Cat Scratch to Vascular Damage: A Rare Case of Bartonella‐Induced Large Vessel Vasculitis

Although Bartonella henselae, the causative agent of cat scratch disease, has been associated with various systemic inflammatory conditions and small-vessel vasculitis—particularly mimicking ANCA-associated vasculitis or presenting in the context of infective endocarditis—large vessel vasculitis (LVV) related to B. henselae has not been reported in the pediatric population to date. Here, we present a pediatric case with a history of cat exposure and confirmed B. henselae infection who subsequently developed large vessel vasculitis during follow-up. This case highlights the need to consider infectious triggers, including Bartonella, in the differential diagnosis of pediatric LVV. A 12-year-old girl was admitted with a 1-month history of right axillary swelling and painful skin lesions on her lower extremities. Approximately 1.5 months prior to admission, she had been scratched by an unvaccinated stray cat. At the time of the incident, she was asymptomatic and received tetanus and rabies prophylaxis. Due to axillary lymphadenopathy, she was prescribed oral amoxicillin-clavulanic acid for 1 week. On admission, her vital signs were as follows: body temperature 36.8°C, heart rate 92 bpm, respiratory rate 18 breaths/min, and blood pressure 110/70 mmHg. On physical examination, ultrasonography revealed a 15 × 40 mm right axillary lymphadenopathy. Purple, painless, non-edematous lesions consistent with erythema nodosum were observed on the anterior tibial surfaces of both legs. Bilateral radial pulses were palpable and symmetric. No bruits were detected on auscultation of the neck or chest. Laboratory findings showed elevated acute phase reactants, with an erythrocyte sedimentation rate (ESR) of 73 mm/h and C-reactive protein (CRP) of 10 mg/L (normal: 0–5 mg/L). Complete blood count revealed a hemoglobin level of 12 g/dL, white blood cell count of 8310/μL, and platelet count of 492 000/μL—all within normal limits. Liver and kidney function tests were normal. Bartonella serology showed IgG positive and IgM negative; antinuclear antibody (ANA) was negative. Initial cervical ultrasonography revealed significant vascular wall thickening in the right common carotid artery, suggestive of vasculitis (Figure 1a: longitudinal view; Figure 1b: transverse view). MRI and Doppler studies demonstrated diffuse wall thickening in the right common carotid artery and minimal pleural effusion. Echocardiography showed a patent foramen ovale (PFO). Thoracoabdominal CT angiography revealed diffuse concentric wall thickening extending from the proximal segment of the superior mesenteric artery to the level of the celiac trunk bifurcation, consistent with vascular involvement. At the 4-week follow-up, the IgG titer had increased threefold. The patient was hospitalized for targeted antibiotic therapy and management of vasculitis secondary to Bartonella infection. Initial treatment with azithromycin was switched to doxycycline, rifampin, and teicoplanin due to insufficient response. Vasculitis treatment included a 3-day pulse of methylprednisolone, followed by maintenance therapy with prednisolone (40 mg/day) and azathioprine (75 mg/day). Following 14 days of teicoplanin and 28 days of doxycycline and rifampin, along with corticosteroid and azathioprine therapy, the patient's clinical condition stabilized, and follow-up imaging demonstrated regression of the lymphadenopathy. At the 3-month follow-up, ultrasonography showed complete resolution of the previously identified vascular involvement (Figure 2). The vascular wall thickening had resolved, with no signs of inflammation or luminal narrowing. Concurrently, the patient's acute phase reactants, including ESR and CRP, had returned to normal levels under the ongoing treatment regimen. At the 6-month follow-up, control CT imaging confirmed complete resolution of the vascular findings, and corticosteroid therapy was discontinued. Although Bartonella henselae is most frequently associated with benign lymphadenopathy, it has been increasingly recognized as a potential trigger for systemic inflammatory responses, including vasculitis. Most reported cases of Bartonella-associated vasculitis involve small vessels and are frequently linked with infective endocarditis, glomerulonephritis, or ANCA-associated vasculitis-like syndromes. Beydon et al. [1] reviewed 16 patients with Bartonella or Coxiella infections who presented with systemic vasculitis; the majority had small-vessel involvement, and only a few exhibited larger vessel abnormalities [1]. Notably, large vessel vasculitis related to Bartonella remains exceedingly rare, especially in children. A similar observation was reported by Houpikian et al. (2005), who described Bartonella as a rare but important cause of culture-negative endocarditis, with associated immune-mediated vasculitic features [2]. Similarly, Fishman et al. (2022) presented a case of Bartonella henselae prosthetic valve endocarditis mimicking p-ANCA-associated necrotizing glomerulonephritis. The patient developed renal and cardiac involvement severe enough to require temporary dialysis, illustrating how Bartonella infection can imitate systemic autoimmune vasculitis, complicating diagnosis and management [3]. To date, the literature contains very limited reports of pediatric LVV potentially triggered by Bartonella infection. In our case, Bartonella infection was confirmed through the development of a compatible clinical picture and a subsequent increase in IgG titers on serial testing. Laboratory findings supported systemic inflammation, and imaging revealed localized vascular involvement. Interestingly, the vascular inflammation was localized to the right common carotid artery, the same side as the axillary lymphadenopathy and the presumed site of the cat scratch. This laterality is consistent with Bartonella's tendency to cause regionalized manifestations, such as lymphadenopathy near the site of inoculation. The literature gives mixed messages about both the best treatment and how long it should be continued [1]. In practice, management really depends on how severe the disease is and on the treating clinician's judgment [4]. For patients with milder signs, a short course of corticosteroids can be helpful [5] When there is a pauci-immune glomerulonephritis–type picture, plasma exchange or cyclophosphamide may be needed [6]. Even in these more serious cases, steroids are usually tapered quickly [4]. In our patient, we also chose to keep corticosteroid use shorter than is typical for other LVV. As for azathioprine, there is no clear evidence on the ideal duration, but we plan to review the need for ongoing therapy and consider stopping it at around 1 year. This case underscores the potential severity of Bartonella infections, particularly when complicated by large vessel vasculitis, and highlights the critical role of a multidisciplinary team, including rheumatologists, infectious disease specialists, and radiologists, in the management of such cases. In this patient, a combination of antibiotic therapy and immunosuppressive treatment proved to be effective in stabilizing the condition. Hulya Ercan Emreol and Veysel Cam were involved in the clinical evaluation of the patient, data collection, and interpretation of the findings. Veysel Cam contributed to the literature review and drafted the initial version of the manuscript. Ozge Basaran supervised the study, critically revised the manuscript for important intellectual content, and served as the corresponding author. All authors read and approved the final version of the manuscript. The authors declare no conflicts of interest. The data that support the findings of this study are available on request from the corresponding author.