Infective endocarditis due to Bartonella bacilliformis associated with systemic vasculitis: a case report

Peñafiel-Sam, Joshua; Alarcón-Guevara, Samuel; Chang-Cabanillas, Sergio; Perez-Medina, Wilkerson; Mendo-Urbina, Fernando; Ordaya-Espinoza, Eloy

doi:10.1590/0037-8682-0042-2017

Cited by 12 publications

(6 citation statements)

References 10 publications

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“…Our literature search identified several other cases that also showed rapid improvement in patients with infective endocarditis and ANCA-mediated disease with the addition of immunosuppressive regimes (Table 1 ). [ 5 , 8 , 12 , 14 , 15 ] As their clinical symptoms worsened, these patients also underwent renal biopsies, which provided histologic evidence of ANCA-mediated disease, including crescentic glomerulonephritis and acute interstitial nephritis (Fig. 1 ) [ 5 , 12 , 14 , 15 ] The kidney is an organ commonly involved in infective endocarditis.…”

Section: Discussionmentioning

confidence: 99%

“…[ 5 , 8 , 12 , 14 , 15 ] As their clinical symptoms worsened, these patients also underwent renal biopsies, which provided histologic evidence of ANCA-mediated disease, including crescentic glomerulonephritis and acute interstitial nephritis (Fig. 1 ) [ 5 , 12 , 14 , 15 ] The kidney is an organ commonly involved in infective endocarditis. Biopsy of the kidney in patients with endocarditis and renal disease can reveal a variety of histologic manifestations, such as postinfectious or vasculitic glomerulonephritis, renal infarction, acute interstitial nephritis, acute tubular necrosis, and others.…”

Section: Discussionmentioning

confidence: 99%

“…For example, infective endocarditis (IE) can induce clinical manifestations of systemic vasculitis and positive ANCA tests, and thereby mimic AAV. [ 3 – 15 ] In the course of endocarditis, the development of ANCA-mediated disease introduces the dilemma of determining the best treatment approach for immune conditions, because the addition of an immunosuppressive drug to therapy in these patients may increase the risk of infection-related death. Thus, whether immunosuppressant therapy should be added to antibiotic treatment has remained controversial.…”

Section: Introductionmentioning

confidence: 99%

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Infective endocarditis mimicking ANCA-associated vasculitis: does it require immunosuppressive therapy?

Shi¹,

Shao

et al. 2020

Medicine

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Rationale: In the course of endocarditis, the development of antineutrophil cytoplasmic antibody (ANCA)-mediated disease introduces the dilemma of determining the best treatment approach for immune conditions, whether immunosuppressant therapy should be added to antibiotic treatment has remained controversial. Patient concerns: A 33-year-old man presented with progressive fever lasting for 7 months, and swelling, pain, and purpura in the arms and legs. The patient showed multiple autoantibodies including cytoplasmic ANCA, antiproteinase 3, rheumatoid factor, and anti-beta 2 glycoprotein I. Blood culture was positive for viridans streptococcus, and renal biopsy revealed glomerulonephritis and interstitial nephritis. Diagnosis: Endocarditis caused by viridans streptococci, ANCA-associated vasculitis, and congenital ventricular septal defect. Interventions: In addition to effective antibiotics, he also received twice intravenous corticosteroids and intravenous immunoglobulin therapy, and a low dose of cyclophosphamide. At last, the patient received congenital ventricular septal defect repair and debridement. Outcomes: The abnormal clinical manifestations, including renal failure and loss of strength, recovered rapidly with corticosteroid therapy in addition to antibiotic treatment. After 6 months without any medications, he remained asymptomatic and was able to live normally. Lessons: In this case with endocarditis and ANCA-associated vasculitis, we highlighted the importance of biopsy and immunosuppressive therapy. Histopathologic examination is required for diagnosis and treatment in such case. Identifying patients who have endocarditis and ANCA positivity with vasculitis pathologic features will require corticosteroid/immunosuppressives in addition to the antibiotics therapy.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Infective endocarditis mimicking ANCA-associated vasculitis: does it require immunosuppressive therapy?

Shi¹,

Shao

et al. 2020

Medicine

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“…We included six original cases of Bartonella infection and 18 patients from the literature review [7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24] . All cases are detailed in Table 1.…”

Section: Bartonella Infectionsmentioning

confidence: 99%

Bartonella and Coxiella infections presenting as systemic vasculitis: case series and review of literature

et al. 2021

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Objectives Coxiella and Bartonella sp. display particular tropism for endothelial or endocardial tissues and an abnormal host response to infections with induced autoimmunity. We aimed, through a case series combined with a comprehensive literature review, to outline characteristics of Coxiella and Bartonella infections presenting as systemic vasculitis. Methods We retrospectively included cases of definite Coxiella and Bartonella infections presenting with vasculitis features and performed a comprehensive literature review. Results Six cases of Bartonella infections were added to 18 cases from literature review. Causative pathogens were mainly B. henselae. Bartonella infection mimicked anti-neutrophil cytoplasmic antibodies (ANCA)-associated vasculitis in 83% with PR3-ANCA and presented as cryoglobulinemic vasculitis in 8%. Glomerulonephritis was present in 92%, and 88% had endocarditis. Complement fractions were low in 82% and rheumatoid factor positive in 85%. Kidney biopsies showed cell proliferation, mostly crescentic, with pauci-immune glomerulonephritis in 29%. Outcome was favorable, with the use of antibiotics alone in one third. Five cases of Coxiella infections were added to 16 from literature review. Sixteen had small-vessel vasculitides, mainly cryoglobulinemia vasculitis in 75%. One patient had polyarteritis nodosa-like vasculitis and four large-vessel vasculitis. Outcome was good except for one death. A highly sensitive next generation sequencing analysis on 3 Coxiella and 2 Bartonella-related vasculitides biopsies did not find any bacterial DNA. Conclusion Coxiella and Bartonella are both able to induce vasculitis but display distinct vasculitis features. Bartonella mimics PR3-ANCA-associated vasculitis in the setting of endocarditis, whereas Coxiella may induce vasculitis involving all vessel sizes.

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“…Clinical and biological vasculitic features are long‐recognized possible manifestations of infective endocarditis. The reported categories include cutaneous LCV, IgA vasculitis, AAV or positive proteinase 3 (PR3) or myeloperoxidase (MPO) ANCA screening. Cerebral vasculitis has been reported in association with Cardiobacterium valvarum endocarditis .…”

Section: Microbiologymentioning

confidence: 99%

Infection‐associated vasculitides

Haq

Pagnoux

2018

Int J of Rheum Dis

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Vasculitides are disorders characterized by inflammation of the vessel walls, often caused by autoimmunity, but sometimes as a result of microbial invasion. Almost all types of microbes including bacteria, viruses, protozoa and fungi have been incriminated in the pathogenesis of vasculitis. Accurate etiological diagnosis is important since immunosuppressive treatment may lead to further deterioration if infection is the cause of vasculitis. Clinical features sometimes provide clues to the etiology. Further evaluation requires a focused and cost-effective plan of laboratory investigation. The investigations aim at establishing the diagnosis of vasculitis and identify the causative organism. An accurate diagnosis of vasculitis optimally requires histological examination and imaging. For infection-associated vasculitis, the identification of the organism requires studies of stained specimens, cultures, and/or detection of antigens and antibodies. Ideally, the treatment involves administration of an appropriate antimicrobial. In non-self-limiting types of vasculitides, glucocorticoids are needed when the symptoms are progressive, with vital organs involvement, and sometimes, when there is no antimicrobial agent of proven efficacy against the incriminated agent. Additional immunosuppressive agents or interventions must be considered when the disease is severe and/or post-infective immune mechanisms are involved in the pathogenesis, e.g., severe HBV-or HCV-associated vasculitides. Available preventative vaccinations are also crucial. The incidence of HBV-associated vasculitides dramatically decreased following HBV vaccination campaigns, and other infection-associated vasculitides may as well in the future.

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Infective endocarditis due to Bartonella bacilliformis associated with systemic vasculitis: a case report

Cited by 12 publications

References 10 publications

Infective endocarditis mimicking ANCA-associated vasculitis: does it require immunosuppressive therapy?

Infective endocarditis mimicking ANCA-associated vasculitis: does it require immunosuppressive therapy?

Bartonella and Coxiella infections presenting as systemic vasculitis: case series and review of literature

Infection‐associated vasculitides

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