Interaction of fluoroquinolones and certain ionophores in broilers: effect on blood levels and hepatic cytochrome p450 monooxygenase activity.

The concomitant administration to broilers of ionophore coccidiostats and certain chemotherapeutic agents may cause deleterious interactions, with toxicosis and death as possible sequelae. In this study, co-administration of the ionophore monensin was not shown to alter blood levels of enrofloxacin or norfloxacin. In addition, exposure to lasalocid was not shown to change blood levels of enrofloxacin. However, norfloxacin + lasalocid co-administration induced aminopyrine N-demethylase (AD) activity by day 5 after the last administration of norfloxacin, and induced a rise of norfloxacin levels in the blood. This rise of blood norfloxacin levels after co-administration of norfloxacin + lasalocid implies that lower levels of norfloxacin could be administered in birds also receiving lasalocid.

Interaction of monensin and sulfadimethoxine in broilers, as mediated by hepatic microsomal cytochrome P-450 monooxygenases.

The influence of monensin + sulfadimethoxine on cytochrome P-450 monooxygenase activity in broilers, and the possible consequences of modification of this system, including changes in blood levels of sulfadimethoxine, influence on the duration of xylazine-ketamine anesthesia, total antioxidant status and superoxide dismutase activity were studied. The results indicate that the combination of monensin + sulfadimethoxine gave a short-term inhibition of microsomal cytochrome P-450 monooxygenase activity but apparently did not influence the metabolism of other (exogenic) substances (ketamine, xylazine), and did not change the state of antioxidant systems or the relative liver weight. There was a rise in blood sulfadimethoxine levels.

Probable toxicosis in cattle in Israel caused by the oak Quercus calliprinos.

A probable outbreak of oak (Quercus calliprinos) toxicosis in a herd of beef cattle--heifers and first-calving cows--grazing in the Judean foothills of Israel is described. Toxicosis probably occurred because of the consumption of oak leaves and buds during a period of pasture scarcity without any feed supplementation. A progressive syndrome of wasting, dullness, anorexia, polyuria, nephrosis, constipation and recumbency, culminating in death, was seen. A high mortality rate of 83% (38/46 animals) was noted. The clinical-pathological findings revealed increases in blood urea, creatinine, aspartate aminotransferase (AST), gamma-glutamyltransferase (GGT), creatine kinase (CK), lactate dehydrogenase (LDH) and inorganic phosphorus. Decreases were found in alkaline phosphatase (ALP), total serum protein, albumin (ALB), triglyceride (TG), calcium (Ca), magnesium (Mg), sodium (Na) and chloride (CI). The main pathological findings were severe nephrosis, chronic interstitial nephritis, and occasional intestinal ulceration. On the basis of epidemiology, clinical signs, clinical-pathological and pathological findings and renal histology, a tentative diagnosis of oak toxicosis was made.

New treatment regimens in organophosphate (diazinon) and carbamate (methomyl) insecticide-induced toxicosis in fowl.

The objective of this work was to determine optimal treatment regimens for organophosphate (OP) or carbamate insecticide toxicoses in fowl using the antidotes atropine sulfate and pralidoxime chloride (2-PAM). Broiler chicks in treatment groups, each comprising 3 replicates of 6-7 birds/replicate, were gavaged on a body weight (BW) basis with the OP and carbamate insecticides, diazinon and methomyl, respectively, at lethal dosages. Treatment groups were injected with either or both of the antidotes at various dosages as soon as clinical signs appeared. Birds appearing healthy 24 h thereafter were regarded as having been treated successfully. At a dosage of 100 mg/kg BW, atropine was mildly toxic and at 200 mg/kg 2-PAM was severely toxic (but not lethal), whereas at dosages of 50 and 100 mg/kg BW, respectively, the antidotes were at their most effective. With diazinon, atropine alone was only partially effective (12/20 survivors), whereas 2-PAM was extremely efficacious. (20/20 survivors); the combination of the 2 antidotes at 2 dosages was slightly less effective (19/20 survivors) than 2-PAM alone. For methomyl toxicity, atropine was largely successful (18/20 survivors), whereas 2-PAM was mostly unsuccessful (10/20 survivors); the combination at high dosage was less effective (15/20 survivors) than atropine alone, but at a low dosage the combination was the most successful (20/20 survivors). The results indicate that anticholinesterase insecticide toxicoses in fowl should not be treated according to textbook recommendations, and antidotal dosage with atropine should be up to 100 times greater than is commonly recommended. The specific cause of the toxicoses should ideally be determined before treatment is given, but as this is often unknown, a combination of antidotes may be the optimal treatment protocol.

Nitrate toxicosis in beef and dairy cattle herds due to contamination of drinking water and whey.

Four cases of rarely reported nitrate toxicosis due to contamination of drinking water or whey were recorded in 2 beef and 2 dairy cattle herds. In the cases associated with water contamination, water containing ammonium nitrate as a fertilizer for irrigating orchards accidentally entered drinking water troughs for cattle through malfunctioning 1-way valves. The whey contamination in 1 instance was caused by transportation in containers which contained traces of concentrated ammonium nitrate; the 2nd case was induced by whey derived from the production of a specialty cheese produced by the incorporation of nitrate. Mortality occurred in 2 herds and abortions in the 2 other herds. Affected cows responded well to treatment, but some animals remained in a deteriorated physical condition for several months.

Acute maduramicin toxicity in calves.

A herd of 277 beef-breed calves in three age groups was mistakenly given the poultry coccidiostat maduramicin in a total mixed ration. It caused an acute toxicosis in which sudden death was the sole clinical finding in most cases. One group of 212 calves aged five to eight months suffered a mortality of 51 per cent in eight days and a total mortality of 56 per cent during the 40 days in which mortality was recorded. Mortality of only 3 per cent was recorded in two other groups of calves aged nine to 16 months in eight days and a total mortality of 11 per cent over the 40-day period.

Lead toxicosis in a captive bottlenose dolphin (Tursiops truncatus) consequent to ingestion of air gun pellets.

A captive bottlenose dolphin (Tursiops truncatus) in a dolphinarium in Tel Aviv, Israel, had signs of anorexia, weight loss and a reluctance to train over a 4-week period in June 1995 and died shortly thereafter. On necropsy, it had an enlarged, yellow discolored liver, and about 55 air gun pellets in the second stomach. The pellets were composed of 40% lead. Samples of liver and kidney cortex contained 3.6 and 4.2 micrograms/g lead, respectively. There was hemosiderosis in the liver and kidneys, status spongiosus in the brain, and vacuolization in the optic nerve; acid-fast intranuclear inclusion bodies were seen in the kidneys. We propose that chronic lead toxicosis had been induced after the gradual dissolution of the lead-based pellets in the acid environment of the stomach.

The inhibitory effects of the fluoroquinolone antimicrobials norfloxacin and enrofloxacin on hepatic microsomal cytochrome P-450 monooxygenases in broiler chickens.

The fluoroquinolone antimicrobials norfloxacin and enrofloxacin were found to inhibit hepatic microsomal cytochrome P-450 monooxygenases in the livers of broiler chickens using dosages as given in commercial flocks. Norfloxacin inhibited the process of N-demethylation of aminopyrine to a greater degree, while enrofloxacin more markedly inhibited hydroxylation of aniline.

Severe hepatopathy in geese and broilers associated with ochratoxin in their feed.

The feeding of a shipment of imported corn was associated with a severe reduction in growth and increased mortality in geese, and increased mortality in broilers. Pathological examinations revealed hepatopathy, visceral gout and mild nephropathy in geese, and in broilers an hepatopathy, which was often severe, and ascites. Samples of feed from affected geese farms were examined for up to 24 mycotoxins, and ochratoxin was found in 6 of 15 samples at levels up to 930 ng/g. The syndrome was experimentally reproduced by feeding geese and broilers suspect feeds with the natural ochratoxin contamination. It is believed that another, unidentified, mycotoxin was the major cause of the hepatotoxicity, and that ochratoxin served in this case as an indicator of a multi-mycotoxin involvement.

The effect of acetylsalicylic acid and cold stress on the susceptibility of broilers to the ascites syndrome.

Acetylsalicylic acid (ASA) inhibits the in vitro formation of many cyclooxygenases, some of which in mammals regulate pulmonary vasoconstriction. Pulmonary vasoconstriction occurs in some species subsequent to hypoxaemia, through the mediation of cyclooxygenases. If this effect also is manifested in broilers, ASA might have a therapeutic potential in ameliorating the pulmonary hypertension syndrome (clinically manifested as the ascites syndrome) induced by, amongst other factors, exposure to low ambient temperatures. Male broilers were fed pellets containing 500 parts/10(6) of ASA from 3 weeks of age. After 1 week, ASA-treated and control (no ASA) groups were moved to a cold environment for 4 weeks. The development of the ascites syndrome was monitored by recording haematocrit and mortality with ascites. The plasma levels of two cyclooxygenases, the prostaglandins PGE2 and PGF2alpha, were measured in birds in the cold-exposed groups. No differences in haematocrit values, overall mortality or plasma prostaglandins levels were noted between the ASA-treated and control groups during the period of cold exposure. There was an increased mortality in the ASA-treated groups during weeks 3 to 4 of cold exposure, indicating possible inhibition of a cyclooxygenase vasodilator, which could exacerbate a possible existing pulmonary vasoconstriction. The protocol of this field trial does not indicate that ASA might be of therapeutic use in preventing the ascites syndrome in broilers.

The effect of feeding dried tomato vines to beef cattle.

Dried Tomato vines (DTV) are used as a feedstuff in some beef cattle in Israel, despite the literature citation that tomato vines contain potentially harmful steroid alkaloids. A small-scale feeding trial over 42 d examined possible deleterious effects of feeding DTV, compared with wheat straw, in beef cows. No differences in hematological values, serum parameters for body weight were seen between the 2 groups. Steroid alkaloid content of the DTV was not examined, but toxic levels of nitrates were found. The main practical hazard in feeding DTV would appear to be from their potentially high nitrate content.

Percutaneous exposure to ethyl parathion in a feral Griffon vulture (Gyps fulvus).

A feral Griffon vulture (Gyps fulvus) was found with tremors, weakness, digit and wing flexion, and an inability to fly. A zero blood cholinesterase activity and a favorable response to treatment with pralidoxime hydrochloride indicated exposure to an anticholinergic pesticide. The bird died after 7 d, and traces of the organophosphate insecticide ethyl parathion were found in the liver and from a blue discolored skin area of the neck. Continuous exposure to ethyl parathion through dermal absorption was presumed the cause of death of the vulture.

The role of microsomal mixed function oxidases in the metabolism and mechanism of action of certain organophosphorus insecticides.

The influence of microsomal mixed function oxidases (MFO) on the biotransformation of pesticides was investigated in experiments with perfusion of isolated rat livers and in whole animals. The pesticides examined were 3 organophosphorus insecticides (OP): S-propyl-O-phenyl-O-ethylthiophosphate (heterophos), a mixture of O,O-dimethyl-O-cyclohexylthionphosphate and O,S-dimethyl-O-cyclohexylthiolphosphate (cyclophos), and dithiophosphonate. The indices of NADPH-dependent hydroxylating systems measured in the microsomal fraction of rat liver homogenates were the activity of aniline hydroxylase, aminopyrine demethylase and the amount of cytochrome P-450. It was shown that not only did the specific chemical structure of the OP and induction or inhibition of MFO determine OP activation and detoxification (and thus its biological action), but also the route and frequency of exposure could influence these parameters.