Biomedical subjects
Publications and source records attributed to P T Hooper.
Rats were fed DL-3-(N-phenylethalamino)-alanine which resulted in kidney lesions histologically identical with those produced by the structurally related compound lysinoalanine. Possible mechanisms for nephrotoxicity are discussed.
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Observations on a runting and stunting syndrome in broiler chickens in Victoria, Australia, based on general observations from 1980 to 1983 on 2244 chickens from 109 affected broiler chicken flocks, are summarised. The details on 156 of these birds from five affected flocks with varying runting percentages are presented. Typically affected birds were presented with atrophy of the pancreas, the thymus and the bursa of Fabricius.
A number of plasma biochemical parameters were examined in five outbreaks of runting in broiler chickens. In four of the five outbreaks, runts showed consistent elevations in plasma amylase activity and reductions in glutathione peroxidase activity. In two of the five outbreaks the plasma vitamin E concentration was reduced, as was the activity of plasma alkaline phosphatase. A highly significant number of runted chickens were found to have pancreatic degeneration, elevated plasma amylase activity and reduced plasma glutathione peroxidase activity, compared with non-runted chickens. The implications of these changes are discussed in relation to the aetiology of runting and stunting syndrome and, in particular, the possible involvement of selenium.
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Utility pigeons on 3 farms were affected by a severe neurological disturbance manifested by fine tremors, rolling gait and incoordination. Affected birds had necrosis of the Purkinje cells of the cerebellar cortex. The birds from the 3 farms had been fed a pelleted diet obtained from a single mix of feed prepared by a stockfeed manufacturer. When feed obtained from the farms was given to utility pigeons under controlled conditions at the laboratory, they suffered the same clinical signs and lesions as seen in birds from the farms. Cross-bred cockerels were not affected when given this feed from day-old to 6 weeks of age. Samples of the feed contained 185 to 226 ppm of the coccidiostat dinitolmide. Utility pigeons given a prepared diet containing a similar level (234 ppm) of dinitolmide developed an identical condition after 3 to 4 weeks feeding. Laying hens were not affected by this feed. Dimetridazole, which was also present in some of the original feed samples, did not exacerbate the condition when included in the diet at a rate of 233 ppm. Production of squabs from the affected farms was dramatically reduced, and many of the breeder had to be culled because of the long-standing neurological disease.
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Spongy degeneration or status spongiosus of the central nervous system (CNS) was described in a number of domestic animal species, notably sheep, cattle, pigs and in one goat. The condition was characterized by diffuse or focal vacuolation, or polymicrocavitation of the CNS, particularly the white matter. The vacuolation showed a well defined pattern of distribution following a number of myelinated tracts in CNS white matter, in isolated fibres crossing grey matter in the brain stem, and along grey and white matter borders in the cerebrum and spinal cord. The vacuoles were not altered by a variety of methods of rapid brain fixation, processing and staining. The appearance of the vacuolation repeatedly favouring the same areas in the CNS in a large number of animals studied, its common origin either by hepatocerebral disease or hyperammonaemia, strongly suggests that CNS spongy degeneration of domestic animals is a distinct disease entity.
Two experiments were completed in which brains and spinal cords from lambs affected with spongy degeneration of the central nervous system (CNS) were analysed for water, sodium and potassium, as measures of cerebral oedema. In a third experiment, lambs with CNS spongy degeneration were tested for permeability of cerebral blood vessels by intravenous injections of Evans blue. The CNS spongy degeneration was produced by poisoning with the hepatotoxic pyrrolizidine alkaloid lasiocarpine. In the first experiment, 2 male lambs were poisoned by lasiocarpine and a third injected with saline alone. One lamb injected with lasiocarpine showed widespread spongy changes in the CNS and the other 2 showed normal brains. In the second experiment, 5 males lambs were poisoned by lasiocarpine and 5 were injected with saline. Three of the 5 poisoned lambs showed widespread spongy changes, a fourth showed minor vascuolation and the remaining 6 had normal brains...
Severe spongy degeneration of the central nervous system (CNS) was seen in 11 cattle, 19 sheep, 4 pigs and 1 goat, associated with a variety of hepatic diseases, particularly those caused by hepatotoxic pyrrolizidine alkaloids. It was also seen in a milder form in 2 of 8 horses examined, 1 dog of 5 dogs examined, and in 1 rabbit only of a large number of laboratory animals examined. This paper reports results of experiments which confirmed initially that the CNS disease cold be caused by pyrrolizidine alkaloid intoxication. This was done by poisoning lambs with lasiocarpine. As the disease was seen in hepatoses not caused by pyrrolizidine alkaloids, the hypothesis that CNS spongy degeneration in lambs could follow any hepatic disease irrespective of its cause, was tested by poisoning lambs with allyl formate, an hepatotoxin chemically unrelated to pyrrolizidine alkaloids. Three of 4 lambs poisoned by the allyl formate showed spongy degeneration in their brains. As the CNS spongy degeneration was an apparent form of hepatocerebral disease, an experiment was conducted to show that the neural disease in sheep was caused by hyperammonaemia. CNS spongy degeneration developed in the brains of all sheep infused intravenously with ammonium acetate, and advanced spongy changes developed in the sheep infused for more than 3 days. The cerebral changes were probably temporary, since sheep infused for 5 days and retained for 3 weeks showed marked regression of vacuolation. Hyperammonaemia caused by intravenous ammonium acetate infusion is a simple, rapid model of CNS spongy degeneration. The syndrome, CNS spongy degeneration caused by hepatic failure and hyperammonaemia, is probably one of the morphologic expressions of hepatocerebral disease in domestic animals and could be an analogue of similar congenital and hepatocerebral diseases in man.