Infection of Fetal Feline Brain Cells in Culture with<i>Bartonella henselae</i>

Muñana, Karen R.; Vitek, Susanne M.; Hegarty, Barbara C.; Kordick, Dorsey L.; Breitschwerdt, Edward B.

doi:10.1128/iai.69.1.564-569.2001

Cited by 21 publications

(17 citation statements)

References 36 publications

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“…B. henselae can invade and colonize human dendritic cells, CD34 progenitor cells, erythrocytes, and vascular endothelial cells (14,28). In vitro intracellular infection of feline microglial cells has also been demonstrated previously (31). In a previous study involving a patient with classical CSD accompanied by encephalopathy, B. henselae DNA was amplified from an epitrochlear mass and from the cerebrospinal fluid (18).…”

Section: Discussionmentioning

confidence: 72%

Bartonella sp. Bacteremia in Patients with Neurological and Neurocognitive Dysfunction

et al. 2008

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We detected infection with a Bartonella species (B. henselae or B. vinsonii subsp. berkhoffii) in blood samples from six immunocompetent patients who presented with a chronic neurological or neurocognitive syndrome including seizures, ataxia, memory loss, and/or tremors. Each of these patients had substantial animal contact or recent arthropod exposure as a potential risk factor for Bartonella infection. Additional studies should be performed to clarify the potential role of Bartonella spp. as a cause of chronic neurological and neurocognitive dysfunction.Bartonella henselae causes a prototypical illness characterized by fever and regional lymphadenopathy following a cat scratch or bite (8, 9). Cat scratch disease (CSD) is usually self-limited, and antibiotic therapy has minimal impact on the clinical course (11, 34). However, a spectrum of neurological manifestations, including ischemic stroke, cerebral arteritis, transverse myelitis, radiculitis, grand mal seizures, epilepsia partialis continua, status epilepticus, coma, and fatal encephalitis, in patients with CSD have been described previously (21,34). Chronic neurological or neurocognitive syndromes associated with persistent Bartonella bacteremia are less well characterized. Neurological symptoms following a cat scratch have also been described in association with B. quintana infection, and recent evidence indicates that cats can harbor B. quintana (6,13,32,37).Although CSD is considered to be self-limiting, persistent intravascular infection of a child with B. henselae for 4 months after a cat scratch has been reported previously (2). Furthermore, we recently described chronic intravascular infection with both B. henselae and B. vinsonii subsp. berkhoffii in immunocompetent people with occupational animal contact and arthropod exposure (5). Cats are the primary reservoir hosts for B. henselae, whereas to date, B. vinsonii subsp. berkhoffii has been isolated only from dogs, coyotes, foxes, or people (9, 27). Domestic and wild canines serve as the primary environmental reservoir for B. vinsonii subsp. berkhoffii, and dogs can be involved in the transmission of B. vinsonii subsp. berkhoffii and B. henselae to people (7,9,10,27,36).In this study, we report the isolation of B. henselae or B. vinsonii subsp. berkhoffii from, or the molecular detection of these pathogens in, blood samples from six people who exhibited a spectrum of neurological and neurocognitive abnormalities. MATERIALS AND METHODSBlood and serum samples from six individuals and cerebrospinal fluid from one patient were submitted by an attending physician to the Intracellular Pathogens Research Laboratory, Center for Comparative Medicine and Translational Research, College of Veterinary Medicine, North Carolina State University, Raleigh, for attempted isolation of a Bartonella species. We used a previously described approach incorporating preenrichment culture of blood in BartonellaAlphaproteobacteria growth medium (BAPGM) and PCR (16). Bacterial isolation, PCR amplification, and cloning were p...

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Section: Discussionmentioning

confidence: 72%

Bartonella sp. Bacteremia in Patients with Neurological and Neurocognitive Dysfunction

et al. 2008

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“…Based on in vitro studies using B. henselae as a prototypical representative of the genus, viable intracellular infection has been documented in several macrophage-like cells, including monocytes, dendritic cells, and microglial cells. [30][31][32] Therefore, based upon previous studies, Bartonella sp. may localize within splenic histiocytes and endothelial cells, but DNA also could be amplified from erythrocytes circulating through the spleen at the time of sample collection.…”

Section: Discussionmentioning

confidence: 97%

“…Based on in vitro studies using B . henselae as a prototypical representative of the genus, viable intracellular infection has been documented in several macrophage‐like cells, including monocytes, dendritic cells, and microglial cells . Therefore, based upon previous studies, Bartonella sp.…”

Section: Discussionmentioning

confidence: 99%

Molecular Prevalence ofBartonella,Babesia, and HemotropicMycoplasmasp. in Dogs with Splenic Disease

Varanat¹,

Maggi²,

Linder

et al. 2011

Veterinary Internal Medicne

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Background: Among diseases that cause splenomegaly in dogs, lymphoid nodular hyperplasia (LNH), splenic hemangiosarcoma (HSA), and fibrohistiocytic nodules (FHN) are common diagnoses. The spleen plays an important role in the immunologic control or elimination of vector-transmitted, blood-borne pathogens, including Bartonella sp., Babesia sp., and hemotropic Mycoplasma sp.Objective: To compare the prevalence of Bartonella sp., Babesia sp., and hemotropic Mycoplasma sp. DNA in spleens from dogs with LNH, HSA, and FHN.Materials and Methods: Paraffin-embedded, surgically obtained biopsy tissues from LNH (N = 50), HSA (N = 50), and FHN (N = 37) were collected from the anatomic pathology archives. Spleens from specific pathogen-free (SPF) dogs (N = 8) were used as controls. Bartonella sp., Babesia sp., and Mycoplasma sp. DNA was amplified by PCR, followed by DNA sequencing.Results: Bartonella sp. DNA was more prevalent in FHN (29.7%) and HSA (26%) as compared to LNH (10%) (P = .019, .0373, respectively) or control spleens (0.0%). The prevalence of Babesia sp. and hemotropic Mycoplasma sp. DNA was significantly lower than Bartonella sp. DNA in HSA (P = .0005, .006, respectively) and FHN (P = .003, .0004, respectively). There was no statistically significant difference in DNA prevalence among the 3 genera in the LNH group.Conclusions: The higher prevalence of Bartonella sp. in FHN and HSA warrants future investigations to determine if this bacterium plays a role in the development of these splenic diseases.

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“…A number of in vitro studies showed that B. henselae can invade diverse cell types such as endothelial cells (120), endothelial progenitor cells (376), epithelial cells (24), hematopoietic progenitor cells (274), monocytes/macrophages (223, 309) (including microglial cells [307]), and even tick cells (40). The ability to manipulate such a variety of cell types is very likely to contribute to the highly diverse illness with a plethora of different symptoms that can arise in human patients suffering from systemic cat scratch disease.…”

Section: The Primary Nichementioning

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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Infection of Fetal Feline Brain Cells in Culture withBartonella henselae

Cited by 21 publications

References 36 publications

Bartonella sp. Bacteremia in Patients with Neurological and Neurocognitive Dysfunction

Bartonella sp. Bacteremia in Patients with Neurological and Neurocognitive Dysfunction

Molecular Prevalence ofBartonella,Babesia, and HemotropicMycoplasmasp. in Dogs with Splenic Disease

Intruders below the Radar: Molecular Pathogenesis of Bartonella spp

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