Canine Babesiosis 85
CHAPTER FIVE
(v) Canine Babesiosis
Remo Lobetti
INTRODUCTION
Canine babesiosis is a tick-borne disease of worldwide
importance, which ranges in severity from relatively
mild to fatal. Although haemolytic anaemia is the
hallmark, several variations and complications can
occur. The causative organism of canine babesiosis is
either Babesia canis or Babesia gibsoni. Three subtypes
or strains of B. canis are recognized, namely, B. canis
canis, B. canis vogeli and B. canis rossi. B. canis canis
and B. canis vogeli occur in Europe and North Africa
respectively, whereas B. canis rossi occurs in southern
Africa (Uilenberg et al., 1989). B. gibsoni occurs in
Asia, North America and North and East Africa
(Taboada, 1998). The genus Babesia was named after
Victor Babes, who in 1887 established the aetiology of
the disease in cattle in Romania. The first report of
canine babesiosis was in South Africa in 1885 by
Hutcheon; however, the parasites were only recog-
nized much later by Purvis in 1896 and Koch in 1897.
LIFE CYCLE
In the adult tick, schizogony occurs in the gut epithelial
cells, resulting in the formation of large merozoites.
These then undergo successive cycles of schizogony
within a variety of cell types, including the oocytes. In
the salivary glands, schizogony results in the forma-
tion of small infective merozoites. After the tick has
attached to a dog (the host) and feeds, the merozoites
in the ticks saliva enter the dogs erythrocytes with the
aid of a specialized apical complex. Once inside the
erythrocyte, the merozoite transforms into a tropho-
zoite, from which further merozoites develop by a
process of merogony. Once divided, they leave the cell
to enter other erythrocytes. Trans-stadial and
transovarial transmission can occur, and it is thought
that a tick can remain infective for several generations.
EPIDEMIOLOGY
Babesiosis is solely a tick-borne disease, with B. canis
canis being transmitted by Dermacentor reticulatus,
B. canis vogeli and B. gibsoni by Rhipicephalus san-
guineus and B. canis rossi by Haemophysalis leachi.
B. canis can affect dogs of all ages, although most cases
are in young dogs. A seasonal variation occurs, with
the highest incidence in the summer months. The
source of infection is carrier ticks, or ticks feeding on
dogs that are either ill or incubating the disease and
then feeding on a susceptible dog (Lobetti, 1998).
Other possible sources of infection are carrier dogs and
blood transfusions.
PATHOGENESIS
The incubation period after exposure to a tick is 1021
days. Intraerythrocytic parasitaemia causes both intra-
vascular and extravascular haemolysis, resulting in
regenerative anaemia, haemoglobinaemia, haemoglob-
inuria and bilirubinuria. Pyrexia also develops, which
is attributed to the release of endogenous pyrogens
after erythrolysis, destruction of the parasite and/or
activation of inflammatory mediators. Splenomegaly
occurs as a result of hyperplasia of the mononuclear
phagocytic system. The haemolytic crisis that devel-
ops results in anaemic hypoxia, anaerobic metabolism
and metabolic acidosis. Compounding the problem is
the fact that the remaining haemoglobin is not func-
tioning optimally, thereby exacerbating the anaemic
hypoxia (Taylor et al., 1993).
The many and varied clinical manifestations of
canine babesiosis are difficult to relate to an organism
that is solely restricted to the erythrocyte. Although the
clinical manifestations are diverse, the mechanisms
promoting them are probably more uniform. Multiple
organ dysfunction syndrome (MODS) is now recog-
nized as the end result of tissue inflammation initiated
by several different conditions, including hypovolae-
mia, septic shock and infectious organisms. Babesiosis
can cause severe tissue hypoxia, with consequent wide-
spread tissue damage and probable release of inflam-
matory mediators. Widespread inflammation and
multiple organ damage can thus occur (Jacobson and
Clark, 1994). The systemic inflammatory response
syndrome (SIRS) that precedes MODS is caused by
excessive release of inflammatory mediators. This
86 Manual of Canine and Feline Haematology and Transfusion Medicine

syndrome is broadly defined and considered to be
present if two or more of the following occur: tachy-
cardia, tachypnoea or respiratory alkalosis, hypother-
mia or hyperthermia and leucocytosis or leucopenia
with a neutrophilic left shift (Cipolle et al., 1993). By
this definition, most cases of babesiosis have SIRS.
In one study, 87% of cases were positive for SIRS,
52% showed single organ damage and 48% had
multiple organ damage (Welzl et al., 1999). Although
outcome was not affected by whether one or multiple
organs showed evidence of damage, specific organ
involvement significantly affected outcome: risk of
death increased 57-fold and fivefold with involve-
ment of the central nervous system and renal dysfunc-
tion, respectively. Liver or muscle damage did not
affect outcome.
CLINICAL MANIFESTATIONS
Canine babesiosis can be clinically classified into
uncomplicated and complicated forms. Uncomplicated
cases typically present with signs relating to acute
haemolysis, including fever, anorexia, depression, pale
mucous membranes, splenomegaly and waterhammer
pulse. This form is further divided into mild, moderate
or severe disease, according to the severity of the
anaemia. A case of mild uncomplicated babesiosis can
progress to become severe uncomplicated, when anae-
mia becomes life threatening. The complicated form of
babesiosis refers to clinical manifestations that are not
easily explained by the haemolytic process alone. Rare
complications include gastrointestinal disturbances,
myalgia, ocular involvement, upper respiratory signs,
cardiac involvement, necrosis of the extremities, fluid
accumulation or disease with a chronic clinical course.
Overlap between the different categories of the com-
plications can also occur.
Acute renal failure
Evidence of renal damage is common in both compli-
cated and uncomplicated cases but does not necessarily
predict renal failure. A recent study showed celluria of
the renal tubular epithelium, enzymuria, proteinuria and
variable azotaemia in dogs with babesiosis without
overt acute renal failure (ARF), although ARF was also
documented in several dogs in the same study (Lobetti
et al., 1999). Acute renal failure in babesiosis typically
presents with anuria or oliguria despite adequate rehy-
dration but is an uncommon complication. An increased
concentration of serum urea alone is an unreliable
indicator of renal insufficiency in babesiosis, as a dis-
proportionate increase in urea, compared with creati-
nine, concentration occurs, which has been related to the
catabolism of lysed erythrocytes. Renal failure is diag-
nosed on the basis of ongoing evaluation of urine
volume, urine analysis and degree of azotaemia.
Cerebral babesiosis
Cerebral babesiosis is defined as the presence of concur-
rent neurological signs in an animal with babesiosis. The
presentation is typically peracute, with clinical signs
being a combination of incoordination, hindquarter
paresis, muscle tremors, nystagmus, anisocoria, inter-
mittent loss of consciousness, seizures, stupor, coma,
aggression, paddling or vocalization (Jacobson and
Clark, 1994). Pathological changes in the brain are
congestion (Figure 5.28), haemorrhage and/or necrosis
(Figure 5.29) and sequestration/pavementing of
parasitized erythrocytes in capillary beds (Figure 5.30).
Coagulopathy
The most consistent haemostatic abnormality in babe-
siosis is profound thrombocytopenia, which is a rou-
tine finding in both complicated and uncomplicated
cases. Despite the degree of thrombocytopenia, clini-
cally apparent haemorrhages are relatively rare. Al-
though disseminated intravascular coagulation (DIC)
has been reported in canine babesiosis, confirmation of
DIC is difficult because of the nature of the underlying
disease process and the reported unreliability of the
human fibrin degradation product test (Jacobson and
Clark, 1994). Clinical signs of DIC are difficult to
recognize until haemorrhages develop in the
hypocoagulable phase, where signs are related to organ
dysfunction induced by microthrombi (Figure 5.31).

Figure 5.30: Histopathological section

Figure 5.28: Brain of a dog that died
from cerebral babesiosis, showing
generalized congestion. (Courtesy of
Dr Anne Pardini, Department of
Pathology, Faculty of Veterinary
Science, University of Pretoria.)
Figure 5.29: Brain of a dog that died
from cerebral babesiosis, showing focal
areas of necrosis. (Courtesy of
Dr Anne Pardini, Department of
Pathology, Faculty of Veterinary
Science, University of Pretoria.)
from a brain of a dog that died from
cerebral babesiosis, showing capillary
blood vessels containing sequestrated
parasitized erythrocytes. (Courtesy of Dr
Anne Pardini, Department of Pathology,
Faculty of Veterinary Science,
University of Pretoria.)

Figure 5.31: Scleral haemorrhage in a dog with babesiosis
complicated by disseminated intravascular coagulation.
Icterus and hepatopathy
In some cases of babesiosis, icterus and increased
concentrations of liver enzymes and bile acids occur,
which are indicative of a liver insult (Miller, 1999).
Whether the insult is due to inflammatory cytokines,
hypoxic damage or a combination of these is not
known. As the icterus (Figure 5.32) does not seem to
be due to haemolysis alone, liver dysfunction seems
to be, at least, contributory. Histopathological changes
usually associated with icterus include both diffuse
and periportal lesions, whereas icteric dogs with
babesiosis show a centrilobular lesion. Hypoxic
insults can cause diffuse hepatocellular swelling,
and thus the hypoxia in severe babesiosis may be
severe enough to cause a hepatopathy.
Figure 5.32: Dog with severe icterus due to babesiosis.
Immune-mediated haemolytic anaemia
Immune-mediated haemolytic anaemia (IMHA) is
the increased destruction of erythrocytes due to
antibodies against the erythrocyte membrane, which
can be either primary (in which the membrane is
normal) or secondary (in which the membrane is
altered and recognized as foreign). Secondary
IMHA is assumed to be the case in babesiosis. The
cardinal feature of babesiosis-associated IMHA is
continuing haemolysis despite successful antibabesial
treatment. Diagnosis is by the in-saline agglutination
test and/or detection of spherocytosis. The Coombs
test is not diagnostic as both uncomplicated cases
and cases complicated with IMHA give a positive
Coombs test result.
Canine Babesiosis 87
Acute respiratory distress syndrome
Acute respiratory distress syndrome (ARDS) is a severe
and frequently catastrophic complication of babesiosis.
Typical clinical signs are a sudden increase in respira-
tory rate (although this may be caused by other factors,
such as pyrexia and acidosis), dyspnoea, moist cough
and blood-tinged frothy nasal discharge. The diagnosis
of ARDS is based on the presence of diffuse pulmonary
infiltrates on thoracic radiographs, hypoxaemia due to
ventilationperfusion mismatch, normal pulmonary
capillary wedge pressure and reduced pulmonary
compliance (Frevert and Warner, 1992). In most clinical
situations, pulmonary wedge pressure, blood gas analy-
sis and compliance cannot be measured. Thus the diag-
nosis of ARDS depends on the recognition of risk
factors for ARDS, thoracic radiographs (Figure 5.33)
and the exclusion of other causes of pulmonary oedema,
especially cardiogenic causes and fluid overload, the
latter particularly where oliguric renal failure is present.
Fluid loads that can be tolerated by normal dogs may
fatally exacerbate pulmonary oedema in ARDS.
Figure 5.33:
Lateral and
dorsoventral
radiographs from a
dog with babesiosis
complicated by
acute respiratory
distress syndrome,
showing severe
pulmonary oedema.
Haemoconcentration
The paradoxical phenomenon of severe intravascular
haemolysis combined with haemoconcentration con-
stitutes the syndrome known as red biliary. Clinical
features are congested mucous membranes, visible
haemoglobinaemia and/or haemoglobinuria and high
88 Manual of Canine and Feline Haematology and Transfusion Medicine

to normal or increased haematocrit (Jacobson and
Clark, 1994). Haemoconcentration has been associ-
ated with other complications, such as cerebral babe-
siosis, DIC, ARF and ARDS. Haemoconcentration in
babesiosis is thought to be due to reduction in blood
volume, because of fluid shifts from the vascular to
the extravascular compartment. As plasma protein
concentrations are normal, plasma, rather than a fil-
trate of plasma, is shifted from the vasculature. The
widespread increase in capillary permeability, which
occurs in SIRS, may play an important role in the
pathogenesis of red biliary.
Hypotension
Dogs with severe and complicated babesiosis are
frequently presented in a state of collapse and clinical
shock, the latter resembling the hyperdynamic phase
of septic shock. In one study, hypotension occurred
frequently in babesiosis, and the presence and sever-
ity of hypotension increased with severity of the
disease (Jacobson et al., 1999). The presence of
hypotension in dogs with complicated babesiosis is
consistent with the hypothesis that inflammatory
mechanisms play a major role in this disease and can
result in a sepsis-like state. It is likely that hypoten-
sion in babesiosis is a combination of vasodilation,
reduced vascular volume due to increased vascular
permeability and/or dehydration, and myocardial
depression. Hypotension can play a role in the patho-
physiology of the disease, as it has been hypothesized
to facilitate parasite sequestration.
CLINICAL PATHOLOGY
The primary haematological abnormalities in canine
babesiosis are anaemia, thrombocytopenia and leu-
cocytosis (Figure 5.34). However, the haematological
profile varies in different parts of the world: in
France, mild anaemia and thrombocytopenia have
been reported. In the Philippines, the only abnormal-
ity reported was mild anaemia. In Nigeria, peracute
cases showed severe anaemia, neutrophilia, lympho-
cytosis and eosinopenia, acute and chronic cases
showed only moderate anaemia, and only mild anae-
mia was present in the chronic cases. In South Africa,
severe anaemia, neutrophilia, monocytosis, eosino-
penia and thrombocytopenia have been reported
(Reyers et al., 1998). The most remarkable differences
observed between these reports were degree of anae-
mia, macrocytosis (representing reticulocytosis) and
leucocytosis in general, but particularly neutrophilia.
Urine analysis may show hypersthenuria, bilirubin-
uria, haemoglobinuria, proteinuria, granular casts
and epithelial cells of the renal tubule. Alterations
in biochemical parameters varies depending on the
severity of the case. Typically, uncomplicated cases
can have no biochemical changes. However, an
increased liver enzyme concentration, hypokalaemia
(in more severely affected cases) and an increased
serum urea concentration with a normal serum creati-
nine concentration may be evident. In complicated
cases, biochemical changes reflect the underlying
complication.
The most commonly reported acidbase distur-
bance in dogs with babesiosis and severe anaemia is
metabolic acidosis. However, studies by Leisewitz et
al. (1999) suggest that a mixed acidbase disturbance
is present in many cases, which would reflect a more
complex pathophysiology than previously assumed.
Dogs with severe babesiosis can show a combination
of abnormalities, including hyperchloraemic meta-
bolic acidosis (low strong ion difference, SID), high
anion gap metabolic acidosis (probably due to
hyperlactataemia), hypoalbuminaemic alkalosis
and hyperphosphataemic acidosis, dilutional acido-
sis and respiratory alkalosis. Respiratory alkalosis
occurs as frequently as metabolic acidosis, and arte-
rial blood pH is a poor indicator of the complexity
of the pathology.

Parameter Mean Standard deviation Range Normal

Haematocrit 20.24 12.81 370 3550%
Reticulocyte count 9.19 7.12 0.144.6 <1%
White cell count 20.09 15.82 0.4109.6 615 x 109/l
Neutrophils 9.318 9.864 075.58 311.5 x 109/l
Band cells 3.453 4.839 049.32 00.3 x 109/l
Lymphocytes 2.439 2.022 023.07 14.8 x109/l
Monocytes 2.419 2.676 022.062 0.151.35 x 109/l
Eosinophils 0.143 0.354 04.088 0.11.25 x 109/l
Platelets 65.12 78.88 1726 200500 x 109/l
Figure 5.34: Haematological parameters from 921 cases of babesiosis due to Babesia canis evaluated at the Onderstepoort
Veterinary Academic Hospital.

DIAGNOSIS
The diagnosis of babesiosis is made by demonstrat-
ing the presence of Babesia organisms within
infected erythrocytes by using Romanowsky-type
stains. Large (2 x 5 m) pear-shaped organisms
(usually present in pairs) are indicative of infection
with B. canis (Figure 5.35), whereas B. gibsoni
appears as smaller (1 x 3 m) single round to oval
organisms (Figure 5.36). Parasites can be detected in
blood smears from peripheral blood as well as central
blood. Serology is a more reliable method for detec-
tion of occult parasitaemias in less endemic areas.
However, as there is serological crossreactivity
between B. canis and B. gibsoni, identification of the
parasite is still necessary.
Figure 5.35: Blood smear from peripheral blood showing
multiple Babesia canis parasites. Diff-Quik stain.
Figure 5.36: Blood smear from peripheral blood showing
multiple Babesia gibsoni parasites. Diff-Quik stain.
THERAPY
The primary therapeutic aim in the treatment of babesio-
sis is the reversal of life-threatening anaemia via blood
transfusions, and elimination or suppression of the
parasite with specific anti-babesial drugs. Mild to
Canine Babesiosis 89
moderate uncomplicated cases require only antibabesial
therapy, severe uncomplicated cases require
antibabesial therapy and blood transfusions, and the
complicated forms of the disease require additional
therapy aimed at treating complications (Figure 5.37).
In mild to moderate uncomplicated cases, noticeable
signs of recovery can be expected within 24 hours of
specific treatment.
Antibabesial therapy
The three recommended and recognized antibabesial
drugs are diminazene aceturate, imidocarb and trypan
blue. Other drugs that have been used are amicarbalide,
euflavine, phenamidine, quinoronium sulphate and
chloroquine. However, due to their poor efficacy
and/or additional adverse effects, these drugs
have been either discontinued or infrequently used
(Swan, 1995).
Diminazene
Diminazene is the drug of choice and is given
intramuscularly at a dosage of 3.5 mg/kg once only.
The drug has a rapid action and a short-lived protective
effect, making it unsuitable for chemoprophylaxis.
Diminazene has a low therapeutic index, with toxicity
resulting in depression or stupor, continuous vocaliza-
tion, ataxia, opisthotonos, extensor rigidity, nystag-
mus and seizures. Nervous signs usually occur 24 to 48
hours after an overdose and are irreversible and poten-
tially fatal.
Imidocarb
Imidocarb can be given either intramuscularly or sub-
cutaneously at a dose of 6 mg/kg. Toxicity can cause
severe renal tubular and hepatic necrosis.
Trypan blue
Trypan blue suppresses parasitaemia and alleviates
clinical signs but does not eliminate infection. Conse-
quently, it is often followed up with diminazene
or imidocarb in an attempt to sterilize the infection.
It is also used in repeated relapses after treatment
with either diminazene or imidocarb. As the drug is
irritant to tissues, it is given strictly intravenously
as a 1% solution, at a dose of 10 mg/kg. Treatment
can be repeated if necessary. Premunity may develop
in some dogs, but relapses can occur at any stage
owing to stress.
Blood transfusions
Transfusions are usually indicated in severe uncom-
plicated cases and in complicated cases that have a
life-threatening anaemia. The decision to transfuse is
based on clinical signs, history and haematological
testing. Clinical signs that would indicate the need
for transfusion are tachycardia, tachypnoea,
waterhammer pulse, weakness and collapse. Although
90 Manual of Canine and Feline Haematology and Transfusion Medicine

Classification Clinical signs Therapeutic principles

Uncomplicated
Mild to moderate Acute haemolysis Antibabesial
Mild/moderate anaemia
Severe Acute haemolytic crisis Antibabesial
Life-threatening anaemia Blood transfusion
Complicated
Acute renal failure Oliguria, anuria or polyuria Antibabesial
Fluids
Diuretics
Dopamine
Cerebral babesiosis Collapsed Antibabesial
Nystagmus Oxygen supplementation
Seizures Barbiturate sedation
Semi-coma, coma Diuretics
Elevation of the head
Coagulopathy May be clinically silent Antibabesial
Bleeding tendency Fresh frozen plasma
Shock, organ dysfunction Heparin
Icterus and hepatopathy Profound bilirubinaemia and bilirubinuria Antibabesial
Yellow discolouration of mucous Blood transfusion
membranes Fluids with potassium and
dextrose
Immune-mediated haemolytic Persistent in-saline agglutination Antibabesial
anaemia Worsening anaemia despite eradication Blood transfusion
of parasites Corticosteroids
Azathioprine
Cyclophosphamide
Intravenous human
gammaglobulin
Acute respiratory distress Sudden onset tachypnoea Antibabesial
syndrome (ARDS, shock lung) Severe dyspnoea Oxygen supplementation
Cough Diuretics
Blood-tinged frothy nasal discharge Pentoxifylline
Colloids
Haemoconcentration (red Peracute onset Antibabesial
biliary) Often collapsed Fluids at double
Severe intravascular haemolysis with maintenance rates
normal or high haematocrit Colloids
Hypotension May not be classic shock Antibabesial
Congestion Blood transfusion
Bounding pulse may be present Fluids
Colloids
Figure 5.37: Clinical manifestations of babesiosis and therapeutic principles.

the haematocrit is the most commonly used indicator
of anaemia, erythrocyte count and haemoglobin
concentration can also be used. There is no set haema-
tocrit at which a transfusion should be given, as it
must be evaluated in conjunction with the clinical
signs and history. Generally, a transfusion is consid-
ered when the haematocrit is 15% or lower and
always indicated when the haematocrit is 10% or
lower. The degree of parasitaemia is not an important
deciding factor, as it often bears little relation to the
degree of anaemia.
Packed red blood cells are the component of choice
for babesiosis. The administration of the plasma com-
ponent of whole blood is unnecessary in most dogs
with babesiosis and can place the patient at risk of
volume overload. If rehydration is required, crystal-

loid replacement solutions are preferable. A blood
transfusion not only has a favourable effect on oxygen
status and acidbase balance in dogs with babesiosis
but also replaces the subfunctional haemoglobin with
functional haemoglobin.
Supportive therapy
Supportive therapy should be based on thorough patient
assessment and ongoing monitoring, appropriate labo-
ratory testing and accepted therapeutic principles for
the complications that may be present: acute renal
failure, immune-mediated haemolytic anaemia, DIC,
hepatopathy, shock and pulmonary oedema.
PREVENTION
The primary means of disease prevention is the control
of the vector tick by routinely dipping or spraying pets,
by using tick collars or spot-on preparations and by
environmental control by spraying the premises. The
newer ectoparasitic agents (such as fipronil) are also
effective.
A vaccine against a specific avirulent strain of
canine babesia is available in France; however, cross
immunity between the different strains of babesia
seems not to occur. It has recently been shown that
protective immunity to a virulent strain is possible,
thus making vaccines from different parasite strains
feasible (Lewis et al., 1995).
Premunity has been recognized as important in
controlling clinical signs of the virulent form of the
disease in endemic areas. Therefore complete eradica-
tion of parasites from infected animals may not be
advantageous in these areas, and thus the use of drugs
to sterilize the infection may be undesirable (Penzhorn,
1994). The role that premunity plays in areas with less
virulent strains is not known.
As babesial organisms can be transmitted by blood
transfusions, it is important that all blood donors are
negative for babesiosis.
Canine Babesiosis 91
REFERENCES AND FURTHER
READING
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