Evolution of inflammatory response and cellular immune responses in a murine model of disseminated blastomycosis

Deepe, George S.; Taylor, Cassandra; Bullock, Ward E.

doi:10.1128/iai.50.1.183-189.1985

Cited by 10 publications

(3 citation statements)

References 21 publications

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“…A few strains used in murine studies of blastomycosis have been deposited with the American Type Culture Collection. These include environmental isolates KL-1 (ATCC 26198) (5,8,11) and MCG-1 (ATCC 32090) (8) and human isolates GA-1 (ATCC 26197) (5, 8, 11) and SCB-2 (ATCC 26199) (5,7,11).…”

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“…Murine models of blastomycosis are fundamental to investigations of pathogenic and immune mechanisms in this chronic mycotic infection. Murine infection has been produced by intravenous (7) and intraperitoneal (16) inoculation of yeast-phase organisms. Studies using models in which infection was induced by yeast-phase B. dermatitidis have shown differences in pathogenicity related to route of inoculation (16), inoculum size (7,11), fungal strain (6,11), and mouse strain (17).…”

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confidence: 99%

“…Murine infection has been produced by intravenous (7) and intraperitoneal (16) inoculation of yeast-phase organisms. Studies using models in which infection was induced by yeast-phase B. dermatitidis have shown differences in pathogenicity related to route of inoculation (16), inoculum size (7,11), fungal strain (6,11), and mouse strain (17). Reports of variance in conidial pathogenicity related to conidial inocula are limited to B. dermatitidis strains KL-1 and 181-2 (D. J. Drutz, P. L. DeMarsh, and C. L. Frey.…”

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Fungal-strain-dependent alterations in the time course and mortality of chronic murine pulmonary blastomycosis

1988

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Intratracheal injection of 104 conidia of Blastomyces dermatitidis strain Mi-A into mice was shown in previous work to induce chronic pulmonary and disseminated infection with histopathologic features of chronic human blastomycosis. Furthermore, 10-fold variations in inoculum density produced marked changes in mean survival times (MSTs), i.e., 32 days at 106, 36 days at 105, 97 days at 104, and 172 days at 103. A second strain (Mi-B) failed to induce death in this model. To assess fungal-strain-dependent virulence, we extended these previous studies to 11 additional human isolates. Groups of male BALB/cByJ mice (6 to 8 weeks old) were injected intratracheally with 104 conidia from each of the 13 strains; the mice were weighed weekly and monitored for mortality, and their lungs were examined histopathologically. Infection rate and mortality were 100% in all groups except for the Mi-B inoculated mice. For strains Mi-B and Mi-A, MST and mortality curves were not significantly different from those observed in our previously reported experiments. Four different survival patterns were noted in infected mice. The shortest MSTs were produced by strains M2-E, M2-B, M2-K, M2-H, and M2-A (24, 26, 26, 27, and 31 days, respectively), and the longest MST was seen in animal groups inoculated with strains M2-J and M2-G (130 and 134 days, respectively). Strains M2-I, M2-F, and M2-D produced intermediate MSTs of 65, 79, and 80 days, respectively. The 107-day MST induced by Mi-A did not differ from strain M2-C-induced MST but differed significantly from the MST produced by the other strains. Pulmonary histopathology was similar in all animals dying with blastomycosis. The wide spectrum in survival times was not related to differences in clinical status of the patient from whom the isolate had been obtained, to fungal inoculum viability, or to individual mouse weight at inoculation. Strain-dependent virulence factors present in these fungal isolates alter the disease course in inbred mice in a fashion similar to that induced by 10-fold inoculum variation of strain Mi-A conidia. These 13 isolates of B. dermatitidis, 1 avirulent and 12 with differing levels of virulence, provide tools for future studies into the nature of fungal virulence determinants in chronic blastomycosis.

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