Damaged Heart Valves Research Articles

Infective Endocarditis by Biofilm-Producing Methicillin-Resistant Staphylococcus aureus—Pathogenesis, Diagnosis, and Management

Infective Endocarditis by Biofilm-Producing Methicillin-Resistant Staphylococcus aureus—Pathogenesis, Diagnosis, and Management

Standardized order set for the management of infective endocarditis.

Infective endocarditis (IE) is a potentially life-threatening infection that affects the inner lining of the heart, particularly the heart valves. Patients with preexisting heart conditions, damaged heart valves, or a history of intravenous drug use are at a higher risk of acquiring IE. A rural acute care facility reported that 68.75% of patients who had a methicillin-resistant Staphylococcus aureus infection were diagnosed with IE. Review of medical records showed that 65% of patients with IE did not have antibiotic start/stop dates and 51% were discharged before the 6-week completion date. The quality-improvement project used a pretest and posttest design. An order set was created based on evidence-based guidelines to assist with the management of patients with IE. The order set included administering intravenous (IV) antibiotics for a minimum of 6 weeks for patients with IE and included a set of recommended weekly follow-up laboratory tests. An order set with the standard of care and reminders in the electronic health records (EHRs) were implemented for the management of IE, including antibiotic start and stop dates and weekly follow-up labs. After implementation, there was an improvement in the completion of IV antibiotics, documentation of start/stop dates for IV antibiotics, and completion of recommended laboratory tests. An order set with the standard of care and reminders in the EHR reduced variations in care and improved patient outcomes by ensuring that all providers were following the same evidence-based guidelines for the management of IE.

Infective Endocarditis Induced – Decompensation of Chronic Liver Disease Presenting as Hepatic Encephalopathy

Abstract Infective endocarditis (IE) occurs in people of older age, with artificial or damaged heart valves, immunocompromised states, and intravenous (IV) drug abusers as major risk factors. This case report describes a rare presentation of IE in a patient with chronic liver disease (CLD). A 38-year-old female with a history of decompensated CLD due to hepatitis C, presented with high-grade fever with chills, abdominal pain, shortness of breath, melena, and altered mental status. On examination, she had signs of hepatic encephalopathy and a systolic murmur in the aortic area. Imaging studies revealed an aortic valve vegetation with moderate aortic regurgitation, and blood cultures were negative. Treatment with meropenem and teicoplanin was started which resulted in clinical improvement. This case highlights the importance of considering IE in patients with CLD presenting with decompensation and suggests that early diagnosis and treatment are crucial in improving outcomes.

Streptococcus mutans PrsA mediates AtlA secretion contributing to extracellular DNA release and biofilm formation in the pathogenesis of infective endocarditis

ABSTRACT The role of secretion chaperone-regulated virulence proteins in the pathogenesis of infective endocarditis (IE) induced by viridans streptococci such as Streptococcus mutans is unclear. In this study, we investigated the contribution of the foldase protein PrsA, a putative parvulin-type peptidyl-prolyl isomerase, to the pathogenesis of S. mutans-induced IE. We found that a prsA-deficient strain had reduced virulence in terms of formation of vegetation on damaged heart valves, as well as reduced autolysis activity, eDNA release and biofilm formation capacity. The secretion and surface exposure of AtlA in vitro was reduced in the prsA-deficient mutant strain, and complementation of recombinant AtlA in the culture medium restored a wild type biofilm phenotype of the prsA-deficient mutant strain. This result suggests that secretion and surface localization of AtlA is regulated by PrsA during biofilm formation. Together, these results demonstrate that S. mutans PrsA could regulate AtlA-mediated eDNA release to contribute to biofilm formation in the pathogenesis of IE.

Chapter 3 - Neurologic complications of rheumatic fever

Sydenham chorea, also known as St. Vitus dance, is a major clinical criterion for the diagnosis of acute rheumatic fever. Clinically, it results in a combination of movement disorders and complex neuropsychiatric symptoms. Cardiac damage due to rheumatic fever may also predispose to neurologic complications later in life. Rheumatic heart disease (RHD) is associated with heart remodeling, cardiac arrhythmias, and ischemic stroke. Furthermore, chronically damaged heart valves are predisposed to infection. Septic brain embolism, a known complication of infective endocarditis, may result in brain ischemia, hemorrhage, and spread of the infection to the brain.

Manganese Depletion Leads to Multisystem Changes in the Transcriptome of the Opportunistic Pathogen Streptococcus sanguinis.

Streptococcus sanguinis is a primary colonizer of teeth and is typically considered beneficial due to its antagonistic relationship with the cariogenic pathogen Streptococcus mutans. However, S. sanguinis can also act as an opportunistic pathogen should it enter the bloodstream and colonize a damaged heart valve, leading to infective endocarditis. Studies have implicated manganese acquisition as an important virulence determinant in streptococcal endocarditis. A knockout mutant lacking the primary manganese import system in S. sanguinis, SsaACB, is severely attenuated for virulence in an in vivo rabbit model. Manganese is a known cofactor for several important enzymes in S. sanguinis, including superoxide dismutase, SodA, and the aerobic ribonucleotide reductase, NrdEF. To determine the effect of manganese depletion on S. sanguinis, we performed transcriptomic analysis on a ΔssaACB mutant grown in aerobic fermentor conditions after the addition of the metal chelator EDTA. Despite the broad specificity of EDTA, analysis of cellular metal content revealed a decrease in manganese, but not in other metals, that coincided with a drop in growth rate. Subsequent supplementation with manganese, but not iron, zinc, or magnesium, restored growth in the fermentor post-EDTA. Reduced activity of Mn-dependent SodA and NrdEF likely contributed to the decreased growth rate post-EDTA, but did not appear entirely responsible. With the exception of the Dps-like peroxide resistance gene, dpr, manganese depletion did not induce stress response systems. By comparing the transcriptome of ΔssaACB cells pre- and post-EDTA, we determined that manganese deprivation led to altered expression of diverse systems. Manganese depletion also led to an apparent induction of carbon catabolite repression in a glucose-independent manner. The combined results suggest that manganese limitation produces effects in S. sanguinis that are diverse and complex, with no single protein or system appearing entirely responsible for the observed growth rate decrease. This study provides further evidence for the importance of this trace element in streptococcal biology. Future studies will focus on determining mechanisms for regulation, as the multitude of changes observed in this study indicate that multiple regulators may respond to manganese levels.

A Study on Dental Caries and Dental Plaques Caused by Streptococcus Mutans, of Patients at Border Guard Hospital Dhaka, Peelkhana

Background: Dental caries is one of the most common chronic infectious diseases in the world. The acids generated through the fermentation of sugar by the microorganisms in dental plaque can decalcify the superficial layers of tooth enamel and can initiate dental caries. Streptococcus mutans have been proposed as the main etiological agents of dental caries .The aim of this study is to identify the main etiological agents of dental caries and plaque which are supposed to be Streptococcus mutans as correlating microorganism.
 Materials and Methods: This cross sectional study was carried out in the Pathology department of Border Guard Hospital, Peelkhana, Dhaka during the period of 1st October, 2018 to 3IST December,2018. Study population was newly enrolled soldiers and their families as male ,female and children in BGB. A total of 50 clinical samples were included in this study. The samples were collected from the Dental outdoor patient department and all laboratory tests were performed at Pathology department of aforementioned hospital. After performing all possible microbiological tests for bacterial isolation, results were recorded.
 Results: Among 50 samples, 46(92%) samples are considered to be positive for Streptococcus viridans and 27(54%) isolates are identified as Streptococci mutans according to ability of producing special kind of exopolysaccharide, lactic acid formation and high salt tolerance tests. Associated organisms (32%) like candida were present in 15(30%) samples and other bacterial colonies were present in 31(62%) samples, along with Streptococcus viridans.
 Conclusion: The finding of this study will help the dentists to treat the patients with chronic caries, dental plaques as they pose the gravest threat when they settle down on damaged heart valves, cause subacute bacterial endocarditis and other infections in various sites including mouth, joints, skin, muscle, and central nervous system after tooth extraction or any other invasive procedure
 J Bangladesh Coll Phys Surg 2020; 38(3): 121-125

The Versatility of Opportunistic Infections Caused by Gemella Isolates Is Supported by the Carriage of Virulence Factors From Multiple Origins.

The molecular basis of the pathogenesis of the opportunistic invasive infections caused by isolates of the Gemella genus remains largely unknown. Moreover, inconsistencies in the current species assignation were detected after genome-level comparison of 16 public Gemella isolates. A literature search detected that, between the two most pathogenic species, Gemella morbillorum causes about twice the number of cases compared to Gemella haemolysans. These two species shared their mean diseases – sepsis and endocarditis – but differed in causing other syndromes. A number of well-known virulence factors were harbored by all species, such as a manganese transport/adhesin sharing 83% identity from oral endocarditis-causing streptococci. Likewise, all Gemellae carried the genes required for incorporating phosphorylcholine into their cell walls and encoded some choline-binding proteins. In contrast, other proteins were species-specific, which may justify the known epidemiological differences. G. haemolysans, but not G. morbillorum, harbor a gene cluster potentially encoding a polysaccharidic capsule. Species-specific surface determinants also included Rib and MucBP repeats, hemoglobin-binding NEAT domains, peptidases of C5a complement factor and domains that recognize extracellular matrix molecules exposed in damaged heart valves, such as collagen and fibronectin. Surface virulence determinants were associated with several taxonomically dispersed opportunistic genera of the oral microbiota, such as Granulicatella, Parvimonas, and Streptococcus, suggesting the existence of a horizontally transferrable gene reservoir in the oral environment, likely facilitated by close proximity in biofilms and ultimately linked to endocarditis. The identification of the Gemella virulence pool should be implemented in whole genome-based protocols to rationally predict the pathogenic potential in ongoing clinical infections caused by these poorly known bacterial pathogens.

Staphylococcus aureus endocarditis: distinct mechanisms of bacterial adhesion to damaged and inflamed heart valves.

The pathogenesis of endocarditis is not well understood resulting in unsuccessful attempts at prevention. Clinical observations suggest that Staphylococcus aureus infects either damaged or inflamed heart valves. Using a newly developed endocarditis mouse model, we therefore studied the initial adhesion of S. aureus in both risk states. Using 3D confocal microscopy, we examined the adhesion of fluorescent S. aureus to murine aortic valves. To mimic different risk states we either damaged the valves with a surgically placed catheter or simulated valve inflammation by local endothelium activation. We used von Willebrand factor (VWF) gene-deficient mice, induced platelet and fibrinogen depletion and used several S. aureus mutant strains to investigate the contribution of both host and bacterial factors in early bacterial adhesion. Both cardiac valve damage and inflammation predisposed to endocarditis, but by distinct mechanisms. Following valve damage, S. aureus adhered directly to VWF and fibrin, deposited on the damaged valve. This was mediated by Sortase A-dependent adhesins such as VWF-binding protein and Clumping factor A. Platelets did not contribute. In contrast, upon cardiac valve inflammation, widespread endothelial activation led to endothelial cell-bound VWF release. This recruited large amounts of platelets, capturing S. aureus to the valve surface. Here, neither fibrinogen, nor Sortase A were essential. Cardiac valve damage and inflammation predispose to S. aureus endocarditis via distinct mechanisms. These findings may have important implications for the development of new preventive strategies, as some interventions might be effective in one risk state, but not in the other.

Genetic variations in innate immunity genes affect response to Coxiella burnetii and are associated with susceptibility to chronic Q fever

ObjectivesChronic Q fever is a persistent infection, mostly of aortic aneurysms, vascular prostheses or damaged heart valves, caused by the intracellular bacterium Coxiella burnetii. Only a fraction of C. burnetii-infected individuals at risk develop chronic Q fever. In these individuals, a defective innate immune response may contribute to the development of chronic Q fever. We assessed whether genetic variations in genes involved in the killing machinery for C. burnetii by macrophages, contribute to the progression to chronic Q fever. MethodsThe prevalence of 66 single nucleotide polymorphisms (SNPs) in 31 genes pivotal in phagolysosomal maturation, bacterial killing and autophagy, was determined in 173 chronic Q fever patients and 184 controls with risk factors for chronic Q fever and serological evidence of a C. burnetii infection. Associations were detected with univariate logistic regression models. To assess the effect of these SNPs on innate responses to C. burnetii, the C. burnetii-induced cytokine production and basal reactive oxygen species production of healthy volunteers was determined. ResultsRAB7A (rs13081864) and P2RX7 loss-of-function SNP (rs3751143) were more common in chronic Q fever patients than in controls. RAB5A (rs8682), P2RX7 gain-of-function SNP (rs1718119), MAP1LC3A (rs1040747) and ATG5 (rs2245214) were more common in controls. In healthy volunteers, RAB7A (rs13081864) and MAP1LC3A (rs1040747) influenced the C. burnetii-induced cytokine production. RAB7A (rs13081864) modulated basal reactive oxygen species production. ConclusionsRAB7A (rs13081864) and P2RX7 (rs3751143) are associated with the development of chronic Q fever, whereas RAB5A (rs8682), P2RX7 (rs1718119), MAP1LC3A (rs1040747) and ATG5 (rs2245214) may have protective effects.

Impact of the duration of antibiotic therapy on relapse and survival following surgery for active infective endocarditis.

Surgery is often required for acute infective endocarditis (IE) to repair or replace damaged heart valves. Traditionally, long courses of antibiotic treatment have been prescribed after surgery for active IE for fear of infecting newly implanted/repaired valves, but the need for this, in the present era of enhanced antimicrobial stewardship, has been questioned. In our institution, the choice and duration of antimicrobial therapy is tailored to individual patients by a multidisciplinary team with an interest in IE. The influence of the duration of postoperative antibiotic therapy on outcomes was studied in patients requiring surgery prior to the completion of a planned course of antibiotic therapy. This was a retrospective observational study on patients with acute IE requiring surgery between January 2004 and December 2015. The primary outcome was relapse. Secondary outcomes were early reoperation and 1-year mortality. In total, 182 IE episodes were included in the final analysis. The median duration of postoperative antibiotic therapy was 23.5 days (interquartile range 12-40 days) and decreased significantly during the period of study (P < 0.001). There were 2 relapses (1.1%) and 18 (9.9%) postoperative deaths within 1 year. Nine (5%) patients underwent early reoperation. The duration of postoperative antibiotic therapy did not affect either the primary or the secondary outcomes. This work supports previous findings that selected patients who require surgery during active IE can be safely given shorter courses of postoperative antibiotics without an impact on relapse of infection or survival.

The Road to Infection: Host-Microbe Interactions Defining the Pathogenicity of Streptococcus bovis/Streptococcus equinus Complex Members.

The Streptococcus bovis/Streptococcus equinus complex (SBSEC) comprises several species inhabiting the animal and human gastrointestinal tract (GIT). They match the pathobiont description, are potential zoonotic agents and technological organisms in fermented foods. SBSEC members are associated with multiple diseases in humans and animals including ruminal acidosis, infective endocarditis (IE) and colorectal cancer (CRC). Therefore, this review aims to re-evaluate adhesion and colonization abilities of SBSEC members of animal, human and food origin paired with genomic and functional host-microbe interaction data on their road from colonization to infection. SBSEC seem to be a marginal population during GIT symbiosis that can proliferate as opportunistic pathogens. Risk factors for human colonization are considered living in rural areas and animal-feces contact. Niche adaptation plays a pivotal role where Streptococcus gallolyticus subsp. gallolyticus (SGG) retained the ability to proliferate in various environments. Other SBSEC members have undergone genome reduction and niche-specific gene gain to yield important commensal, pathobiont and technological species. Selective colonization of CRC tissue is suggested for SGG, possibly related to increased adhesion to cancerous cell types featuring enhanced collagen IV accessibility. SGG can colonize, proliferate and may shape the tumor microenvironment to their benefit by tumor promotion upon initial neoplasia development. Bacteria cell surface structures including lipotheichoic acids, capsular polysaccharides and pilus loci (pil1, pil2, and pil3) govern adhesion. Only human blood-derived SGG contain complete pilus loci and other disease-associated surface proteins. Rumen or feces-derived SGG and other SBSEC members lack or harbor mutated pili. Pili also contribute to binding to fibrinogen upon invasion and translocation of cells from the GIT into the blood system, subsequent immune evasion, human contact system activation and collagen-I-binding on damaged heart valves. Only SGG carrying complete pilus loci seem to have highest IE potential in humans with significant links between SGG bacteremia/IE and underlying diseases including CRC. Other SBSEC host-microbe combinations might rely on currently unknown mechanisms. Comparative genome data of blood, commensal and food isolates are limited but required to elucidate the role of pili and other virulence factors, understand pathogenicity mechanisms, host specificity and estimate health risks for animals, humans and food alike.

In vitro biomechanical and hydrodynamic characterisation of decellularised human pulmonary and aortic roots.

The use of decellularised biological heart valves in the replacement of damaged heart valves offers a promising solution to reduce the degradation issues associated with existing cryopreserved allografts. The purpose of this study was to assess the effect of low concentration sodium dodecyl sulphate decellularisation on the in vitro biomechanical and hydrodynamic properties of cryopreserved human aortic and pulmonary roots. The biomechanical and hydrodynamic properties of cryopreserved decellularised human aortic and pulmonary roots were fully characterised and compared to cellular human aortic and pulmonary roots in an unpaired study. Following review of these results, a further study was performed to investigate the influence of a specific processing step during the decellularisation protocol ('scraping') in a paired comparison, and to improve the method of the closed valve competency test by incorporating a more physiological boundary condition. The majority of the biomechanical and hydrodynamic characteristics of the decellularised aortic and pulmonary roots were similar compared to their cellular counterparts. However, several differences were noted, particularly in the functional biomechanical parameters of the pulmonary roots. However, in the subsequent paired comparison of pulmonary roots with and without decellularisation, and when a more appropriate physiological test model was used, the functional biomechanical parameters for the decellularised pulmonary roots were similar to the cellular roots. Overall, the results demonstrated that the decellularised roots would be a potential choice for clinical application in heart valve replacement.

AtlA Mediates Extracellular DNA Release, Which Contributes to Streptococcus mutans Biofilm Formation in an Experimental Rat Model of Infective Endocarditis.

Host factors, such as platelets, have been shown to enhance biofilm formation by oral commensal streptococci, inducing infective endocarditis (IE), but how bacterial components contribute to biofilm formation in vivo is still not clear. We demonstrated previously that an isogenic mutant strain of Streptococcus mutans deficient in autolysin AtlA (ΔatlA) showed a reduced ability to cause vegetation in a rat model of bacterial endocarditis. However, the role of AtlA in bacterial biofilm formation is unclear. In this study, confocal laser scanning microscopy analysis showed that extracellular DNA (eDNA) was embedded in S. mutans GS5 floes during biofilm formation on damaged heart valves, but an ΔatlA strain could not form bacterial aggregates. Semiquantification of eDNA by PCR with bacterial 16S rRNA primers demonstrated that the ΔatlA mutant strain produced dramatically less eDNA than the wild type. Similar results were observed with in vitro biofilm models. The addition of polyanethol sulfonate, a chemical lysis inhibitor, revealed that eDNA release mediated by bacterial cell lysis is required for biofilm initiation and maturation in the wild-type strain. Supplementation of cultures with calcium ions reduced wild-type growth but increased eDNA release and biofilm mass. The effect of calcium ions on biofilm formation was abolished in ΔatlA cultures and by the addition of polyanethol sulfonate. The VicK sensor, but not CiaH, was found to be required for the induction of eDNA release or the stimulation of biofilm formation by calcium ions. These data suggest that calcium ion-regulated AtlA maturation mediates the release of eDNA by S. mutans, which contributes to biofilm formation in infective endocarditis.

Infective endocarditis: Importance of molecular biological techniques in etiological diagnosis

To investigate the specific features of conventional bacteriological methods and current molecular biological techniques for the etiological diagnosis of infective endocarditis (IE). Examinations were made in 53 patients treated at City Clinical Hospital Sixty-Four, Moscow Healthcare Department, in 2012-2015 who underwent simultaneous bacteriological and molecular biological (polymerase chain reaction (PCR) or PCR with further sequencing) examinations of blood or resected cardiac valve tissues. The investigation included 53 patients (31 men; median age, 62 years) with IE (Duke 2009); its primary form was observed in 32 (60.4%) patients. Blood bacteriological tests and PCR assays were positive in 28 (52.8%) and 34 (64.2%) patients, respectively. There were concordant results in 21 of the 28 positive blood culture cases and discordant results in 7 (25%); at the same time 3 cases showed a compete discordance in the detected causative agents (the growth of Enterococcus spp. was revealed by bacteriological examination and that of Staphylococcus spp., Streptococcus spp., and Escherichia coli by DNA PCR) and a pathogen could not be identified by DNA PCR in 4 patients who had positive blood bacteriological results. The positive PCR results for cocci and fungi were obtained in 10 of the 25 (47.2%) examinees with culture-negative IE. Rare causative agents were not revealed. The tissues obtained from 8 resected damaged heart valves displayed a wider spectrum of pathogens than did blood samples, which was associated with the formation of bacterial films. The etiological agent of IE was revealed in venous blood by bacteriological examination in 52.8% of the examinees, by PCR in 64.2%, and by either in 71.7%. There were concordant and discordant results in 67.9 and 32.1% of the patients, respectively; among whom 18.9% were found to have pathogen DNA revealed by PCR in culture-negative IE.

Инфекционный эндокардит: проблемы диагностики и лечения

Results of the clinical study involving 458 patients (from 12 to 75 years, mean age 49 +/- 9.3 years) with various forms of infective endocarditis (IE) have been summarized. Integrated echocardiography was the principal non-invasive method of presurgical diagnosis of the disease. Sensitivity of transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE) were 96% and 97.9% in patients with primary IE, 59% and 92% in patients with secondary IE and 2.7% and 90% in patients with prosthetic endocarditis, respectively. Results of echocardiography were confirmed during intrasurgical revision and histological study of removed valves. However, we have not found correlation between size, location, shape, mobility of vegetations, and risk of embolic events. Integrated echocardiography contributed to the correct diagnosis and also provided the possibility to determine the necessity of surgery and to schedule it in time. The main goals of surgery in IE heart valves are complete removal/sanitation of infected tissue and restoration or replacement of damaged heart valves. Overall hospital mortality was 8.1%. Mortality among patients operated in the active stage of IE and during remission was 10.5 and 7.1%, respectively. Surgical treatment in the active phase of IE is indicated in patients with factors of high risk, when the possibility of cure with antibiotics is unlikely, as well as in patients with high chances of recovery according to the state of organs and systems.

Infective endocarditis

Infective endocarditis (IE) is a severe bacterial infection of the endocardial surface of the heart; it usually involves damaged or synthetic heart valves. Improvement in surgical and medical therapeutics have been encouraging, however, if managed poorly it can still have a poor prognosis. In the developed world, rheumatic heart disease is an uncommon risk factor whereas intravenous drug use, degenerative valvular disease in the elderly population and use of prosthetic heart valves are becoming more common. In terms of the microbiological cause of IE, Staphylococcus aureus is the most common cause in the Western world. It is therefore important for GPs to be aware of and be able to identify these risk factors. This article aims to examine the pathophysiology, risk factors, changing trends in epidemiology and recent guidelines on the management of IE.

Cells for tissue engineering of cardiac valves.

Heart valve tissue engineering is a promising alternative to prostheses for the replacement of diseased or damaged heart valves, because tissue-engineered valves have the ability to remodel, regenerate and grow. To engineer heart valves, cells are harvested, seeded onto or into a three-dimensional (3D) matrix platform to generate a tissue-engineered construct in vitro, and then implanted into a patient's body. Successful engineering of heart valves requires a thorough understanding of the different types of cells that can be used to obtain the essential phenotypes that are expressed in native heart valves. This article reviews different cell types that have been used in heart valve engineering, cell sources for harvesting, phenotypic expression in constructs and suitability in heart valve tissue engineering. Natural and synthetic biomaterials that have been applied as scaffold systems or cell-delivery platforms are discussed with each cell type. Copyright © 2015 John Wiley & Sons, Ltd.

Circulation: Clinical Summaries.

Circulation: Clinical Summaries.

İnfantta Gastrik Cerrahi Sonrası Gelişen Streptococcus gordonii Bakteremisi

Streptococcus gordonii is a viridans group streptococci of the S. sangius group that is normally a non-pathogenic inhabitant of the oral cavity and occasionally the gastrointestinal tract. S. gordonii is well-known for its ability to colonize damaged heart valves and cause bacterial endocarditis, but it rarely causes positive blood cultures in patients that undergo diagnostic procedures involving the gastrointestinal tract, such as sigmoidoscopy and gastroduodenoscopy. Herein we report a 5-month-old patient with bacteremia due to S. gordonii following a surgery for malrotation. The source of S. gordonii infection was thought to be the malrotation surgery. To the best of our knowledge, the literature does not include any pediatric cases of S. gordonii bacteremia following a gastric surgery.