Quantitative Analysis of Proliferation and Excretion of Bartonella quintana in Body Lice, Pediculus humanus L.

Seki, Naomi; Kasai, Shinji; Saito, Noriko; Komagata, Osamu; Mihara, Morihiro; Sasaki, Toshinori; Tomita, Takashi; Sasaki, Tsuguo; Kobayashi, Mutsuo

doi:10.4269/ajtmh.2007.77.562

Cited by 35 publications

(47 citation statements)

References 18 publications

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“…Transmission to humans is thought to occur mostly indirectly via contaminated flea feces that are inoculated via a cat scratch ("cat scratch disease") (89). It was shown for both human body lice and cat fleas that B. quintana and B. henselae, respectively, can replicate in their digestive systems and are shed in the arthropod feces (139,145,398). More general, it is obvious that other hematophagous arthropods are capable of transmitting Bartonella as long as the bacteria can survive within these vectors and make productive contact with new host individuals.…”

Section: Host Specificitymentioning

confidence: 99%

Intruders below the Radar: Molecular Pathogenesis of Bartonella spp

2012

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SUMMARY Bartonella spp. are facultative intracellular pathogens that employ a unique stealth infection strategy comprising immune evasion and modulation, intimate interaction with nucleated cells, and intraerythrocytic persistence. Infections with Bartonella are ubiquitous among mammals, and many species can infect humans either as their natural host or incidentally as zoonotic pathogens. Upon inoculation into a naive host, the bartonellae first colonize a primary niche that is widely accepted to involve the manipulation of nucleated host cells, e.g., in the microvasculature. Consistently, in vitro research showed that Bartonella harbors an ample arsenal of virulence factors to modulate the response of such cells, gain entrance, and establish an intracellular niche. Subsequently, the bacteria are seeded into the bloodstream where they invade erythrocytes and give rise to a typically asymptomatic intraerythrocytic bacteremia. While this course of infection is characteristic for natural hosts, zoonotic infections or the infection of immunocompromised patients may alter the path of Bartonella and result in considerable morbidity. In this review we compile current knowledge on the molecular processes underlying both the infection strategy and pathogenesis of Bartonella and discuss their connection to the clinical presentation of human patients, which ranges from minor complaints to life-threatening disease.

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Section: Host Specificitymentioning

confidence: 99%

Intruders below the Radar: Molecular Pathogenesis of Bartonella spp

2012

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“…The louse excretes B. quintana in its feces during feeding, and feces containing B. quintana are inoculated into the louse bite when the human scratches the bite. B. quintana forms a biofilm-like structure in the louse feces, allowing prolonged bacterial survival within the fecal environment (9).…”

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confidence: 99%

The Bartonella quintana Extracytoplasmic Function Sigma Factor RpoE Has a Role in Bacterial Adaptation to the Arthropod Vector Environment

Abromaitis

Koehler

2013

J Bacteriol

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Bartonella quintana is a vector-borne bacterial pathogen that causes fatal disease in humans. During the infectious cycle, B. quintana transitions from the hemin-restricted human bloodstream to the hemin-rich body louse vector. Because extracytoplasmic function (ECF) sigma factors often regulate adaptation to environmental changes, we hypothesized that a previously unstudied B. quintana ECF sigma factor, RpoE, is involved in the transition from the human host to the body louse vector. The genomic context of B. quintana rpoE identified it as a member of the ECF15 family of sigma factors found only in alphaproteobacteria. ECF15 sigma factors are believed to be the master regulators of the general stress response in alphaproteobacteria. In this study, we examined the B. quintana RpoE response to two stressors that are encountered in the body louse vector environment, a decreased temperature and an increased hemin concentration. We determined that the expression of rpoE is significantly upregulated at the body louse (28°C) versus the human host (37°C) temperature. rpoE expression also was upregulated when B. quintana was exposed to high hemin concentrations. In vitro and in vivo analyses demonstrated that RpoE function is regulated by a mechanism involving the anti-sigma factor NepR and the response regulator PhyR. The ⌬rpoE ⌬nepR mutant strain of B. quintana established that RpoE-mediated transcription is important in mediating the tolerance of B. quintana to high hemin concentrations. We present the first analysis of an ECF15 sigma factor in a vector-borne human pathogen and conclude that RpoE has a role in the adaptation of B. quintana to the hemin-rich arthropod vector environment.

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“…For trial 2, the absence of B. henselae in all fleas on day 9 was anticipated and accompanied by the absence of bacteria in their feces on days 8 and 9. Similarly, in a previous study, no B. quintana DNA was detected in louse feces on either day 5, 7, 9, or 11 after infection (34).…”

Section: Discussionmentioning

confidence: 99%

“…Similarly, R. felis has recently been shown to replicate in the digestive tract of C. felis in the first stage of infection, and then to migrate to the hemolymph, disseminating to the excretory system (Malpighian tubules, hindgut, and rectal ampulla) and reproductive tissues (36). At present, the survival of B. henselae in excreted feces is estimated to last for at least 3 days in the environment (20) and could be possible because of the aggregation of the bacteria in a biofilm on the surface of the feces, as suggested for B. quintana on louse feces (34). Nevertheless, the dispersion of B. henselae within the cat flea and B. henselae excretion have not yet been fully investigated.…”

Section: Discussionmentioning

confidence: 99%

“…directly from patient tissues (30)(31)(32). The artificial membrane feeding system allowing experimental infection has also been used to investigate several vector-pathogen interactions, like those involving Xenopsylla cheopis and Yersinia pestis, Pediculus humanus and B. quintana, and Ixodes ricinus and B. henselae (5,33,34). In the case of B. henselae, it is known that its acquisition by C. felis can already occur from 3 h after the start of a contaminated blood meal (19).…”

Section: Discussionmentioning

confidence: 99%

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Assessment of Persistence of Bartonella henselae in Ctenocephalides felis

Bouhsira

Franc

Boulouis

et al. 2013

Appl Environ Microbiol

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c Bartonella henselae (Rhizobiales: Bartonellaceae) is a Gram-negative fastidious bacterium of veterinary and zoonotic importance. The cat flea Ctenocephalides felis (Siphonaptera: Pulicidae) is the main recognized vector of B. henselae, and transmission among cats and humans occurs mainly through infected flea feces. The present study documents the use of a quantitative molecular approach to follow the daily kinetics of B. henselae within the cat flea and its excreted feces after exposure to infected blood for 48 h in an artificial membrane system. B. henselae DNA was detected in both fleas and feces for the entire life span of the fleas (i.e., 12 days) starting from 24 h after initiation of the blood meal. Bartonella henselae is a Gram-negative facultative intracellular bacterium of veterinary and zoonotic importance distributed worldwide (1). At present, its major competent vector is the cat flea, Ctenocephalides felis (2). Viable B. henselae or its DNA has also been detected in several other blood-feeding arthropods, such as ticks (Dermacentor spp., Ixodes spp.) (3-6) and biting flies (Haematobia spp., Stomoxys spp.) (7); however, no evidence of the role of these insects as competent vectors exists. Cats, particularly kittens, represent the major reservoir of B. henselae (8). Infected cats are usually asymptomatic but experience chronic recurring bacteremia (9). Clinical signs observed after experimental infection of cats include febrile illness, transient anemia, neurological dysfunction, and endocarditis (10-12).In humans, B. henselae is the causative agent of cat scratch disease (CSD), a syndrome characterized by a persistent regional lymphadenopathy that is usually self-limiting within 2 to 4 months in immunocompetent patients (13). However, infected immunocompromised individuals (such as those with AIDS or organ transplant recipients) can develop severe vasoproliferative tumors known as bacillary angiomatosis and bacillary peliosis (13,14,15).Although the prevalence of B. henselae infection in cats fluctuates significantly, the highest levels of infection occur in temperate regions where conditions are most favorable for the development of C. felis (1,16,17). The seroprevalence of antibodies against B. henselae in healthy cat populations ranges from 25 to 45% throughout the world (17). Nonetheless, in North America, where C. felis is endemic, seroprevalence was reported to reach up to more than 90% in some cat colonies (18). Fleas acquire B. henselae during their blood meal on highly bacteremic cats (16). Once in the arthropod vector, the bacterium seems to replicate within the gut and is then excreted in the feces (19,20). While transmission by flea saliva still requires further investigation (21), the exposure to infected flea feces appears to be the main route of infection for cats and, accidentally, humans (22-24). B. henselae can also be inoculated into the skin of a naive host via scratching or biting by a flea-contaminated carrier animal (16,20,25).Knowledge of the kinetics of B. henselae in C. f...

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Quantitative Analysis of Proliferation and Excretion of Bartonella quintana in Body Lice, Pediculus humanus L.

Cited by 35 publications

References 18 publications

Intruders below the Radar: Molecular Pathogenesis of Bartonella spp

Intruders below the Radar: Molecular Pathogenesis of Bartonella spp

The Bartonella quintana Extracytoplasmic Function Sigma Factor RpoE Has a Role in Bacterial Adaptation to the Arthropod Vector Environment

Assessment of Persistence of Bartonella henselae in Ctenocephalides felis

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