Envenomation of domestic animals by snakes occurs frequently in certain geographic areas.However, reports describing clinical signs, clinicopathologic abnormalities, therapeutic approaches, and outcomes are sparse. This review summarizes various snake families, venom types associated with harmful snakes, and the significant hematologic, hemostatic, and biochemical abnormalities associated with envenomation. Hematologic abnormalities include RBC membrane abnormalities, hemolysis, hemoconcentration, leukogram changes, and platelet abnormalities, specifically thrombocytopenia.Coagulopathies associated with snake envenomation are well described in human medicine, and many studies have demonstrated properties of venoms that lead to both procoagulation and anticoagulation.As expected, similar abnormalities have been described in domestic animals. Biochemical abnormalities are associated with the effects of venom on tissues such as liver, skeletal and cardiac 2 muscle, vascular endothelium, and kidney as well as effects on protein components and cholesterol.This comprehensive review of clinicopathologic abnormalities associated with envenomation and their relationship to characterized venom constituents should be useful both in the diagnosis and management of envenomation and serve as a foundation for future research in this field.

Objective -To investigate hemostatic changes in dogs envenomed by cytotoxic (African puffadder) and neurotoxic snakes (snouted cobra) using thromboelastography (TEG) and plasma-based coagulation assays. Design -Prospective observational clinical study. Setting -University teaching hospital. Animals -Eighteen client-owned dogs; 9 envenomed by African puffadder (Bitis arietans) and 9 by snouted cobra (Naja annulifera). Ten healthy dogs served as controls. Interventions -None. Measurements and Main Results -Blood was collected at presentation and 24 hours post envenomation. Platelet count, TEG, prothrombin time, activated partial thromboplastin time (aPTT), antithrombin activity, and fibrinogen (Fib) and C-reactive protein (CRP) concentrations were measured. Outcomes were analyzed using linear mixed models at 5% significance. At presentation, R time was significantly prolonged in the puffadder group compared to the cobra (P = 0.01) and control groups (P = 0.05). Platelet count was significantly lower in the puffadder compared to the cobra (P = 0.04) and control groups (P = 0.001), respectively. Antithrombin activity was significantly decreased in the puffadder (P = 0.002) and cobra groups (P = 0.004) compared to the control group. Both prothrombin time and activated partial thromboplastin time were significantly prolonged in the cobra group compared to the control group (P = 0.03 for both). The TEG variables, maximum amplitude (MA) and G, were significantly increased 24 hours post envenomation in the puffadder group compared to their values at presentation (P = 0.05 for both). Fib and CRP concentrations were significantly increased 24 hours post envenomation in both snake-envenomed groups. Conclusions -Prolonged clot initiation was a common feature in puffadder-envenomed dogs at presentation and this was likely venom induced. Snouted cobra-envenomed dogs were normo-to hypercoagulable at presentation. Dogs from both puffadder and cobra groups progressed to a more hypercoagulable by 24 hours post envenomation, most likely due to marked inflammation as indicated by the increased Fib and CRP concentrations. TEG proved a sensitive tool for detecting abnormal hemostasis in snake-envenomed dogs.

Renal dysfunction in dogs envenomed by snakes has mostly been evaluated using routine serum and urine renal markers. Generally, these are not able to detect the renal damage at an early stage and their sensitivity is affected by hemolysis, hematuria and pigmenturia. Selective use of urinary biomarkers can provide early information on severity and stage of renal injury caused by nephrotoxic substances before major decline in renal function occurs. Therefore, the aim of this study was to evaluate venom-induced renal damage using urinary markers of glomerular (urinary albumin (uAlb), immunoglubin G (IgG) and Creactive protein (uCRP)) and proximal tubular dysfunction (urinary retinol binding protein (uRBP)) and compare these markers with routine renal markers (serum urea (BUN) and creatinine (sCr), urinary specific gravity (USG) and urinary protein to creatinine ratio (UPC)).Nineteen dogs envenomed by either neurotoxic or cytotoxic snakes and ten clinically healthy dogs were included in this study. Urinary markers were measured using previously validated commercially available ELISA kits. Among measured routine renal markers a significant difference between snake -envenomed and healthy dogs was noted only in UPC, but in the presence of hematuria and hemoglobinuria, differentiation between prerenal and renal proteinuria was not possible. The urinary biomarkers uAlb, uIgG and uRBP in snakeenvenomed dogs were significantly increased (P<0.05) when compared to healthy dogs at admission, whereas 24 h after envenomation only uCRP was significantly elevated. Using urinary /markers, results of this study showed that snake venom evokes renal dysfunction at the glomerular and tubular region of the nephron.

Theileriosis is a tick-borne disease caused by a piroplasma of the genus Theileria that can causeanaemia and thrombocytopenia. Its clinical importance for dogs’ remains poorly understood,as only some develop clinical signs. In this study, physical and laboratory findings, treatment and outcomes of six client-owned diseased dogs presented at the Onderstepoort Veterinary Academic Hospital are described retrospectively. In the dogs, Theileria species (n = 4)and Theileria equi (n = 2) were detected by a polymerase chain reaction (PCR)-reverse blothybridisation assay in blood samples, whilst PCR for Babesia, Anaplasma and Ehrlichia were negative. The most common physical findings were pale mucous membranes (five out of six dogs), bleeding tendencies (five out of six dogs) and lethargy (three out of six dogs). All dogs were thrombocytopenic [median 59.5 x 109/L (range 13–199)] and five out of six dogs were anaemic [median haematocrit 18% (range 5–32)]. Bone marrow core biopsies performed in two dogs showed myelofibrosis. Theileriosis was treated with imidocarb dipropionate and the suspected secondary immune-mediated haematological disorders with prednisolone and azathioprine. Five dogs achieved clinical cure and post-treatment PCR performed in three out of five dogs confirmed absence of circulating parasitaemia. An immune-mediated response to Theileria species is thought to result in anaemia and/or thrombocytopenia in diseased dogs with theileriosis. A bleeding tendency, most likely secondary to thrombocytopenia and/or thrombocytopathy, was the most significant clinical finding in these cases. The link between thrombocytopenia, anaemia and myelofibrosis in theileriosis requires further investigation and theileriosis should be considered a differential diagnosis for dogs presenting with anaemia and/or thrombocytopenia in endemic tick-borne disease areas.