Corynebacterial Pseudotuberculosis in Mice

Abstract

The susceptibility of mice to experimental infection with Corynebacterium kutscheri was studied by comparing the host response to this organism of mice obtained from 31 different colonies, representing 15 different genetic types. A standardized infective dose, administered intravenously, made it possible to separate the animals into two sharply differentiated groups. All the animals of the following colonies died: Swiss Lynch, Swiss R/J, A/Jax, Princeton, RFVL, and CF1 (SPF). All the animals of the following colonies survived: CFW, ICR, Balb/C, BSVS, BRVR, RIII, YBR/He, DBA/2 (from 3 different colonies), and C57B1/6 (from 12 different colonies). The two highly inbred strains, Swiss Lynch and C57Bl/6, were selected as prototypes of susceptible and resistant animals respectively, for more detailed studies. Following injection of an infective dose of 0.2 x 10–4 ml of culture of C. kutscheri, all Swiss Lynch animals died within 3 to 11 days (the majority within 4 to 7 days); whereas all C57Bl/6 animals survived. The outcome of the infection in each strain was independent of age and sex of the animals. In Swiss Lynch animals, the corynebacteria multiplied rapidly in lungs, liver, kidneys, and to some extent in the spleen. In C57Bl/6 mice, there was no increase of the corynebacterial population in the lungs, liver, or spleen, but multiplication occurred in the kidneys during the early phase of the infectious process with resultant abscess formation. However, the renal infection soon subsided leaving no residual pathology. C. kutscheri could not be recovered from any organs of C57Bl/6 mice sacrificed 16 days after infection. Homogenates of organs from Swiss Lynch mice obtained while the infection was progressing contained only typical C. kutscheri. In contrast, the lungs and livers of similarly infected C57Bl/6 animals occasionally yielded large numbers of small translucent colonies distinctly different from those of typical corynebacteria. The use of mouse strains differing markedly in response to experimental infection with C. kutscheri is presented as a biologic model lending itself to further studies concerning factors which condition resistance to corynebacterial pseudotuberculosis, a disease of practical importance for investigators conducting experiments with murine species.

Microbial Persistence

“…This question of the microbial states during latent and dormant infections has been discussed elsewhere (6,7) and is considered in detail in a more recent report by Pierce-Chase, Fauve, and Dubos (12). The fact that these acid-fast forms were readily demonstrable at the end of therapy in those 26 wk drug regimen experiments in which there has been no revival at all, casts some doubt on the possibility that they represent revivable tubercle bacilli.…”

The Role of Complement in Resistance to Endogenous and Exogenous Infection With a Common Mouse Pathogen, Corynebacterium Kutscheri

“…This study utilizes a common mouse pathogen, Corynebacterium kutscheri, which causes an often fatal pseudotuberculosis in mice. Pierce-Chase, Fauve, and Dubos have recently demonstrated large strain differences in susceptibility to disease caused by this organism (13). The same workers also showed that corynebacterial pseudotuberculosis could be activated by the hydrocorfisone treatment of mice harboring latent C. kutscheri (14).…”

“…Saline-treated mice were sacrificed upon the death of corresponding hydrocortisone-treated mice. The kidneys, livers, lungs, hearts, and spleens of experimental and control mice were examined for the macroscopically visible yellow-white nodules characteristic of pseudotubercuiosis caused by infection with C. k~sched (13)(14)(15). Impression smears of the above named organs were stained and examined for corynebacterial-like microorganisms.…”

“…Portions of the above named organs were minced in Petri dishes using sterile technique, and incubated in veal infusion broth for 48 hr at 37°C (13). Aliquots of the broth cultures were then streaked on veal infusion agsr and incubated overnight at 37°C.…”

“…Treatment with Hydrocortisone.--Since resistance to injected C. kutsckeri is dependent upon the presence of that organism in the latent state within the host (13,14), it was suspected that both B10.D2 sublines were carriers of latent C. kutsckeri. In order to test that hypothesis, B10.D2 mice were treated with hydrocorfisone, which has been shown to activate latent C. kutsckeri and thereby to induce pseudotuberculosis (14).…”