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Chapter 28 : Regulating the Transition of Out of the Host

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Abstract:

Properly mediating the transition between host and environment is of particular importance to toxigenic , as it encounters numerous physical and biological stresses during these transitions. Interestingly, there is evidence that has evolved to preemptively prepare itself for this transition by turning off virulence genes and turning on environmental survival genes while still in the human host. This chapter focuses heavily on the genetic changes the bacterium undergoes as it transitions out of the host and into the aquatic environment. To better understand the changes in gene expression that occur during the transition out of the host, the chapter first discusses the state of gene expression prior to this transition. This prior, acute stage of infection within the small intestine is when multiplies on the epithelium and expresses virulence factors. Over the course of an infection, waterborne pathogens undergo two major transitions, environment to host and host to environment. During both of these transitions, they experience major physiochemical and nutrient stresses. The chapter focuses on the model pathogen , whose life cycle is studied in depth, and reveals fascinating adaptive and evolutionary strategies for moving between host and environment. Determination of where and how and other waterborne pathogens are persisting in the environment and the mechanisms by which they cycle between environment and host will allow us to more rationally plan public health interventions with maximum effectiveness.

Citation: McDonough E, Bradley E, Camilli A. 2013. Regulating the Transition of Out of the Host, p 566-585. In Vasil M, Darwin A (ed), Regulation of Bacterial Virulence. ASM Press, Washington, DC. doi: 10.1128/9781555818524.ch28
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Figure 1

Simple life cycle of toxigenic . cells present in contaminated freshwater sources are ingested and cause cholera in humans. The bacteria replicate in the small intestine and are shed back into the environment in rice water stool (RWS). The shed bacteria return to the aquatic environment to initiate another infection cycle. Key chemical differences between these environments are listed and measurements of the typical chemical composition of these environments are presented in Table 1 . doi:10.1128/9781555818528.ch24f1

Citation: McDonough E, Bradley E, Camilli A. 2013. Regulating the Transition of Out of the Host, p 566-585. In Vasil M, Darwin A (ed), Regulation of Bacterial Virulence. ASM Press, Washington, DC. doi: 10.1128/9781555818524.ch28
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Figure 2

Quorum sensing and starvation conditions coordinate the expression of many genes. cells are capable of monitoring their population density by production of small molecules known as autoinducers ( ). The two known autoinducers in are labeled as AI-1 and AI-2. At low cell densities, concentrations of these autoinducers are low. Under these conditions, the response regulator LuxO is phosphorylated by the Lux sensor kinases LuxQ and LuxU and the Cqs sensor kinase CqsS, leading to the production of the sRNAs ( ). The sRNAs interfere with mRNA translation, leading to reduced levels of this transcription factor. At high cell densities, autoinducers produced by the Lux and Cqs systems are present at high concentrations. Under these conditions LuxU, LuxQ, and CqsS act as phosphatases for LuxO, causing inactivation of the response regulator and lowered sRNA levels, which leads to increased levels of HapR. HapR has a number of regulator targets in , including activation of chemotaxis and flagellar genes ( ), as well as repression of ( ). AphA is a transcription factor required for transcription ( ), which encodes a membrane-bound transcription factor that is required to activate ToxT expression ( ). ToxT is the major transcriptional activator of virulence genes, and it leads to production of cholera toxin (CT) and the toxin-coregulated pilus (TCP) ( ). Stationary-phase signals at high cell density, including slowed growth and nutrient limitation, lead to increased levels of active CRP. In turn, CRP increases activation of HapR and induces activation of RpoS ( ). RpoS contributes to the activation of the chemotaxis and flagellar genes, which are hypothesized to be involved in detachment and escape from the intestinal epithelium at late times of infection ( ). RpoS also regulates genes for glycogen biosynthesis ( ) and genes important for survival in the environment ( ). doi:10.1128/9781555818524.ch28f2

Citation: McDonough E, Bradley E, Camilli A. 2013. Regulating the Transition of Out of the Host, p 566-585. In Vasil M, Darwin A (ed), Regulation of Bacterial Virulence. ASM Press, Washington, DC. doi: 10.1128/9781555818524.ch28
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Figure 3

cAMP-CRP repression and ToxT autoregulation create the bistable expression pattern of . Upon transition into a host, in vivo signals, possibly including bile salts, temperature, or pH, are sensed through TcpP/H and ToxR/S ( ). These transcription factors activate transcription of the gene from its own promoter. Subsequently, ToxT, the major virulence regulator in , induces expression from the promoter. Read-through transcription from this operon promoter, which is directly upstream of , results in an increase in mRNA and ToxT protein levels. This generates a situation where expression is amplified in a positive feedback loop, which is proposed to stochastically generate bacteria that express high levels of ToxT ( ). Stationary-phase signals, presumably sensed late in infection, are thought to be responsible for extinguishing this regulatory cascade. Carbon limitation sensed though the phosphorylated glucose-specific PTS system (PTS glu) stimulates adenylate cyclase (cya), which increases the pool of cAMP within the cell. Consequently, cAMP can bind and activate the catabolite repressor protein (CRP) ( ). The cAMP-CRP complex directly inhibits the expression of TcpP/H ( ). As illustrated in Fig. 2 , cAMP-CRP indirectly enhances the expression of HapR ( ), which also acts to indirectly reduce TcpP/H expression. It is proposed that cAMP-CRP also inhibits expression from the promoter by an undetermined mechanism ( ). This is hypothesized to dampen the ToxT autoregulatory circuit in a portion of the population (approximately 50%), leading to shutoff of virulence gene expression ( ). doi:10.1128/9781555818524.ch28f3

Citation: McDonough E, Bradley E, Camilli A. 2013. Regulating the Transition of Out of the Host, p 566-585. In Vasil M, Darwin A (ed), Regulation of Bacterial Virulence. ASM Press, Washington, DC. doi: 10.1128/9781555818524.ch28
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Figure 4

Transcriptional changes of during infection. During the course of infection, is hypothesized to undergo numerous transcriptional changes. After initial attachment, bacteria express high levels of the major virulence regulator, ToxT ( ). ToxT activates virulence and colonization genes, which allow the bacterium to elaborate the toxin-coregulated pilus (TCP) and cholera toxin (CT) ( ). Additionally, these cells exhibit fast growth ( ). As cell density increases and nutrients become limiting, HapR and cAMP-CRP are hypothesized to inhibit virulence gene expression and begin the process of exit from the small intestine ( ). While this occurs, RpoS and HapR enhance the expression of factors for chemotaxis and motility, which allow the bacteria to escape the mucosal epithelial layer ( ). As is shed in RWS, chemotaxis becomes repressed and the bacteria enter a hyperinfectious state ( ). During this transition from the intestinal mucosal layer to RWS, the bacteria regulate genes important for environmental survival ( ). The regulators important for this transition remain to be determined, although RpoS and PhoB may be key players in this transcriptional shift ( ). doi:10.1128/9781555818524.ch28f4

Citation: McDonough E, Bradley E, Camilli A. 2013. Regulating the Transition of Out of the Host, p 566-585. In Vasil M, Darwin A (ed), Regulation of Bacterial Virulence. ASM Press, Washington, DC. doi: 10.1128/9781555818524.ch28
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Figure 5

Dissemination and transmission of in areas of endemic infection. persists in the environment primarily in estuarine waters (salt concentrations greater than 0.1%) ( ). is hypothesized to persist long-term in biofilms associated with chitinous surfaces ( ) or in a viable but nonculturable state (VBNC) ( ). Weather events and disruption of freshwater ecosystems by human activity ( ) can lead to contamination of freshwater reservoirs where can survive for at least short periods ( ). Cholera epidemics begin with ingestion of from contaminated water sources. Hyperinfectious spread of freshly shed is hypothesized to rapidly amplify the number of infected patients during an outbreak ( ). Improper waste management can lead to continued contamination of drinking-water sources, which prolongs the epidemic. doi:10.1128/9781555818524.ch28f5

Citation: McDonough E, Bradley E, Camilli A. 2013. Regulating the Transition of Out of the Host, p 566-585. In Vasil M, Darwin A (ed), Regulation of Bacterial Virulence. ASM Press, Washington, DC. doi: 10.1128/9781555818524.ch28
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Tables

Generic image for table
Table 1

Comparison of physiochemical parameters of typical environments for

Citation: McDonough E, Bradley E, Camilli A. 2013. Regulating the Transition of Out of the Host, p 566-585. In Vasil M, Darwin A (ed), Regulation of Bacterial Virulence. ASM Press, Washington, DC. doi: 10.1128/9781555818524.ch28
Generic image for table
Table 2

genes induced late in the infant-mouse model of colonization

Citation: McDonough E, Bradley E, Camilli A. 2013. Regulating the Transition of Out of the Host, p 566-585. In Vasil M, Darwin A (ed), Regulation of Bacterial Virulence. ASM Press, Washington, DC. doi: 10.1128/9781555818524.ch28

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