Pathology, Diagnosis, and Treatment of Anthrax in Humans

Guarner, Jeannette; Rı́o, Carlos del

doi:10.1002/9780470891193.ch13

Cited by 5 publications

(3 citation statements)

References 61 publications

(76 reference statements)

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“…Since the host environment changes with the progression of infection, it would be of interest to investigate gene expression under such conditions. For instance, inhalational anthrax can cause dyspnea ( 62 , 63 ), which could result in hypoxemia and hypercapnia ( 64 , 65 ). Whereas we performed transcriptomic profiling under a high-CO 2 environment, analysis under other host-like environments during infection or directly from the infected host ( 66 ) would provide insightful information.…”

Section: Discussionmentioning

confidence: 99%

Direct Regulons of AtxA, the Master Virulence Regulator of Bacillus anthracis

et al. 2021

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Section: Discussionmentioning

confidence: 99%

Direct Regulons of AtxA, the Master Virulence Regulator of Bacillus anthracis

et al. 2021

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“…The eschars develop from small painless, itchy lesions that occur about 3 to 5 days after infection [16,17]. These lesions will then develop edema and later develop a black necrotic center, known as an eschar [17,18]. After the appearance of the eschar, the host will present with fever, malaise, and lymphadenitis [18].…”

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confidence: 99%

“…These lesions will then develop edema and later develop a black necrotic center, known as an eschar [17,18]. After the appearance of the eschar, the host will present with fever, malaise, and lymphadenitis [18].…”

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confidence: 99%

Opening moves: early events in anthrax pathogenesis and their consequences for dissemination

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Bacillus anthracis is a Gram positive sporulating bacterium that is the causative agent of anthrax. Early steps in dissemination are understudied due to the asymptomatic and asynchronous nature of B. anthracis infections. The goals of these studies are to establish a model of the early steps of B. anthracis infections and examine how the initial site of infection and exotoxin production affect bacterial dissemination. In these studies, a mouse model was used in combination with a bioluminescent signature tagged library to determine how B.anthracis disseminates through the host and the roles of an exotoxin component, lethal factor, in colonization and dissemination. This library allowed for real time observation of dissemination and analysis of bacterial population dynamics. In the first set of experiments, mice were infected via inhalational or subcutaneous routes with the tagged library to determine how the bacterial population changed during dissemination. In inhalational and subcutaneous infections, the disseminated population was comprised of a small subset of the original library.This indicated the presence of a population bottleneck, a random decrease in genetic diversity during the infection. Surprisingly, the diminishment and location of the bottleneck varied depending on the initial site of infection. This suggested B. anthracis exploits multiple host environments and some sites may be more permissive for dissemination than others. In the second set of experiments, mice were infected with a signature tagged library where a portion of clones lacked lethal factor. Lethal factor is known to be an important virulence factor as deletion results in attenuated or complete loss of virulence in most animal models. Host survival increased when < 10% of the library produced lethal factor, but few other differences were observed. Furthermore, decreases in the proportion of lethal factor producing clones led to fewer clones disseminating. These findings suggest that a threshold of lethal factor must be ii produced for colonization and dissemination to occur in vivo. In total, this work provides an understanding of how B. anthracis is able to rapidly disseminate from a several tissues and gives insights in where future therapeutics should be focused to reduce disease incidence.iii

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