First Report of Micrococcus luteus Native Valve Endocarditis Complicated With Pulmonary Infarction in a Pediatric Patient: Case Report and Literature Review

To the Editors: A 9-year-old girl affected by anti-MOG positive bilateral optic neuropathy, treated during the acute phase with methylprednisolone, prednisone and plasmapheresis and in preventive treatment since July 2019 with monthly Intravenous Immunoglobulin infusions, has been transferred to our Pediatric Department for a Micrococcus Luteus-positive endocarditis and a pulmonary thrombo-embolic infarct (see Figure 1; Video, Supplemental Digital Content 1, https://links.lww.com/INF/E418). The source of infection was a port-a-cath CVC positioned for the Immunoglobulin infusions. Clinical history started in summer 2020 with low-grade fever, diarrhea and vomiting with pain in the region of the catheter and increase in inflammatory markers. A transesophageal echocardiogram (TEE) showed the catheter in an endocavitary position with a big atrial eversion (suspected kinking) that reached the tricuspid valvular plane; it also described an isoechoic, homogeneous image, fixed on the right atrial floor at the outlet of the inferior vena cava, measuring approximately 0.6 cm, compatible with a thrombus (Figure 1A and 1C). Empirical therapy with Ceftriaxone and Vancomycin was started and subsequently continued with Vancomycin and Meropenem. Prophylactic antithrombotic therapy with enoxaparin was introduced, and the catheter was removed. Cultures of both the tip and the medial part positive for Micrococcus Luteus. Therapy with vancomycin was continued intravenously at a daily dosage of 2 g, with measurements of vancomycin trough levels (target value 15–20 µg/mL). Therapy with piperacillin/tazobactam was started at a dosage of 100 mg/kg every 6 hours. The newly performed thoracic angio-CT scan showed a defective opacification of the arterial branches of the anterior, lateral and posterior segments of the right inferior lobe, occluded by hypoechoic material of embolic nature; a further filling defect due to pulmonary embolism was described at the level of the bifurcation of the medium lobar branch into its dorsal apical and posterior basal segments. Hypoechoic areas of necrotic nature were detected in the dorsal apical and posterior basal segments (Figure 1D). Due to pulmonary embolism, enoxaparin dose was switched from prophylactic to therapeutic. A screening for thrombophilia gave negative results. The follow-up tests showed increased creatininemia (from 0.6 to 1.03 mg/dL) and proteinuria. Due to a suspected vancomycin-related acute renal toxicity, daily administration of the drug was adjusted and subsequently definitively suspended after approximately 4 total weeks of therapy. Predischarge TEE no longer documented the mobile sessile thrombotic formation in the right atrium located in the sinus between the Eustachian and the Thebesian valve, described previously, thus highlighting a remission of endocarditis.FIGURE 1.: Right atrial thrombus attached to the atrial wall. A: Transesophageal echocardiographic image of the right atrium (bicaval view) demonstrating a clot (arrow) adherent to the wall of the recess between EV and Tebesio valve. B: Transesophageal echocardiographic image after 25 days demonstrating persistence of the clot (arrow) although smaller in size. C: Transesophageal echocardiographic image after 10 days demonstrating the complete resolution of the clot. D: Pulmonary infarction on chest computed tomography. EV indicates Eustachian valve; IVC, inferior vena cava.Micrococcus Luteus is rarely a cause of infective endocarditis. Only 18 cases on prosthetic valve have been described (more common as Micrococcus has the ability to form a biofilm on the prosthetic material),1 1 case of a native mitral valve in a patient with multiple risk factors2 and 2 on native aortic valve in patients receiving immunosuppressive therapy.3,4 Thus, this is the first pediatric case of endocarditis due to Micrococcus Luteus described in the literature. There is currently no therapeutic protocol for Micrococcus luteus endocarditis; however, according to previous cases reported in the literature and in consideration of the antimicrobial susceptibility, it is believed that the treatment of choice is vancomycin in combination with rifampicin.5 Empirical therapy with vancomycin seemed to have solved the infectious picture in our child; however, it was necessary to adjust the dose of the drug due to the development of acute renal damage, up to suspension before the completion of the 4 weeks of therapy. Native valve endocarditis related to atypical pathogens is uncommon in pediatric practice; however, due to the increasing complexity and chronicity of pediatric patients related to both diagnostic and therapeutic improvements (eg, chronic immunosuppressive therapies and use of invasive devices, as happened in our case), facing unusual scenarios are becoming more frequent. This case shows the effectiveness of our treatment, thus providing a new source of supporting bibliography for the management of future pediatric cases.