Bacterial pathogens play an important role in causing respiratory disease in domestic poultry species. In many cases, the bacterial component of a respiratory disease colonizes the respiratory system only after a primary viral or environmental insult. Colonization of the airsacs of a chicken by Escherichia coli following an infectious bronchitis virus infection is an example of secondary bacterial invasion. In other cases, the bacterial component of the respiratory disease is the primary initiating cause of the disease. Examples of primary bacterial respiratory disease are infectious coryza in chickens and fowl cholera in chickens and turkeys.

One hundred forty-eight Pasteurella multocida isolates from four southeastern states and California were serotyped by a gel diffusion precipitin test. The isolates were predominantly from turkeys and chickens. Sixty-eight percent of the isolates had antigenic characteristics of serotypes 3 and 4 (3 X 4). In turkeys, 76% of the isolates were 3 X 4, and serotype 3 was second (17%) in frequency. In chickens, 54% of the isolates were 3 X 4 and 19% were serotype 1.

Two serotype 3,4:A strains of Pasteurella multocida that differ in virulence in turkeys were examined for their ability to invade epithelial cell monolayers grown in tissue culture. Both organisms were comparably adherent to cells of turkey kidney origin. However, the virulent strain (86-1913) penetrated primary turkey kidney epithelial cell monolayers at 10 times the level of the low-virulence vaccine strain. The virulent strain was also able to invade porcine epithelial cells (PK15) and feline epithelial cells (CRFK) in cell culture. Neither organism invaded rabbit epithelial cells (RK13). Invasion of turkey cells was prevented by inhibition of bacterial protein or RNA synthesis but not by pretreatment of the monolayers with periodate, trypsin, or neuraminidase. Invasion might be a mechanism of pathogenicity for this organism, contributing to colonization or virulence.

No abstract

One-day-old poults were placed on littler on which poults had previously developed diarrhea, increased mortality, and stunting. Small intestines, pancreas, and liver were evaluated histologically. Morphometric evaluations were conducted to determine villous length and crypt depth. Poults were evaluated for malabsorption utilizing D-xylose and lipid absorption tests. Compared with controls, the gastrointestinal tract of affected birds was grossly distended, was fluid-filled, and had thin, flaccid walls on days 5 and 8. Ceca were distended with brown watery fluid and gas on days 5, 8, and 12. No histologic lesions were present in the liver, pancreas, or pancreatic ducts, and only mild inflammatory changes were present in the small intestine. Villous atrophy and crypt hypertrophy were present in the small intestine on days 5, 8, 12, 16, and 21. Morphometry revealed significant decreases in villous lengths and increases in crypt depth throughout the trial. D-Xylose and lipid absorption were significantly decreased on days 8 and 11. Intestinal epithelial damage by infectious agents with subsequent villous atrophy is postulated to have produced malabsorptive diarrhea.