The pathogenesis of tularemia was studied in groups of rhesus monkeys ( Macaca mulatta ) that inhaled graded 10-fold doses ranging from 10 through 10 6 organisms of Francisella tularensis 425, a strain highly virulent for the white mouse but of reduced virulence for the domestic rabbit. Mean incubation periods ranged from 3 to 6 days followed by acute illness lasting 5 to 11 days with subsequent recovery of most animals. The higher inhaled doses resulted in shorter incubation periods, longer and more severe acute illnesses, and 18% mortality at the highest dose. Strain 425 multiplied in the lungs, disseminated to the regional lymph nodes, and became systemic. Maximal bacterial populations in tissues were reached by the 7th day after exposure of the animals regardless of the number of organisms inhaled. F. tularensis was no longer recoverable from any of six tissues examined 2 months after exposure. The most significant tissue changes occurred in the lungs; these consisted of foci of liquefaction necrosis, lobular consolidation, and pleural effusion and adhesions. The data indicate that the inhaled dose of strain 425 determined the maximal growth of the organism in the lungs which in turn influenced the severity of the usually self-limiting pneumonia and systemic infection. Although the monkey is less resistant to tularemia than is man, this laboratory animal when infected with F. tularensis 425 provides a useful model for the self-limiting type of human pulmonary tularemia usually observed in Europe and Asia but to a lesser extent in North America.
Signs, bacterial multiplication and dissemination, and pathologic changes were correlated following intracutaneous inoculation of rabbits with l03 cells of Pasteurella tularensis SCHU S4. The infectious process could be divided into four phases: (i) adaptation, (ii) regional infection, (iii) hematogenic dissemination and focal spread, and (iv) septicemia. The organisms became established at the inoculation site during the first 8 hours; they spread to regional lymph n-des and multiplied rapidly during the 8th to 30th hours.Clinical disease coincided with generalization of the process and early pathologic changes.Septicemia was marked by impairment of organ functions, rapid bacterial proliferation and metastasis, progressive anatomic pathologic changes, and terminated in death 103 to 145 hours after inoculation.Bacterial populations per or an in regional lymph nodes, liver, spleen, and lungs were between 10 and l0e at time of decth and did not differ appreciably among animals dying as early as 103 or as late as 145 hours after inoculation. Icterus that developed during the septicemic period resulted primarily from hepatocellular damage.
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