Molecular Detection of Bartonella henselae for the Diagnosis of Cat Scratch Disease and Bacillary Angiomatosis of the Conjunctiva

Cornea ◽  
2011 ◽  
Vol 30 (7) ◽  
pp. 807-814 ◽  
Author(s):  
Bradley M Mitchell ◽  
Ramon L Font
Keyword(s):  
Molecular Detection ◽  
Bartonella Henselae ◽  
Cat Scratch Disease ◽  
Bacillary Angiomatosis

The Bartonella henselae sucB gene encodes a dihydrolipoamide succinyltransferase protein reactive with sera from patients with cat-scratch disease

2004 ◽  
Vol 53 (12) ◽  
pp. 1221-1227 ◽  
Author(s):  
Christine M Litwin ◽  
Joel M Johnson ◽  
Thomas B Martins
Keyword(s):  
Coxiella Burnetii ◽  
Brucella Melitensis ◽  
Bartonella Henselae ◽  
Immunoblot Analysis ◽  
Cross Reactivity ◽  
Cosmid Library ◽  
Cat Scratch Disease ◽  
Igg Antibodies ◽  
Bacillary Angiomatosis ◽  
Dihydrolipoamide Succinyltransferase

Bartonella henselae is a recently recognized pathogenic bacterium associated with cat-scratch disease, bacillary angiomatosis and bacillary peliosis. A recombinant clone expressing an immunoreactive antigen of B. henselae was isolated by screening a genomic DNA cosmid library by Western blotting with sera pooled from patients positive for B. henselae IgG antibodies by indirect immunofluorescence (IFA). The deduced amino acid sequence of the 43.7 kDa encoded protein was found to be 76.3 % identical to the dihydrolipoamide succinyltransferase enzyme (SucB) of Brucella melitensis. SucB has been shown to be an immunogenic protein during infections by Brucella melitensis, Coxiella burnetii and Bartonella vinsonii. The agreement between reactivity with a recombinant SucB fusion protein on immunoblot analysis and the results obtained by IFA was 55 % for IFA-positive sera and 88 % for IFA-negative sera. Cross-reactivity was observed with sera from patients with antibodies against Brucella melitensis, Mycoplasma pneumoniae, Francisella tularensis, Coxiella burnetii and Rickettsia typhi.

scholarly journals Development of an Immunoglobulin M Capture-Based Enzyme-Linked Immunosorbent Assay for Diagnosis of Acute Infections with Bartonella henselae

2008 ◽  
Vol 16 (2) ◽  
pp. 282-284 ◽  
Author(s):  
John G. Hoey ◽  
Fernando Valois-Cruz ◽  
Hannah Goldenberg ◽  
Yekaterina Voskoboynik ◽  
Jenna Pfiffner ◽  
...  
Keyword(s):  
Antibody Response ◽  
Immunosorbent Assay ◽  
Bartonella Henselae ◽  
Immunoglobulin M ◽  
Enzyme Linked Immunosorbent Assay ◽  
Cat Scratch Disease ◽  
Specific Enzyme ◽  
Negative Patient ◽  
Bacillary Angiomatosis ◽  
Acute Infections

ABSTRACT We describe the development of an immunoglobulin M-specific enzyme-linked immunosorbent assay for the detection of an early antibody response to Bartonella henselae, the causative agent of cat scratch disease, bacillary angiomatosis, and endocarditis. This assay discriminates between B. henselae-positive and -negative patient samples with sensitivity and specificity values of 100% and 97.1%, respectively.

scholarly journals Murine Model of Bartonella henselae Infection in the Immunocompetent Host

1998 ◽  
Vol 66 (11) ◽  
pp. 5534-5536 ◽  
Author(s):  
T. Regnath ◽  
M. E. A. Mielke ◽  
M. Arvand ◽  
H. Hahn
Keyword(s):  
Immune Response ◽  
Liver Tissue ◽  
Bartonella Henselae ◽  
Granulomatous Inflammation ◽  
Peliosis Hepatis ◽  
Cat Scratch Disease ◽  
Immunocompetent Host ◽  
Bacillary Angiomatosis ◽  
Model Following ◽  
Intraperitoneal Infection

ABSTRACT Bartonella henselae is an emerging pathogen causing cat scratch disease, bacillary angiomatosis, and peliosis hepatis. Progress in understanding the pathogenesis of and the immune response to these infections has been limited by the lack of an animal model. Following intraperitoneal infection of C57BL/6 mice withB. henselae, organs were cleared of cultivatable bacteria within 6 days. In contrast, B. henselae DNA could be detected in liver tissue for at least 3 months. Liver tissue showed granulomatous inflammation reaching its highest degree of intensity during the fourth week of infection and resolving within 12 weeks postinfection. This mouse model is applicable to the study of the pathogenesis of B. henselae and the immune response to this pathogen in the immunocompetent host.

scholarly journals Serological and molecular detection of Bartonella henselae in specimens from patients with suspected cat scratch disease in Italy: A comparative study

PLoS ONE ◽  
2019 ◽  
Vol 14 (2) ◽  
pp. e0211945 ◽  
Author(s):  
Valeria Allizond ◽  
Cristina Costa ◽  
Francesca Sidoti ◽  
Sara Scutera ◽  
Gabriele Bianco ◽  
...  
Keyword(s):  
Comparative Study ◽  
Molecular Detection ◽  
Bartonella Henselae ◽  
Cat Scratch Disease

scholarly journals Analysis of Bartonella Adhesin A Expression Reveals Differences between Various B. henselae Strains

2006 ◽  
Vol 75 (1) ◽  
pp. 35-43 ◽  
Author(s):  
Tanja Riess ◽  
Günter Raddatz ◽  
Dirk Linke ◽  
Andrea Schäfer ◽  
Volkhard A. J. Kempf
Keyword(s):  
Bartonella Henselae ◽  
Matrix Proteins ◽  
Peliosis Hepatis ◽  
Cat Scratch Disease ◽  
Head Region ◽  
Membrane Anchor ◽  
Bacillary Angiomatosis ◽  
Frameshift Deletion ◽  
Genetic Modifications ◽  
Head Neck

ABSTRACT Bartonella henselae causes cat scratch disease and the vasculoproliferative disorders bacillary angiomatosis and peliosis hepatis in humans. One of the best known pathogenicity factors of B. henselae is Bartonella adhesin A (BadA), which is modularly constructed, consisting of head, neck/stalk, and membrane anchor domains. BadA is important for the adhesion of B. henselae to extracellular-matrix proteins and endothelial cells (ECs). In this study, we analyzed different B. henselae strains for BadA expression, autoagglutination, fibronectin (Fn) binding, and adhesion to ECs. We found that the B. henselae strains Marseille, ATCC 49882, Freiburg 96BK3 (FR96BK3), FR96BK38, and G-5436 express BadA. Remarkably, BadA expression was lacking in a B. henselae ATCC 49882 variant, in strains ATCC 49793 and Berlin-1, and in the majority of bacteria of strain Berlin-2. Adherence of B. henselae to ECs and Fn reliably correlated with BadA expression. badA was present in all tested strains, although the length of the gene varied significantly due to length variations of the stalk region. Sequencing of the promoter, head, and membrane anchor regions revealed only minor differences that did not correlate with BadA expression, apart from strain Berlin-1, in which a 1-bp deletion led to a frameshift in the head region of BadA. Our data suggest that, apart from the identified genetic modifications (frameshift deletion and recombination), other so-far-unknown regulatory mechanisms influence BadA expression. Because of variations between and within different B. henselae isolates, BadA expression should be analyzed before performing infection experiments with B. henselae.

Other bacterial diseasesCat-scratch disease

2011 ◽  
Author(s):  
Michel Drancourt
Keyword(s):  
Lymph Nodes ◽  
Bartonella Henselae ◽  
Severe Disease ◽  
Formal Description ◽  
Cat Scratch Disease ◽  
Bacillary Angiomatosis ◽  
Children And Young Adults ◽  
Eye Infection ◽  
Rough Play ◽  
Spleen Enlargement

Cat-scratch disease (CSD) is a worldwide zoonoses caused by infection with the bacterium, Bartonella henselae. The formal description of the disease by Debré in 1950 (Debré et al. 1950) corresponds to the most frequently diagnosed form of the disease. Cats are the main reservoir for B. henselae and transmission is via Ctniocephalides felis. Humans usually become infected after being scratched or bitten by a cat and is most frequently seen in children and young adults.CSD is a self-limiting illness which often begins with a small papule developing at the site of cat scratch or bite within 3-14 days of the infection. Nearby lymph nodes, usually neck, axillary or groin, become swollen and can persist for several months. It may take up to 7 weeks for the enlarged lymph nodes to appear and individuals may not recall any cat scratch or bite. In healthy cases antibiotics are not indicated.About 5-10% of patients may develop other forms of CSD including eye infection characterised by conjunctivitis and swollen lymph nodes, rash, liver and spleen enlargement, and more rarely encephalitis. Immunosuppresed patients may develop more severe disease, such as bacillary angiomatosis.General advice for preventing CSD includes avoiding rough play with cats, particularly kittens. Cat scratches and bites should be washed immediately with water and soap and cats should not be allowed to lick open wounds.

scholarly journals Bartonella henselae Persistence within Mesenchymal Stromal Cells Enhances Endothelial Cells Activation and Infectability Amplifying the Angiogenic Process.

2021 ◽  
Author(s):  
Scutera Sara ◽  
Mitola Stefania ◽  
Sparti Rosaria ◽  
Salvi Valentina ◽  
Grillo Elisabetta ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Mesenchymal Stromal Cells ◽  
Stromal Cells ◽  
Cytokine Production ◽  
Bartonella Henselae ◽  
Antimicrobial Properties ◽  
Cat Scratch Disease ◽  
Angiogenic Potential ◽  
Bacillary Angiomatosis

Some bacterial pathogens can manipulate the angiogenic response, suppressing or inducing it for their own ends. In humans, B. henselae is associated with cat-scratch disease and vasculoproliferative disorders such as bacillary angiomatosis and bacillary peliosis. Although endothelial cells (ECs) support the pathogenesis of Bartonella , the mechanisms by which Bartonella induces EC activation are not completely clear, as well as the possible contribution of other cells recruited at the site of infection. Mesenchymal stromal cells (MSCs) are endowed with angiogenic potential and play a dual role in infections exerting antimicrobial properties but also acting as a shelter for pathogens. Here we delved into the role of MSCs as reservoir of Bartonella and modulator of EC functions. B. henselae readily infected MSCs and survived in perinuclear bound vacuoles for up to 8 days. Infection enhanced MSC proliferation and the expression of EGFR, TLR2 and NOD1, proteins that are involved in bacterial internalization and cytokine production. Secretome analysis revealed that infected MSCs secreted higher levels of the proangiogenic factors VEGF, FGF-7, MMP-9, PIGF, serpin E1, TSP-1, uPA, IL-6, PDGF-D, CCL5 and CXCL8. Supernatants from B. henselae -infected MSCs increased the susceptibility of ECs to B. henselae infection and enhanced EC proliferation, invasion and reorganization in tube-like structures. Altogether, these results candidate MSCs as a still underestimated niche for B. henselae persistent infection and reveal a MSC-EC crosstalk that may contribute to exacerbate bacterial-induced angiogenesis and granuloma formation.

scholarly journals Bartonella henselae Induces NF-κB-Dependent Upregulation of Adhesion Molecules in Cultured Human Endothelial Cells: Possible Role of Outer Membrane Proteins as Pathogenic Factors

2001 ◽  
Vol 69 (8) ◽  
pp. 5088-5097 ◽  
Author(s):  
Oliver Fuhrmann ◽  
Mardjan Arvand ◽  
Alexander Göhler ◽  
Michael Schmid ◽  
Matthias Krüll ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Outer Membrane ◽  
Adhesion Molecule ◽  
Cell Activation ◽  
Bartonella Henselae ◽  
Outer Membrane Proteins ◽  
Adhesion Molecule Expression ◽  
Cat Scratch Disease ◽  
Bacillary Angiomatosis

ABSTRACT The endothelium is a specific target for Bartonella henselae, and endothelial cell infection represents an important step in the pathogenesis of cat scratch disease and bacillary angiomatosis. Mechanisms of Bartonella-endothelial cell interaction as well as signaling pathways involved in target cell activation were analyzed. B. henselae strain Berlin-1, isolated from bacillary angiomatosis lesions of a human immunodeficiency virus-infected patient, potently stimulated human umbilical cord vein endothelial cells (HUVEC), as determined by NF-κB activation and enhanced adhesion molecule expression. These effects were accompanied by increased PMN rolling on and adhesion to infected endothelial cell monolayers, as measured in a parallel-plate flow chamber assay. Monoclonal antibodies against E-selectin significantly reduced PMN rolling and adhesion. In our hands, B. henselae Berlin-1 was substantially more active than the typing strain B. henselae ATCC 49882. E-selectin and ICAM-1 upregulation occurred for up to 9 days, as verified by Northern blotting and cell surface enzyme-linked immunosorbent assay. Induction of adhesion molecules was mediated via NF-κB activation and could be blocked by a specific NF-κB inhibitor. Additional studies indicated that B. henselae-induced effects did not require living bacteria or Bartonella lipopolysaccharides. Exposure of HUVEC to purified B. henselae outer membrane proteins (OMPs), however, reproduced all aspects of endothelial cell activation. In conclusion, B. henselae, the causative agent of cat scratch disease and bacillary angiomatosis, infects and activates endothelial cells. B. henselae OMPs are sufficient to induce NF-κB activation and adhesion molecule expression followed by enhanced rolling and adhesion of leukocytes. These observations identify important new properties of B. henselae, demonstrating its capacity to initiate a cascade of events culminating in a proinflammatory phenotype of infected endothelial cells.

Bacillary Angiomatosis

1995 ◽  
Vol 104 (8) ◽  
pp. 668-672 ◽  
Author(s):  
John G. Batsakis ◽  
Jae Y. Ro ◽  
Elizabeth E. Frauenhoffer
Keyword(s):  
Head And Neck ◽  
Acquired Immunodeficiency Syndrome ◽  
Opportunistic Infections ◽  
Epidemiologic Studies ◽  
Cat Scratch Disease ◽  
Bacterial Agent ◽  
Bacillary Angiomatosis ◽  
Mucous Membranes ◽  
Acquired Immunodeficiency ◽  
Immunodeficiency Syndrome

The acquired immunodeficiency syndrome and other causes of immunosuppression have ushered in a variety of opportunistic infections. One of these is bacillary angiomatosis, a vasoproliferative lesion whose principal causative agent is Rochalimaea henselae. Bacillary angiomatosis, while preponderantly a cutaneous affliction, can be systemic, including involvement of the head and neck mucous membranes. Molecular technology and epidemiologic studies used to identify the bacterial agent of bacillary angiomatosis have also uncovered R henselae as the organism responsible for most cases of cat-scratch disease. Why the same organism promotes two different histopathologic lesions, as seen in bacillary angiomatosis and cat-scratch disease, is unknown.

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