The effect of coccidian infection on the gut microflora of Nubian goat kids.

Enteric coccidiosis was experimentally induced in Nubian goat kids by the oral inoculation of 1.5 x 10(6) sporulated oocysts of five mixed Eimeria species. Diarrhoea was the major manifestation of the disease, which terminated fatally within 19 to 25 days postinfection. Faecal excretion of oocysts was first detected on day 8 (mean 58 x 10(2)) with a maximum shedding (mean 16.39 x 10(5)) on day 14 post-infection. In addition, noticeable alterations were further observed on the normal constituents of the gut microflora in coccidia-infected kids. These changes were characterized by progressive reduction of the Gram-positive population from 84% pre-infection to 24.3% after the onset of diarrhoea. On the other hand, the Gramnegative population was conversely increased from 16% pre-infection to 75.7% after diarrhoea. At this stage (diarrhoea) E. coli was the most dominant organism amongst the various constituents of the gut microflora.

Neurotoxic potential of six organophosphorus compounds in adult hens.

The neurotoxic potential of trichlorfon, diazinon, phosmet, dichlorvos, phosphamidon and coumaphos was evaluated for their ability to inhibit brain neurotoxic esterase (NTE) activity in adult hens. Leptophos was used as a reference neurotoxic agent. All compounds were administered at high single oral doses and the NTE and acetylcholinesterase (AchE) activities were measured at 24 h and 6 w later. With the exception of leptophos, all compounds produced severe cholinergic signs associated with > 80% inhibition of brain AchE at 24 h. On the other hand, brain NTE activity was 86% inhibited by leptophos and to lesser extents by trichlorfon (76%), phosphamidon (74%), coumaphos (70%) and dichlorvos (70%). However, none of the latter compounds produced clinical delayed neurotoxicity as was observed with leptophos. It was concluded that trichlorfon, phosphamidon, coumaphos and dichlorvos are potentially neurotoxic because of their ability to inhibit brain NTE activity, but the extent of inhibition required for development of clinical delayed neurotoxicity (> 80%) is not likely to occur with any of these compounds due to their severe cholinergic activity.

Susceptibility to homologous reinfection with Fasciola gigantica in goats.

Goats previously infected with 100 viable Fasciola gigantica metacercariae and treated with rafoxanide (Ranide, 7.5 mg/kg) at week 4 were not protected against subsequent homologous challenge with 250 metacercariae administered two weeks later. Reinfection resulted in more severe hepatic lesions and a higher percentage of flukes recovered as compared with primarily infected controls. However, the size of flukes originating from the second (challenge) infection was considerably reduced. The plasma enzyme activity of aspartate amino-transferase (AST), glutamate dehydrogenase (GD) and sorbitol dehydrogenase (SD) increased to a similar extent with primary and challenge infections. However, the plasma antibody response to F. gigantica was less pronounced in reinfected goats.

The effect of induced liver, kidney and lung lesions on the toxicity of levamisole and diazinon in calves.

Liver damage in calves, produced by the oral administration of the flukecide, carbon tetrachloride, increased the toxic effect of diazinon but not of levamisole, whereas the presence of a renal tubular lesion caused by mercuric chloride enhanced the toxicity of both commonly used anthelmintic compounds. The toxicity of diazinon was increased in calves with a lung lesion caused by oral dosing with tryptophan, an agent implicated in 'fog fever' of cattle.

Comparative effect of certain organophosphorus compounds and other chemicals on whole blood, plasma and tissue cholinesterase activity in goats.

Cholinesterase (ChE) activity was measured in whole blood, plasma and certain tissues of goats experimentally poisoned with certain organophosphates, organochlorines, heavy metals and anthelmintic drugs. The enzyme activity was only inhibited by the organophosphorus compounds and not by any of the other substances used. The greatest inhibition occurred in the brain, although the blood ChE activity was concurrently inhibited in a similar degree.

Organophosphorus compounds. II. Metabolic considerations.

Organophosphorus compounds are esters of alcohols with phosphoric acids or anhydrides of phosphoric acids with some other acids. The most important groups are the phosphates, phosphorothionates, phosphorothioates, phosphoroamidates, phosphorochloridate and phosphonates. The metabolism of phosphorothionates and phosphorothioates involves initial activation (oxidative desulphuration) followed by hydrolysis of the active metabolites. Activation is carried out by the action of microsomal oxidases, and degradation is performed by different types of hepatic and plasma esterases.

Organophosphorus compounds. I. Toxicity in domestic animals.

Organophosphorus compounds with various aspects of their modes of action, toxicity and antidotal treatment have been briefly reviewed. Their clinical, pathological and biochemical effects on different species of domestic animals are also described.

Effect of pretreatment with hepatic microsomal enzyme inducers on the toxicity of diazinon in calves.

The pretreatment of calves with a single dose of 10 mg kg-1 dieldrin or 21 daily doses of 10 mg kg-1 phenobarbitone increased the toxicity of diazinon as reflected by the development of more severe clinical signs and greater depression in whole blood cholinesterase activity in the pretreated calves. Induction by dieldrin or phenobarbitone of the hepatic microsomal enzyme amidopyrine-N-demethylase was also accompanied by a concurrent rise in the liver carboxylesterase activity.

Some effects of imidocarb in goats.

Clinically normal Nubian goats were given the antiprotozoal drug imidocarb at single intramuscular doses of 6, 12, 18 and 24 mg/kg, and the various clinical, biochemical and pathological manifestations were recorded. At a dose of 6 mg/kg the drug produced no change in any of the parameters studied. At higher doses, the drug produced dose dependent changes which included increased heart and respiratory rates, increased defaecation, urination, depression, incoordination of movement, weakness of the hindlegs, recumbency, and finally death. Just prior to death, there was a significant decrease in the number of erythrocytes, and in packed cell volume, and haemoglobin concentration. In plasma there was an increase in the activity of aspartate transaminase, urea and creatinine concentrations and inhibition of cholinesterase activity. The main histopathological changes were associated with hepatic and renal damage. Three goats were pre-treated with atropine sulphate (1 mg/animal) and after one hour given imidocarb intramuscularly at a dose of 12 mg/kg. The changes were similar but much less severe when compared with those in animals given imidocarb alone at the same dose.