A small gram-negative motile bacillus was isolated from laboratory poults affected by acute respiratory disease (rhinotracheitis) of turkeys. The bacterium was inoculated intranasally into susceptible day-old poults; the poults developed typical clinical signs of acute respiratory disease, and the bacterium was reisolated. This same bacterium was isolated from commercial poults with typical signs of acute respiratory disease but not from poults of similar age which were clinically normal. The bacterium has not been identified taxonomically. We conclude that it is a primary etiologic agent for acute respiratory disease of turkey poults.

Cell-associated Marek's disease (MD) vaccine was suspended at dilutions normally used for vaccination in seven commercially available diluents and in tryptose phosphate broth. The stability of diluted vaccines was determined by assay in cell cultures subjected to 0 to 37 C for 0 to 90 minutes. Optimum holding temperatures for MD vaccine virus survival varied with the specific diluents employed. Some diluents afforded greatest survival when dilution was at 0 C and held at 0 C, while others performed best when dilution was at 25 C followed by cooling and holding at 0 C. Diluents which allowed greatest survival when tested at 37 C also performed well under other temperature regimes. Spectinomycin dihydrochloride pentahydrate and various buffering compounds were added to commercial diluents used for diluting MD vaccine. Additives producing osmolality of 745 mOsm/kg and higher markedly reduced vaccine virus survival. The adverse effects of high osmotic pressure were accentuated by extended holding time, elevated incubation temperature, and physical manipulations including mechanical mixing or expressing through a syringe and needle. Satisfactory MD vaccine virus survival was afforded by a commercial diluent especially formulated to accommodate the pH osmolality changes produced by adding spectinomycin dihydrochloride pentahydrate.

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The course of changes within the upper respiratory tracts of turkey poults experimentally infected with Alcaligenes faecalis was studied. The initial change observed (5 days post-inoculation) was colonization of the upper respiratory tract by the bacterium. Changes in the nasal turbinates and trachea were first apparent as a focal loss of cilia but subsequently developed into a general loss of cilia (11 days post-inoculation). Eventually, the entire ciliated epithelial layer in the cranial region of the trachea was lost (13 days post-inoculation). With the loss of cilia and ciliated cells, a highly viscous mucus was able to accumulate in the anterior one-half to two-thirds of the trachea. In addition, changes in the gross structure of the trachea (flaccid trachea) were observed in all poults inoculated with A. faecalis. There was an apparent gradation in the severity of these changes from severe in the cranial region of the trachea to mild in the region just anterior to the bronchial bifurcation. The observations resulting from A. faecalis infection indicated two major tracheal changes responsible for the chronic and sometimes severe nature of this disease. These changes included a loss of ciliary activity and a flaccid trachea which together resulted in the accumulation and stasis of mucus and tracheal collapse.

A virus with physical and biological characteristics of an adenovirus was isolated from turkey poults with respiratory disease. The virus was ether-resistant and incorporated [3H] thymidine. Electron microscopy revealed virions of icosahedral configuration, approximately 78 nm in diameter, within the nuclei of infected cells. The virus produced cytopathology in turkey kidney cells, but did not produce observable disease when inoculated into commercial turkey poults or specific-pathogen-free embryonated chicken eggs. Virus-neutralization tests indicated widespread exposure to the virus in North Carolina turkey populations.