Yersinia pestis can infect the Pawlowsky glands of human body lice and be transmitted by louse bite.

Yersinia pestis, the causative agent of plague, is a highly lethal vector-borne pathogen responsible for killing large portions of Europe's population during the Black Death of the Middle Ages. In the wild, Y. pestis cycles between fleas and rodents; occasionally spilling over into humans bitten by infectious fleas.

Role of the phospholipase D (Ymt) in the initial aggregation step of biofilm formation in the flea.

Unlabelled: Transmission of by fleas depends on the formation of condensed bacterial aggregates embedded within a gel-like matrix that localizes to the proventricular valve in the flea foregut and interferes with normal blood feeding. This is essentially a bacterial biofilm phenomenon, which at its end stage requires the production of a exopolysaccharide that bridges the bacteria together in a cohesive, dense biofilm that completely blocks the proventriculus. However, bacterial aggregates are evident within an hour after a flea ingests , and the bacterial exopolysaccharide is not required for this process.

Acid phosphatase-like proteins, a biogenic amine and leukotriene-binding salivary protein family from the flea Xenopsylla cheopis.

The salivary glands of hematophagous arthropods contain pharmacologically active molecules that interfere with host hemostasis and immune responses, favoring blood acquisition and pathogen transmission. Exploration of the salivary gland composition of the rat flea, Xenopsylla cheopis, revealed several abundant acid phosphatase-like proteins whose sequences lacked one or two of their presumed catalytic residues. In this study, we undertook a comprehensive characterization of the tree most abundant X.

and Plague: some knowns and unknowns.

Since its first identification in 1894 during the third pandemic in Hong Kong, there has been significant progress of understanding the lifestyle of , the pathogen that is responsible for plague. Although we now have some understanding of the pathogen's physiology, genetics, genomics, evolution, gene regulation, pathogenesis and immunity, there are many unknown aspects of the pathogen and its disease development. Here, we focus on some of the knowns and unknowns relating to and plague.

Characterization and CRISPR/Cas9-mediated genetic manipulation of neutrophils derived from Hoxb8-ER-immortalized myeloid progenitors.

Neutrophils represent a first line of defense against a wide variety of microbial pathogens. Transduction with an estrogen receptor-Hoxb8 transcription factor fusion construct conditionally immortalizes myeloid progenitor cells (NeutPro) capable of differentiation into neutrophils. This system has been very useful for generating large numbers of murine neutrophils for in vitro and in vivo studies.

A Role for Early-Phase Transmission in the Enzootic Maintenance of Plague.

Yersinia pestis, the bacterial agent of plague, is enzootic in many parts of the world within wild rodent populations and is transmitted by different flea vectors. The ecology of plague is complex, with rodent hosts exhibiting varying susceptibilities to overt disease and their fleas exhibiting varying levels of vector competence. A long-standing question in plague ecology concerns the conditions that lead to occasional epizootics among susceptible rodents.

Reevaluation of the Role of Blocked Oropsylla hirsuta Prairie Dog Fleas (Siphonaptera: Ceratophyllidae) in Yersinia pestis (Enterobacterales: Enterobacteriaceae) Transmission.

Prairie dogs in the western United States experience periodic epizootics of plague, caused by the flea-borne bacterial pathogen Yersinia pestis. An early study indicated that Oropsylla hirsuta (Baker), often the most abundant prairie dog flea vector of plague, seldom transmits Y. pestis by the classic blocked flea mechanism.

Integrated analysis of the sialotranscriptome and sialoproteome of the rat flea Xenopsylla cheopis.

Over the last 20 years, advances in sequencing technologies paired with biochemical and structural studies have shed light on the unique pharmacological arsenal produced by the salivary glands of hematophagous arthropods that can target host hemostasis and immune response, favoring blood acquisition and, in several cases, enhancing pathogen transmission. Here we provide a deeper insight into Xenopsylla cheopis salivary gland contents pairing transcriptomic and proteomic approaches. Sequencing of 99 pairs of salivary glands from adult female X.

Exploring and Mitigating Plague for One Health Purposes.

Purpose Of Review: In 2020, the Appropriations Committee for the U.S. House of Representatives directed the CDC to develop a national One Health framework to combat zoonotic diseases, including sylvatic plague, which is caused by the flea-borne bacterium .

Identification of a substrate-like cleavage-resistant thrombin inhibitor from the saliva of the flea Xenopsylla cheopis.

The salivary glands of the flea Xenopsylla cheopis, a vector of the plague bacterium, Yersinia pestis, express proteins and peptides thought to target the hemostatic and inflammatory systems of its mammalian hosts. Past transcriptomic analyses of salivary gland tissue revealed the presence of two similar peptides (XC-42 and XC-43) having no extensive similarities to any other deposited sequences. Here we show that these peptides specifically inhibit coagulation of plasma and the amidolytic activity of α-thrombin.

Acquisition of yersinia murine toxin enabled Yersinia pestis to expand the range of mammalian hosts that sustain flea-borne plague.

Yersinia murine toxin (Ymt) is a phospholipase D encoded on a plasmid acquired by Yersinia pestis after its recent divergence from a Yersinia pseudotuberculosis progenitor. Despite its name, Ymt is not required for virulence but acts to enhance bacterial survival in the flea digestive tract. Certain Y.

Poor vector competence of the human flea, Pulex irritans, to transmit Yersinia pestis.

Background: The human flea, Pulex irritans, is widespread globally and has a long association with humans, one of its principal hosts. Its role in plague transmission is still under discussion, although its high prevalence in plague-endemic regions and the presence of infected fleas of this species during plague outbreaks has led to proposals that it has been a significant vector in human-to-human transmission in some historical and present-day epidemiologic situations. However, based on a limited number of studies, P.

Molecular and Genetic Mechanisms That Mediate Transmission of by Fleas.

The ability to cause plague in mammals represents only half of the life history of . It is also able to colonize and produce a transmissible infection in the digestive tract of the flea, its insect host. Parallel to studies of the molecular mechanisms by which is able to overcome the immune response of its mammalian hosts, disseminate, and produce septicemia, studies of -flea interactions have led to the identification and characterization of important factors that lead to transmission by flea bite.

Comparison of the transmission efficiency and plague progression dynamics associated with two mechanisms by which fleas transmit Yersinia pestis.

Yersinia pestis can be transmitted by fleas during the first week after an infectious blood meal, termed early-phase or mass transmission, and again after Y. pestis forms a cohesive biofilm in the flea foregut that blocks normal blood feeding. We compared the transmission efficiency and the progression of infection after transmission by Oropsylla montana fleas at both stages.

Antibody Opsonization Enhances Early Interactions between Yersinia pestis and Neutrophils in the Skin and Draining Lymph Node in a Mouse Model of Bubonic Plague.

Bubonic plague results when is deposited in the skin via the bite of an infected flea. Bacteria then traffic to the draining lymph node (dLN) where they replicate to large numbers. Without treatment, this infection can result in highly fatal septicemia.

Transcriptomic profiling of the digestive tract of the rat flea, Xenopsylla cheopis, following blood feeding and infection with Yersinia pestis.

Yersinia pestis, the causative agent of plague, is a highly lethal pathogen transmitted by the bite of infected fleas. Once ingested by a flea, Y. pestis establish a replicative niche in the gut and produce a biofilm that promotes foregut colonization and transmission.

Correction: Comparative Ability of Oropsylla montana and Xenopsylla cheopis Fleas to Transmit Yersinia pestis by Two Different Mechanisms.

[This corrects the article DOI: 10.1371/journal.pntd.

Intravital Confocal Microscopy of Dermal Innate Immune Responses to Flea-Transmitted Yersinia pestis.

The technique known as intravital microscopy (IVM), when used in conjunction with transgenic mice expressing fluorescent proteins in various cell populations, is a powerful tool with the potential to provide new insights into host-pathogen interactions in infectious disease pathogenesis in vivo. Yersinia pestis, the causative agent of plague, is typically deposited in a host's skin during feeding of an infected flea. IVM has been used to characterize the innate immune response to Y.

Differential Gene Expression Patterns of and during Infection and Biofilm Formation in the Flea Digestive Tract.

Yersinia pestis, the etiologic agent of plague, emerged as a fleaborne pathogen only within the last 6,000 years. Just five simple genetic changes in the Yersinia pseudotuberculosis progenitor, which served to eliminate toxicity to fleas and to enhance survival and biofilm formation in the flea digestive tract, were key to the transition to the arthropodborne transmission route. To gain a deeper understanding of the genetic basis for the development of a transmissible biofilm infection in the flea foregut, we evaluated additional gene differences and performed transcriptional profiling of Y.

Infectious blood source alters early foregut infection and regurgitative transmission of Yersinia pestis by rodent fleas.

Fleas can transmit Yersinia pestis by two mechanisms, early-phase transmission (EPT) and biofilm-dependent transmission (BDT). Transmission efficiency varies among flea species and the results from different studies have not always been consistent. One complicating variable is the species of rodent blood used for the infectious blood meal.

"Fleaing" the Plague: Adaptations of Yersinia pestis to Its Insect Vector That Lead to Transmission.

Interest in arthropod-borne pathogens focuses primarily on how they cause disease in humans. How they produce a transmissible infection in their arthropod host is just as critical to their life cycle, however. Yersinia pestis adopts a unique life stage in the digestive tract of its flea vector, characterized by rapid formation of a bacterial biofilm that is enveloped in a complex extracellular polymeric substance.

Characterization of Interactions with Human Neutrophils .

is a gram-negative, zoonotic, bacterial pathogen, and the causative agent of plague. The bubonic form of plague occurs subsequent to deposition of bacteria in the skin by the bite of an infected flea. Neutrophils are recruited to the site of infection within the first few hours and interactions between neutrophils and have been demonstrated .

Comparative Ability of Oropsylla montana and Xenopsylla cheopis Fleas to Transmit Yersinia pestis by Two Different Mechanisms.

Background: Transmission of Yersinia pestis by flea bite can occur by two mechanisms. After taking a blood meal from a bacteremic mammal, fleas have the potential to transmit the very next time they feed. This early-phase transmission resembles mechanical transmission in some respects, but the mechanism is unknown.

Ecological Opportunity, Evolution, and the Emergence of Flea-Borne Plague.

The plague bacillus Yersinia pestis is unique among the pathogenic Enterobacteriaceae in utilizing an arthropod-borne transmission route. Transmission by fleabite is a recent evolutionary adaptation that followed the divergence of Y. pestis from the closely related food- and waterborne enteric pathogen Yersinia pseudotuberculosis A combination of population genetics, comparative genomics, and investigations of Yersinia-flea interactions have disclosed the important steps in the evolution and emergence of Y.