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Epidemiological and microbial trends of infective endocarditis in western Norway: a 7-year prospective observational study

BMC Infectious Diseases volume 24, Article number: 702 (2024) Cite this article

Abstract

Background

In this prospective, observational study, we aimed to investigate epidemiologic and microbial trends of infective endocarditis in western Norway.

Methods

Clinical and microbiological characteristics of 497 cases of infective endocarditis from 2016 through 2022 were investigated. Categorical data were analysed using Chi-squared tests. Survival data were analysed using multiple Cox regression and reported using hazard ratios.

Results

The mean age was 67 years, and 74% were men. The annual incidence rates varied from 10.4 to 14.1 per 100,000 inhabitants per year. Infective endocarditis on native valves was observed in 257 (52%) of the cases, whereas infective endocarditis on prosthetic valves and/or cardiac implantable electronic devices was observed in 240 (48%) of the cases: infection on surgically implanted bioprostheses was observed in 124 (25%) of the patients, infection on transcatheter aortic valve implantation was observed in 47 (10%) patients, and infection on mechanical valves was observed in 34 (7%) cases. Infection related to cardiac implantable electronic devices was observed in a total of 50 (10%) cases.

Staphylococcus aureus and viridans streptococci were the most common microbial causes, and isolated in 145 (29%) and 130 (26%) of the cases, respectively.

Enterococcal endocarditis showed a rising trend during the study period and constituted 90 (18%) of our total cases of infective endocarditis, and 67%, 47%, and 26% of the cases associated with prosthetic material, transcatheter aortic valve implantation and cardiac implantable electronic devices, respectively.

There was no significant difference in 90-day mortality rates between the native valve endocarditis group (12%) and the group with infective endocarditis on prosthetic valves or cardiac implants (14%), p = 0.522. In a model with gender, age, people who inject drugs, microbiology and type of valve affected, only advanced age was significantly associated with fatal outcome within 90 days.

Conclusions

The incidence of infective endocarditis, and particularly enterococcal endocarditis, increased during the study period. Enterococci appeared to have a particular affinity for prosthetic cardiac material. Advanced age was the only independent risk factor for death within 90 days.

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Background

Infective endocarditis (IE) has a considerable burden on critical healthcare resources with estimated in-hospital mortality rates up to 18% [1]. The epidemiology is changing, probably due to increasing age in the IE- population, a lower threshold for heart valve surgery, and increased diagnostic awareness [1, 2]. During the last decade, the prevalence of enterococcal endocarditis (EE) has increased, the importance of which is also reflected in the revised Duke-ISCVID criteria, where the identification of Enterococcus faecalis is proposed as a major criterion for IE [2,3,4,5]. Our previous study, retrospectively covering IE in western Norway during the period 1996–2015, showed increasing overall annual incidence rates of IE from 4.6 – 7.4 per 100.000 inhabitants and a significant increase in enterococcal endocarditis (EE) from 4 to 13% during the two decades [6].

To follow the most recent IE trends, explore correlations in more detail, and propose possible explanations for the observed changes, we prospectively collected and investigated comprehensive clinical and microbiological data from a total of 497 patients treated for IE in our region in western Norway from 2016 through 2022. The main aims of the present study were to investigate clinical features and microbial causes of IE, risk factors for fatal outcome, and predictors of native valve endocarditis (NVE) and prosthetic valve endocarditis (PVE), including IE on transcatheter aortic valve implantation (TAVI) and cardiac implantable electronic devices (CIED).

Materials and methods

Study setting and population

Clinical and microbiological data from 497 IE cases in the period 2016 through 2022 were prospectively collected. All patients were recruited from the tertiary care hospital Haukeland University Hospital (HUH) or the secondary care hospital Haraldsplass Deaconess Hospital (HDH), both located in the municipality of Bergen, western Norway. The population of the catchment area increased from 513,038 to 547,458 during the study period [7]. In addition, HUH has a regional responsibility for IE-patients with a complicated clinical course requiring multidisciplinary evaluation by infectious disease specialists, cardiologists and cardiothoracic surgeons for the entire Health Region West, comprising 1.1 million inhabitants [7]. To minimize referral bias, only patients belonging to the catchment areas of HUH or HDH were included in the incidence calculations whereas all patients were included in the statistical analysis to reflect the patient composition of the total sample.

All patients included were ≥ 18 years of age. Cases were identified upon admission and included when the diagnosis of definite or possible IE according to the modified Duke criteria and the 2015 ESC guidelines, was established [8, 9]. Both patients with definite and possible IE were included, as patients in both groups received similar treatment, in line with the national guidelines for antimicrobial therapy of endocarditis in Norway [10]. Repeated IE included both relapse and reinfection. Sample collection procedures and antibiotic treatment practices remained unchanged during the study period. The study was approved by the Regional Committee for Medical Research Ethics Western Norway (REK Vest, approval no. 2015/ 1170). Written, informed consent was obtained from all patients.

All-cause mortality at 90 days was chosen as the main endpoints since death within this relatively wide timeframe was considered the most sensible parameter for the estimation of IE-related death, in line with previous publications [11, 12]. Secondary aims were predictors of NVE and PVE including CIED-IE and factors affecting the outcome in these two groups (NVE versus PVE/CIED-IE).

Microbial isolates

All microbial isolates were cultured from blood, and matrix-assisted laser desorption/ionization – time of flight (Maldi-TOF MS) was used for microbial speciation. In patients undergoing surgery, the excised valves were routinely cultured. All culture-negative valves were investigated using broad-range amplification of the bacterial 16S rRNA directly from the sample DNA, followed by Sanger sequencing (direct 16S rRNA sequencing).

Statistics

Data were analysed using IBM SPSS Statistics, Version 29.0.2.0 (Armonk, NY: IBM Corp). Continuous variables are presented as mean ± standard deviation and categorical variables as proportions. Groups were compared by Student’s t-test for continuous variables and Chi-squared tests for categorical variables. Survival was analysed by using univariable and multivariable Cox regression models and the results are reported using the hazard ratio (HRs) with 95% confidence intervals (CIs). A two-sided p-value ≤ 0.05 was considered statistically significant.

Results

Clinical characteristics

Baseline characteristics and outcomes are displayed in Table 1. The mean age was 67 years, and 366 (74%) of the patients were male. Eighty-one patients (16%) were people who inject drugs (PWID). Prior IE was documented in 85 patients (17%), diabetes mellitus in 75 (15%), dental visits within the last 6 months prior to admission as reported by the patients in 53 (11%) and 14 (3%) of the patients were treated with haemodialysis. A total of 50 patients (10%) with a mean age of 61 years, were referred from the tertiary care centre Stavanger University Hospital. In this cohort, 20 (40%) patients had a PVE/CIED-IE.

Table 1 Clinical characteristics, bacterial aetiology, and outcomes for the total IE group, NVE and PVE/CIED-IE in western Norway in the period 2016–2022
Full size table

As shown in Fig. 1, the annual incidence rates varied from 10.4–14.1 per 100 000 inhabitants per year in the period 2016–2022, with the lowest incidence in 2020.

Fig. 1
figure 1

Incidence of infective endocarditis per 100 000 persons per year in western Norway in the period from 2016–2022

Full size image

The aortic and mitral valves were affected in 338 (68%) and 103 (21%) of the patients, respectively. Among the aortic endocarditis cases were 23 patients with concomitant aortic and mitral valve infection, 14 patients with infection both on the aortic valve and a CIED, four patients with infection both on the aortic and tricuspid valve, and one patient with concomitant aortic and pulmonary valve infection. The tricuspid valve was affected in 58 (12%) patients whereas pulmonal valve endocarditis was evident in only three patients. Based on findings from echocardiography or positron emission tomography-computed tomography (PET-CT), several combinations of concomitant valve infections and combinations of valve and CIED infection were observed (Fig. 2).

Fig. 2
figure 2

Distribution of infective endocarditis on different valves in western Norway in the period 2016–2022

Full size image

NVE accounted for 257 (52%) of the cases, whilst 240 (48%) of the patients had PVE/CIED-IE. The mean age was significantly lower in the NVE than in the PVE/CIED-IE group (67 ± 18 vs. 72 ± 14, p < 0.001). Females accounted for 80 (31%) of the NVE patients and 51 (21%) of the PVE/CIED-IE patients (p = 0.012).

In the NVE group, 33 patients (13%) had a history of active malignancy detected within the last 5 years preceding admission, whilst 50 patients (21%) in the PVE/CIED-IE group had a similar history of malignancy (p = 0.017). Prostate/urogenital cancer and gastrointestinal cancer were most common in both groups (Table 1). The prevalence of newly detected malignancies during the hospital stay was 4% of patients in both groups (p = 0.918); the majority of which were gastrointestinal cancers.

IE on surgically implanted bioprostheses was identified in 124 (25%) patients, whereas TAVI-IE was identified in 47 (10%), and IE on a mechanical valve was identified in 34 (7%) patients. CIED-IE was identified in a total of 50 (10%) cases; in 24 (48%) of these, the infection was restricted to the CIED. Among the remaining cases of CIED-IE there was concomitant involvement of either a prosthetic (n = 15) or native (n = 11) valve. The mean time from TAVI-procedure to the development of IE was 1.4 years (± 1.2 years), cefazolin was used for antibacterial prophylactic treatment, and given 15–30 min prior to the procedure.

A total of 160 patients (32%) had surgical treatment for IE. Of these, 131 (81%) patients received biological prostheses, whereas mechanical prostheses were preferred in 24 patients (15%) (Table 1). Mitral valve repair was performed in 16 (3%) of the cases, tricuspid valve repair in two, whereas 29 patients (6%) had an aortic vascular graft implanted concomitantly with a valve.

Mortality rates

Thirty-day mortality was 42 (9%) whereas 65 patients (13%) died within 90 days after admission. A total of 192 patients (39%) died during the study period, with a mean follow-up of 3.2 years (± 2.3).

There was no significant difference in 90-day mortality rates between the NVE group and the PVE/CIED-IE group (12% versus 14%, p = 0.522) (Table 1).

A Cox regression analysis of mortality was performed, with administrative censoring at day 90 and surgery with mechanical or biological valve as a time-dependent covariate. In a model with gender, age, PWID, microbiological findings and type of valve affected, only high age (HR 1.04 per year, 95% CI 1.02–1.07, p < 0.001), was statistically significantly associated with fatal outcome (Table 2).

Table 2 Results from Cox regression analysisa of risk factors for fatal outcome in 497 patients treated for IE in western Norway in the period 2016 – 2022
Full size table

Microbiological findings

Staphylococcus aureus (S. aureus) was the most common bacterium, identified in 145 (29%) of the cases, followed by viridans streptococci in 130 (26%), enterococci in 90 (18%) and non-viridans streptococci in 35 (7%) of the cases. Thirty-six (7%) of the cases were culture negative (Table 1). Among the 90 cases of EE, Enterococcus faecalis was identified in 83 (92%), Enterococcus faecium in 6 (7%) and Enterococcus hirae in one case.

Enterococci were identified more often in PVE/CIED-IE than in NVE (25% vs. 12%, p < 0.001), whereas S. aureus was more frequently associated with NVE than PVE/CIED (38% vs. 20%, p < 0.001). In total, 67% of the IE cases related to cardiac prostheses and/or intracardial electronic devices were caused by enterococci.

The prevalence of different bacteria according to type of valve affected—categorized as native valve, surgically implanted bioprostheses, TAVI, mechanical prostheses and CIED are shown in Table 3.

Table 3 Microbial aetiology according to type of infected valves for patients with NVE, PVE and CIED IE in western Norway from 2016–2022
Full size table

Enterococci were more frequently identified in TAVI-IE (47%) than in the other groups (12%–26%). Staphylococcus aureus was more often associated with NVE (37%) and CIED (40%) than the other groups (13%–19%). Viridans streptococci were more often identified in NVE (30%) and in surgically implanted bioprotheses (30%) than in the other groups (3%-21%).

Microbial growth from the excised valves was obtained in 22 (14%) of the 160 operated patients, whereof enterococci constituted 9 (41%). Mean time from admission to surgery was shorter in the enterococcal group than in the S. aureus group (10 days ± 13 vs. 19 days ± 28, p = 0.022). All bacterial isolates cultured from the valves had already been recovered from blood cultures. Bacterial DNA was detected in 136 (85%) valve biopsies and provided microbial identification for eight culture negative cases.

A total of 55 patients were admitted with repeated IE. Relapse within 6 months occurred in two patients, whereas 53 patients had reinfection more than 6 months after the previous event. The mean time to reinfection was 3.3 years (± 2.3 years). Repeated IE was more frequently associated with PVE than NVE (n = 33, 60% vs. n = 22, 40%) but the difference was not significant, (p = 0.065). Staphylococcus aureus more often caused repeated IE in the NVE group than in the PVE/CIED-IE group (64% vs 15%, p < 0.001) whereas enterococci more often caused repeated IE in the PVE/CIED-IE group than in the NVE group (36% vs 9%, p = 0.023, supplementary Table 1).

Discussion

This prospective observational study investigated a large number of IE patients from one out of four Health Regions in Norway. Together with our recent retrospective study from the same region our data provides a complete description of developments in the incidence rates, clinical characteristics and microbiological findings associated with IE in our community over a period of three decades [6]. We found a rising incidence of IE related to prosthetic valves or cardiac implants and in the elderly population, and our data also illustrate a noteworthy increase in enterococcal endocarditis (EE).

Nearly 50% of TAVI-related IE was caused by enterococci, as compared to only 13% caused by S. aureus. These numbers differ considerably from those reported in previous studies and recent reviews, where S. aureus was reported as the major causative microbe in TAVI-IE, accounting for 20–30% of the cases, closely followed by enterococci, accounting for 13–25% [11, 13,14,15,16,17]. Furthermore, enterococci were the causative bacteria in 26% of our patients with CIED-IE, where the most prevalent microbe was S. aureus (40%). Surprisingly, coagulase negative staphylococci accounted for only one case in this group. The relatively high proportion of enterococcal CIED-IE also differed from that reported in previous studies, where S. aureus and CoNS were reported to cause as much as 60–70% of the total CIED-infections and enterococci were only identified in approximately 4% [1, 4, 18, 19]. Our EE patients resembled those in previous studies regarding comorbidities, age, and male predominance [3, 15].

An association between urologic or colorectal malignancies and enterococcal bacteriemia as well as an association between urologic procedures and EE has been described [20, 21]. Among our EE patients, a recent urologic procedure was registered for only 7%, and a novel malignancy was only diagnosed in six cases during the diagnostic work-up, three of which were gastrointestinal and only one prostatic. Taken together, we have not been able to identify any plausible underlying reasons for the higher incidence of EE in our material compared to previous studies. Nevertheless, our data strongly support that the empirical antibiotic regimen for suspected IE on TAVI or CIED should include effective coverage of enterococci. Further studies are warranted to identify risk factors for EE on foreign material.

Staphylococcus aureus was significantly more often identified in patients with NVE than PVE/CIED-IE (38% vs. 21%, p < 0.001). The identification of S. aureus in 18% of IE cases on mechanical valves differed from that found in a recent study on PVE in Sweden, where S. aureus accounted for 36% of IE on mechanical valves [22]. Although our patient sample was smaller (240 vs. 780 patients) and from a regional study and not nationwide registry, it is interesting to note such differences in microbial epidemiology of PVE between countries with supposedly similar demographics and clinical patient characteristics.

A total of 160 patients received valve replacement surgery. Bacterial DNA was detected in 136 (85%) of the valve biopsies and provided microbial identification for eight culture negative cases. Of the 22 tissue samples with continued per operative growth despite adequate antimicrobial therapy from admission, enterococci were identified in 9 (41%) and S. aureus in 6 (27%), respectively. Clearly, the small numbers do not allow firm conclusions, but we might speculate that this finding reflects enterococci and S. aureus as particularly difficult to eradicate from endocardial surfaces and foreign implants due to their capability of biofilm formation, although specific virulence factors for IE in these two bacteria have not yet been identified [23,24,25].

In our population, repeated endocarditis was observed in 55 patients. Among these, S. aureus and enterococci were the most frequent cause of repeated NVE and PVE/CIED-IE, respectively. Relapse of EE has been reported in as much as 10% of the patients, and valve replacement therapy has been found to be a protective factor against one-year relapse and death in this group [26]. Despite a clinical indication for surgery of EE, this is often not performed due to high age, risk, and frailty of the patient [11]. Reinfections with enterococci are frequent but less prevalent in patients treated with combination therapy with amoxicillin-gentamicin or amoxicillin-ceftriaxone compared to monotherapy with ampicillin [26]. Furthermore, a beneficial effect of suppressive antimicrobial treatment for EE has been documented [15]. Based on this, guidelines clarifying the indication for suppressive therapy after the first EE event should be established, as such a treatment option could possibly prevent repeated long-term hospital admissions for old and multimorbid patients.

The highest mortality rates were seen among our cases with IE caused by non-viridans streptococci and S. aureus with 30-day mortality rates of 11% and 10%, and 90-day mortality rates of 23% and 16%, respectively. IE caused by non-viridans streptococci and in particular beta-haemolytic streptococci (BHS), have been associated with in-hospital mortality rates between 13–20% in comparable studies [6, 27, 28]. The clinical presentation of IE caused by BHS resemble that of IE caused by S. aureus, with more often an initial dysregulated immune response to infection and need for more aggressive therapy and surgery than IE caused by viridans group streptococci [28, 29]. Interestingly, Streptococcus dysgalacticae accounted for 51% of IE caused by non-viridans streptococci in our patient cohort. This bacterium is increasingly associated with invasive infections, and is currently the fifth most common cause of bloodstream infections in our region [30].

In our previous study, the mean age of our IE-population increased from 58 to 60 years during the two decades 1996–2005 vs. 2006–2015 whilst 30-day mortality remained 13% and unchanged [6]. In the present study, the mean age increased to 67 years whilst 30-day mortality rate was 9% and lower than expected from comparable populations [31,32,33]. The reason for this rather striking increase in mean age in only seven years, is not known but noteworthy, as only advanced age remained an independent risk factor for increased 90 days mortality in the fully adjusted model.

We observed annual incidence rates of IE from 10.4 to 14.1 per 100 000 inhabitants per year, with a peak in 2019. Thereafter, a decline was observed in 2020, which we believe was partially associated with the SARS-CoV-2 pandemic. One might assume that the lock-down of the society prevented people from seeking medical care during the first pandemic wave, although Norway had a lower pandemic burden than most other countries. A similar trend for acute hospital admissions has been described in the United Kingdom (UK), although IE-specific data were not presented [34]. Furthermore, remote consulting was widely implemented among general practitioners in the UK in 2020 [35]. This might have led to diagnostic delay in complicated cases, as described in a case report on IE [36]. Our results might suggest that the Covid-19 pandemic influenced the availability of health-care services even in resourceful countries. However, both 30- and 90-day mortality rates were comparable in the period before and after 2019.

A previous study comparing IE in Northern and Southern Europe, documented a significant rise in EE over time, but did not identify major microbiological differences between regions [37]. Whilst IE in high-income countries reflects advances in highly specialized medicine, with an increasing number of patients with intracardial devices, rheumatic heart disease and congenital heart disease are still reported as the most common predisposing condition for IE in developing countries, although documentation is scarce [38, 39].

In the present study, only cases from a limited geographical region in a high-income country with a semi-decentralized structure of the specialist care were included. Therefore, the transferability to other regions might be questioned. Furthermore, this was an observational study without an age- and comorbidity matched control group, thus prohibiting a comparison of overall mortality rates at the end of the follow-up period. Nevertheless, we feel that the study provides important information on the epidemiology, patient characteristics, and microbial aetiology of IE, and will hopefully pave the way for future studies on this important infectious disease.

Conclusion

The incidence of infective endocarditis increased during the study period, but the mortality rates were relatively low. High age was the only independent risk factor for death within 90 days. Staphylococcus aureus was the most frequent bacterial cause overall, but the incidence of EE increased significantly during the study period and was particularly associated with PVE and CIED-IE. Further studies to identify risk factors for EE, and especially in those patients with TAVI and CIED, is warranted.

Availability of data and materials

The datasets used and analysed during the current study are available from the corresponding author on reasonable request.

Abbreviations

IE:

Infective endocarditis

CIED:

Cardiac implantable electronic devices

EE:

Enterococcal endocarditis

Duke-ISCVID:

Duke-International Society of Cardiovascular Infectious Diseases

NVE:

Native valve endocarditis

PVE:

Prosthetic valve endocarditis

TAVI:

Transcatheter aortic valve implantation

HUH:

Haukeland university hospital

HDH:

Haraldsplass deaconess hospital

Maldi-TOF MS:

matrix-assisted laser desorption/ionization Time of flight

RNA:

Ribonucleic acid

DNA:

Deoxyribonucleic acid

PWID:

People who inject drugs

S. aureus:

Staphylococcus aureus

BHS:

Betahaemolytic streptococci

SARS-CoV-2:

Severe acute respiratory syndrome coronavirus 2

UK:

United Kingdom

References

  1. Delgado V, Ajmone Marsan N, de Waha S, Bonaros N, Brida M, Burri H, . . . Borger MA. 2023 ESC Guidelines for the management of endocarditis. Eur Heart J. 2023;44(39):3948–4042.

  2. Fowler VG, Durack DT, Selton-Suty C, Athan E, Bayer AS, Chamis AL, . . . Miro JM. The 2023 Duke-International Society for Cardiovascular Infectious Diseases Criteria for Infective Endocarditis: Updating the Modified Duke Criteria. Clin Infect Dis. 2023;77(4):518–26.

  3. Fernández-Hidalgo N, Escolà-Vergé L, Pericàs JM. Enterococcus faecalis endocarditis: what’s next? Future Microbiol. 2020;15:349–64.

    Article  PubMed  Google Scholar 

  4. Pericàs JM, Llopis J, Muñoz P, Gálvez-Acebal J, Kestler M, Valerio M, et al. A Contemporary Picture of Enterococcal Endocarditis. J Am Coll Cardiol. 2020;75(5):482–94.

    Article  PubMed  Google Scholar 

  5. Dahl A, Fowler VG, Miro JM, Bruun NE. Sign of the Times: Updating Infective Endocarditis Diagnostic Criteria to Recognize Enterococcus faecalis as a Typical Endocarditis Bacterium. Clin Infect Dis. 2022;75(6):1097–102.

    Article  PubMed  Google Scholar 

  6. Jordal S, Kittang BR, Salminen PR, Eide GE, Kommedal Ø, Wendelbo Ø, . . . Sjursen H. Infective endocarditis in Western Norway: a 20-year retrospective survey. Infect Dis (Lond). 2018;50(10):757–63.

  7. Statistisk Sentralbyrå. 2024. Available from: www.ssb.no/befolkning/folketall/statistikk. Accessed 21.02.2024.

  8. Li JS, Sexton DJ, Mick N, Nettles R, Fowler VG Jr, Ryan T, et al. Proposed modifications to the Duke criteria for the diagnosis of infective endocarditis. Clin Infect Dis. 2000;30(4):633–8.

    Article  CAS  PubMed  Google Scholar 

  9. Habib G, Lancellotti P, Antunes MJ, Bongiorni MG, Casalta JP, Del Zotti F, et al. 2015 ESC Guidelines for the management of infective endocarditis: The Task Force for the Management of Infective Endocarditis of the European Society of Cardiology (ESC). Endorsed by: European Association for Cardio-Thoracic Surgery (EACTS), the European Association of Nuclear Medicine (EANM). Eur Heart J. 2015;36(44):3075–128.

    Article  PubMed  Google Scholar 

  10. Helsedirektoratet. Nasjonal faglig retningslinje for bruk av antibiotika i sykehus. 2021. Accessed 10.06.2024.

  11. Strange JE, Østergaard L, Køber L, Bundgaard H, Iversen K, Voldstedlund M, et al. Patient Characteristics, Microbiology, and Mortality of Infective Endocarditis After Transcatheter Aortic Valve Implantation. Clin Infect Dis. 2023;77(12):1617–25.

    Article  PubMed  PubMed Central  Google Scholar 

  12. Corcorran MA, Stewart J, Lan K, Gupta A, Glick SN, Seshadri C, et al. Correlates of 90-Day Mortality Among People Who Do and Do Not Inject Drugs With Infective Endocarditis in Seattle, Washington. Open Forum infect Dis. 2022;9(5):ofac150.

    Article  PubMed  PubMed Central  Google Scholar 

  13. Summers MR, Leon MB, Smith CR, Kodali SK, Thourani VH, Herrmann HC, et al. Prosthetic Valve Endocarditis After TAVR and SAVR: Insights From the PARTNER Trials. Circulation. 2019;140(24):1984–94.

    Article  PubMed  Google Scholar 

  14. Regueiro A, Linke A, Latib A, Ihlemann N, Urena M, Walther T, et al. Association Between Transcatheter Aortic Valve Replacement and Subsequent Infective Endocarditis and In-Hospital Death. JAMA. 2016;316(10):1083–92.

    Article  PubMed  Google Scholar 

  15. Garofoli N, Joly V, Le Pluart D, Hobson CA, Beaumont AL, Lariven S, et al. Enterococcal endocarditis management and relapses. JAC-Antimicrobial Resistance. 2024;6(2):dlae033.

    Article  PubMed  PubMed Central  Google Scholar 

  16. Del Val D, Panagides V, Mestres CA, Miró JM, Rodés-Cabau J. Infective Endocarditis After Transcatheter Aortic Valve Replacement: JACC State-of-the-Art Review. J Am Coll Cardiol. 2023;81(4):394–412.

    Article  PubMed  Google Scholar 

  17. Del Val D, Abdel-Wahab M, Mangner N, Durand E, Ihlemann N, Urena M, et al. Infective Endocarditis Caused by Staphylococcus aureus After Transcatheter Aortic Valve Replacement. Can J Cardiol. 2022;38(1):102–12.

    Article  PubMed  Google Scholar 

  18. Baddour LM, Epstein AE, Erickson CC, Knight BP, Levison ME, Lockhart PB, et al. Update on cardiovascular implantable electronic device infections and their management: a scientific statement from the American Heart Association. Circulation. 2010;121(3):458–77.

    Article  PubMed  Google Scholar 

  19. Hussein AA, Baghdy Y, Wazni OM, Brunner MP, Kabbach G, Shao M, et al. Microbiology of Cardiac Implantable Electronic Device Infections. JACC Clin Electrophys. 2016;2(4):498–505.

    Article  Google Scholar 

  20. Mohee AR, West R, Baig W, Eardley I, Sandoe JA. A case-control study: are urological procedures risk factors for the development of infective endocarditis? BJU Int. 2014;114(1):118–24.

    Article  PubMed  Google Scholar 

  21. Cabiltes I, Coghill S, Bowe SJ, Athan E. Enterococcal bacteraemia ‘silent but deadly’: a populationbased cohort study. Intern Med J. 2020;50(4):434–40.

  22. Berisha B, Ragnarsson S, Olaison L, Rasmussen M. Microbiological etiology in prosthetic valve endocarditis: A nationwide registry study. J Intern Med. 2022;292(3):428–37.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  23. Caixeta Magalhães Tibúrcio AA, Paiva AD, Pedrosa AL, Rodrigues WF, Bernardes da Silva R, Oliveira AG. Effect of sub-inhibitory concentrations of antibiotics on biofilm formation and expression of virulence genes in penicillin-resistant, ampicillin-susceptible Enterococcus faecalis. Heliyon. 2022;8(10):e11154.

    Article  PubMed  PubMed Central  Google Scholar 

  24. Johansson D, Rasmussen M. Virulence factors in isolates of Enterococcus faecalis from infective endocarditis and from the normal flora. Microb Pathog. 2013;55:28–31.

    Article  CAS  PubMed  Google Scholar 

  25. Bastien S, Meyers S, Salgado-Pabón W, Giulieri SG, Rasigade JP, Liesenborghs L, et al. All Staphylococcus aureus bacteraemia-inducing strains can cause infective endocarditis: Results of GWAS and experimental animal studies. J Infect. 2023;86(2):123–33.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  26. Danneels P, Hamel JF, Picard L, Rezig S, Martinet P, Lorleac’h A, et al. Impact of Enterococcus faecalis Endocarditis Treatment on Risk of Relapse. Clin Infect Dis. 2023;76(2):281–90.

    Article  CAS  PubMed  Google Scholar 

  27. Fernández Hidalgo N, Gharamti AA, Aznar ML, Almirante B, Yasmin M, Fortes CQ, et al. Beta-Hemolytic Streptococcal Infective Endocarditis: Characteristics and Outcomes From a Large, Multinational Cohort. Open Forum Infect Dis. 2020;7(5):ofaa120.

    Article  PubMed  PubMed Central  Google Scholar 

  28. Ruch Y, Hansmann Y, Riegel P, Lefebvre N, Mazzucotelli JP, Douiri N, et al. Virulence of beta-hemolytic streptococci in infective endocarditis. Infection. 2020;48(1):91–7.

    Article  CAS  PubMed  Google Scholar 

  29. Sendi P. Infective endocarditis caused by Streptococcus agalactiae: time for beta-hemolytic streptococci to follow treatment recommendations for S. aureus? Eur J Clin] Microbiol Infect Dis. 2019;38(3):419–22.

    Article  PubMed  Google Scholar 

  30. Oppegaard O, Glambek M, Skutlaberg DH, Skrede S, Sivertsen A, Kittang BR. Streptococcus dysgalactiae Bloodstream Infections, Norway, 1999–2021. Emerg Infect Dis. 2023;29(2):260–7.

    Article  PubMed  PubMed Central  Google Scholar 

  31. Murdoch DR, Corey GR, Hoen B, Miro JM, Fowler VG Jr, Bayer AS, et al. Clinical presentation, etiology, and outcome of infective endocarditis in the 21st century: the International Collaboration on Endocarditis-Prospective Cohort Study. Arch Intern Med. 2009;169(5):463–73.

    Article  PubMed  PubMed Central  Google Scholar 

  32. Erdem H, Puca E, Ruch Y, Santos L, Ghanem-Zoubi N, Argemi X, et al. Portraying infective endocarditis: results of multinational ID-IRI study. Eur J Clin Microbiol Infect Dis. 2019;38(9):1753–63.

    Article  CAS  PubMed  Google Scholar 

  33. Chu VH, Cabell CH, Benjamin DK Jr, Kuniholm EF, Fowler VG Jr, Engemann J, et al. Early predictors of in-hospital death in infective endocarditis. Circulation. 2004;109(14):1745–9.

    Article  PubMed  Google Scholar 

  34. Shah SA, Mulholland RH, Wilkinson S, Katikireddi SV, Pan J, Shi T, et al. Impact on emergency and elective hospital-based care in Scotland over the first 12 months of the pandemic: interrupted time-series analysis of national lockdowns. J R Soc Med. 2022;115(11):429–38.

    Article  PubMed  PubMed Central  Google Scholar 

  35. Murphy M, Scott LJ, Salisbury C, Turner A, Scott A, Denholm R, et al. Implementation of remote consulting in UK primary care following the COVID-19 pandemic: a mixed-methods longitudinal study. Br J Gen Pract. 2021;71(704):e166–77.

    Article  PubMed  PubMed Central  Google Scholar 

  36. Demetriades P, Ridley P, Yazdani F, Duckett S. Challenges of remote consultations: a delayed diagnosis of aortic valve endocarditis complicated by recurrent intracranial events. BMJ Case Rep. 2022;15(2):e248287. https://doi.org/10.1136/bcr-2021-248287.

  37. Ambrosioni J, Hernández-Meneses M, Durante-Mangoni E, Tattevin P, Olaison L, Freiberger T, et al. Epidemiological Changes and Improvement in Outcomes of Infective Endocarditis in Europe in the Twenty-First Century: An International Collaboration on Endocarditis (ICE) Prospective Cohort Study (2000–2012). Infect Dis Ther. 2023;12(4):1083–101.

    Article  PubMed  PubMed Central  Google Scholar 

  38. Mutagaywa RK, Vroon JC, Fundikira L, Wind AM, Kunambi P, Manyahi J, et al. Infective endocarditis in developing countries: An update. Front Cardiovasc Med. 2022;9:1007118.

    Article  PubMed  PubMed Central  Google Scholar 

  39. Bin Abdulhak AA, Baddour LM, Erwin PJ, Hoen B, Chu VH, Mensah GA, et al. Global and regional burden of infective endocarditis, 1990–2010: a systematic review of the literature. Glob Heart. 2014;9(1):131–43.

    Article  PubMed  Google Scholar 

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Acknowledgements

We would like to thank our colleagues at the clinical wards for help in inclusion of the patients. We would also express our great gratitude to all the patients who participated – without you, this study would not have been possible to perform.

Funding

Open access funding provided by University of Bergen.

Author information

Authors and Affiliations

  1. Section of Infectious Diseases, Department of Medicine, Haukeland University Hospital, Bergen, Norway

    Stina Jordal

  2. Department of Clinical Science, University of Bergen, Bergen, Norway

    Stina Jordal, Rune Haaverstad & Bård Reiakvam Kittang

  3. Department of Microbiology, Haukeland University Hospital, Bergen, Norway

    Øyvind Kommedal

  4. Section of Cardiothoracic Surgery, Department of Cardiology, Haukeland University Hospital, Bergen, Norway

    Rune Haaverstad & Pirjo-Riitta Salminen

  5. Department of Cardiology, Haukeland University Hospital, Bergen, Norway

    Sahrai Saeed & Einar Skulstad Davidsen

  6. Centre for Clinical Research, Haukeland University Hospital, Bergen, Norway

    Karl Ove Hufthammer

  7. Department of Medicine, Haraldsplass Deaconess Hospital, Bergen, Norway

    Bård Reiakvam Kittang

Authors
  1. Stina Jordal
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  2. Øyvind Kommedal
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  8. Bård Reiakvam Kittang
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Contributions

S.J., Ø.K. and B.R.K. designed the study, S.J. and B.R.K. included patients, drafted and revised the manuscript, S.J. and K.O.H. performed the statistical analysis. Ø.K. was the major collaborator in the microbiological services and revised the manuscript. R.H. and P.R.S. performed cardio-thoracic evaluation and revised the manuscript. E.S.D. and S.S. performed the cardiological evaluation and revised the manuscript. All authors reviewed the manuscript.

Corresponding author

Correspondence to Stina Jordal.

Ethics declarations

Ethics approval and consent to participate

The study was approved by the Regional Committee for Medical Research Ethics Western Norway (REK Vest, approval no. 2015/ 1170). Written, informed consent was obtained from all patients.

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Not applicable.

Competing interests

The authors declare no competing interests.

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Jordal, S., Kommedal, Ø., Haaverstad, R. et al. Epidemiological and microbial trends of infective endocarditis in western Norway: a 7-year prospective observational study. BMC Infect Dis 24, 702 (2024). https://doi.org/10.1186/s12879-024-09596-3

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  • DOI: https://doi.org/10.1186/s12879-024-09596-3

Keywords

BMC Infectious Diseases

ISSN: 1471-2334

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