Biomedical subjects
Publications and source records attributed to J E Sander.
A 27-year-old woman with a recent diagnosis of multiple sclerosis developed several episodes of noncardiogenic pulmonary edema over a 3-month period, each requiring intubation and ventilatory support. The development and subsequent resolution of an isolated lesion at the obex was correlated with the episodes. The literature regarding the anatomical basis of neurogenic pulmonary edema is reviewed.
Reports of brain computed tomography (CT) findings in spongy degeneration describe radiolucent changes of the cerebral white matter, but have not described changes in the posterior fossa. We describe an infant with spongy degeneration in whom CT scans detected brainstem, cerebellar, and cerebral white matter radiolucencies before the diagnosis was established. The posterior fossa CT findings resembled the periventricular changes described in subacute necrotizing encephalomyelopathy (SNE). As the patient's initial clinical findings were consistent with SNE, the similarity of the posterior fossa radiolucencies was misleading. Without basal ganglia or thalamic involvement, or without variability in their appearance over time, posterior fossa periventricular radiolucencies are not diagnostic of a specific degenerative disorder.
One-day-old broiler chicks were housed on litter treated with 0, 0.9, 3.6, or 7.2 kg of boric acid per 9.3 m2 of floor space. After 15 days, average body weights were 340.7 g, 278.1 g, and 213.2 g for chickens exposed to 0, 3.6, and 7.2 kg boric acid/9.3 m2, respectively (P < or = 0.05). Feed conversion was 1.68 and 2.29 in chickens exposed to 0 and 7.2 kg boric acid/9.3 m2 (P < or = 0.05). In a second experiment, after birds ingested feed treated with 2500 and 5000 ppm of boric acid for 2 weeks, body weights were 254.8 g and 149.6 g, respectively. The chickens in the control group weighed an average of 285.0 g (P < or = 0.05). The 5000 ppm treatment group had a feed conversion of 1.70, vs. 1.45 in the controls (P < or = 0.05). A dose-related feathering abnormality was evident in treated chickens. No significant histopathologic changes were observed. Livability, weight gain, and feed conversion were not adversely affected in broilers as a result of exposure to litter treated with boric acid at recommended levels of 0.4-0.9 kg/9.3 m2.
The acute oral mean lethal dose of boric acid in 1-day-old chickens was found to be 2.95 +/- 0.35 g/kg of body weight, which classifies this product as only slightly toxic to chickens. One-day-old broiler chicks were housed in floor pens in which litter had been treated with 0, 0.9, 3.6, or 7.2 kg of boric acid per 9.9 m2 of floor space. Boron residue levels in brain, kidney, liver, and white muscle were not statistically elevated following a 15-day exposure period. Boron residue levels in the same types of tissue were not significantly elevated in chicks fed 500 ppm or 1250 ppm boric acid in feed ad libitum for 3 weeks; however, residues were significantly higher in chicks fed 2500 ppm or 5000 ppm boric acid. These data indicate that broilers grown on boric acid-treated litter do not consume enough boric acid to cause elevated boron levels in tissues.
Pasteurella multocida, the etiologic agent of fowl cholera, was isolated from six broiler flocks in Georgia during summer 1988. The flocks ranged in age from 20 to 46 days, represented four companies, and spanned a distance of 50 miles. Increased mortality and lameness were the clinical signs present in all affected flocks. Bacterial isolation and agar gel precipitation for somatic antigen serotyping revealed that three of the cases were caused by serotype 1,3, two by serotype 3,4, and one by serotype 3. To prove the virulence of these organisms, two isolates were selected to challenge 5-week-old broilers. Mortality and lameness resulted from this challenge, and P. multocida was reisolated.