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Canine babesiosis: introduction to a potential new disease

threat
Author : Vanessa Biggle

Categories : Companion animal, Vets

Date : April 11, 2016

Since the introduction of the Pet Travel Scheme, babesiosis has been diagnosed with
increasing frequency in dogs resident in the UK after travelling from enzootic areas of
Europe (Shaw et al, 2003). However, a fatal case was confirmed in a dog residing in Kent
with no history of foreign travel (Holm et al, 2006).

Dermacentor reticulatus. Image: © Dark Raptor.

The APHA and Public Health England are investigating an outbreak of canine babesiosis in
Harlow, Essex – and this has affected many animals that have never left the UK.

A tick removed from one of the dogs was sent to the APHA, confirming its identification of

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Dermacentor reticulatus – a species reported in several locations in Wales and southern England.
The tick was infected with Babesia canis, distinct from other Babesia species that infect dogs
(Phipps et al, 2016).

Babesiosis is a tick-borne disease of worldwide significance that affects humans and other
mammals. Canine Babesia are morphologically classified into large and small forms. There are
three antigenically different subspecies of B canis – the species typically affecting dogs in Europe,
although other species exist.

Various species of ticks can transmit Babesia, with D reticulatus being the vector of B canis canis,
the subspecies found in continental Europe. This tick is also referred to as the marsh tick and is
distributed across Europe from the Atlantic Ocean to Kazakhstan.

Babesiosis can affect dogs of all ages, although disease mostly occurs in young dogs. The
incubation period varies from 10 days to 21 days for B canis. The female ticks feed on the host for
approximately one week and will have usually left the host before disease develops (Schoeman
and Leisewitz, 2006).

Transmission of sporozoites from the salivary glands of a feeding tick into the subcutaneous
tissues and bloodstream of the canine host is the route by which most dogs are infected with
canine babesiosis. Once they are inside the host’s bloodstream, the parasites invade, feed, and
multiply within erythrocytes during repeated phases of asexual reproduction, releasing merozoites
that find and invade more red cells.

Transmission back to a vector may occur at any time parasitaemia exists; ticks are infected with
piroplasms when they take a blood meal from a parasitaemic host. After ingestion by the tick, the
piroplasms continue to develop by sexual reproduction and maturation, eventually migrating to the
cells of the tick’s salivary glands in readiness for the next feeding, or to its ovaries for transovarial
transmission to the next generation of ticks (Irwin, 2010).

Although vector-borne transmission is the natural means of infection, it has also been reported in
some Babesia species via transplacental transmission to neonates, via blood transfusions and
between fighting dogs (Schoeman and Leisewitz, 2006; Irwin, 2010).

Clinical signs
Severity of disease depends on the species of Babesia, the presence of concurrent infections and
the age and immune status of the patient. Disease presentation varies widely from peracute to
chronic and may be subclinical (Schoeman and Leisewitz, 2006). Most dogs develop haemolytic
anaemia and/or thrombocytopaenia (Irwin, 2010).

Clinical signs include pallor, tachycardia, tachypnoea, depression, anorexia, weakness,

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splenomegaly and pyrexia. It is thought the clinical signs are the result of tissue hypoxia following
anaemia and a concomitant systemic inflammatory response syndrome caused by cytokine
release. The pathogenesis of the anaemia is not completely understood. Extra and intravascular
haemolysis occurs, but other mechanisms, such as poor bone marrow response, are also thought
to occur (Schoeman and Leisewitz, 2006; Irwin, 2010).

The anaemia does not correlate with the level of parasitaemia. Dogs tend to start to improve after
parasiticidal treatment, although the haematocrit values generally drop further before starting to
increase. In some cases there is an additional immune mediated breakdown of red blood cells.

Dogs showing positive saline agglutination reactions need to be carefully monitored for rapid
decreases in haematocrit (Schoeman and Leisewitz, 2006).

Clinical findings in canine babesiosis include:

loss of appetite and depression

pale mucous membranes
tachycardia
tachypnoea
pyrexia
splenomegaly
collapse
icterus
discoloured (red) urine (Schoeman and Leisewitz, 2006; Lobetti, 2010; Irwin, 2010)

Babesia canis piroplasm stage infecting Giemsa-stained red blood cells of a dog.

The severe form of disease is characterised by marked haemolytic anaemia, severe acid-base
abnormalities with frequent secondary multi-organ failure and complications, such as acute kidney
injury, hepatopathy with marked icterus, hypoglycaemia, acute respiratory distress syndrome,

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cerebral pathology and additional immune-mediated red blood cell destruction (Schoeman and
Leisewitz, 2006).

Complications associated with the disease include:

hypoglycaemia
hepatopathy and marked icterus
pancreatitis
immune-mediated haemolytic anaemia
hypovolaemia
multiple-organ dysfunction
respiratory distress syndrome
cerebral signs
acute kidney injury
severe mixed acid-base abnormalities
disseminated intravascular coagulation (Schoeman and Leisewitz, 2006; Lobetti, 2010;
Irwin, 2010)

Diagnosis
Diagnosis of acute B canis infection is based on the clinical presentation and demonstration of
intracellular parasites on Diff-Quick-stained thin capillary blood smears. Large Babesia are typically
seen as paired pyriform to round bodies, although some red blood cells can contain up to eight
bodies. Parasitaemia has been shown to be higher in capillaries compared with central blood at
presentation. Blood samples taken at the ear margin may, therefore, be more representative
(Schoeman and Leisewitz, 2006).

In more chronic cases, parasitaemia may be below the microscopic detection limit (Schoeman and
Leisewitz, 2006; Irwin, 2010). In these cases, diagnosis may be achieved through positive indirect
fluorescent antibody titres or PCR (although false negatives can occur), together with history and
physical examination findings. Examination of thick smears, or along the periphery of the blood
smear, may assist in the detection of parasites (Schoeman and Leisewitz, 2006).

Active infection may be demonstrated by confirming increasing antibody titres over two to three
weeks. Diagnosis should not be purely made on seropositivity, as clinically normal dogs from
endemic areas may be seropositive. In dogs that have never left the UK, seropositivity would
provide good evidence of current infection (Schoeman and Leisewitz, 2006).

Other blood smear findings typically reflect the underlying regenerative haemolytic anaemia, such
as anisocytosis, polychromasia and reticulocytosis. The regenerative response takes three to five
days so, in acute disease, a non-regenerative (pre-regenerative) anaemia may be apparent.
Thrombocytopenia is a hallmark of disease and is often marked (Schoeman and Leisewitz, 2006).

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Spherocytosis may be seen in dogs with secondary immune-mediated haemolytic anaemia and a
left shift neutrophilia may be seen due to a marked systemic inflammatory response (Schoeman
and Leisewitz, 2006).

Elevation of liver enzymes may occur in cases with hepatopathies. Serum potassium is frequently
low, especially in icteric cases. Serum bilirubin concentrations are elevated in relation to the degree
of anaemia and accompanying hepatopathy. Azotaemia may be present in dehydrated patients and
those with acute kidney injury. Urinalysis may demonstrate bilirubinuria, haemoglobinuria,
proteinuria, renal tubular epithelial cells and granular cysts. Acid-base imbalances are common,
especially metabolic acidosis and respiratory alkalosis (Schoeman and Leisewitz, 2006).

Laboratory findings in canine babesiosis include:

low haematocrit, haemoglobin and red cell count

normoblastemia
reticulocytosis
spherocytosis
leukopenia (in the early stages)
left-shift neutrophilia lymphocytosis
marked thrombocytopenia
in-saline positive red blood cell agglutination
elevated liver enzymes
elevated serum bilirubin
hypoglycaemia
raised serum amylase and lipase
raised urea (often with normal creatinine)
hypokalaemia
mild hypoalbuminaemia and hyperglobulinaemia
acid-base abnormalities, most commonly mixed metabolic acidosis and respiratory alkalosis
(Schoeman and Leisewitz, 2006; Lobetti, 2010).

Treatment and prognosis

The primary goals of treatment are to eliminate the parasite and reverse life-threatening anaemia.
Imidocarb dipropionate can be administered as a single dose of 7.5mg/kg or at 7mg/kg given twice,
14 days apart IM (Schoeman and Leisewitz, 2006). Alternative dosing schedules and medications
have also been reported.

However, a 100% safe and efficacious treatment is not available. Treated dogs should be regarded
as potentially affected for life, as it is difficult to completely cure the disease (Irwin, 2010) despite
resolution of clinical signs.

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Patients with mild or moderate anaemia may only require parasitic medications. Markedly anaemic
animals, or those with any of the previously mentioned complications, will require additional
supportive treatments (Schoeman and Leisewitz, 2006).

Approximately 85% to 90% of canine patients worldwide survive the illness. Dogs developing
complications can, however, have a poor prognosis despite interventions (Schoeman and
Leisewitz, 2006).

Prevention
Educating owners on examining their pets daily for the presence of ticks should be strongly
recommended, as the tick must feed on the host for at least three days to transmit B canis
(Schoeman and Leisewitz, 2006).

Identification of tick-infested areas and their avoidance should be promoted. This can help to
reduce the exposure of dogs to the ticks; however, other wild mammals will still face exposure and
could potentially move infected ticks over widespread distances.

A variety of tickicidal and tick repellent products are commercially available for veterinary use.

Dog owners can also send any found ticks to Public Health England’s Tick Surveillance Scheme for
identification (Phipps et al, 2016).

Significant research will be required to ascertain the underlying cause surrounding this outbreak
and whether it is related to the removal in 2012 of the requirement of tick treatment prior to entry
into the UK of pets travelling from Europe.

Please note the drug mentioned in this article is used under the cascade.

References

Holm LP et al (2006). Fatal babesiosis in an untravelled British dog, Veterinary Record

159(6): 179-180.
Irwin PJ (2010). Canine babesiosis, Veterinary Clinics of North America: Small Animal
Practice 40(6): 1,141-1,156.
Lobetti R (2010). Tropical diseases. In Ettinger SJ and Feldman EC (eds), Textbook of
Veterinary Internal Medicine (7th edn), Missouri: Saunders Elsevier, 1,002-1,005.
Phipps LP et al (2016). Tickborne diseases: Babesia canis detected in dogs and associated
ticks from Essex, Veterinary Record 178(10): 243-244.
Schoeman J and Leisewitz A (2006). Disease risks for the travelling pet: babesiosis, In
Practice 28: 384-390.
Shaw SE et al (2003). Review of exotic infectious diseases in small animals entering the

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 United Kingdom from abroad diagnosed by PCR, Veterinary Record 152(6): 176-177.

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