(II) METABOLIC HYPOPHOSPHATAEMIA (Post-parturient hemoglobinuria in cows) (Hemoglobinuria of pregnant buffaloes)

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Prof Mohamed Ghanem Professor of Veterinary Internal Medicine Head of Department of Animal Medicine Faculty of Veterinary Medicine Benha University

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(II) METABOLIC HYPOPHOSPHATAEMIA (Post-parturient hemoglobinuria in cows) (Hemoglobinuria of pregnant buffaloes)

Definition:

It is a metabolic haemolytic disease of lactating cattle, and pregnant buffaloes, characterized clinically by hypophosphataemia and intravascular haemolysis of erythrocytes.

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Incidence, occurrence and predisposing factors:

1- The disease affect mostly cattle and

buffaloes. 2- The disease occur 3-4 weeks after

parturition in cows. While occur in "mid-ten." gestation period in buffaloe.

3-The disease mostly affect aged and senile cattle and buffaloes and age incidence usually between 5-10 years old.

Heavy milk production predispose to the-disease.

Seasonal occurrrence

6- Feeding plants or rations which are normally low in phosphorous and high in calcium content, like feeding Green Barseem (Alfa alfa or clover) exclusively for long period may extend up to 4-6 months predispose to the occurrence of the disease particularly in Egypt (Beest, Turnips, Kale in Europe).

7- The disease have a seasonal occurrence in Egypt usually associated with late spring (April-May).

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Etiology

1- The exact cause of the disease is "unknown"

2- The basic biochemical findings in the disease is low inorganic phosphorous level in blood of affected animals (hypophosphataemia).

3- Hypophosphataemia may develop due to "inadequate" intake of phosphorous in ration which may be exacerbated by ingestion of high calcium in ration.

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Pathogenesis (1)

The cause of intravascular haemolysis of erythrocytes is "unexplained", but may be attributed to:

a) Increased fragility of red cells due to inadequacy of phosphorous for formation of phospholipids member of erythrocytes.

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Pathogenesis (2)

b) Haemolytic factors of "saponins"" present in Alfa Alfa leaves (e.g of haemolytic factors are thiocynate, nitrate and sulfoxides toxins).

These toxins causes irreversible oxidative changes in haemoglobin, leading to formation of what is called Heinz-bodies.

Red cells which containing these H.R. are removed by spleen for haemolysis.

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Clinical signs

I- The animal voiding "dark red-brown" to almost "black" urine.

2-The animal eat and milk normally for 24 hours after the appearance of hemoglobinuria.

3- Pale m.m., or even ecteric m.m. in severe cases (due to haemolytic jaundice).

4- Tachycardia and increased pulse, and respiration rates above normal ranges.

5- Normal rectal temperature.

6- Recumbency after an acute course of 3-5 days.

7- The disease slowly recovered as convalescence is prolonged for up 3-4 weeks (chronic cases) and pica is often observed during this stage.

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Yellow staining of the conjunctiva and valva MM in severe cases of hypophosphatemia.

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Diagnosis (1) History

(II) Clinical signs

(III) Laboratory diagnosis:

(A) Urinanalysis:

I- Benzidine test for detection of blood in urine (+ve)blue.

2- Centrifugation of urine sample --- > persistant red column ---Haememoglobinurea

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(B) Blood analysis

1- Estimation of blood haemoglobin ----> drop to 5 mg% (N=4-7 mg%)

2-Estimation of blocd haemoglohin --->drop to 5 gm% (Normal 10-12 gmo)

3- Determination of total erythrocyte count --->drop to 2 millions (Normal 5-8 millions)

4- Determination of PCV (Haematocrit value ------ > drop to 2.5 voIume %(N= about 35)

Estimation of serm bilirubin and blood urea……> raised.

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Differential diagnosis

The disease must be differentiated from other causes of haemoglobinurea e.g Bebesiosis

leptospirosis,

clocstridium haemolyticm ,

copper poisoning,

onion poisoning

water intoxication.

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Treatment

1- Change the diet which is rich in calcium by another diet rich in phosphorous e.g bran instead of barseem.

2- Elevation of serurm inorganic phosphorous level by: a) I/V injection of 60 gram Na acid phosphate in 300

dist. water. Followed by: b) S/C of similar dose ; times with 12 hours intervals.

Followed by; c ) Oral similar dose till disappearance of

haemoglobinurea.

3- Bone meal 120 gram twice daily till disappear-ance of haemoglobinurea (but expensive treat-ment)

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4- I/V calcium hypophosphate in glucose solution (prepared by dissolving 30 gram in 10% glucose).

5- The use of commercial useful preparation e.g: Tonophosphan (Hochest) 20 ml I/V or I/M till disappearance of haemoglobinurea.

- Phospho-20 (Verbac) 15 m1 of haemoglobinurea

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Prevention of the disease

Aged or senile lactating cows, or pregnant buffaloes must given as a prephylaxis half the therapeutic dose of sodium acid phosphate (30 pm) or bone meal (60 gm).

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Questions