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The South African form of severe and complicated canine babesiosis: Clinical advances 1994–2004 Linda S. Jacobson

Abstract Babesia (canis) rossi infection is common in dogs in South Africa, and frequently causes severe, life-threatening disease. Acidemia, persistent hyperlactatemia, hemoconcentration, elevated creatinine, cerebral babesiosis, pulmonary edema and pancreatitis are all associatedwith mortality rates above 30%, compared with overall mortality of 12% in admitted cases. Although half the admitted cases are severely anemic, hemoconcentration is associated with far higher mortality. Cerebral babesiosis is uncommon, but carries a poor prognosis. The pathological mechanism has been suggested to be endothelial cell damage and necrosis, followed by segmental microvascularnecrosis with perivascular edema and hemorrhage. Renal involvement in babesiosis resembles the functional renal failure of sepsis. Hypotension is common, and other cardiovascular disturbances have been documented. Cerebellar ataxia, rhabdomyolysis and pancreatitis are recently identified complications. While the previous categorization into “severe” (life-threatening anemia) and “complicated”(complications not directly attributable to anemia) disease has proved useful, the distinction is artificial and probably unnecessary. An updated approach to classification is suggested, aimed at grouping animals by severity and prognosis, and using simple measures, such as clinical collapse and abnormal breathing, as much as possible. Although inflammatory mechanisms are undoubtedly important in thepathophysiology of babesiosis, there can be little doubt that tissue hypoxia plays a major role in the disease process.

Article Outline 1. Introduction 1.1. Background 1.2. Parasites 2. Epidemiology 2.1. Signalment and incidence 2.2. Outcome 3. Red cells, parasites, and paradoxes 3.1. Anemia 3.2. Parasitemia 3.3. Hemoconcentration 4. Metabolic derangements 4.1. Hyperlactatemia and hypoglycemia 4.2.Acid-base disturbances 4.3. Altered hemostasis 5. Organ involvement

5.1. Systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome 5.2. Central nervous system 5.3. Renal involvement 5.4. Cardiovascular system 5.5. Acute pancreatitis 5.6. Icterus and hepatopathy 6. Effects of babesiosis on laboratory testing 7. Inflammatory mechanisms 8. Conclusions 8.1. Clinicalclassification 8.2. Pathophysiology Acknowledgements References

1. Introduction 1.1. Background South Africa is home to a particularly severe form of canine babesiosis that clinically resembles Plasmodium falciparum malaria (Malherbe and Parkin, 1951, Maegraith et al., 1957 and Clark and Jacobson, 1998). A clinical classification system was proposed in 1994 (Jacobson and Clark, 1994), based looselyon the WHO classification for malaria (Warrell et al., 1990). Babesiosis was classified as uncomplicated if the clinical changes could be attributed directly to hemolytic anemia. Uncomplicated babesiosis was sub-classified as mild if anemia was mild to moderate, and severe if anemia was life-threatening. Complicated cases were those with problems that were not directly attributable to acutehemolysis. Complications recognized at that time were acute renal failure, cerebral babesiosis, coagulopathy, icterus and hepatopathy, immune-mediated hemolytic anemia, peracute babesiosis, pulmonary edema, “red biliary” (hemoconcentration), and shock. The 1994 review (Jacobson and Clark, 1994) argued for a “unifying mechanism” for what had hitherto been a confusing welter of apparently unrelatedcomplications. It was hypothesized that, as with malaria, much of the disease process in babesiosis could be explained by the host inflammatory response to the parasite, rather than the parasite itself. This would explain similarities between disparate conditions in host species with similar inflammatory responses, as well as similarities, within species, between conditions such as babesiosis,...