Relevant bibliographies by topics / Infective endocarditis

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
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  6. Reports

Academic literature on the topic 'Infective endocarditis'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "Infective endocarditis"

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Hoyer, Andrew, and Michael Silberbach. "Infective Endocarditis." Pediatrics in Review 26, no. 11 (November 2005): 394–400. http://dx.doi.org/10.1542/pir.26-11-394.

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Danilowicz, D. "Infective Endocarditis." Pediatrics in Review 16, no. 4 (April 1, 1995): 148–54. http://dx.doi.org/10.1542/pir.16-4-148.

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Davies, Patrick. "Infective endocarditis." Nursing Standard 8, no. 35 (May 25, 1994): 54–55. http://dx.doi.org/10.7748/ns.8.35.54.s61.

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Baig, Wazir, and Jonathan Sandoe. "Infective endocarditis." Clinical Medicine 10, no. 2 (April 2010): 188–91. http://dx.doi.org/10.7861/clinmedicine.10-2-188.

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Lang, Selwyn, and Arthur Morris. "Infective Endocarditis." Drugs 34, no. 2 (August 1987): 279–88. http://dx.doi.org/10.2165/00003495-198734020-00005.

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Miner, Pamela D. "INFECTIVE ENDOCARDITIS." Nursing Clinics of North America 29, no. 2 (June 1994): 269–83. http://dx.doi.org/10.1016/s0029-6465(22)02732-3.

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Sheppard, Mary N. "Infective endocarditis." Diagnostic Histopathology 28, no. 4 (April 2022): 199–208. http://dx.doi.org/10.1016/j.mpdhp.2022.01.003.

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Hoyer, Andrew, and Michael Silberbach. "Infective Endocarditis." Pediatrics In Review 26, no. 11 (November 1, 2005): 394–400. http://dx.doi.org/10.1542/pir.26.11.394.

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Danilowicz, Delores. "Infective Endocarditis." Pediatrics In Review 16, no. 4 (April 1, 1995): 148–54. http://dx.doi.org/10.1542/pir.16.4.148.

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A high level of suspicion is of utmost importance in the diagnosis of endocarditis, particularly in the patient at risk who may have received antibiotic treatment for the prodrome. Treatment with adequate levels of a bactericidal drug based on an identified organism will give the highest percentage of cures. Early treatment may prevent damage to cardiac structures and lessen further complications related to emboli or progressively enlarging vegetations. The combination of a high-risk patient with either resistant bacterial endocarditis or fungal [See table in the PDF file] endocarditis carries a higher morbidity and will account for most of the mortality. Although not an ideal answer, SBE prophylaxis is justified from observations in animals and should be recommended strongly to the parents and to the patient as she or he gets older. Because an increasing number of children survive their congenital heart defects but remain at risk for acquiring SBE and because an increasing number of preterm infants and neonates are exposed to indwelling catheters, the pediatrician will continue to see IE presenting as both a diagnostic dilemma and an acute treatment problem. The emergence of children who are human immunodeficiency virus-positive or who have acquired immunodeficiency syndrome has increased the group at immunologic risk, as has an increasing population of children surviving organ transplants. These children can present more often with infections caused by nosocomial, resistant agents because of their frequent hospitalizations, and they may have a variety of opportunistic infections from organisms that normally are not pathogens. Unfortunately, a higher mortality rate can be expected among these children. The diagnosis of IE is made even more of a challenge because it accounts for only about 1/1000 to 1/4500 hospital admissions to pediatric services. In tertiary care hospitals that have an active pediatric cardiac service, the numbers may be higher. The most important element in diagnosing endocarditis remains its early consideration as a possibility in any child who has a persistent unexplained febrile illness and its being the first consideration in a high-risk child.
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Tseluiko, V. I. "Infective endocarditis." Medicine of Ukraine, no. 4(210) (June 9, 2017): 33–41. http://dx.doi.org/10.37987/1997-9894.2017.4(210).222047.

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Dissertations / Theses on the topic "Infective endocarditis"

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Mansur, Alfredo Jose. "Avaliação da probabilidade de óbito em portadores de endocardite infecciosa." Universidade de São Paulo, 1987. http://www.teses.usp.br/teses/disponiveis/5/5131/tde-21072014-100754/.

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Foram estudados 300 episódios de endocardite infecciosa (EI) em 288 pacientes acompanhados no Instituto do Coração do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, no período de outubro de 1978 a agosto de 1986, com o intuito de avaliar a probabilidade de óbito e assim identificar os pacientes sob maior risco de evolução desfavorável. As idades dos pacientes variaram entre 0,2 a 78 (média de 30, desvio padrão de 16,06) anos, correspondentes a pacientes do sexo masculino em 185 (62%) episódios e feminino em 115 (38%). Procedeu-se a análise univariada (testes de qui quadrado e exato de Fischer, análise de variância) para se identificar variáveis cujas distribuições diferissem quanto a mortalidade, para em seguida realizar a análise multivariada com o emprego de regressão logística, a fim de estimar a probabilidade de óbito. Para isso, foi desenvolvido um modelo estatístico e aplicado a casuística e, a casos hipotéticos, para o estudo conceitual. Não houve diferença de distribuição significativa quanto a mortalidade em relação a idade, sexo, tempo decorrido entre o início dos sintomas e a hospitalização, presença de antecedente de manipulação possível de induzir a bacteriemia, informação de lesão cutânea na história clínica, uso prévio de antimicrobiano, presença de petéquias, esplenomegalia, dimensão da área cardíaca na radiografia de tórax, presença de vegetação no ecocardiograma, duração da antibioticoterapia pre-operatória, portadores de aneurisma micótico, embolia arterial sistêmica, infecção em câmaras cardíacas direitas em relação à infecção de câmaras cardíacas esquerdas, infecção em prótese valvar antes ou depois de quatro meses de seu implante, infecção em prótese aórtica em relação à infecção de prótese mitral, prótese única em relação à dupla prótese, velocidade de eritrossedimentação, taxa de hemoglobina no sangue, taxas de gamaglobulina e creatinina séricas. Houve diferença significativa quanto à mortalidade considerando-se o estado cardíaco anterior à EI, a localização da EI, os agentes etiológicos, a alteração no exame do fundo de olho, o número de complicações, a taxa de mucoproteína e albumina séricas e a taxa de leucócitos do sangue, os portadores de infecção em prótese valvar em relação à infecção em estrutura natural. Na análise multivariada foram empregados o estado cardíaco anterior à EI (portadores de valvopatia, de prótese valvar cardíaca, de cardiopatias congênitas, e pacientes sem evidência de cardiopatia prévia), o agente etiológico [estreptococos, Staphylococcus aureus, outras bactérias (incluindo-se as bactérias gram-negativas, gram-positivas excetuando-se os estreptococos e os estafilococos, e os Staphylococcus epidermis) e os portadores de EI com hemoculturas negativas], a presença ou ausência de complicações e as taxas de leucócitos do sangue, de mucoproteína e de albumina séricas. O modelo estatístico desenvolvido, que incorporou informações do estado cardíaco anterior à EI, do agente etiológico, das complicações e da taxa de leucócitos do sangue, era aplicável a 229 episódios e permitiu prever adequadamente 158 entre 173 evoluções de pacientes que receberam alta hospitalar e 27 entre 56 evoluções de enfermos que faleceram; estimar como alta hospitalar 29 pacientes que faleceram e como óbito 15 pacientes que receberam alta hospitalar, classificando corretamente 185 dos 229 episódios. Aplicado a pacientes hipotéticos dos diferentes subgrupos considerados na análise o modelo demonstra, com base em nossa experiência, que a probabilidade de óbito será maior nos portadores de prótese valvar cardíaca, endocardite por microorganismos agrupados como \"outras bactérias\" (bactérias gram-negativas, Staphylococcus epidermidis, e outras bactérias gram positivas excetuando-se estafilococos e estreptococos) e por Staphylococcus aureus, na presença de complicações. À presença de complicações foi a variável que exerceu maior influência na probabilidade de óbito; a sua ausência minimiza sobremaneira essa probabilidade qualquer que seja o estado cardíaco anterior à EI e o agente etiológico. Nossos dados permitem sugerir que considerando de modo simultâneo e conjunto o estado cardíaco anterior à EI, o agente etiológico, a presença ou ausência de complicações e a taxa de leucócitos do sangue contribuem na avaliação prognóstica em portadores de EI. Entre essas variáveis, a participação da presença de complicações e a mais ressaltada. Na ausência de complicações a probabilidade de óbito reduz-se acentuadamente.
In order to assess the probability of death in the course of infective endocarditis we studied 300 episodes involving 288 patients, followed from October 1978 up to August 1986. The ages ranged from 0.2 to 78 (mean 30, standard deviation 16.06) years; 185 (62%) episodes occurred in male patients and 115 (38%) in female patients. As a first step we tested several variables against mortality through univariated analysis (chi square test, Fisher\'s exact test, analysis of variance). The variables showing significant differences in the univariated test were then submitted to multivariate analysis (logistic regression), to develop a statistical model to assess the contribution of each of the selected variable to the probability expression and to identify the probability of death for each patient. There was no significant difference in mortality related to age, sex, time elapsed between onset of symptoms and hospital admission, previous manipulation usually associated with bacteremia, information of cutaneous lesions, previous antimicrobial therapy, petechiae, splenomegaly, cardiac dimensions on chest roentgenogram, vegetations detected on echocardiogram, pre operative antibiotic therapy, presence of my cotic aneurysm, arterial embolism, right sided vs. left sided endocarditis, erythrocyte sedimentation rate, blood hemoglobin, serum gama globulin, serum creatinin, early prosthetic valve infection vs. late prosthetic valve infection, prosthetic aortic valve vs. prosthetic mitral valve, single prosthesis vs. two prosthesis. There was significant difference in mortality related to cardiac status before the endocarditis, etiologic agent, fundoscopic abnormality on indirect ophtalmoscopy, frequency of complications. serum mucoprotein, serum albumin, blood leukocyte count, prosthetic valve endocarditis in relation to native valve endocarditis. The model developed through logistic regression included the cardiac status before the endocarditis (valvular heart disease, congenital heart disease, prosthetic heart valves or no known heart disease}, etiologic agent (streptococci, Staphylococcus aureus, other bacteria, negative blood cultures), presence of complications, blood leukocyte count. The model could be applied to 229 episodes. It detected correctly the evolution in 185 of 229 episodes, and identified 158 in 173 patients discharged from the hospital as well as 27 in 56 patients who died. There was also prevision for hospital discharge in 29 patients who died and for death in 15 patients discharged from the hospital. The probability of death is higher in patients with prosthetic heart valve, when the etiologic agent is the Staphylococcus aureus and the group of gram negative bacteria, gram positive bacteria other than streptococci and staphylococci and Staphylococcus epidermis, in the presence of complications. In conclusion, the informations provided by cardiac status before the endocarditis, etiologic agent, presence or absence of complications and blood leukocyte count may be useful in the assessment of the outcome of patients with infective endocarditis.
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Watkin, Richard. "The diagnosis of infective endocarditis." Thesis, University of Birmingham, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.408833.

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Carey, Andrew J., Devin Johnson, George Obeng, Zia Rahman, Abdul Hannan, and Jack Goldstein. "A Classic Presentation of Infective Endocarditis." Digital Commons @ East Tennessee State University, 2018. https://dc.etsu.edu/asrf/2018/schedule/140.

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Introduction: Advances in modern medicine have enabled early detection of infective diagnosis through blood cultures and echocardiography, which have been standardized by the widely accepted Modified Duke Criteria and have enabled rapid administration of antibiotics. As a consequence, the well-discussed and often variable clinical findings have become less common and have relegated to minor criteria in diagnosis. Fever is the single most common presenting symptom, whereas more specific signs such as petechiae may be seen in only 20-40% of patients. Even more rare are the pathognomonic Janeway lesions, Roth spots, and Osler nodes. Here we present a case in which early diagnosis was established through minor criteria manifest upon physical exam, and we highlight the timely insight provided from physical exam. Case: A 29-year-old man was admitted to the hospital for altered mental status, fever, vomiting, diarrhea, and vertigo. His past medical history included IV drug abuse, thrombotic thrombocytopenia, Hepatitis C, and seizures. Upon admission, his encephalopathy progressed rapidly, and he was mechanically ventilated and started on hemodialysis. Blood cultures grew Methicillin sensitive Staphylococcus aureus and Elizabethkingia meningosepticum and susceptibilities were attained. Echocardiography showed 3.1 cm vegetation on the aortic valve. By the Modified Duke Criteria, the diagnosis of infective endocarditis was confirmed. Discussion: The increasing incidence of complex infective endocarditis—including polymicrobial infection as well as the increasing resistance to antibiotic therapy—poses challenges to the rapid assessment and treatment necessary to mitigate the multi-organ involvement and the devastating consequences of septic emboli. Developments in medical technology have expedited both the diagnosis and treatment of infective endocarditis, which has subsequently decreased the extent and frequency of classical signs. Nonetheless, this case illustrates the unavoidable vitality of the physical exam, because this patient’s quick and clear presentation enabled diagnosis solely through physical exam. Empiric antibiotic treatment was started promptly and subsequently adjusted based on culture and susceptibilities.
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Daga, Shruti. "Host-pathogen interactions influencing susceptibility to infective endocarditis." Thesis, University of Edinburgh, 2010. http://hdl.handle.net/1842/27859.

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Introduction: Bacterial-platelet-fibrin complexes (vegetations), form on cardiac valves in infective endocarditis and are associated with increased morbidity and mortality. Although the mechanisms of bacterium-platelet adhesion, platelet activation and aggregation that are likely to contribute to vegetation formation have been identified, experimental conditions employed in these studies do not accurately reflect bacterial growth in the human vasculature. In addition, the contribution of host genetic factors such as platelet receptor polymorphisms to the pathogenesis of infective endocarditis is unknown. Considering that Staphylococcus aureus is now the most common cause of infective endocarditis associated with a poor prognosis, the contribution of bacterial and host factors to bacterium-platelet interactions, platelet activation and severity of infective endocarditis were analysed. Methods and results: Influence of bacterial growth environment on S. aureus-platelet interactions: Platelet aggregometry was performed with a range of S. aureus clinical and genetically modified isolates grown in nutrient broth and whole human blood. Some strains grown in nutrient broth failed to induce platelet aggregation, whereas all S. aureus isolates induced platelet aggregation after growth in blood. S. aureus surface proteins clumping factors A and B, serine-aspartate repeats C, D and E, iron-regulated surface determinants A and B and staphylococcal protein A were not essential for platelet aggregation induced by S. aureus grown in human blood, but the lag time to aggregation was increased in a strain containing mutations in genes encoding fibronectin-binding proteins A and B. Correlation between platelet activation and susceptibility to infective endocarditis: Platelet activation was determined in patients with infective endocarditis using flow cytometry. Platelet P-selectin expression was reduced in patients with infective endocarditis as compared to healthy volunteers, but was higher in patients requiring surgery. Influence of host genetic polymorphisms on S. aureus-platelet interactions and outcome in infective endocarditis: Flow cytometry and platelet aggregometry were performed to determine the role of specific platelet receptor GPIIIa piAI/A2, GPIb Kozak sequence, human platelet antigen (HPA)-2, variable number of tandem repeats (VNTR) and FcγRIIa H131R polymorphisms in S. aureus-platelet interactions. The GPIIIa P1A1/A1 genotype, FcγRIIa H allele and GPIb Kozak sequence polymorphism were associated with increased S. aureus-induced platelet aggregation. GPIb VNTR alleles influenced aggregate formation in vitro and development of vegetations in patients with infective endocarditis. The GPIb HPA-2a/2a genotype was associated with increased incidence of the composite clinical end-point of embolism, heart failure, need for surgery and mortality in patients with infective endocarditis. Conclusions: These studies have indicated that host and bacterial factors influence infective endocarditis and S. aureus-platelet interactions under conditions reflective of the host environment. Bacterial factors expressed during growth in human blood, host platelet activation levels and platelet receptor polymorphisms may represent novel prognostic markers and therapeutic targets in infective endocarditis.
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Mohee, Amar Raj. "Infections in urological practice : bacteraemia and infective endocarditis." Thesis, University of Leeds, 2014. http://etheses.whiterose.ac.uk/6839/.

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Introduction. It is known that infections may occur after urological instrumentation, as some patients develop infective symptoms. The purpose of this study was to investigate bacteraemia in patients undergoing transurethral resection of the prostate (TURP) and catheter manipulation, using contemporary culture methods. Another aim was to explore the potential for molecular methods to detect, identify and quantify bacteraemia. We aim to evaluate the association between urological instrumentation and the development of infective endocarditis (IE). Methods. Microbiological molecular methods to identify and quantify bacteria in blood were developed. Blood samples were collected at different time points during the procedure from patients undergoing TURP and catheter manipulation to evaluate the presence of bacteria using both the culture and molecular methods. The association between risk factors (patient and procedural) and bacteraemia was analysed statistically. A case-control model was used to assess the association between the development of IE and a number of risk factors, including urological instrumentation. Results. Bacteraemia occurred in both sets of patients though most patients were asymptomatic. In the TURP group, bacteraemia occurred within the first twenty minutes of the procedure in spite of antibiotics prophylaxis. In the catheter manipulation group, bacteraemia was present even prior to any urological manipulation. The case-control model demonstrated an association between urological instrumentation and the development of IE. Conclusion. This study has shown that bacteraemia during urological instrumentation is more prevalent than previously thought but is largely asymptomatic. Moreover, antibiotic prophylaxis in TURP patients fails to stop a significant proportion of intra-procedure bacteraemias. Asymptomatic bacteraemia may explain the statistical association between urological instrumentation and IE has been demonstrated.
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Ekdahl, Christer. "Infective Endocarditis : aspects of pathophysiology, epidemiology, management and prognosis." Doctoral thesis, Linköping : Department of Clinical and Experimental Medicine, Linköping University, 2008. http://www.bibl.liu.se/liupubl/disp/disp2008/med1017s.pdf.

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Vesey, Peter Mark. "Antigen expression of oral streptococci associated with infective endocarditis." Thesis, University of Newcastle Upon Tyne, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.324795.

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de, Villiers Marthinus Coenraad. "The changing landscape of infective endocarditis in South Africa." Master's thesis, Faculty of Health Sciences, 2019. http://hdl.handle.net/11427/31498.

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Background. Little is known about the current clinical profile and outcomes of patients with infective endocarditis (IE) in South Africa. Methods. We conducted a retrospective review of the records of patients admitted to Groote Schuur Hospital between 2009 and 2016 fulfilling universal criteria for definite or possible IE, in search of demographic, clinical, microbiological, echocardiographic, treatment and outcome information. Results. 105 patients fulfilled the modified Duke criteria for IE. The median age of the cohort was 39 years (IQR 29-51), with a male preponderance (61.9%). The majority of patients (72.4%) had left-sided native valve endocarditis, 14% had right-sided disease, and 13.3% had prosthetic valve endocarditis. A third of the cohort had rheumatic heart disease. Although 41.1% of patients with left-sided disease had negative blood cultures, the three most common organisms cultured in this subgroup were Staphylococcus aureus (18.9%), Streptococcus spp. (16.7%) and Enterococcus spp. (6.7%). Participants with right-sided endocarditis were younger (29 years (IQR 27-37)), were predominantly intravenous drug users (IVDU; 73.3%) and the majority cultured positive for S. aureus (73.3%) with frequent septic pulmonary complications (40.0%). The overall in-hospital mortality was 16.2%, with no deaths in the group with right-sided endocarditis. Predictors of death in our patients were heart failure (OR 8.16, CI 1.77-37.70; p=0.007) and an age > 45 years (OR 4.73, CI 1.11- 20.14; p=0.036). Valve surgery was associated with a reduction in mortality (OR 0.09, CI 0.02-0.43; p=0.003). Conclusions. Infective endocarditis in a typical teaching tertiary care centre in South Africa remains an important clinical problem. In this setting, it continues to affect mainly young people with post-inflammatory valve disease and congenital heart disease. IE is associated with an in-hospital mortality that remains high. Intravenous drug-associated endocarditis caused by S. aureus is an important IE subset, comprising approximately 10% of all cases, a fact which was not reported 15 years ago, and culture-negative endocarditis remains highly prevalent. Heart failure in IE carries significant risk of death and needs a more intensive level of care in hospital. Finally, cardiac surgery was associated with reduced mortality, with the largest impact in those patients with heart failure.
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Wong, Chloe. "Patients Diagnosed with Infective Endocarditis: A Retrospective Chart Review." The Ohio State University, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu1591717038456204.

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Turner, Lauren. "Identification of Virulence Determinants for Streptococcus sanguinis Infective Endocarditis." VCU Scholars Compass, 2008. http://scholarscompass.vcu.edu/etd/1560.

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Streptococcus sanguinis is the second most common causative agent of bacterial infective endocarditis (IE). Risk of S. sanguinis IE is dependent on pre-disposing damage to the heart valve endothelium, which results in deposition of clotting factors for formation of a sterile thrombus (referred to as vegetation). Despite medical advances, high mortality and morbidity rates persist. Molecular characterization of S. sanguinis virulence determinants may enable development of prevention methods. In a previous screen for S. sanguinis virulence determinants by signature-tagged mutagenesis (STM) an attenuated mutant was identified with a transposon insertion in the nrdD gene, encoding an anaerobic ribonucleotide reductase. Evaluation of this mutant, as well as an nrdD in-frame deletion mutant, JFP27, by a soft-agar growth assay confirmed the anaerobic growth sensitivity of these strains. These studies suggest that an oxygen gradient occurs at the site of infection which selects for expression of anaerobic-specific genes at the nexus of the vegetation. The random STM screen failed to identify any favorable streptococcal surface-exposed prophylactic candidates. It was also apparent that additional genetic tools were required to facilitate the in vivo analyses of mutant strains. As it was desirable to insert antibiotic resistance markers into the chromosome, we identified a chromosomal site for ectopic expression of foreign genes. In vitro and in vivo analyses verified that insertion into this site did not affect important cellular phenotypes. The genetic tools developed facilitated further in vivo screening of S. sanguinis cell wall-associated (Cwa) protein mutants. A directed application of STM was employed for a comprehensive analysis of this surface protein class in the rabbit model of IE. Putative sortases, upon which Cwa proteins are dependent for cell surface localization, were also evaluated. No single S. sanguinis Cwa protein was determined essential for IE by STM screening; however competitiveness for colonization of the infection site was reduced for the mutant lacking expression of sortase A. The studies described here present a progressive picture of S. sanguinis IE, beginning with surface protein-dependent colonization of the vegetation in early IE, that later shifts to a bacterial persistence in situ dependent on condition-specific housekeeping genes, including nrdD.
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Books on the topic "Infective endocarditis"

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L, Brusch John, ed. Infective endocarditis. New York: Oxford University Press, 1996.

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Habib, Gilbert, ed. Infective Endocarditis. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-32432-6.

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Siniawski, Henryk. Active Infective Aortic Valve Endocarditis with Infection Extension. Heidelberg: Steinkopff, 2006. http://dx.doi.org/10.1007/3-7985-1629-4.

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L, Dominguez Claudia, and Ramos Alba M, eds. Bacterial endocarditis: Etiology, pathogenesis, and interventions. New York: Nova Science Publishers, 2008.

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An atlas of infective endocarditis: Diagnosis and management. Pearl River, N.Y., USA: Parthenon Pub. Group, 1995.

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Endocarditis essentials. Sudbury, Mass: Jones & Bartlett Learning, 2011.

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Steven, Bolling, and Vlessis Angelo A, eds. Endocarditis: A multidisciplinary approach to modern treatment. Armonk, NY: Futura, 1999.

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Shorrock, Patricia Joan. Surface properties of enterococcus faecalis in relation to infective endocarditis. Birmingham: Aston University. Department of Pharmaceutical Sciences, 1990.

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Mitral valve prolapse: Benign syndrome? [Barrie, Ont.]: Wellington House Press, 1990.

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Infective Endocarditis. Academic Press, 1988.

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Book chapters on the topic "Infective endocarditis"

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Tleyjeh, Imad M., and Aref A. Bin Abdulhak. "Definition and Epidemiology of Infective Endocarditis." In Infective Endocarditis, 3–13. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-32432-6_1.

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Hayley, Bradley, and Kwan Leung Chan. "Infectious Complications in Infective Endocarditis." In Infective Endocarditis, 123–36. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-32432-6_10.

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Kang, Duk-Hyun. "Embolic Complications in Infective Endocarditits." In Infective Endocarditis, 137–48. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-32432-6_11.

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Snygg-Martin, Ulrika. "Neurological Complications in Infective Endocarditis." In Infective Endocarditis, 149–68. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-32432-6_12.

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Marechaux, Sylvestre, and Christophe Tribouilloy. "Prosthetic Valve Endocarditis." In Infective Endocarditis, 171–86. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-32432-6_13.

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Arif, Sana, Larry M. Baddour, and M. Rizwan Sohail. "Cardiac Device Related Endocarditis." In Infective Endocarditis, 187–205. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-32432-6_14.

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Vilacosta, Isidre, Carmen Olmos Blanco, Cristina Sarriá Cepeda, Javier López Díaz, Carlos Ferrera Durán, and José Alberto San Román Calvar. "Right-Heart Endocarditis." In Infective Endocarditis, 207–22. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-32432-6_15.

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Lancellotti, Patrizio. "Non-bacterial Thrombotic Endocarditis." In Infective Endocarditis, 223–29. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-32432-6_16.

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Kuijpers, Joey Mike, Berto J. Bouma, and Barbara J. M. Mulder. "Infective Endocarditis in Congenital Heart Disease." In Infective Endocarditis, 231–44. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-32432-6_17.

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Fournier, Pierre-Edouard, George Watt, Paul N. Newton, Cristiane C. Lamas, Pierre Tattevin, and Didier Raoult. "Blood Culture-Negative Endocarditis." In Infective Endocarditis, 245–58. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-32432-6_18.

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Conference papers on the topic "Infective endocarditis"

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Ganesan, D., H. Grewal, A. Goodman, and I. G. Amzuta. "A Quintessential Masquerader of Infective Endocarditis." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a3766.

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Nigri, R., A. Barajas-Ochoa, W. Roque, R. Bembry, S. Rashid, and M. S. Ayyala. "Septic Pulmonary Emboli Secondary to Infective Endocarditis." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a3921.

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Al-Alwan, A., V. Sirpal, S. N. Yarrarapu, H. A. Fichadiya, C. H. Vyas, R. Tiperneni, and F. Heis. "Citrobacter Koseri Infective Endocarditis with Septic Endophthalmitis." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a1644.

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Moreno, Albino, Raquel Valdés, Luis Jiménez, Enrique Vallejo, Salvador Hernández, and Gabriel Soto. "Infective endocarditis detection through SPECT/CT images digital processing." In SPIE Medical Imaging, edited by Stephen Aylward and Lubomir M. Hadjiiski. SPIE, 2014. http://dx.doi.org/10.1117/12.2043765.

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Khan, J. J., M. D. Hashmi, S. Elmahdy, and C. Barnett. "Murmur in Infective Endocarditis: Not What You Might Think." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a3421.

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Li, W., and J. Yusuff. "An Uncommon Cause of Infective Endocarditis - Group G Streptococcus." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a3463.

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Shaikh, F., W. Shamsi, K. Bibi, and P. P. Patel. "A Valve That Suddenly Leaked- Chordal Rupture from Infective Endocarditis." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a3484.

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Xenakis, J., K. Amlani, and H. Mopuru. "Infective Endocarditis Secondary to Skin Popping Complicated by Septic Emboli." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a3983.

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Eyermann, R. "Valid Comparison of Infective Endocarditis (IE) Risk Constellations: Current Data." In 50th Annual Meeting of the German Society for Thoracic and Cardiovascular Surgery (DGTHG). Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1725809.

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Westhofen, S., E. Girdauskas, Y. Alassar, C. Detter, H. Reichenspurner, and L. Conradi. "Isolated Repair versus Replacement for Infective Native Mitral Valve Endocarditis." In 49th Annual Meeting of the German Society for Thoracic and Cardiovascular Surgery. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1705417.

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Reports on the topic "Infective endocarditis"

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AlBakri, Aref, Auswaf Ahsan, Manoj Vengal, KR Ashir, Abdul Majeed, and Hanan Siddiq. Antibiotic Prophylaxis before Invasive Dental Procedures for Patients at High-Risk of Infective Endocarditis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2022. http://dx.doi.org/10.37766/inplasy2022.7.0011.

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Review question / Objective: The aim of the present systematic review and meta-analysis is to determine whether there is a genuine clinical need for Antibiotic Prophylaxis(AP) for the prevention of Infective Endocarditis(IE) in high-risk individuals (particularly those with demonstrable structural heart diseases or valve surgery) undergoing invasive dental procedures. Information sources: PubMed, Science Direct, British Dental Journal and Cochrane Register of Controlled Trials. Search terms used included various combinations of the following subject headings and title or abstract keywords – prophylactic antibiotics, antibiotic prophylaxis, antimicrobial, dentist, extraction, implant, infective endocarditis, or bacterial endocarditis.
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Splitter, Gary A., Menachem Banai, and Jerome S. Harms. Brucella second messenger coordinates stages of infection. United States Department of Agriculture, January 2011. http://dx.doi.org/10.32747/2011.7699864.bard.

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Aim 1: To determine levels of this second messenger in: a) B. melitensiscyclic-dimericguanosinemonophosphate-regulating mutants (BMEI1448, BMEI1453, and BMEI1520), and b) B. melitensis16M (wild type) and mutant infections of macrophages and immune competent mice. (US lab primary) Aim 2: To determine proteomic differences between Brucelladeletion mutants BMEI1453 (high cyclic-dimericguanosinemonophosphate, chronic persistent state) and BMEI1520 (low cyclicdimericguanosinemonophosphate, acute virulent state) compared to wild type B. melitensisto identify the role of this second messenger in establishing the two polar states of brucellosis. (US lab primary with synergistic assistance from the Israel lab Aim 3: Determine the level of Brucellacyclic-dimericguanosinemonophosphate and transcriptional expression from naturally infected placenta. (Israel lab primary with synergistic assistance from the US lab). B. Background Brucellaspecies are Gram-negative, facultative intracellular bacterial pathogens that cause brucellosis, the most prevalent zoonosis worldwide. Brucellosis is characterized by increased abortion, weak offspring, and decreased milk production in animals. Humans are infected with Brucellaby consuming contaminated milk products or via inhalation of aerosolized bacteria from occupational hazards. Chronic human infections can result in complications such as liver damage, orchitis, endocarditis, and arthritis. Brucellaspp. have the ability to infect both professional and non-professional phagocytes. Because of this, Brucellaencounter varied environments both throughout the body and within a cell and must adapt accordingly. To date, few virulence factors have been identified in B. melitensisand even less is known about how these virulence factors are regulated. Subsequently, little is known about how Brucellaadapt to its rapidly changing environments, and how it alternates between acute and chronic virulence. Our studies suggest that decreased concentrations of cyclic dimericguanosinemonophosphate (c-di-GMP) lead to an acute virulent state and increased concentrations of c-di-GMP lead to persistent, chronic state of B. melitensisin a mouse model of infection. We hypothesize that B. melitensisuses c-di-GMP to transition from the chronic state of an infected host to the acute, virulent stage of infection in the placenta where the bacteria prepare to infect a new host. Studies on environmental pathogens such as Vibrio choleraeand Pseudomonas aeruginosasupport a mechanism where changes in c-di-GMP levels cause the bacterium to alternate between virulent and chronic states. Little work exists on understanding the role of c-di-GMP in dangerous intracellular pathogens, like Brucellathat is a frequent pathogen in Israeli domestic animals and U.S. elk and bison. Brucellamust carefully regulate virulence factors during infection of a host to ensure proper expression at appropriate times in response to host cues. Recently, the novel secondary signaling molecule c-di-GMP has been identified as a major component of bacterial regulation and we have identified c-di-GMP as an important signaling factor in B. melitensishost adaptation. C. Major conclusions, solutions, achievements 1. The B. melitensis1453 deletion mutant has increased c-di-GMP, while the 1520 deletion mutant has decreased c-di-GMP. 2. Both mutants grow similarly in in vitro cultures; however, the 1453 mutant has a microcolony phenotype both in vitro and in vivo 3. The 1453 mutant has increased crystal violet staining suggesting biofilm formation. 4. Scanning electron microscopy revealed an abnormal coccus appearance with in increased cell area. 5. Proteomic analysis revealed the 1453 mutant possessed increased production of proteins involved in cell wall processes, cell division, and the Type IV secretion system, and a decrease in proteins involved in amino acid transport/metabolism, carbohydrate metabolism, fatty acid production, and iron acquisition suggesting less preparedness for intracellular survival. 6. RNAseq analysis of bone marrow derived macrophages infected with the mutants revealed the host immune response is greatly reduced with the 1453 mutant infection. These findings support that microlocalization of proteins involved in c-di-GMP homeostasis serve a second messenger to B. melitensisregulating functions of the bacteria during infection of the host.
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