Elsevier

Anaerobe

Volume 72, December 2021, 102459
Anaerobe

Case Reports
Pacemaker infection and endocarditis due to Parvimonas micra: A case report and systematic review

https://doi.org/10.1016/j.anaerobe.2021.102459Get rights and content

Highlights

  • Parvimonas micra is commonly recognized as an oral pathogen.

  • Sometimes serious complications due to P. micra infection can occur.

  • We present a case of pacemaker infection and endocarditis due to P. micra.

  • We also present a systematic review of endocarditis due to P. micra.

  • Clinicians should be attentive to recurrent infection during follow-up.

Abstract

Infective endocarditis caused by Parvimonas micra is rare. Its clinical features are presented in this systematic review. We also describe the case of an 82-year-old man with infective endocarditis and pacemaker infection due to P. micra. There are some reports of recurrence during antimicrobial therapy; hence, careful follow-up is necessary.

Introduction

Infective endocarditis (IE) is associated with high morbidity and mortality [[1], [2], [3]] and is defined as a systemic septic disease with various manifestations [4]. The risk factors for endocarditis include increasing age [5], male sex [6], poor dentition [7], and cardiac implantable electronic devices [8]. Permanent pacemaker (PPM)-related infection has been recognized since the 1970s [9], with an occurrence of 1.19% during the lifetime of a device [10]. Cardiac device infective endocarditis (CDIE) has remarkably higher mortality than cardiac device infections without endocarditis. Approximately 60–80% of the pathogens causing CDIE belong to staphylococcal species; other Gram-positive cocci only account for 4% cases [11].

Parvimonas micra (P. micra), a Gram-positive anaerobic coccus, is part of the normal commensal flora in the oral cavity and gastrointestinal tract [12]. Despite its low virulence, some patients may develop bacteremia [13], lung abscess [14], meningitis [15], cerebral and brain abscesses [16], spondylodiscitis [17], and iliopsoas abscesses [18]. P. micra endocarditis is uncommon, with few reports published previously [19,20]. Additionally, their pathogenic implication remains underestimated owing to slow growth and difficulty in identification.

This is the first report of right-sided IE caused by P. micra involving a pacemaker. The strength of this review is informing us of the clinical features regarding prognosis, recurrence, or complications of IE by P. micra. Herein, we present a case of pacemaker infection and describe its clinical characteristics in a systematic review of P. micra endocarditis.

An 82-year-old man presented with acute onset of fever and dizziness. His past medical history included pacemaker implantation due to sick sinus syndrome, synthetic graft replacement for an abdominal aortic aneurysm two decades ago, and hypertension. The patient was on aspirin (100 mg, once daily) and olmesartan medoxomil (10 mg, once daily) at admission. He was a social drinker without any smoking history. He was a businessman, currently retired, living in his retirement home, and originally independent in his daily activities using a cane. On admission, he was in acute distress, with clear consciousness; temperature, 38.4 °C; blood pressure, 114/75 mmHg; pulse rate, 74 beats/min (not pacemaker rhythm); respiratory rate, 18 breaths/min; and oxygen saturation, 94% at room temperature. Physical examination revealed a grade III diastolic murmur that was mostly audible in the left third intercostal space. He had poor oral hygiene and dental caries. No immunological phenomena (Roth spots or Osler nodes) or vascular phenomena (Janeway lesions, conjunctival petechiae, or splinter hemorrhage) were observed. Lungs were clear on auscultation, and he had no abnormal abdominal findings. Neurological findings showed no sensory or motor deficits and no central nervous system abnormalities. Laboratory investigations revealed the following: total white blood cell count (WBC), 15,000/μL (WBC differential: 87% neutrophils, 4% lymphocytes, 6% monocytes, and 3% eosinophils); hemoglobin, 13.3 g/dL; platelet, 121,000/μL; aspartate aminotransferase, 19 U/L; alanine aminotransferase, 8 U/L; lactate dehydrogenase, 314 IU/L; total bilirubin, 1.4 mg/dL; alkaline phosphatase, 189 IU/L; blood urea nitrogen, 18 mg/dL; creatinine, 0.96 mg/dL; and C-reactive protein, 2.51 mg/dL. HIV and rheumatoid factor were negative. Urinalysis was negative for urinary white or red blood cells and nitrites, and urine bacteriology test was negative. Contrast-enhanced computed tomography (CT) of the chest-abdomen-pelvis area revealed no inflammation or artificial blood vessel infection. After admission, empirical ceftriaxone administration was initiated (2.0 g intravenously [IV]) every 24 h).

Blood cultures on admission grew clusters of Gram-positive cocci on day 5. Transthoracic echocardiography revealed moderate tricuspid valvular regurgitation without signs of vegetation; however, on day 7, transesophageal echocardiography (TEE) revealed vegetation on the tricuspid valve and pacemaker lead (mainly the atrial lead) (Fig. 1). Therefore, ceftriaxone was replaced with ampicillin (2.0 g, IV, every 4 h) and gentamicin (180 mg, IV, every 24 h). On day 12, we removed the pacemaker and leads surgically and inserted a temporary pacemaker. On day 13, the blood cultured pathogen in the admission sample was confirmed as P. micra on matrix-assisted laser desorption/ionization and time-of-flight mass spectrometry (MALDI-TOF MS) (Bruker Daltonic, Bremen, Germany). Since the patient was receiving appropriate antimicrobial regimens, the culture pathogen tests for the pacemaker body and leads were negative. Modified Duke criteria [21] supported the diagnosis of endocarditis—one major criterion (evidence of endocardial involvement) and three minor criteria (predisposing heart condition, fever>38 °C, and microbiologic evidence). With known susceptibility results, gentamicin was terminated after a total of 6 days, and the subsequent antimicrobial regimen was revised to ampicillin (2.0 g, IV, every 4 h) alone. Follow-up blood cultures were negative. On day 22, a repeat TEE showed new vegetation on the temporary pacemaker lead and tricuspid valve (Fig. 2). As the patient did not need temporary pacemaker, it was removed entirely. The patient's clinical signs and symptoms improved, and ampicillin (2.0 g, IV, every 4 h) was continued for 6 weeks after removing the temporary pacemaker; no subsequent antimicrobials were necessary. The patient's regular medications remained unchanged during hospitalization and after discharge. The patient was discharged on day 64 without any sequelae, and no infection or cardiac events recurred during the 12 months of follow-up.

Two authors independently reviewed the titles and abstracts of database records, retrieved full texts for eligibility assessment, and extracted data (Fig. 3). The respective search strategies for PubMed, Embase, and Ichusi-web are described in Fig. 3; 28 articles were retrieved. After removing duplicates and irrelevant reports, four articles were selected [22,23]. After full-text evaluation, four articles comprising four patients were included (Fig. 3 and Table 1).

Section snippets

Discussion

P. micra was originally classified as Peptostreptococcus micros. The classification of the Gram-positive anaerobic cocci (GPAC) group has been remarkably transformed by a new genetic classification method based on the 16S rRNA gene sequence introduced in the late 1990s. Thereafter, P. micros was reclassified as P. micra in 2006 [24]. GPAC are low-virulence bacilli frequently detected as Gram-negative anaerobic rods (GNAR), but their pathogenic implication remains underestimated because of slow

Ethics approval and consent to participate

The treatment for the patient was performed in accordance with the tenets of the Declaration of Helsinki. The patient reported in the study provided written informed consent for all procedures.

Consent for publication

The patient enrolled in the study provided written informed consent for the publication of his clinical details and accompanying images. A copy of the written informed consent is available for the journal.

Availability of data and materials

Not applicable.

Funding

Ethics approval and consent to participateThis research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

Authors' contributions

T.S. wrote a draft of the manuscript. K.I., T.M., Y.K., and N.M. supervised the study and edited the manuscript. Y.K., H.A., and N.K. were the attending physicians of this patient. F.K. and K.I. participated in the literature review. All authors reviewed the final manuscript and approved its contents.

Declaration of competing interest

The authors have no financial disclosures or conflicts of interest to declare.

Acknowledgements

Not applicable.

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