By prof Mohamed Ghanem: Red urine as a common metabolic disorder in lactating cattle in spring season. A fatal diseases if not treated properly

1. (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.

4. 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