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We report the first documented case of endocarditis in a man infected with Bartonella alsatica, which causes bacteremia in healthy wild rabbits. B. alsatica was identified by serology and culture and by PCR of an aortic valve specimen. B. alsatica should be added to the list of zoonotic agents of blood culture-negative endocarditis.
Cat scratch disease (CSD) is a frequent clinical outcome of Bartonella henselae infection in humans. Recently, two case reports indicated Bartonella clarridgeiae as an additional causative agent of CSD. Both pathogens have been isolated from domestic cats, which are considered to be their natural reservoir. B. clarridgeiae and B. henselae can be distinguished phenotypically by the presence or absence of flagella, respectively. Separation of the protein content of purified flagella of B. clarridgeiae by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and immunoblot analysis indicated that the flagellar filament is mainly composed of a polypeptide with a mass of 41 kDa. N-terminal sequencing of 20 amino acids of this protein revealed a perfect match to the N-terminal sequence of flagellin (FlaA) as deduced from the sequence of the flaA gene cloned from B. clarridgeiae. The flagellin of B. clarridgeiae is closely related to flagellins of Bartonella bacilliformis and several Bartonella-related bacteria. Since flagellar proteins are often immunodominant antigens, we investigated whether antibodies specific for the FlaA protein of B. clarridgeiae are found in patients with CSD or lymphadenopathy. Immunoblotting with 724 sera of patients suffering from lymphadenopathy and 100 healthy controls indicated specific FlaA antibodies in 3.9% of the patients' sera but in none of the controls. B. clarridgeiae FlaA is thus antigenic and expressed in vivo, providing a valuable tool for serological testing. Our results further indicate that B. clarridgeiae might be a possible etiologic agent of CSD or lymphadenopathy. However, it remains to be clarified whether antibodies to the FlaA protein of B. clarridgeiae are a useful indicator of acute infection.
Bartonella spp. have been identified as aetiological agents in culture-negative infective endocarditis (IE). Coxiella burnetii may cause chronic Q-fever with endocarditis, 334 blood samples collected from 329 patients (334 episodes) with IE diagnosed between 1984 and 1996 in Göteborg, Sweden, were investigated for antibodies to Bartonella spp. and C. burnetii. 71 of the episodes (21%) were blood culture negative. A microimmunofluorescence assay revealed immunoglobulin G (IgG) antibodies to Bartonella in 13 of the culture verified episodes and in 2 of the culture-negative episodes. Three of the patients had IgG antibodies to > or = 200 in the blood culture-verified group, but none had a titre > or = 800, the cut-off level for Bartonella endocarditis. One patient had elevated antibodies to C. burnetii, diagnosing chronic Q-fever endocarditis. In conclusion, serologically verified Bartonella endocarditis is not prevalent in western Sweden and Q-fever endocarditis is rare.
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We report a case of endocarditis in a human infected with Bartonella vinsonii subsp. berkhoffii, which causes bacteremia and endocarditis in dogs. Bacterial identification was established by PCR amplification and sequencing of an intergenic spacer region (ITS1), 16S ribosomal DNA, and a gene encoding citrate synthase (gltA). Bartonella antibodies were detected by immunofluorescence.
BACKGROUND: Cat scratch disease neuroretinitis is caused by infection by Bartonella henselae. To demonstrate B. henselae infection, serologic examination is commonly used, but sometimes serologic examination is not adequate for correct diagnosis. Here we present a case of cat scratch disease neuroretinitis confirmed by polymerase chain reaction in addition to serologic examination. CASE: A 55-year-old woman, presenting with headache and high fever, had noticed visual disturbance. The best-corrected visual acuity in her right eye was 0.01. Meningitis, optic neuritis and retinitis were observed and she was treated with oral prednisolone. After repeated questioning, the patient remembered being scratched by a cat. Systemic examination focusing on B. henselae infection was conducted and B. henselae-specific immunoglobulin (Ig) G, but not IgM, was detected in both serum and cerebrospinal fluid. To confirm B. henselae infection, polymerase chain reaction (PCR) analysis using cerebrospinal fluid was performed and the presence of B. henselae-specific DNA was demonstrated. From these results, we diagnosed cat scratch disease neuroretinitis and treated the patient with minocycline hydrochloride together with prednisolone. Following this treatment regimen, the patient's condition improved, and the best-corrected visual acuity in her right eye increased to 0.6 five months after the onset. CONCLUSION: The PCR technique is useful to correctly diagnose cat scratch disease neuroretinitis, if patients exhibit marginal data on B. henselae-specific antibody titer.
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Human bartonellosis is a classically biphasic disease caused by infection with the alpha-2 Proteobacteria Bartonella bacilliformis, which is phylogenetically related to the etiologic agents of cat scratch disease, bacillary angiomatosis, and trench fever. In Ecuador, typical bartonellosis has remained endemic for the past century in highland provinces near the Peruvian border. During the past six years, public health officials have noted an increasing number of atypical cases in which monophasic verrucous cutaneous disease is the only clinical manifestation. Epidemiologic, immunologic, histopathologic, and molecular biological studies have confirmed the presence of sporadic, atypical bartonellosis in residents of the lowland province of Manabi, where archeologic evidence exists of bartonellosis in pre-Colombian times. Between 1987 and 1995, 11 cases of cutaneous bartonellosis were investigated and serologic studies were done on 224 persons from five villages, two lowland and three highland. In the lowland village of Pajan in the province of Manabi, there was a 21% seropositivity proportion in contacts of index cases. These combined data suggest that bartonellosis is significantly under-reported due to the existence of mild clinical disease, possibly associated with less virulent bacterial strains, which are now disseminating or re-emerging in previously disease-free areas.
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Bartonella henselae is the causative agent of cat scratch disease (CSD), a self-limiting condition characterized by a subacute regional lymphadenopathy that may develop into disseminated bartonellosis in immunocompromised subjects. Mice experimentally infected with B. henselae display typical liver and spleen granulomas rich in T cells and macrophages. So far there are no data on the interaction between bartonellae and macrophages. In order to clarify this topic, we investigated the interaction of B. henselae with J774, a mouse macrophage cell line. Analysis of bacterial uptake by functional assays and transmission electron microscopy indicates that bartonellae can enter and survive inside J774. Entry occurred within 30 min postinfection and reached a plateau at 160 min. Infection of J774 was followed by a dose-dependent release of the proinflammatory cytokines tumor necrosis factor alpha, interleukin 1beta (IL-1beta), and IL-6. Bartonellae persisted intracellularly without loss of viability for at least 8 h, and their number slightly decreased 24 h postinfection. Gamma interferon (IFN-gamma) treatment of J774 significantly decreased the number of recoverable bacteria at 8 and 24 h. This enhancement of macrophage bactericidal activity was associated with nitric oxide (NO) release and was prevented by the addition of the competitive inhibitor of NO synthesis N(G)-monomethyl L-arginine. These findings suggest that IFN-gamma-mediated activation of macrophages may be important for the clearing of B. henselae infection and that anti-B. henselae microbicidal activity of IFN-gamma-activated macrophages is mediated to a large extent by NO production.
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People infected with human immunodeficiency virus (HIV) are at increased risk for bacterial infections due to HIV-associated immunologic defects. Bacterial infections were found to be, both a predictor of progression to AIDS and a substantial cause of mortality in pre-AIDS stages. Most bacterial infections are caused by Streptococcus pneumoniae, Haemophilus influenzae, Salmonella spp. and Pseudomonas aeruginosa. Rhodococcus equi, Nocardia spp., Campylobacter spp. and Bartonella spp. are less common. Data derived from two AIDS Clinical Trials Group studies showed that the most common bacterial infections were sinusitis (8.5 per 100 episodes per person years [py]), bacterial pneumonia (5.0 per 100 py), bronchitis (4.1 per 100 py) and soft tissue infections (3.5 per 100 py). In this review clinical characteristics and treatment recommendations according to data available in the literature for these infections are summarized.
Rochalimaea henselae and R. quintana are associated clinically with proliferative neovascular lesions. The effect of Rochalimaea species on human umbilical vein endothelial cell (HUVEC) proliferation and migration was evaluated in vitro. Cocultivation of Rochalimaea organisms with HUVECs resulted in enhanced HUVEC proliferation. Fibroblast proliferation was unaffected by R. henselae. HUVECs were also stimulated to migrate by Rochalimaea. When R. henselae organisms were disrupted and subjected to centrifugation, the ability to enhance HUVEC proliferation and migration was localized to the particulate, noncytosolic fraction. Trypsin treatment of this fraction diminished its stimulatory activity. These data suggest that the neovascular manifestations of infection with Rochalimaea are likely caused by the production of an angiogenic factor by these bacteria.