THE USE OF AMITRAZ IN THE CONTROL OF AN OUTBREAK OF SARCOPTIC MANGE IN A COLONY OF KOALAS

SUMMARY: An outbreak of sarcoptic mange in a colony of koalas was effectively controlled by the topical application of amitraz as a 0.025% aqueous suspension. Several koalas died in the 9 months preceding treatment, with lesions suggestive of Sarcoptes scabiei ; however, no further deaths occurred following treatment and there was complete recovery of all affected animals.     

Plasma and urine disposition and dose proportionality of ceftiofur and metabolites in dogs after subcutaneous administration of ceftiofur sodium

Nine male dogs (10.3–13.5 kg body weight) were randomly assigned to three groups of three dogs each and administered ceftiofur sodium subcutaneously as a single dose of 0.22, 2.2, or 4.4 mg ceftiofur free acid equivalents/kg body weight. Plasma and urine samples were collected serially for 72 h and assayed for ceftiofur and metabolites (derivatized to desfuroylceftiofur acetamide) using high-performance liquid chromatography. Urine concentrations remained above the MIC ₉₀ for Escherichia coll (4.0 μg/mL) and Proteus mirabilis (1.0 μg/mL) for over 24 h after doses of 2.2 mg/kg (8.1 μg/mL) and 4.4 mg/kg (29.6 μg/mL), the interval between treatments for ceftiofur sodium in dogs, whereas urine concentrations 24 h after dosing at 0.22 mg/kg (0.1 mg/Ib) were below the MIC ₉₀ for E.coli and P. mirabills (0.6 μg/mL). Plasma concentrations were dose-proportional, with peak concentrations of 1.66 ± 0.0990 μg/mL, 8.91 ± 6.42 μg/mL, and 26.7 ± 1.07 μg/mL after doses of 0.22, 2.2, and 4.4 mg/kg, respectively. The area under the plasma concentration versus time curve, when normalized to dose, was similar across all dosage groups.     

Immunocytological confirmation of a diagnosis of canine distemper using cells in urine

Immunofluorescent staining of epithelial cells present in urine of early clinical cases of canine distemper confirmed the presumptive diagnosis by revealing fluorescing intracytoplasmic inclusions. Positive results were not obtained in urine samples from control dogs nor from samples from dogs ill for more than three weeks. The urine samples, with added preservative, still yielded positive results after 5 days storage at 37°C or 21 days storage at 18°C.     

Human rhodopsin

Human rhodopsin in aqueous solution has lambda(max). of 493 mmicro and is lower in the spectrum than the rhodopsins of all other known vertebrates, with the exception of certain deep-sea fishes. Its molar extinction is 40,000 +/- 800. Like other rhodopsins, it bleaches to a mixture of opsin and all-trans retinene and is resynthesized by incubating opsin with neo-b (11-cis) retinene. The regenerated rhodopsin has the same lambda(max). as the extracted pigment; this is due, therefore, not to an unusual retinene but to a characteristic human opsin. The regeneration in solution from opsin and neo-b retinene is a second-order reaction with a half-time, at 29.5 degrees C, of about 2.5 minutes. This is much faster than the synthesis of rhodopsin in the living human eye, and faster than human rod dark-adaptation; the rate of both processes in vivo must be limited by reactions which precede the union of neo-b retinene with opsin, the final step in rhodopsin synthesis. In the rods, rhodopsin is virtually in the solid state-highly oriented in close relation with other highly oriented molecules. In this situation its spectrum is displaced toward the red (lambda(max) 500 mmicro) and is narrower than in solution. For light entering the rods axially, rhodopsin has also a considerably increased extinction, some 1.5 times higher than when randomly oriented. The spectrum of rhodopsin in rods agrees well in form and position with the spectral sensitivity of human rod vision, measured at the retinal surface.