Production and characterization of VP4/VP7 reassortant swine rotaviruses derived from Gottfried and OSU parental strains.

The ability of viral glycoproteins (VP) VP4/VP7 reassortant swine rotaviruses (RV) to induce cross-neutralizing antibody against parental serotypes was investigated in guinea pigs. Using selective culture conditions, we produced 10 reassortant viruses that contained gene segment 4 of the OSU RV strain and gene segment 9 of the Gottfried RV strain. These reassortant RV grew to high titer in cell culture and were neutralized by monospecific antisera against both parental RV strains. The reassortant RV were chemically inactivated with binary ethylenimine, adjuvanted with aluminum hydroxide, and used to produce antisera in guinea pigs. The hyperimmune antisera had high neutralization titer against both parent RV strains. These results indicate that several of the reassortant RV may be capable of inducing neutralizing antibodies to VP4 and VP7 and may have future use as bivalent vaccine strains.

Resistance of the rabbit to dietary pyrrolizidine (Senecio) alkaloid.

Rabbits were fed Senecio jacobaea for 263 days. Total intake of the plant averaged 112.5% of initial body weight. No gross lesions, or changes in serum protein and albumin occurred. Microscopic changes in liver tissue were seen. Two rabbits injected with 150 mg Senecio pyrrolizidine alkaloid/kg body weight died in less than 24 hours. The resistance of the rabbit to chronic Senecio intoxication, but not to injected alkaloid, suggests that alkaloid absorption may be low in this species.

An experimental approach to surgery of the equine fetlock and its associated structures.

An illustrated approach to the medial aspect of the equine fetlock joint is described, whereby the collateral ligaments are transected. This approach is suggested as a possible technique for metatarsal or metacarpal bone fracture repair by retrograde pinning, arthrodesis of the fetlock joint and other joint and sesamoid bone surgery. The histological evidence of satisfactory healing is presented and the advantages and disadvantages are discussed.

Induction of pulmonary edema and emphysema in goats by intraruminal administration of 3-methylindole.

The effects of intraruminal administration of 3-methylindole (3MI; skatole) were determined in goats. The 3MI was given to 4 goats at the dose level of 0.3 g/kg of body weight, to 2 goats at 0.2 g/kg, and to 2 goats at 0.1 g/kg; 3 nontreated goats were used as controls. Clinical signs of acute progressive respiratory tract disease were seen in all treated goats. Goats given the largest dose of 3MI (0.3 g/kg) died between 5 and 11 hours after treatment; those given smaller doses (0.2 and 0.1 g/kg) died between 79 and 92 hours. Increased plasma concentrations of 3MI were detected in goats give 0.1 or 0.2 g/kg within 3 hours after administration. By 24 and 36 hours, the concentrations of 3MI in the plasma decreased to low or nondetectable amounts and remained low for the duration of the experiment. Clinical signs of respiratory distress in the goats progressed after 3MI had been cleared from the plasma. Diffuse pulmonary edema and hydrothorax were extensive in goats which died early in the course of the experimentally induced disease. In goats which died at later stages, the lungs were firm and had less watery transudate. Temporal variations in the nature of pulmonic changes were even more obvious by microscopic examination. Diffuse pulmonary edema was the predominant early change. Small foci of emphysema were apparently caused by overdistention of some clusters of alveoli. Marked septal thickening and proliferation of alveolar cells were the prominent changes in goats which died between 79 and 92 hours after treatment. Incubation of L-tryptophan with caprine ruminal fluid resulted in formation of indoleacetic acid, indole, and 3MI. Similar incubations did not convert indoleacetic acid to 3MI. Control incubations showed 3MI as a fermentation metabolite, indicating it exists in caprine ruminal fluid in vivo. Results demonstrated that goats are susceptible to intraruminal administration of 3MI. The transitory appearance of 3MI in the plasma associated with progressive respiratory tract disease was similar to observations in cattle give 3MI. Clinical signs and lesions seen at necropsy were qualitatively similar to those reported in cattle given tryptophan and indoleacetic acid.

Pulmonary edema and emphysema in cattle after intraruminal and intravenous administration of 3-methylindole.

Intraruminal and intravenous administration of 3-methylindole (3MI; skatole) caused interstitial pulmonary edema and emphysema in cattle. In 3 adult heifers given the intraruminal dose of 0.2 g of 3 MI per kilogram of body weight, clinical signs of respiratory disease appeared between 6 and 12 hours after dosing, and death due to pulmonary edema and emphysema occurred at 33, 69, and 72 hours. The mean plasma concentration of 3MI became maximal (18.5 mug/ml) at 3 hours and then decreased to low concentrations by 48 hours. In 2 heifers given an intraruminal dose of 0.1 g of 3MI/kg, clinical signs developed, but they did not die during the 96-hour experiment. The mean plasma concentration of 3 MI became maximal (16.8 mug/ml) at 3 hours and decreased to 1.6 and 0.4 mug/ml at 12 and 36 hours, respectively. At necropsy of the heifers, the lung were large, firm, dark red, and heavier than normal. Diffuse pulmonary edema was the predominant change in cattle which died early, and interstitial emphysema was more severe at later stages of the disease. During the early stages, alveoli were overdistended, and a few more ruptured. Most alveolar spaces were filled with proteinaceous residue, but the alveolar septums were smooth and of normal thickness. At later stages, proliferation of alveolar cells was observed, and alveolar septums were thickened. In 3 cows given 0.06 g of 3MI/kg by jugular infusion, clinical signs appeared in all cows, and 1 cow died of pulmonary edema and emphysema 56 hours after the infusion was started. Severe pulmonary lesions seen in all of the cows given a 3MI infusion were similar to those in the cows given an intraruminal dose of 3MI. The mean plasma concentration of 3MI increased to 10.7 mug/ml at 9 hours after starting the infusion and decreased to 0.5 mug/ml at 18 hours. The results indicate that 3MI, a product of ruminal tryptophan fermentation, can cause pulmonary edema and interstitial emphysema in cattle and support the hypothesis that 3MI is the causative agent in tryptophan-induced pulmonary disease.

Ruminal and plasma concentrations of 3-methylindole associated with tryptophan-induced pulmonary edema and emphysema in cattle.

Five Hereford cows were given an intraruminal dose of L-tryptophan (0.35 g/kg of body weight), and 2 cows were used as controls. Of the 5 treated cows, 3 developed clinical signs of interstitial pul monary edema, and emphysema and severe pulmonary lesions were seen at necropsy after 96 hours. Another cow developed moderate clinical signs and pulmonary lesions, and the remaining cow had few clinical signs and mild pulmonary lesions. The severity of clinical signs in each cow was related to the severity of pulmonary lesions at necropsy. The 3-methylindole (3MI) was present in ruminal fluid and plasma within 6 hours after administration of tryptophan, and the concentrations increased to 3.0 and 9.0 mug/ml within 12 to 24 hours. Severity of pulmonary lesions was related to maximal concentration and duration of 3MI in the plasma. At necropsy, gross lesions were characterized by diffuse, pulmonary edema and interstital emphysema; and the lungs were dark red, firm, and heavier than normal. Predominant microscopic changes included accumulation of proteinaceous residue, hypertrophy and hyperplasia of alveolar lining epithelium, thickening of alveolar septums, and emphysematous thickening of interstitial tissues. These changes were similar to previously reported 3MI-induced pulmonary lesions. The presence of 3MI in ruminal fluid and plasma after administration of tryptophan and the relationship between concentration of 3MI and severity of clinical signs indicate that 3MI is the principal metabolite of ruminal fermentation which leads to the development of acute pulmonary edema and emphysema in cattle given tryptophan.

Induction of pulmonary edema and emphysema in cattle and goats with 3-methylindole.

Microorganisms from rumen converted L-tryptophan and indoleacetic acid to 3-methylindole in vitro. Oral doses of 3-methylindole caused interstitial pulmonary edema and emphysema in cattle and goats. Intravenous infusion of this metabolite also induced pulmonary disease in cattle. These results demonstrate than an end product of ruminal fermentation of tryptophan can induce acute pulmonary disease in cattle and goats.