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Occipitoatlantoaxial malformation was diagnosed in a 19-month-old mare of Appaloosa breeding and in a 3-year-old Quarter Horse gelding. Both horses had abnormal head and neck carriage since birth, but neurologic deficits did not become evident clinically until the horses reached 2 and 3 years of age, respectively. Palpation and manipulation of the base of the skull and cervical area proved to be useful diagnostically. Movement could not be elicited at the atlantooccipital joint but, in comparison with clinically normal horses, the range of dorsoventral motion at the atlantoaxial joint was increased. Alternate subluxation and relocation of this joint generated audible clicking sounds. Radiography revealed symmetric atlantooccipital fusion, with modification of the atlas, atlantoaxial joint, and axis. These findings were confirmed at necropsy.

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The effect of IV amitraz on the transit of barium sulfate through the stomach and duodenum as well as amitraz-induced bradycardia was studied in 4 dogs. Control transit time and heart rates were determined after IV injection of dimethyl sulfoxide (0.1 ml/kg), which was subsequently used as the vehicle for amitraz administration. The time for barium sulfate to move from the stomach to the duodenojejunal junction was 6.1 +/- 1.3 minutes (mean +/- SEM). An IV injection of amitraz (1 mg/kg) prolonged the transit time to 251.2 +/- 27.0 minutes, and induced marked bradycardia for at least 60 minutes. During the amitraz-induced prolongation of gastrointestinal transit, there were no vigorous gastric contractions for at least 180 minutes. Yohimbine, an alpha 2-adrenergic blocking agent, given IV 20 minutes after amitraz administration, at a dosage of 0.1 mg/kg, reversed both the gastrointestinal and bradycardic effects of amitraz. It was concluded that 1) amitraz causes decreased gastrointestinal motility and bradycardia, and 2) yohimbine may be useful in the control of the untoward reactions caused by amitraz administration.

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Rhodococcus (Corynebacterium) equi pneumonia is diagnosed by thoracic auscultation, radiographic and hematologic examination, and transtracheal aspiration. Treatment may be unsuccessful because of the organism's tendency to cause pulmonary abscesses. A 2-month-old, depressed, anorectic, febrile Quarter Horse colt, previously unresponsive to penicillin therapy, had loud, moist breath sounds in the ventral lung fields. Chest radiographs revealed pneumonia. Based on culture and sensitivity tests on organisms isolated from transtracheal washes, chloramphenicol and erythromycin, and then oral trimethoprim-sulfadiazine, were given, in addition to supportive therapy. The animal was fully recovered within 2 months.

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The effects of yohimbine and doxapram on xylazine-induced prolongation of gastroduodenal transit of barium sulfate were studied in 5 dogs. Base-line transit time was determined while the dogs were non-sedated and undisturbed; the time for barium sulfate to move from the stomach to the duodenojejunal junction was 5.6 +/- 4.0 minutes (mean +/- SD). An IV injection of xylazine (1 mg/kg) prolonged the transit time to 95.0 +/- 14.6 minutes. During the xylazine-induced prolongation of gastroduodenal transit, there were no vigorous gastric or intestinal peristaltic contractions for at least 60 minutes. Yohimbine, an alpha 2-adrenergic blocking agent, given IV at a dosage of 0.1 mg/kg, reversed the gastrointestinal and sedative effects of xylazine. Doxapram hydrochloride, an analeptic, given IV at a dosage of 5.5 mg/kg, prolonged the transit time to 43.0 +/- 22.8 minutes. When doxapram was given in combination with xylazine, it potentiated the gastrointestinal effect of xylazine, and further prolonged the transit time to 148.0 +/- 32.7 minutes. It was concluded that yohimbine is effective as an antidote to reverse the xylazine-induced prolongation of gastrointestinal transit, whereas doxapram has no value in this respect.

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The effect of xylazine on the transit of barium sulfate through the stomach and duodenum was evaluated in 4 dogs. Base-line transit time was determined while the dogs were nonsedated and undisturbed; the mean time for barium sulfate to move from the stomach to the duodenojejunal junction was 4.8 +/- 1.2 minutes. An IV injection of xylazine (1 mg/kg) prolonged the mean transit time to 157 +/- 37.8 minutes. During the xylazine-induced prolongation of gastrointestinal transit, there were no vigorous contractions for at least 90 minutes. Yohimbine, an alpha 2-adrenergic-blocking agent, given IV at a dosage of 0.1 mg/kg, did not affect gastrointestinal motility. It did, however, prevent both the gastrointestinal and sedative effects of xylazine. Atropine methylnitrate given IV at a dosage of 1 mg/kg prolonged the transit time to 13.8 +/- 2.4 minutes. After atropine methylnitrate injection, the gastrointestinal tract was more flaccid than with xylazine administration. The prolongation of transit induced by atropine methylnitrate was not prevented by yohimbine. It was concluded that gastrointestinal radiographic findings in animals under the influence of xylazine should be interpreted cautiously.

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A 10-month-old dwarfed male pup born of large-breed parents with normal stature had congenital goiter. Hypothyroidism due to failure to form organic iodine was diagnosed based on low serum thyroxine and triiodothyronine assays, radiographic findings in the epiphyses, and an abnormal perchlorate discharge test. Replacement of thyroid hormone resulted in more than 450% increase in body weight and a 600% increase in shoulder height over an 8-month period of treatment. A relapse in mental and physical condition occurred when hormone replacement therapy was later withdrawn. Postmortem findings are described.

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