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Zinc Phosphide Poisoning in Poultry
108
THE VETERINARY JOURNAL
Miller, Murdock and Heishmann (1939): I .A.V.M.A., 95, p. 749. Palmer (1942): North Amer. Vet., 23, 12, p. 776. Posgay (1936): Kozi. Oesszehas. elet. es Kortan Kore/),ol., 26, p. 545. Ramsay (1938) : Canad. I .. Comp o Med., 2, p. 129. Roberts (1944): Comell Vet., 34, 2, p. 131. Sanders (1942) : N orlh A mer. Vet., 23, 3, p. 195. - - (1943): Ibid, 24, p. 40. Schalm (1940): !.A.v.M.A., 97, p. 20. - - (1941): A·mer. I. Vet. Res., 2, p. 117. - - (1942) : 1.A.v.M.A .., 100, p. 323. Schmidt (1937): Bert. tierarzt. Wschnt., October 22, p. 665. Schmidt and Hoernsdorf (1937) : Berl. tierarztl. W schnt., 19, p. 713. Schnorf (1925): Schweiz. Arch. f. Tier., 47, p. 25. Schoepe (1940): Berl. Munich Tierarztl. W scht!t., April 5, p. 160. Seelemann : Die Sireptol.orfen l:nfektionen des Euters. Schaft Hanover, 1932. Seelemann and Siemonsen (1933): Arch. wiss. V. prakt. Tie"hlk ., 67, p. 10. - - (1938a): Ibid, 74, p. 41. .....0..-- (l938b) : Bert. tierarzl. W SCMlt., October 22, p. 243. - - (1939): Tierarzll. Rdsch., 45, p. 105. Seelemann and Wutzler (1939): A rch. wiss. prakt. Tierheilk., 75, p. 124. Stable forth (1938): Agr. Prog.. , IS, pp. 8·15. - - (1939): Vet. Rec., 51, 15; pp. 469·475. Stable forth and Hignett (1942): Vet. Rec., 54, 51, p. 525. Sta ble forth and Scorgie (1938): Vet . Rec., 23, 50, p . 66J. Stableforth, Hignett, Watts, Paterson, Cunningham, Edwards, Malcom and Roach (1942) :' Vet. Rec., 54, 52, p. 539. Steck (1931) : S chweiz. Arch .. f. Tier, 73, p. 109. - - (1934): T welfth International Veterinary Congress, New York, 1934. Vol. 11, p.. 494. - - (1936): Schweiz. Arch. Tierhlk., 78, p. 555. - - (1937): Schw eiz. Arch. Tierhlk., 79, p. 1. - - (1938): Berl. tierarzt. Wschnt ., October 22, p. 360. Steven son (1939): Canad. 1. Compo Med., 3, p. 147. Stewart (1940): Aust. Ve l. I., 16, p. 108. Teinstone, Bliss, Ott and Long (1938): Th e lohn Hopkins Hospital, 62, p. 565. Tripp and Lawrence (1942): Cornell Vet., 32, I, p. 90. Udall, Johnson and Ferguson (1943) : Ibid, 33, 2, p. 209. Veenbass and Sjollema (1939): Tijdschr. Diergeneesk, 66, p. 70. Weirether, Anderson, Johnson, Plastridge and Jungherr (1941): Amer. I. Vel . Res., 2, p. 141.. Wolf and Leskien (1936-7) : Disch. tierarztl. W schnt., 44, p. 870, and 45, p. 292.
ZINC PHOSPHIDE POISONJING IN POULTRY By
J.
D. BLAXLAND and R. F. GORDON, Weybridge .
IT is a comparatively frequ ent occurrence to receive in the routine post-· mortem department carcases of fowls in which the macroscopic lesions areconsistent wIth acute chemical poisoning. In the past, most of these cases have been associated with the use of phosphorus or arsenical preparations fo r the· destruction of vermin. Usually the post-mortem findings ha ve been characteristic' and it has been possible to dempnstrate the presence of these substances in the ingesta. Recently, however, since the introduction of zinc phosphide as a vermin poison, carcases have been received in which the post-mortem lesions, although, again suggestive of acute poisoning, were not consistent with those previously' found in cases of arsenical or phosphorus poisoning, whil st qualitative chemical tests for these substances were negative. On several oceasions there was a history of zinc phosphide, either as a paste or as "sausage," having been useo. on the premises. In order to ascertain the degree of toxicity of zinc phosphide for poultry and to observe the symptoms and post-mortem lesions, if any, a number of birds were dosed experimentally.
ZINC PHOSPHIDE POISONING
109
Procedure
Ten birds in all were dosed orally with varying amounts of zinc phosphide. The compound in its normal state, as a dark grey fine powder, was washed straight into the birds' crop with small quantities of tap water using a glass funnel and a short length of rubber tubing. The dosage and results are shown in Table 1. Bird R.I.R. 9 W .L. 9 W.L. Q W .L. Q
5 4 4 5
We ight lb. 8 oz. lb. 8 oz. lb. 4 oz. lb. 3 oz.
R.I.R. 9 W.L. Q R.I.R. 9 R .I.R. Q R.I.R. Q RI.R·9
4 5 4 5 5 4
lb. lb. lb. lb. Lb. lb.
12 oz. 4 8 2 5
oz. oz. oz. oz.
TABLE I Dose
Remit
1 g. 0.5 g. 0.25 g. 0.125 g.
(15 gra ins approx.) ) ( 8 ) ( 4 ) ( 2
0.125 g. 0.06 g. 0.06 g. 0.06 g.
( 2 ( 1 ( 1 (1
0.03 g . ( ! 0.03 i!:. ( !
) )
~) )
Dosed 4.0 p.m ., died overnight. Died 3 hours after dosing. Dosed 4.0 p.m., died overnight. Alive 16 hours after dosing, ·b ut died in 18 hours. Dosed 3.0 p.m., died overnight. No effect. Dosed 4.0 p.m., died overnigh t. Dosed 4.0 p.m ., died overnight. No effect. No effect.
Symptoms
Death occurred within a variable period of 3-18 hours after dosage . In some cases the crops were full, and this probably played a part in delaying the onset of symptoms and of death, e.g., one of the two birds receiving a dose of 0 .125 g. Symptoms, however, were not particularly characteristic, although one bird-that receiving a dose of 0.5 g.-showed a greatly increased respiratory rate accompanied by gasping through its open beak. In all cases death was preceded by partial coma. Post-mortem Findings
In the alimentary tract, the gas phosphine is liberated from zinc phosphide :and it was the unpleasant pungent odour of this gas from the crop and gizzard contents wh ich was the most characteristic finding. In birds which had received t he larger doses, the odour seemed to pervade the whole carcase. It was discernible in all but two cases, i.e., the bird receiving 0 .125 g. in which death was delayed for 18 hours and one of those receiving 0.06 g. The macroscopic lesions were those of a general cardiac collapse, the flesh a nd visceral organs having a dirty, greasy and rather fevered appearance. The hearts were either flaccid or slightly dilated, with engorgement of the co ronary blood vessels. T he liver and kidneys were dark in colou r and markedly congested. In two cases, one having had 0.125 g. and the other 0.06 g., there was a n extensi·ve sero-fibrinous exudate from the liver capsule. The lungs were somewhat <:edematous with serous fluid in the pleural cavity. Congestion of these organs was not so marked, but in one bird there were patches of hremorrhage on the lung surface. In most cases there were a few petechial hremorrhages on the surface of the myocardium, and the blood vessels of the mesentery and ovary were engo rged. Cases Encountered in R outine Post-mortem Diagnosis
During the past year thirteen cases have been received from different parts of the country. The general macroscopic appearance and findings were as described in birds experimentally dosed. Again the most characteristic finding was the strong odour of phosphine from the crop and gizzard contents. In a few cases, probably owing to a smaller quantity of poisoned bait having been ingested or to delay in despatch of the carcase to the laboratory, the odour
110
THE VETERINARY JOURNAL
was not discernible or not sufficiently pronounced to enable a diagnosis to be made. The sero-ftbrinous exudate does not appear to be a feature of naturally poisoned birds, but congestion of the lungs was rather more marked than in those experimentally dosed. Differential Diagnosis
The four commonest causes of acute poisomng in poultry encountered in the routine department are phosphorus, arsenic, zinc phosphide and cacao bean residues. Differential diagnosis in typical cases is not difficult. features are tabulated in Table II.
The chief characteristic
T,A BLE II Post-mortem lesions.
Odour.
Phosphorus Carcase and visceral o~gans rather Jaundiced with advanced fatty d e g eneration of the li ve r.
C h a r a cteri stic odour of wet matches. Visible fum e s when the gizzard is opened.
Arsenic Carcase and visceral organs congested and rather wet in appearance. Inten se inflammation of th e subepithelial layer of the gizzard with separation of the horny epithelium from the underlying tissues by a s e r 0 - gelatinous exudate. (Gordon and T o w n so n, 1938.) Nothing.
Zinc Phosphide Carcase and visceral organs congested and rather greasy In appearance.
Cacao Residu~s Visceral organs con g est e d. CE sop hagu·s. crop and gizzard fuJI o f dark chocolate mcoloured gesta.
Pungent odou r of phosphine. No v i s i b le f umes.
Odour of chocola te.
In the first three cases the autopsy findings are confirmed by qualitative chemical tests. A recently devised test for the presence of zinc phosphide is described in the accompanying paper. Summary ( 1) Thirteen suspected cases of zinc phosphide poisoning in poul-try were encountered in the routine diagnosis department during the last twelve months. (2) Symptoms and post-mortem changes in birds experimentally dosed with zinc phosphide are described. (3) 'T his substance was found to be an extremely toxic compound for poultry. (4) The minimum lethal dose was approximately 1 grain for a 5 lb. bird (l / 5th gr. per lb. body weight), or 20-30 milligrams per kilo body weight. (5) Differential diagnosis of phosphorus, arsenic, zinc phosphide and cacao residues poisoning is discussed briefly. REFERENCES Townson, W. K., and Gordon, R. F.: "Acute Arsenical Poisoning 1938, 50, No. 14, 403-404.
In
Fowls," Vet. Rec.,
THE VETERINARY JOURNAL
Miller, Murdock and Heishmann (1939): I .A.V.M.A., 95, p. 749. Palmer (1942): North Amer. Vet., 23, 12, p. 776. Posgay (1936): Kozi. Oesszehas. elet. es Kortan Kore/),ol., 26, p. 545. Ramsay (1938) : Canad. I .. Comp o Med., 2, p. 129. Roberts (1944): Comell Vet., 34, 2, p. 131. Sanders (1942) : N orlh A mer. Vet., 23, 3, p. 195. - - (1943): Ibid, 24, p. 40. Schalm (1940): !.A.v.M.A., 97, p. 20. - - (1941): A·mer. I. Vet. Res., 2, p. 117. - - (1942) : 1.A.v.M.A .., 100, p. 323. Schmidt (1937): Bert. tierarzt. Wschnt., October 22, p. 665. Schmidt and Hoernsdorf (1937) : Berl. tierarztl. W schnt., 19, p. 713. Schnorf (1925): Schweiz. Arch. f. Tier., 47, p. 25. Schoepe (1940): Berl. Munich Tierarztl. W scht!t., April 5, p. 160. Seelemann : Die Sireptol.orfen l:nfektionen des Euters. Schaft Hanover, 1932. Seelemann and Siemonsen (1933): Arch. wiss. V. prakt. Tie"hlk ., 67, p. 10. - - (1938a): Ibid, 74, p. 41. .....0..-- (l938b) : Bert. tierarzl. W SCMlt., October 22, p. 243. - - (1939): Tierarzll. Rdsch., 45, p. 105. Seelemann and Wutzler (1939): A rch. wiss. prakt. Tierheilk., 75, p. 124. Stable forth (1938): Agr. Prog.. , IS, pp. 8·15. - - (1939): Vet. Rec., 51, 15; pp. 469·475. Stable forth and Hignett (1942): Vet. Rec., 54, 51, p. 525. Sta ble forth and Scorgie (1938): Vet . Rec., 23, 50, p . 66J. Stableforth, Hignett, Watts, Paterson, Cunningham, Edwards, Malcom and Roach (1942) :' Vet. Rec., 54, 52, p. 539. Steck (1931) : S chweiz. Arch .. f. Tier, 73, p. 109. - - (1934): T welfth International Veterinary Congress, New York, 1934. Vol. 11, p.. 494. - - (1936): Schweiz. Arch. Tierhlk., 78, p. 555. - - (1937): Schw eiz. Arch. Tierhlk., 79, p. 1. - - (1938): Berl. tierarzt. Wschnt ., October 22, p. 360. Steven son (1939): Canad. 1. Compo Med., 3, p. 147. Stewart (1940): Aust. Ve l. I., 16, p. 108. Teinstone, Bliss, Ott and Long (1938): Th e lohn Hopkins Hospital, 62, p. 565. Tripp and Lawrence (1942): Cornell Vet., 32, I, p. 90. Udall, Johnson and Ferguson (1943) : Ibid, 33, 2, p. 209. Veenbass and Sjollema (1939): Tijdschr. Diergeneesk, 66, p. 70. Weirether, Anderson, Johnson, Plastridge and Jungherr (1941): Amer. I. Vel . Res., 2, p. 141.. Wolf and Leskien (1936-7) : Disch. tierarztl. W schnt., 44, p. 870, and 45, p. 292.
ZINC PHOSPHIDE POISONJING IN POULTRY By
J.
D. BLAXLAND and R. F. GORDON, Weybridge .
IT is a comparatively frequ ent occurrence to receive in the routine post-· mortem department carcases of fowls in which the macroscopic lesions areconsistent wIth acute chemical poisoning. In the past, most of these cases have been associated with the use of phosphorus or arsenical preparations fo r the· destruction of vermin. Usually the post-mortem findings ha ve been characteristic' and it has been possible to dempnstrate the presence of these substances in the ingesta. Recently, however, since the introduction of zinc phosphide as a vermin poison, carcases have been received in which the post-mortem lesions, although, again suggestive of acute poisoning, were not consistent with those previously' found in cases of arsenical or phosphorus poisoning, whil st qualitative chemical tests for these substances were negative. On several oceasions there was a history of zinc phosphide, either as a paste or as "sausage," having been useo. on the premises. In order to ascertain the degree of toxicity of zinc phosphide for poultry and to observe the symptoms and post-mortem lesions, if any, a number of birds were dosed experimentally.
ZINC PHOSPHIDE POISONING
109
Procedure
Ten birds in all were dosed orally with varying amounts of zinc phosphide. The compound in its normal state, as a dark grey fine powder, was washed straight into the birds' crop with small quantities of tap water using a glass funnel and a short length of rubber tubing. The dosage and results are shown in Table 1. Bird R.I.R. 9 W .L. 9 W.L. Q W .L. Q
5 4 4 5
We ight lb. 8 oz. lb. 8 oz. lb. 4 oz. lb. 3 oz.
R.I.R. 9 W.L. Q R.I.R. 9 R .I.R. Q R.I.R. Q RI.R·9
4 5 4 5 5 4
lb. lb. lb. lb. Lb. lb.
12 oz. 4 8 2 5
oz. oz. oz. oz.
TABLE I Dose
Remit
1 g. 0.5 g. 0.25 g. 0.125 g.
(15 gra ins approx.) ) ( 8 ) ( 4 ) ( 2
0.125 g. 0.06 g. 0.06 g. 0.06 g.
( 2 ( 1 ( 1 (1
0.03 g . ( ! 0.03 i!:. ( !
) )
~) )
Dosed 4.0 p.m ., died overnight. Died 3 hours after dosing. Dosed 4.0 p.m., died overnight. Alive 16 hours after dosing, ·b ut died in 18 hours. Dosed 3.0 p.m., died overnight. No effect. Dosed 4.0 p.m., died overnigh t. Dosed 4.0 p.m ., died overnight. No effect. No effect.
Symptoms
Death occurred within a variable period of 3-18 hours after dosage . In some cases the crops were full, and this probably played a part in delaying the onset of symptoms and of death, e.g., one of the two birds receiving a dose of 0 .125 g. Symptoms, however, were not particularly characteristic, although one bird-that receiving a dose of 0.5 g.-showed a greatly increased respiratory rate accompanied by gasping through its open beak. In all cases death was preceded by partial coma. Post-mortem Findings
In the alimentary tract, the gas phosphine is liberated from zinc phosphide :and it was the unpleasant pungent odour of this gas from the crop and gizzard contents wh ich was the most characteristic finding. In birds which had received t he larger doses, the odour seemed to pervade the whole carcase. It was discernible in all but two cases, i.e., the bird receiving 0 .125 g. in which death was delayed for 18 hours and one of those receiving 0.06 g. The macroscopic lesions were those of a general cardiac collapse, the flesh a nd visceral organs having a dirty, greasy and rather fevered appearance. The hearts were either flaccid or slightly dilated, with engorgement of the co ronary blood vessels. T he liver and kidneys were dark in colou r and markedly congested. In two cases, one having had 0.125 g. and the other 0.06 g., there was a n extensi·ve sero-fibrinous exudate from the liver capsule. The lungs were somewhat <:edematous with serous fluid in the pleural cavity. Congestion of these organs was not so marked, but in one bird there were patches of hremorrhage on the lung surface. In most cases there were a few petechial hremorrhages on the surface of the myocardium, and the blood vessels of the mesentery and ovary were engo rged. Cases Encountered in R outine Post-mortem Diagnosis
During the past year thirteen cases have been received from different parts of the country. The general macroscopic appearance and findings were as described in birds experimentally dosed. Again the most characteristic finding was the strong odour of phosphine from the crop and gizzard contents. In a few cases, probably owing to a smaller quantity of poisoned bait having been ingested or to delay in despatch of the carcase to the laboratory, the odour
110
THE VETERINARY JOURNAL
was not discernible or not sufficiently pronounced to enable a diagnosis to be made. The sero-ftbrinous exudate does not appear to be a feature of naturally poisoned birds, but congestion of the lungs was rather more marked than in those experimentally dosed. Differential Diagnosis
The four commonest causes of acute poisomng in poultry encountered in the routine department are phosphorus, arsenic, zinc phosphide and cacao bean residues. Differential diagnosis in typical cases is not difficult. features are tabulated in Table II.
The chief characteristic
T,A BLE II Post-mortem lesions.
Odour.
Phosphorus Carcase and visceral o~gans rather Jaundiced with advanced fatty d e g eneration of the li ve r.
C h a r a cteri stic odour of wet matches. Visible fum e s when the gizzard is opened.
Arsenic Carcase and visceral organs congested and rather wet in appearance. Inten se inflammation of th e subepithelial layer of the gizzard with separation of the horny epithelium from the underlying tissues by a s e r 0 - gelatinous exudate. (Gordon and T o w n so n, 1938.) Nothing.
Zinc Phosphide Carcase and visceral organs congested and rather greasy In appearance.
Cacao Residu~s Visceral organs con g est e d. CE sop hagu·s. crop and gizzard fuJI o f dark chocolate mcoloured gesta.
Pungent odou r of phosphine. No v i s i b le f umes.
Odour of chocola te.
In the first three cases the autopsy findings are confirmed by qualitative chemical tests. A recently devised test for the presence of zinc phosphide is described in the accompanying paper. Summary ( 1) Thirteen suspected cases of zinc phosphide poisoning in poul-try were encountered in the routine diagnosis department during the last twelve months. (2) Symptoms and post-mortem changes in birds experimentally dosed with zinc phosphide are described. (3) 'T his substance was found to be an extremely toxic compound for poultry. (4) The minimum lethal dose was approximately 1 grain for a 5 lb. bird (l / 5th gr. per lb. body weight), or 20-30 milligrams per kilo body weight. (5) Differential diagnosis of phosphorus, arsenic, zinc phosphide and cacao residues poisoning is discussed briefly. REFERENCES Townson, W. K., and Gordon, R. F.: "Acute Arsenical Poisoning 1938, 50, No. 14, 403-404.
In
Fowls," Vet. Rec.,