35].
Diversity among Babesia canis strains
Differences in virulence
Differences in the clinical manifestations of disease may
reflect different Babesia strains. This is best evidenced in
B. bovis, for which it has been possible to select for strains
that are less virulent than the parent strain. This selection
process involves repeated passage through splenecto-
mized calves and is being used in the production of live
vaccines against B. bovis in cattle [36]. In addition to
differences in virulence, it was also shown that there
are antigenic differences between B. bovis strains. The
occurrence of antigenically different strains has been
suggested to explain vaccination failures in Australia in
the period 1985–1990 [37]. Likewise, strain diversity in B.
canis could explain the variable clinical picture seen in
affected dogs in France [11]. Direct evidence of the exis-
tence of strains of B. canis with variable virulence has
recently been reported from Poland. Based on differences
in part of the 18S ribosomal RNA gene, isolates of B. canis
could be separated into two genetically different groups: A
and B [17]. It was later shown that thrombocytopenia, one
of the first hematological signs of natural and experimen-
tal B. canis infection [11,27], was statistically different
between the two genetic groups [26]. In addition, there was
a strong correlation between the extent of thrombocytope-
nia and increases in body temperature, accelerated pulse
rate and discoloration of urine. These data support the
hypothesis that virulence is indeed different between
Refs. strains of B. canis.
[76]
[7] Genetic diversity
[3] With the development of molecular biological tools it be-
[4] came possible to analyze the diversity of B. canis strains at
[87] the genetic level. Analysis of more than 90 isolates from
[88] France revealed that based on diversity of the Bc28 gene,
[9,89,90] three genetically distinct groups could be defined, Bc28-A,
Bc28-B (predominant) and Bc28-3403 [38]. Similar analy-
sis of over 200 isolates from Central Europe revealed that
only genetic groups Bc28-A and Bc28-B were prevalent,
with a slight predominance of Bc28-A (B. Carcy, unpub-
lished). The analysis did not allow a correlation with
virulence to be established; however, a correlation with
functional protective immunity in vaccination challenge
studies is apparent (discussed below).
Antigenic diversity
Vaccination challenge experiments have indicated that
antigenic diversity is present in B. canis strains. Dogs
vaccinated with soluble parasite antigens (SPA) derived
from the supernatant of in vitro cultures of B. canis strain
A parasites were protected against homologous challenge
infection, but not against challenge infection with a heter-
ologous B. canis strain B [39,40]. This indicates that there
are functional antigenic differences between B. canis
strains [2]. Antigenic diversity may be related to allelic
diversity, where by different parasite clones express dis-
tinct members of a particular protein family, such as the
MSA-1 and MSA-2 merozoite surface antigens [38]. Ho-
mologous recombination during sexual stages in the tick
vector is likely to be the molecular mechanism involved in
the generation of such antigenic diversity, although gene
organization analysis suggests that other mechanisms
may also contribute [41].
Antigenic variation
A further and distinct mechanism for the generation of
antigenic diversity takes place via a dynamic genetic pro-
cess operating at the clonal level. This phenomenon has
been described for several protozoan parasites, including
B. bovis [42], where antigenic molecules are not expressed
at the merozoite surface but are instead expressed at the
surface of the infected erythrocytes, and may therefore
play a role in the specific adhesion of infected erythrocytes

Table 2. Geographic distribution of different Babesia species and their vectors

Species Geographic distribution Vector Refs. and comments
Babesia canis Europe, Asia Dermacentor reticulatus [6,9,13,16,91]
Babesia rossi Africa Haemaphysalis leachii [92]
Babesia vogeli Africa, Europe, Asia, Australia, Rhipicephalus sanguineus [5,6,9,17–19,93–97]
North and South America
Babesia sp. (Coco) United States Unknown [3]
Babesia gibsoni Worldwide Haemaphysalis sp. [7,87,89,98,99]
Rhipicephalus sp.
Babesia conradae California Rhipicephalus sanguineus? [90]
Babesia microti-like Southern Europe Most probably Ixodes hexagonus? Discovered 10 years ago in Spain and
(Theileria annae) named Babesia microti-like or Babesia
annae. Renamed Theileria annae based
on molecular phylogenetic analysis [9,19,88,100].

100
Review
to the capillary endothelium of particular organs, a process
termed sequestration. It is believed that this process plays
a role in sustaining low-level chronic infection in immune
animals, which helps to maintain immunity [43]. Although
antigenic variation has not been shown for B. canis, low-
level chronic infection occurs in dogs experimentally
infected with B. canis or B. vogeli parasites [44,45]. In
the latter it was further shown that immunity in these dogs
was prolonged compared to dogs treated after initial infec-
tion to clear the parasites [45]. In the field, dogs are faced
with several antigenically diverse B. canis parasite fami-
lies of variable virulence, and these have evolved mecha-
nisms that allow survival in (partially) immune dogs.
Pathophysiology of the disease
Canine babesiosis is generally classified into uncomplicat-
ed and complicated forms. Whereas uncomplicated babe-
siosis appears to be a consequence of anemia, complicated
canine babesiosis is characterized by pathologic changes in
a number of organs (MODS). In recent years increasing
numbers of researchers have proposed that a uniform
mechanism leads to different clinical manifestations
[22,28,46]. This is based on the hypothesis that SIRS
(leading to MODS) is a pathophysiological mechanism that
underlies the different presentations of babesiosis. Recent
publications have shown that both uncomplicated and
complicated babesiosis due to B. canis are associated with
host inflammatory responses [27,46].
Uncomplicated babesiosis
Subjects infected with Babesia parasites develop anemia.
The mechanism that leads to the anemic state is complex
and involves erythrocyte depletion as a result of parasite
multiplication, hemodilution, localization in the spleen,
(autoimmune) hemolysis, erythrophagocytosis and im-
paired erythropoiesis [47]. Anemia may lead to tissue
anoxia, and this is considered to be the hallmark of babe-
siosis [28]. There are indications that oxidative stress and
lipid peroxidation play a role in the pathogenesis of anemia
in some protozoan diseases [48]. Excess lipid peroxidation
in biological membranes compromises their structural
integrity, with loss of fluidity, decrease in membrane po-
tential and increased permeability to ions [49]. These
changes can lead to rupture of the membrane and release
of cell contents [50]. Mata (M.M. Mata, M.V.Sc. Thesis,
Haryana Agriculture University, 1990) argued that lipid
peroxidation causes an accumulation of oxidative ions in
red blood cells that causes their lysis.
Many parasites including protozoa are sensitive to oxi-
dative stress. Sensitivity to oxidative stress has been
reported in malaria [51], hepatozoonosis [52], tropical
theileriosis [53] and bovine babesiosis [54]. Reactive oxy-
gen species (ROS) and reactive nitrogen species (RNS) are
powerful oxidants and nitrating species that can inactivate
enzymes and initiate lipid peroxidation and nitration,
which in turn lead to free-radical chain reactions that
further damage membranes, nucleic acids and proteins
[55]. These processes can ultimately lead to parasite death
[51,52]. As a defense mechanism, parasites produce com-
pounds and antioxidant enzymes that directly neutralize
ROS and RNS. Over recent years, several antioxidant and
Trends in Parasitology March 2012, Vol. 28, No. 3
detoxification systems of parasitic protozoa have been
identified and their roles in parasite survival have been
investigated [55]. The so-called ‘redox proteins’ were
shown to be essential for the survival of protozoan para-
sites. Furthermore, oxidative stress may negatively affect
organ injury and overall survival [56]. Malondialdehyde is
an end product of polyunsaturated fatty acid oxygenation
and is a reliable and commonly used biomarker for asses-
sing lipid peroxidation [57]. Serum malondialdehyde
levels were found to be elevated significantly in canine
babesiosis [58].
Products of oxidative stress may thus contribute to
protective immune responses against the parasite if pro-
duced in optimal amounts [52,53], but can also contribute
to pathogenesis when produced in excess [54]. Therefore,
the important element for favorable outcome in babesiosis
may be the balance between oxidant and antioxidant
processes.
Different levels of parasitemia have been reported in
numerous studies of canine babesiosis. Anemia in canine
babesiosis is not proportional to parasitemia [33,59,60].
The established fact that the quantity of destroyed ery-
throcytes is much higher than the degree of parasitemia
suggests that destruction takes place of both parasitized
and unparasitized erythrocytes [61]. In one study, all
patients showed a level of parasitemia of below 1% [62].
Another study reported that higher levels of parasitemia
correlated with worse clinical scores [63], and the degree
of parasitemia was significantly higher in the dogs that
died. In an experimental study of canine babesiosis
caused by B. canis, all dogs developed low-grade para-
sitemia (less than 1%) [27]. In studies of canine babesiosis
in Croatia, all patients with uncomplicated babesiosis had
a level of parasitemia below 1% (I. Kiš, Ph.D. Thesis,
University of Zagreb, 2007). In a study in Croatia of septic
shock due to babesiosis, seven of 10 dogs had a level of
parasitemia above 1%, whereas three had a level below
1% [32]. Given that all the dogs in this study died, it would
seem that a low level of parasitemia does not guarantee a
favorable outcome, but that a level of parasitemia greater
than 1% is associated with poor outcome. One of the
proposed mechanisms that could lead to the development
of septic shock in babesiosis, and subsequently increase
the risk of poor outcome, is related to the parasite itself.
The association between a higher level of parasitemia and
shock raises the question of whether the two are causally
related. In experimental B. canis infection, the onset of
the acute phase reaction appeared to be related to the
infectious dose, although the acute phase response was
ultimately triggered in all cases, irrespective of dose [27].
The arguments for the inflammatory response are sup-
ported by the fact that acute-phase protein production is
increased in canine babesiosis and can be used as a
predictive marker for disease risk and to monitor the
response to treatment [46]. Nevertheless, the concentra-
tion of C-reactive protein (CRP) did not show prognostic
value because it was not associated with outcome in
babesiosis caused by B. rossi [64].
The timing of the different triggers may lead to different
outcomes: high infectious doses trigger an early inflamma-
tory response that could push the system out of balance.
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Review
However, severe parasitemia is unlikely to be the sole
trigger of circulatory collapse in canine babesiosis, espe-
cially because some dogs with low levels of parasitemia are
known to develop shock [27,32,63]. It has been suggested
that this response is triggered by SPA released into the
plasma during infection [2,27].
Host inflammatory response
Because babesiosis, as with human malaria caused by
Plasmodium falciparum, can be classified as protozoal
sepsis [65,66], it was suggested that the inflammatory
mechanisms in this disease are similar to those of other
septic conditions clinically characterized by SIRS and
MODS. This could explain similarities between various
diseases such as babesiosis, malaria, sepsis, multiple trau-
ma and burns [22]. These similarities have provoked
scientists to revise the original definition of sepsis as being
caused exclusively by bacteria. It is now considered that
sepsis is SIRS with the confirmed presence of an infectious
agent in the blood [65]. SIRS is described in naturally
occurring as well as in experimental canine babesiosis
[23,27,30], and although the role of SIRS in systemic
inflammation and the development of MODS have not
been disputed, the criteria for defining SIRS remain con-
troversial [67–72]. One flaw in the definition of SIRS is that
it might identify patients with systemic inflammatory
disease, but the presence or absence of SIRS has little
value in predicting outcome [73]. The cut-off values for the
parameters of SIRS are a major issue in veterinary medi-
cine because the normal values for temperature, heart rate
and respiratory rate vary in dogs, owing in part at least to
significant variations in their size [74]. This is especially a
problem in babesiosis because anemia, which is often
present in canine babesiosis, significantly increases heart
and respiratory rate. Another problem regarding SIRS is
that a significant number of dogs with babesiosis are SIRS-
negative [23,30], and therefore could not be considered to
have sepsis according to current definitions. Because both
uncomplicated and complicated babesiosis appear to be the
result of host inflammatory responses [27,46,64], in these
cases the concept of SIRS fails to identify patients with
demonstrated systemic inflammation. Moreover, some
SIRS-negative dogs develop MODS [23,30]. SIRS, sepsis,
severe sepsis and septic shock are clinical entities that are
considered to represent the progression of the inflamma-
tory response, and therefore an animal with babesiosis
that is both SIRS-negative and MODS-positive cannot be
clinically classified according to the present definitions.
Multiple organ dysfunction syndrome is documented in
canine babesiosis caused by B. rossi and B. canis [23,30,32].
As emphasized for the concept of SIRS, the MODS criteria
are also controversial. For example, the creatinine level
has been widely used for identifying renal failure. Howev-
er, prerenal azotemia with no structural kidney damage
can also lead to elevated serum creatinine concentrations,
and creatinine values are therefore insufficiently specific to
establish renal failure. In addition, in experimental B.
canis infection it was shown that creatinine levels decrease
in the early phase of the disease [27,75]. Liver failure is
commonly diagnosed from elevated concentrations of
liver enzymes, but this in our opinion is also not specific.
102
Trends in Parasitology March 2012, Vol. 28, No. 3
Bilirubin concentration is a much better indicator of liver
damage, but is problematic in canine babesiosis because of
hemolysis. All these facts confirm the need to revise the
criteria for SIRS and MODS in veterinary medicine and to
develop a uniform and reliable scoring system for inflam-
matory responses (SIRS, MODS, sepsis, septic shock) to be
able to compare these conditions between different veteri-
nary centers or different countries.
Canine babesiosis – how many diseases?
For a long time it was widely accepted that babesiosis caused
by B. rossi is a disease different from babesiosis caused by B.
canis. Most importantly, with B. rossi infections there is a
higher risk of developing complications and a significantly
higher rate of mortality [22,28,59,76,77]. By comparison,
infection with B. canis was considered to cause a predomi-
nantly mild disease with high seroprevalence ranges (20–
85%) in endemic areas [9,78,79] and low rate of clinical
disease [80]. Reviewing the results of studies of babesiosis
caused by B. canis throughout Europe demonstrated a wide
range of mortality rates, varying from 1.5 to 20%. The
highest mortality rates are found in Hungary (20%) [29]
and Croatia (11–13.9%) (I. Kiš, Ph.D. Thesis, University of
Zagreb, 2007) [43], and the lowest in France (1.5%) [80]. The
reported mortality rate in the Netherlands is 17% [15] and
9% in Portugal [17], but these numbers should be inter-
preted with caution. Regarding the study of canine babesio-
sis in the Netherlands, it is important to emphasize that
because diagnosis of babesiosis in three of the four dogs that
died was only established postmortem, these animals there-
fore did not receive any antibabesial treatment. For the
Netherlands study, diagnosis of babesiosis in three of the
four dogs that died was only established postmortem, and
these animals therefore did not receive any antibabesial
treatment. Considering the fact that only one dog with
confirmed babesiosis died in that study, the actual mortality
rate was 5%. In addition, reported mortality rates for dogs
with babesiosis in Portugal should be interpreted in light of
the fact that two of four dogs that died were euthanized
without treatment, the third was infected with B. vogeli,
Erlichia canis and Leishmania infantum, and the fourth
was infected with B. canis and Leishmania infantum. From
these data, the actual mortality rate in Portugal for B. canis
infection without coinfection was low. Therefore, B. canis
disease in both the Netherlands and Portugal can be con-
sidered to be mild.
By contrast, the clinical manifestations, complications
and mortality rate of B. canis infection in Hungary and
Croatia are more similar to those of South African canine
babesiosis caused by B. rossi than to B. canis infections in
other European countries. Overall, it seems that canine
babesiosis caused by B. canis in Europe is not a single
disease, and instead has at least two clinically different
disease manifestations, one mild, in which multiple organ
failure is absent, and a second that is severe and that is
generally complicated by MODS and hypotension. The an-
swer to the question ‘why is it like this?’ might lie in the
parasite itself, the host, or in host–parasite interplay. Re-
garding the parasite itself, it has been demonstrated that
different Babesia species, subspecies or isolates can produce
disease of markedly different severity [77]. Moreover,
Review
significant differences in disease outcome and prognosis
have been observed following infection with different strains
of a single species of Babesia (B. rossi) [81].
Regarding the host response, it was reported that in
some human patients with malaria, organ system dysfunc-
tion may develop and evolve even after the parasites have
been eradicated from the blood by specific therapy [82].
This observation supports the hypothesis that inflamma-
tory mediators are involved because immunoinflammatory
processes set in motion by fulminant infection may at times
be self-perpetuating, even when the parasites have been
eliminated by treatment. It is clinically important to un-
derstand that the proinflammatory state of the acute phase
response (SIRS) also initiates anti-inflammatory media-
tors (compensatory anti-inflammatory response syndrome,
CARS). The extent of the pro- and anti-inflammatory
events should be balanced and proportional to the insult.
However, some factors (i.e. constitutional, genetic, and/or
environmental) may generate an inadequate reaction
(over-reaction and under-reaction). The balance between
SIRS and CARS plays a crucial role in resolving the infec-
tion, but the pro- and anti-inflammatory mechanisms are
often dysregulated for reasons that are not entirely under-
stood. To summarize, the differences in clinical manifesta-
tions of babesiosis appear to be the result of the interplay of
parasite–host interactions. If the animal responds quickly
with robust inflammatory cytokine production, the para-
site may be quickly controlled, but if the proinflammatory
response is inadequate, then surviving parasites will con-
tinue to trigger that response, resulting in the clinical
picture of MODS. This reflects failure of the proinflamma-
tory cytokine response to be switched off in time, leading to
ongoing damage to host tissues and organs. This could
explain why vaccination with SPA is effective: the second-
ary antibody response could limit further triggering of the
proinflammatory response initiated by SPA [2].
Proinflammatory and anti-inflammatory cytokine profile
Infectious agents induce tissue macrophages, monocytes,
mast cells, endothelial cells, platelets and other reactive
cell elements to produce various proinflammatory media-
tors. Of these, tumor necrosis factor-a (TNF-a), interleu-
kin-1 (IL-1) and IL-6 are the most widely known. IL-4 and
IL-10 turn off monocyte/macrophage production of TNF-a,
IL-1 and IL-6. Early events in the inflammatory response
also induce the production of cortisol, another potent anti-
inflammatory mediator. Through the combined action of
these mechanisms, the acute phase response leads to
resolution of the infection [83]. A major role of proinflam-
matory cytokines has been reported in human [84], bovine
[85], equine [86] and canine babesiosis (T. Vaughan-Scott,
M.Med.Vet. Thesis, University of Pretoria, 2001) [27].
However, the only proinflammatory cytokine that has been
investigated in canine babesiosis is TNF-a. Furthermore,
the only anti-inflammatory mediator studied in canine
babesiosis is cortisol. The principal limitations of the
aforementioned studies are that only single pro- and an-
ti-inflammatory mediators have been studied, and the
research was carried out on different samples, thus pre-
cluding investigation of their interactions and possible
correlations between them. The final limitation is that
Trends in Parasitology March 2012, Vol. 28, No. 3
the majority of these studies were carried out on dogs
infected with B. rossi.
Concluding remarks
In summary, the balance between SIRS and CARS is of
utmost importance, and it would be prudent to investigate
several pro- and anti-inflammatory mediators in the same
samples before drawing conclusions regarding possible
interactions and correlations between them. It will be
crucial to relate the outcome of canine babesiosis to the
onset, magnitude and durations of SIRS and CARS (and
their elements). From the European point of view, it is
important to conduct these studies on B. canis. In addition,
it will be important to conduct such studies in different
European countries on patients with genetically charac-
terized B. canis strains.
Acknowledgments
Theo P. Schetters is Invited Professor at the Laboratoire de Biologie
Cellulaire et Moléculaire of the University of Montpellier 1, Montpellier
(France).
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