South African canine babesiosis is caused by the virulent Babesia canis rossi. In recent years, this common disease has been detected in 12% of dogs presented at the outpatients' division of the University of Pretoria's (Onderstepoort) Veterinary Academic Hospital, and 31% of the affected dogs have been hospitalized as seriously ill. Of these hospitalized cases, 50% had severe anaemia at presentation, 32% had moderate anaemia and 18% were non-anaemic (often polycythaemic), frequently with central-nervous-system signs or multiple organ failure. A retrospective survey of 662 hospitalized cases revealed that the haematology, clinical biochemistry and patient profile (signalment) of the severely anaemic dogs were distinct from those of the non-anaemic, indicating that the babesiosis in these two groups of dogs should be viewed as two different disease in terms of the postulated, underlying, 'pathomechanisms'. The severely anaemic dogs exhibited hypoxic hepatic disease and an increase in serum urea (without a concomitant increase in creatinine), seldom had profound electrolyte imbalances and tended to have a much more profound leucocytosis, consisting of a left-shifted inflammatory leucogram, with higher numbers of circulating metamyelocytes, lymphocytosis and monocytosis. In contrast, the non-anaemic dogs exhibited severe azotaemia (which could be of renal or pre-renal origin) and often showed a marked electrolyte disturbance (reflecting acid-base abnormalities) and a very mild leucocyte response; such dogs often presented as leucopenic, many being lymphocytopenic. These results indicate that the severely anaemic dogs had developed haemolytic disease (possibly immune-mediated), whereas the non-anaemic dogs had developed an acute and overwhelming inflammatory response. The mean age of the non-anaemic dogs (2.66 years) was less than the dogs in the 'severe anaemia group' (0.83 years). Dogs belonging to the traditional fighting breeds (bull terriers, pit bull terriers and Staffordshire bull terriers) were noticeably over-represented in the non-survivors of the acute inflammatory response, possibly indicating an underlying genetic basis for the different presentations. It is evident that the inflammatory-response disease presentation, which is similar to complicated falciparum malaria in humans, amy serve as an animal model for the disease.