Canine babesiosis in South Africa is caused by the tick-borne intraerythrocytic protozoan parasites, Babesia rossi and Babesia vogeli.1 The disease typically causes a haemolytic anaemia with a course ranging from mild to peracutely fatal. The different subspecies differ in their pathogenicity with B. rossi often responsible for a fatal infection despite intensive treatment, whereas B. vogeli usually causes a mild clinically insignificant infection.1,2 In South Africa, the virulent form of canine babesiosis is usually caused by B. rossi and can be associated with various complications.3 These complications include acute renal failure (ARF), cerebral babesiosis, coagulopathies like disseminated intravascular coagulation (DIC), icterus, hepatopathy, immune-mediated haemolytic anaemia (IMHA), acute respiratory distress syndrome (ARDS), haemoconcentration, shock, pancreatitis and hypoglycaemia.3 The complications are thought to result from a more global systemic inflammatory response syndrome (SIRS) present in most cases of canine babesiosis.4 The SIRS is mediated by cytokines, nitric oxide and free oxygen radicals and could eventually progress to a multiple organ dysfunction syndrome (MODS).2 Using the criteria for SIRS, 87% of complicated canine babesiosis cases in South Africa were categorised as suffering from SIRS.4 Of the cases identified with organ damage/dysfunction, 52% had single organ involvement and the remaining 48% had MODS.4
Because of the varied and sometimes unpredictable course of the disease, it would be very useful if clinicians could have a way of measuring disease severity and possible disease outcomes. This will enable them to optimise therapy preemptively and also to give the owners an indication of possible prognosis and financial implications and likelihood of response to therapy.
Various studies have investigated parameters of disease severity and outcome, some of which were found useful as predictors of mortality or were associated with fatal outcome in canine babesiosis.1,2
Tumour necrosis factor (TNF) concentration was associated with clinical severity as well as the degree of parasitaemia1 In three dogs with hypoglycaemia TNF was dramatically elevated.3 There was no significant association between TNF and outcome in these cases.
Although nitric oxide is proposed to be a mediator of MODS, which could be present in cases with complicated canine babesiosis, reactive nitrogen intermediates (RNI) did not correlate with the severity of disease or outcome.1 RNI measurements were, however, higher in cases with babesiosis when compared to healthy laboratory dogs.3
Higher capillary and venous parasitaemia together with a collapsed state were associated with mortality.1,2 There was a significant positive correlation between high parasitaemia and mortality. Capillary parasitaemias were significantly higher than venous parasitaemias, and it is therefore recommended to obtain peripheral samples for diagnostic purposes.
Hypoglycaemia defined as a blood glucose level below 3.3 mmol/l was seen in 20% of cases.2 Patients that present in a state of collapse, paediatric patients and patients with severe anaemia or icterus were more likely to have hypoglycaemia.2 Cases with hypoglycaemia show signs of neurological disease, including decreased consciousness, weakness, ataxia and even seizures. Hypoglycaemia could be fatal, but can be treated quite easily. These cases can show a dramatic response to intravenous glucose supplementation. Continued monitoring of blood glucose levels are very important and should be done until stable clinical improvement is noted.
Blood lactate is elevated in approximately 50% of hospitalised cases.2 In these patients, lactate levels can easily exceed 10 mmol/l, but with intensive therapy, this level decreases by at least 50% or even to normal within the first few hours after admission. Lactate that fails to decrease below 4.4 mmol/l by 24 hours was associated with death in all cases.2
Cardiac troponin I could be associated with a poor outcome, as a study in dogs indicated that cardiac troponin I was higher in the three non-survivors in the study.2 There was an association between cardiac troponin I and cardiac histological changes, clinical disease severity and survival.3
Mortality was shown to be associated with endocrine parameters. Significantly higher median cortisol and adrenocortical trophic hormone (ACTH) concentrations were recorded in non-survivors.2 All dogs with cortisol concentrations below 260 nmol/l survived, whereas 55% of dogs with serum cortisol above 400 nmol/l died. In almost all the dogs that did not survive, lower thyroxin (T4) and free thyroxin (fT4) concentrations were recorded when compared to the survivors.1,2
Outcome is not affected by the severity of the anaemia or the presence of SIRS, MODS, and IMHA.1,2 Although severe anaemia was not associated with death, in the absence of anaemia, the risk of death was increased.3 "Red biliary" is a paradoxical phenomenon seen in some patients where there is haemoconcentration with elevated haematocrits rather than anaemia despite the presence of intravascular haemolysis. "Red biliary" is associated with higher mortality. It is thought that there is a shift of protein rich fluid from within the vasculature into the extravascular space.3
Collapse is associated with poor outcome and hypotension correlates with disease severity, yet, blood pressure has not been shown to be a predictor of mortality.1 Hypotension was seen mainly in complicated cases. The presence of hypotension will have implications for therapy and ongoing monitoring of the patient. It may prove to be useful as a serially measured parameter in conjunction with other measurements of severity and prognosis.3
C-reactive protein (CRP) is a useful predictor of disease severity and outcome in various other diseases; however, there was no significant difference in mean CRP concentration between survivors and non-survivors with babesiosis at admission.1 There was also no significance in the relationship between the magnitude of change in CRP concentration 24 hours after admission, and the number of days of hospitalisation in survivors.
Acidaemia also increases the risk of death and 60% of dogs with pH < 7.32 died compared to only 22% of cases that showed alkalaemia (pH > 7.44).3
Changes in alkaline phosphatase (ALP) and alanine aminotransferase (ALT) are often present and ALT levels are significantly higher in non-survivors when compared to survivors.3
The presence of damage or insufficiency in certain organs is associated with increased chances of death in many cases. Patients diagnosed with pulmonary edema had the highest fatality rate followed by cases with central nervous system involvement and cases with renal shut down.4 Fifty-six percent of fatal cases were diagnosed with pulmonary edema.3
True renal failure is rare in canine babesiosis, but "renal involvement" defined by elevated admission creatinine (> 150 μmol/l) is seen in 34% of dogs with complicated babesiosis.3 The risk of death was increased 5 times in cases that had elevated creatinine.4 In these cases, creatinine remains elevated despite adequate fluid therapy. The presence of oliguria is said to be an ominous sign.3
Involvement of the central nervous system (CNS) increased the risk of death 57 times.4 Mortality rates for cases identified with cerebral babesiosis reach > 80%.3 It is important to first rule out hypoglycaemia as the cause of the CNS signs due to the fact that the 2 complications can present with similar clinical pictures.
The presence of pancreatitis is often associated with other complications and has a significant mortality rate of 32%.3
Clinicians treating patients for canine babesiosis can consider all of these parameters when deciding on therapies and when owners require prognostic information. At the Onderstepoort Veterinary Academic Hospital, blood glucose is monitored in every case admitted with canine babesiosis. Lactate is measured serially to monitor response to therapy and to help determine prognosis. Many clinicians also make use of acid-base monitoring. Monitoring and therapy is individualised for each patient in order to optimise the chances of survival.
1. Koster L, van Schoor M, Goddard A, Thompson P, Matjila P, Kjelgaard-Hansen M. C-reactive protein in canine babesiosis caused by Babesia rossi and its association with outcome. J South Afr Vet Assoc. 2009;80(2):1–5.
2. Schoeman J. Canine babesiosis. Onderstepoort J Vet Res. 2009;76:59–66.
3. Jacobson L. The South African form of severe and complicated canine babesiosis: clinical advances 1994–2004.Vet Parasitol. 2006;138:126–39.
4. Welzl C, Leisewitz A, Jacobson L, Vaughn-Scott T, Myburgh E. Systemic inflammatory response syndrome and multiple organ damage/dysfunction in complicated canine babesiosis. J South Afr Vet Assoc. 2001;72:158–162.