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An Extracellular Polysaccharide Locus Required for Transmission of Bordetella bronchiseptica.

ABSTRACT: Background:The lack of animal models to experimentally study how infectious agents transmit between hosts limits our understanding of what makes some pathogens so contagious. Methods:We recently developed a Bordetella bronchiseptica mouse model to study transmission and have used it to assess, for the first time, which of several well-studied "virulence factors" common to classical Bordetella species contribute to transmission. Results:Among 13 mutants screened, a mutant lacking an extracellular polysaccharide (EPS) locus consistently failed to transmit. The loss of EPS had no obvious effect on in vitro characteristics of growth, adherence, cytotoxicity, or serum resistance, though it profoundly reduced the ability of the mutant to colonize the lower respiratory tract of mice. While wild-type B. bronchiseptica was shed from colonized mice and efficiently transmitted to cage-mates, the mutant colonized less efficiently, shed at lower numbers, and consequently did not transmit to naive animals. Conclusions:These results have important implications for potential roles of polysaccharides in the pathogenesis and transmission of Bordetella species as well as other respiratory pathogens. Cases of pertussis (whooping cough) caused by Bordetella pertussis are on the rise, and understanding factors that contribute to their spread is critical to its control.

SUBMITTER: Dewan KK

PROVIDER: S-EPMC5853889 | biostudies-literature | 2017 Oct

REPOSITORIES: biostudies-literature

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An Extracellular Polysaccharide Locus Required for Transmission of Bordetella bronchiseptica.

Dewan Kalyan K KK Taylor-Mulneix Dawn L DL Hilburger Lindsay J LJ Rivera Israel I Preston Andrew A Harvill Eric T ET

The Journal of infectious diseases 20171001 7

<h4>Background</h4>The lack of animal models to experimentally study how infectious agents transmit between hosts limits our understanding of what makes some pathogens so contagious.<h4>Methods</h4>We recently developed a Bordetella bronchiseptica mouse model to study transmission and have used it to assess, for the first time, which of several well-studied "virulence factors" common to classical Bordetella species contribute to transmission.<h4>Results</h4>Among 13 mutants screened, a mutant la ...[more]

PMID: 28973366

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Project description:Whooping cough is resurging in the United States despite high vaccine coverage. The rapid rise of Bordetella pertussis isolates lacking pertactin (PRN), a key vaccine antigen, has led to concerns about vaccine-driven evolution. Previous studies showed that pertactin can mediate binding to mammalian cells in vitro and act as an immunomodulatory factor in resisting neutrophil-mediated clearance. To further investigate the role of PRN in vivo, we examined the functions of pertactin in the context of a more naturally low dose inoculation experimental system using C3H/HeJ mice that is more sensitive to effects on colonization, growth and spread within the respiratory tract, as well as an experimental approach to measure shedding and transmission between hosts. A B. bronchiseptica pertactin deletion mutant was found to behave similarly to its wild-type (WT) parental strain in colonization of the nasal cavity, trachea, and lungs of mice. However, the pertactin-deficient strain was shed from the nares of mice in much lower numbers, resulting in a significantly lower rate of transmission between hosts. Histological examination of respiratory epithelia revealed that pertactin-deficient bacteria induced substantially less inflammation and mucus accumulation than the WT strain and in vitro assays verified the effect of PRN on the induction of TNF-α by murine macrophages. Interestingly, only WT B. bronchiseptica could be recovered from the spleen of infected mice and were further observed to be intracellular among isolated splenocytes, indicating that pertactin contributes to systemic dissemination involving intracellular survival. These results suggest that pertactin can mediate interactions with immune cells and augments inflammation that contributes to bacterial shedding and transmission between hosts. Understanding the relative contributions of various factors to inflammation, mucus production, shedding and transmission will guide novel strategies to interfere with the reemergence of pertussis.

Dataset Information

An Extracellular Polysaccharide Locus Required for Transmission of Bordetella bronchiseptica.

Publications

An Extracellular Polysaccharide Locus Required for Transmission of Bordetella bronchiseptica.

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