Arthropod-borne infectious diseases of the dog and cat
Crystalline fluid therapy should be given with caution
in anaemic patients in order to avoid causing further
haemodilution or exacerbating respiratory distress.
Oxygen therapy does not alleviate the hypoxia in anaemic
states but is indicated for the therapy of pulmonary
oedema in complicated babesiosis. Bicarbonate therapy
continues to attract controversy and its use is best
restricted to institutions where acid-base status can be
regularly assessed and interpreted. Organ dysfunction
associated with complicated babesiosis should be
managed according to the general guidelines provided in
current critical care manuals. A detailed review pertaining
to the supportive treatment of canine babesiosis has been
published (see Further reading, p. 146). Glucocorticoids,
including dexamethasone and prednisolone (or
prednisone), have been recommended by some authors
but their benefits in babesiosis are currently unproven.
Prevention and control
As with any tick-transmitted disease, removing all
possibility of exposure to the vector is the best way to
prevent babesiosis. However, this is rarely achievable in
endemic areas despite attentive ectoparasite control.
Regular spraying, dipping or bathing with topical
acaricidal preparations in accordance with the
manufacturers’ instructions should be practised in regions
where tick challenge is continual. For dogs that are
visiting tick-enzootic regions for a short time, and in cats
that may have increased susceptibility to the toxicity of
many acaricidal preparations, fipronil spray or ‘spot-on’
is a suitable choice, with a reasonable prophylactic effect.
Owners should be encouraged to search their pets daily
for ticks and, once found, to physically remove and
dispose of them. Tick ‘removers’ have become available
commercially in recent years and the use of these devices
(and the wearing of gloves) may help to reduce the chance
of inadvertent exposure of the owner to other potentially
infectious agents within the tick (e.g. Borrelia species).
Several drugs have been investigated for their
prophylactic potential against babesiosis, yet none have
been consistently reliable in this regard. Experimental
studies have suggested that a single dose of imidocarb
dipropionate (6 mg/kg) protects dogs from Babesia
challenge for up to eight weeks, and that doxycycline at
5 mg/kg/day ameliorates the severity of disease when
challenged with virulent B. canis. Higher doses of both
drugs may protect more effectively for longer periods but
the potential toxicity of imidocarb and the overuse of
doxycycline would be of concern. Reliance on such
strategies cannot be recommended.
Vaccines made from cell culture-attenuated antigens
have been developed for immunization against B. canis
canis and are available commercially. While these
vaccines do not prevent infection, they limit the
parasitaemia and ameliorate the clinical signs and
laboratory changes that occur after acute infection. The
use of vaccines containing B. canis canis antigen only is
restricted to Europe, as cross-protection against other
Babesia parasites of dogs (e.g. B. canis rossi and
B. gibsoni) does not develop. However, when mixed
B. canis canis and B. canis rossi antigens are incorporated
into a vaccine, heterologous protection is induced.
Zoonotic potential/public health significance
Babesiosis is an emerging zoonosis in many parts of the
world yet, with a few exceptions, the babesial parasites of
companion animals have not been implicated in zoonotic
transmission. The majority of human cases of babesiosis
in North America are associated with B. microti, a
natural parasite of rodents, and these are typically mild or
asymptomatic except in those individuals who are
immunocompromised or splenectomized. In Europe,
human babesiosis is less common but is associated with
greater morbidity (and mortality) and is usually caused by
the bovine pathogen B. divergens. In 1991 an acute
malaria-like syndrome in a human patient on the west
coast of the USA was attributed to a new Babesia-like
piroplasm, designated WA-1. Molecular phylogenetic
analysis has revealed that WA-1 is closely related to the
small canine piroplasms (Table 11, p. 64) and falls within
a cluster that includes Theileria equi (B. equi). A similar
piroplasm, designated CA-1, was discovered in several
splenectomized humans in California and is related to, yet
distinct from, WA-1 and B. gibsoni. Serological surveys
have been used to investigate the prevalence of babesial
infections in regions where clinically apparent cases have
occurred. Surveys of blood donors have shown 3–8%
prevalence for B. microti and up to 16% prevalence of
antibodies against the WA-1 organism.
CYTAUXZOONOSIS
Background, aetiology and epidemiology
Cytauxzoonosis is a tick-transmitted protozoal disease of
clinical importance for domestic cats in southern regions
of the USA. The causative agent is Cytauxzoon felis,
which is recognized to have both pre-erythrocytic and
erythrocytic phases of its life cycle in the vertebrate host.
The exoerythrocytic stage of the life cycle has led to its
taxonomic classification within the family Theileriidae, in
the order Piroplasmida. Members of the genus
Cytauxzoon are differentiated from Theileria species
based on the fact that schizogony in Cytauxzoon occurs
in macrophages, while schizogony in Theileria occurs in
lymphocytes. However, it is clear that C. felis not only
shares morphological characteristics with organisms of
the genera Theileria and Babesia but it is also closely
related on a molecular basis to the smaller piroplasms B.
rodhaini and T. equi (formerly Babesia equi).
The natural hosts are the North American wildcat
species such as the bobcat (Lynx rufus) and Florida
panther (Puma concolor coryi) and it is thought that
transmission of C. felis to domestic cats represents the
inadvertent infection of a dead-end host. Natural C. felis
infection may result from transmission by an attached
tick, ingestion of infected ticks or by inoculation of
Babesiosis and cytauxzoonosis
64
infected blood or tissue during fights, notably with
bobcats. The highest incidence of disease occurs during
early summer through to autumn, corresponding to the
time when ticks are most active. More than one individual
in a multicat household may be affected and it is wise to
check the other cats when the disease is first diagnosed.
The life cycle of C. felis is poorly understood. It is
suspected that Dermacentor variabilis is the principal
vector for natural transmission and is responsible for
injecting infective sporozoites from its salivary glands into
the mammalian host. Schizonts develop primarily within
tissue histiocytes in many organs and go on to release
merozoites, which invade monocytes and erythrocytes. In
cats that survive initial infection, low-level erythrocytic
parasitaemias can persist for many years.
Pathogenesis
65
Infection of domestic cats with the schizogenous stage
typically results in a rapidly progressive systemic disease
with a high mortality rate. In natural infections with
C. felis there is an apparent variation in pathogenicity
that may be associated with geographical location. In one
recent report, 18 cats living in an area near the northern
border of Arkansas and Oklahoma survived natural
infection and developed chronic parasitaemia. The
pathogenesis of cytauxzoonosis is attributed to the
schizogenous phase that causes mechanical obstruction to
blood flow through various organs, notably the lungs,
and results in a shock-like state. Vascular occlusion and
damage are further associated with the release of
inflammatory mediators and development of DIC.
Intravascular and extravascular haemolysis occur as a
result of erythrocyte invasion by merozoites.
Clinical signs
64, 65 Ventrodorsal (64) and lateral (65) radiographs of the
thorax of a cat with cytauxzoonosis. The pulmonary vessels
are enlarged and appear increased in number. The margins
are slightly hazy due to a moderate diffuse increase in
interstitial opacity, with a mild bronchial component. Faint
pleural fissure lines indicate a small volume of pleural effusion.
(Radiographs courtesy Dr N Lester).
The tissue schizont phase of infection with C. felis is
responsible for the clinical signs. Soon after infection,
affected cats develop non-specific signs such as anorexia,
lymphadenopathy, fever and lethargy, but the course of
the disease is usually rapid, with the onset of a severe
clinical syndrome characterized by dehydration, pallor,
dyspnoea, icterus, recumbency and death. Thoracic
radiographs may reveal enlarged and tortuous pulmonary
vessels as a result of vascular occlusion by the tissue stages
(64, 65). Usually, by the time the cat is presented, it is
severely ill. Most cats die within 9–15 days following
infection by virulent strains, regardless of treatment.
Arthropod-borne infectious diseases of the dog and cat
Diagnosis
The diagnosis of cytauxzoonosis is made by the
identification of erythrocytic piroplasms in blood smears
stained with Wright’s stain or Giemsa (66). There is no
serological assay commercially available at the current
time. Parasitaemias are typically low (1–4%), although in
some acute infections as many as 25% of the red cells may
be infected. C. felis is a small piroplasm (Table 11, p. 64)
that must be differentiated from Babesia felis, which is
very similar in size and appearance, by light microscopy;
however, B. felis is confined geographically to southern
Africa. C. felis appears in a number of morphological
varieties including the signet-ring form, bipolar oval
forms, tetrads and dark-staining ‘dots’, the latter of which
may be mistaken for a more common and widespread
parasite of cats, Mycoplasma (Haemobartonella) species,
the cause of feline infectious anaemia. A unique, yet
uncommon, finding in cytauxzoonosis is the appearance
of tissue phase schizonts in blood smears and buffy coat
preparations. However, these forms are best demonstrated in impression smears from bone marrow, spleen or
lymph nodes, where they are typically numerous (67).
Haematology and serum biochemistry abnormalities
are typical of haemolytic anaemia. Initially, the anaemia is
normochromic and normocytic but it progresses to a
strong regenerative response, characterized by the
presence of nucleated red cells by the time of death.
Moderate to severe leucopenia is typical and
thrombocytopenia, sometimes profound, is commonly
reported with or without DIC. Prolongation of clotting
times (PT and APTT) has been recorded and has been
used to support a diagnosis of disseminated intravascular
coagulation (DIC), but concentrations of fibrin
degradation products (FDP) are variable. The plasma
appears icteric on the last day or two of life and is
associated with a high serum concentration of bilirubin.
Other clinicopathological changes that have been
recorded in cases of cytauxzoonosis include
hyperglycaemia, hypokalaemia, hypocholesterolaemia
and elevations in serum ALT and AP; however, these
changes may be minimal in acutely affected individuals
that typically die before such abnormalities are recorded.
Necropsy findings in cats that have died of
cytauxzoonosis include pallor and icterus of the tissues,
petechial and ecchymotic haemorrhages on the serosal
surfaces of organs, oedematous lymph nodes and lungs,
and hepatosplenomegaly. The diagnosis may be
confirmed by histological examination of the tissues.
Large numbers of mononuclear phagocytes containing
schizonts are visible in the veins of most organs, including
the liver, lung, spleen, lymph nodes, kidneys and CNS.
Treatment and control
The diagnosis of cytauxzoonosis carries a grave
prognosis, with high mortality rates despite treatment. Of
the specific therapies that appear to help ameliorate the
disease, imidocarb dipropionate and diminazine aceturate
have shown most promise (Table 18). It is suggested that
66
66 Cytauxzoon felis piroplasms in a domestic cat with terminal
cytauxzoonosis (Oklahoma, USA). (Specimen courtesy Dr
J Meinkoth)
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