Effect of Streptomycin on Susceptibility of Intestinal Tract to Experimental Salmonella Infection.

Bohnhoff, Marjorie; Drake, Barbara L.; Miller, Claire A.

doi:10.3181/00379727-86-21030

Cited by 310 publications

(202 citation statements)

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“…It will be noted that the experiment with mixed inocula does not provide an answer, for it can only estimate the number of bacteria which initiate each fatal infection. The following three experiments suggest that in this system the bacteria initiating fatal infections may have been the only bacteria which passed from the gut to the tissues where they were of maximal virulence: ( a ) the resistance of mice to oral infection by the Str+ variant is greatly lowered when the normal gut flora is previously altered by giving streptomycin by mouth (Bohnhoff, Drake & Miller, 1954;Meynell, 1955). The LD50 dose of the Str+ variant of Salmonella typhimurium was decreased in this way from c. 5 x lo5 to 1.2 organisms.…”

Section: Discussionmentioning

confidence: 99%

The Applicability of the Hypothesis of Independent Action to Fatal Infections in Mice given Salmonella typhimurium by Mouth

Meynell

1957

Journal of General Microbiology

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SUMMARY:Mice were challenged by mouth with a suspension containing equal numbers of streptomycin-sensitive (Str-) and streptomycin-resistant (Str+) variants of Salmonella typhimurium. These variants were of equal virulence but the Str+ variant grew more slowly in Vivo than the Str-variant. The LD50 dose contained c. 5 x lo6 bacteria. Heart blood obtained from mice dying from many LD50 doses nearly always contained a great excess of the S t r variant, but blood from mice dying from less than one LD 50 dose contained either Str-, Str+, or a mixture of Strand Str+ variants. The appearance of the Str+ variant alone in the latter mice strongly suggests that these fatal infections were initiated by a very small number of organisms or possibly by a single organism. It is therefore concluded that these organisms were acting independently. In this system, it is likely that any bacterium which enters the tissues from the gut can initiate a fatal infection and that the probability of effecting such an entrance almost entirely determines the probability of an inoculated bacterium causing a fatal infection.The inoculation of a partially resistant host with many bacteria will often cause a fatal infection when the inoculation of one bacterium is very unlikely to do so. Of several hypotheses advanced to account for this phenomenon, the most satisfactory appears to be that described elsewhere (Meynell & Stocker, 1957) as the 'hypothesis of independent action' which postulates ( a ) that bacteria act independently after inoculation, and (b) a mean probability (1 > p > 0) per inoculated bacterium of initiating a fatal infection which is constant and unaffected by the number of bacteria inoculated. On this hypothesis therefore, there will always be a chance that the death of a host inoculated with many bacteria will be caused by the progeny of only one of the inoculated bacteria. Although many of the inoculated bacteria may multiply to some extent, the total toxic effect of their clones will never be fatal and will be negligible compared to the toxic effect of the clone descended from only one of the inoculated bacteria. The progenitor of this clone may thus be said to have initiated the fatal infection.A well-known alternative hypothesis is that of the minimal lethal dose which postulates that if the dose exceeds a critical minimum size, death is inevitable; while if it is smaller than the minimum, the host is certain to survive. Thus, a lethal dose might be supposed to saturate the host defences so that death follows the multiplication either of all the inoculated bacteria or of those bacteria not needed for saturation. I n the latter case, a fatal infection could * Present address.

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Section: Discussionmentioning

confidence: 99%

The Applicability of the Hypothesis of Independent Action to Fatal Infections in Mice given Salmonella typhimurium by Mouth

Meynell

1957

Journal of General Microbiology

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“…In 1955, Bohnhoff et al (1955) already demonstrated that mice with intact endogenous bacterial colonization require 100 000 times higher inocula to establish Salmonella enterica infection compared with streptomycin-treated mice, a mechanism known as 'colonization resistance' (Buffie and Pamer, 2013). Several mechanisms have been proposed to explain such symbiont-mediated interference with the growth of pathogens (Haine, 2008;Hamilton and Perlman, 2013).…”

Section: Introductionmentioning

confidence: 99%

Bacteria–bacteria interactions within the microbiota of the ancestral metazoan Hydra contribute to fungal resistance

et al. 2014

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Epithelial surfaces of most animals are colonized by diverse microbial communities. Although it is generally agreed that commensal bacteria can serve beneficial functions, the processes involved are poorly understood. Here we report that in the basal metazoan Hydra, ectodermal epithelial cells are covered with a multilayered glycocalyx that provides a habitat for a distinctive microbial community. Removing this epithelial microbiota results in lethal infection by the filamentous fungus Fusarium sp. Restoring the complex microbiota in gnotobiotic polyps prevents pathogen infection. Although mono-associations with distinct members of the microbiota fail to provide full protection, additive and synergistic interactions of commensal bacteria are contributing to full fungal resistance. Our results highlight the importance of resident microbiota diversity as a protective factor against pathogen infections. Besides revealing insights into the in vivo function of commensal microbes in Hydra, our findings indicate that interactions among commensal bacteria are essential to inhibit pathogen infection.

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“…It is thought that these anaerobes keep the overall density of facultative anaerobic bacteria (i.e., Enterobacteriaceae) rather low (<<10 8 cfu/g), a condition termed colonization resistance (CR) (12)(13)(14). Thus, in complex bacterial ecosystems, low densities of donor and recipient bacteria may lower the frequency of direct bacterial encounters and thus decrease the chance of conjugation-mediated HGT.…”

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confidence: 99%

Gut inflammation can boost horizontal gene transfer between pathogenic and commensal Enterobacteriaceae

Stecher

Denzler

Maier

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

409

399

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The mammalian gut harbors a dense microbial community interacting in multiple ways, including horizontal gene transfer (HGT). Pangenome analyses established particularly high levels of genetic flux between Gram-negative Enterobacteriaceae. However, the mechanisms fostering intraenterobacterial HGT are incompletely understood. Using a mouse colitis model, we found that Salmonella-inflicted enteropathy elicits parallel blooms of the pathogen and of resident commensal Escherichia coli. These blooms boosted conjugative HGT of the colicin-plasmid p2 from Salmonella enterica serovar Typhimurium to E. coli. Transconjugation efficiencies of ∼100% in vivo were attributable to high intrinsic p2-transfer rates. Plasmid-encoded fitness benefits contributed little. Under normal conditions, HGT was blocked by the commensal microbiota inhibiting contact-dependent conjugation between Enterobacteriaceae. Our data show that pathogen-driven inflammatory responses in the gut can generate transient enterobacterial blooms in which conjugative transfer occurs at unprecedented rates. These blooms may favor reassortment of plasmid-encoded genes between pathogens and commensals fostering the spread of fitness-, virulence-, and antibiotic-resistance determinants.bacterial evolution | hospital-acquired infection | mucosal immune response | plasmid spread

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Effect of Streptomycin on Susceptibility of Intestinal Tract to Experimental Salmonella Infection.

Cited by 310 publications

References 0 publications

The Applicability of the Hypothesis of Independent Action to Fatal Infections in Mice given Salmonella typhimurium by Mouth

The Applicability of the Hypothesis of Independent Action to Fatal Infections in Mice given Salmonella typhimurium by Mouth

Bacteria–bacteria interactions within the microbiota of the ancestral metazoan Hydra contribute to fungal resistance

Gut inflammation can boost horizontal gene transfer between pathogenic and commensal Enterobacteriaceae

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