Respiratory pathogenesis of Pasteurella Multocida in turkeys Public Deposited

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  • Pasteurella multocida causes diseases in many animal species including fowl cholera, a septicemic disease of poultry and other birds. Pathogenesis of the disease has been studied by many investigators by the systemic administration of the organism in poultry. However, only a few studies have been done as to the respiratory pathogenesis of the organism. The objective of the study was to investigate the fate of P. multocida after the intratracheal administration in turkeys The fate of four strains of Pasteurella multocida was studied after their intratracheal inoculation in young adult turkeys. Viable bacterial counts were made in respiratory tissues as well as in the liver, spleen and blood at 6 and 9 hrs after the inoculation of approximately 10⁹ viable organisms of each strain. A virulent, encapsulated strain, P-1059, invaded systemically by 6 hrs postinoculation (PI) and multiplied vigorously in all tissues and organs examined. A blue colony mutant of P-1059, T-325, which does not possess a thick layer of capsule, as well as CU vaccine strain, invaded the parenchymal organs, but did not show significant increase in viable counts at 9 hrs PI compared with at 6 hrs PI. Another vaccine strain, M-9, also invaded blood and internal organs by 6 hrs PI, however, its viable counts showed no significant change between 6 and 9 hrs PI, or in some tissues significant decrease at 9 hrs PI. The results indicate that all the four strains possess high capacity to invade respiratory tissues with varying capacity to persist in host tissues. The lesions caused by two strains of Pasteurella multocida (P-1059 and M-9) were observed after their intratracheal inoculation in young adult turkeys. The lesions were observed in the respiratory organs at 0, 0.25, 0.5, 1, 2, 3, and 6 hrs after inoculation of approximately 10⁹ viable organisms of each strain. Both virulent strain, P-1059 and non-virulent vaccine strain, M-9, have capacity to invade and multiply in the tissues examined. Macroscopicly, the lesions in the lung and in the airsac were found as early as 1 hr PI, including the infected lung was foamy and the airsac became cloudy. They became more severe by 2 to 6 hrs PI. Microscopicly, hecerophiles were present, occasionally, in the lung, trachea and airsac by 0 to 1 hr after inoculation. Then they became more severe by 2 to 6 hrs PI. By 6 hrs PI, there were diffuse heterophiles infiltration in the trachea, lung, anc airsac. The lung vascular was edema. The trachea ciliate and mucous gland was cystic or hyperplasia, and the airsac shewed increased in thickness and cloudiness. These results of study indicate that the lesion caused by P-1059 and vaccine strain, M-9, were not significantly different.
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