Development of Experimental Myopia in Chicks in a Natural Environment.

PURPOSE: The hypothesis that outdoor exposure might protect against myopia has generated much interest, although available data find only modest clinical efficacy. We tested the effect of outdoor rearing on form-deprivation myopia in chicks, a myopia model markedly inhibited by high-intensity indoor laboratory lighting. METHODS: Unilaterally goggled cohorts of White Leghorn chicks were maintained in a species-appropriate, outdoor rural setting during daylight hours to the extent permitted by weather. Control chicks were reared indoors with incandescent lighting. Besides ocular refraction and ultrasound, we determined dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC) content in retina and vitreous and measured mRNA expression levels of selected clock and circadian rhythm-related genes in the retina/RPE. RESULTS: Myopia developed in the goggled eyes of all cohorts. Whereas outdoor rearing lessened myopia by 44% at 4 days, a protective effect was no longer evident at 11 days. Outdoor rearing had no consistent effect on retinal or vitreous content of dopamine or DOPAC. Conforming to prior data on form-deprivation myopia, retina and vitreous levels of DOPAC were reduced in goggled eyes. Compared with contralateral eyes, the retinal expression of clock and circadian rhythm-related genes was modestly altered in myopic eyes of chicks reared indoors or outdoors. CONCLUSIONS: Outdoor rearing of chicks induces only a partial decrease of goggle-induced myopia that is not maintained, without evidence that retinal dopamine metabolism accounts for the partial myopia inhibition under these outdoor conditions. Although modest, alterations in retinal gene expression suggest that studying circadian signals might be informative for understanding refractive mechanisms.

Evaluation of the efficacy of a live fowlpox-vectored infectious laryngotracheitis/avian encephalomyelitis vaccine against ILT viral challenge.

Infectious laryngotracheitis (ILT) is caused by an alphaherpesvirus, and latency can be produced by previous exposure to vaccine virus. The main sites of latency for the ILT virus have been shown to be the trigeminal ganglion and the trachea. Reactivation of latent virus is one factor related to the production of clinical signs. The development of a genetically engineered ILT vaccine has been suggested for many years as a tool to eliminate viral latency. Several approaches have been suggested. Included among them is the development of a thymidine kinase-deficient mutant or the insertion of ILT viral glycoproteins into a viral vector such as a poxvirus. A commercially available, live, fowlpox-vectored infectious laryngotracheitis + avian encephalomyelitis (FP-LT+AE) vaccine was used in field trials in leghorn pullet flocks and evaluated by tracheal challenge in a laboratory setting with the use of the National Veterinary Services Laboratory (Ames, IA) ILT challenge virus. Interference of the pigeon pox vaccine, which is often administered concurrently with fowlpox vaccine, was also evaluated when given in conjunction with the FP-LT+AE vaccine. Overall, the results indicate that the FP-LT+AE vaccine provides adequate protection against ILT viral challenge. Proper administration is essential. In one flock, inadequate protection was most likely a result of either poor vaccine administration or previous exposure to pox virus. In addition, the simultaneous administration of pigeon pox vaccine did not appear to interfere with protection against ILT viral challenge.