Haemoglobinuria and hypophosphataemia in postparturient dairy cows without dietary deficiency of phosphorus

Abstract

SUMMARY Postparturient haemogloblnuria occurred in 11 Holstein‐Friesian cows in 8 dairy herds in East Gippsland, Victoria. The affected cows had a wide range of ages, body condition and production level. Seven of 9 cows sampled were hypophosphataemic, 4 of 8 cows examined had Heinz bodies present in erythrocytes and strong ketonuria was present in 6 of 10 urine samples tested. Herdmates having similar calving dates had mostly normal serum phosphorus levels and none had Heinz bodies. There was no evidence for dietary phosphorus (P) deficiency, hypocuprosis or excessive P drain from high production being predisposing factors. There were no cruciferous plants in the diet. Haemolysis persisted in 4 cows despite treatment to raise serum P levels. An hyposthesis is proposed for the sporadic nature and clinical manifestations of the disease. This is based on mechanisms of hypophosphataemia occurring in man and mechanisms of Heinz body formation and haemolysis in other circumstances. We suggest that hypophosphataemia occurs following recovery from preparturient keto‐acidosis caused by undernutrition in late pregnancy and then becoming nutritionally replete in the early postparturient period. Circulating oxidants may cause erythrocyte damage which may be predisposed to by hypophosphataemia.

Evaluation of the correlation between serum biochemical values and liver ultrasonographic indices in periparturient cows with different body condition scores

“…Inorganic phosphorus is a component of phospholipids, phosphoproteins, nucleic acids, and ATP. 48 Provision of phosphorus and vitamin B 12 can improve energy metabolism of periparturient dairy cows, which signifies the role of inorganic phosphorus during this period. 46 In addition, postparturient hypophosphatemia has been associated with an increasing fatty infiltration of the liver.…”

Red Blood Cell Phosphate Concentration and Osmotic Resistance During Dietary Phosphate Depletion in Dairy Cows

“…The proposed mechanism is a marked drop in red blood cell (RBC) adenosine triphosphate (ATP) and 2,3‐diphosphoglycerate (2,3‐DPG) synthesis in bovine RBCs in states of P depletion presumably because of insufficient availability of intracellular phosphate (Pi) . Red blood cells require ATP among other things to control the cell volume and deformability through active extrusion of sodium . A decrease in the ATP concentration in P‐depleted human RBCs to 15% of normal values resulted in decreased osmotic resistance of RBCs, spherocytosis, and intravascular hemolysis .…”

“…Studies investigating osmotic resistance of RBCs in cattle with clinical PPH yielded conflicting results . Furthermore, hypophosphatemia has been reported in many but not all cases of PPH and response to treatment with phosphate salts is variable in affected animals . A number of alternative etiologies of PPH have been proposed, including the ingestion of beet pulp products or cruciferous plants containing saponins, copper‐molybdenum imbalances as reported in cases of PPH in New Zealand or oxidative stress causing increased RBC membrane permeability and hemolysis …”

Post parturient hemoglobinuria in a sheep flock

“…Simultaneous serum copper, selenium and molybdenum deficiency with hypophosphatemia have been observed in buffalos with PPH (Akhtar et al, 2007b;Mahmood et al, 2013). Circulating oxidants have also caused erythrocyte damage in hypophosphatemic dairy cows (Jubb et al, 1990). Almost all cows develop hemoglobinuria two to four weeks after calving (Radostits et al 2007), whereas buffalos develop hemoglobinuria before or after parturition (Pirzada and Hussain, 1998;Reddy et al, 2014).…”