Abstract
Escherichia coli is a rare cause of infectious endocarditis. We report a clinical case of E. coli endocarditis of a native mitral valve in a young 26-year-old woman with a recurrent urinary tract infection who had a high fever for one week despite probabilistic treatment with amoxcillin-clavulanic acid 3 g per day. The patient was successfully treated with antibiotics and recovered without surgery.
Keywords: Endocarditis, Mitral valve, Native, Urinary tract infection, Escherichia coli
Background
Infectious endocarditis (IE) caused by Escherichia coli (E.coli) is rare, despite the frequency of septicaemia due particularly to this bacterium. E. coli is the causative microorganism in approximately 0.51 % of cases of IE [1]. Thirty-six cases of E. coli native valve IE that met the Duke criteria were reported in the literature from 1909 to 2002, and urinary tract infection was the most common cause of endocarditis due to E. coli [2]. The low incidence of E. coliIE has been attributed to the inability of this bacterium to adhere to the endocardium as well as the existence of antibodies to E. coli in normal serum [3]. Notably, however, the number of > 70-year-old patients with E. coli IE has recently increased, and about 70 % of affected patients are older women [2]. In addition, the mortality rate of E. coli IE (21 %) is higher than that of IE due to Haemophilus spp, Aggregatibacter spp, Cardiobacterium hominis, Eikenella corrodens, and Kingela spp (HACEK group). [1,4].
We report a clinical case of E. coli endocarditis of a native mitral valve in a young 26-year-old woman with a recurrent urinary tract infection who had a high fever for one week despite probabilistic treatment with amoxcillin-clavulanic acid 3 g per day.
Case report
The patient, 26 years old woman, had been presenting for one week a high fever despite probabilistic treatment with amoxcillin-clavulanic acid 3 g per day, asthenia, chills, palpitations, general alteration of state, without any notion of chest pain and syncope. The anamnesis reported a notion of untreated stomatological affection and recurrent urinary tract infections. The initial clinical examination found the patient to be febrile at 39.9 °C, blood pressure at 10/6 mmHg, heart rate at 130bat/min and respiratory rate at 24 cycles/min. Cardiovascular examination revealed stetho-acoustic semiology of mitral and aortic insufficiency. Transthoracic and transoesophageal echocardiography revealed the presence of a vegetation at the mitral valve (18 × 12 mm) (Fig. 1).
Fig. 1.
Infective endocarditis of the mitral valve in para-sternal long axis section.
A chest radiograph showed no obvious signs suggesting pneumonia or pulmonary congestion. Electrocardiography showed sinus tachycardia and no other abnormalities. Laboratory tests showed a white blood cell count of 15,500/mm3 with neutrophilic polynuclear predominance, C-reactive protein at 316 mg/dl, procalcitonin at 24 μg/L, hypochromic microcytic anemia with normal ferritin levels. Blood cultures were done by collecting three consecutive blood samples at intervals of one hour. The blood culture bottles were incubated at 37 °C for 18−24 h. The broth was subcultured on to 5% sheep blood agar and Bromocresol purple and incubated at 37 °C. After 18 h of incubation, Bromocresol purple agar medium showed lactose-fermenting colonies, about 2−3 mm in diameter. Colonies on blood agar were grey and non-haemolytic. They were found to be Gram-negative, motile, pleomorphic, coccobacilli, which were oxidase negative and catalase positive. An API 20E® gallery (Bio- Mérieux, Marcy l'étoile France) allowed the identification of 98.9 % E. coli with excellent identification (Code5144572). Culture of the urine also grew E. coli with a colony count of >106 CFU/mL. The sputum culture showed no significant growth of pathogenic bacteria.
The antibiogram was carried out by diffusion method in Mueller-Hinton agar medium in compliance with the recommendations of EUCAST 2020. The study of antibiotic sensitivity showed that this strain was resistant to ampicillin, ticarcillin and amoxicillin-clavulanic acid, sensitive to ceftriaxone, cefotaxime, imipenem, gentamicin, amikacin, ciprofloxacin, norfloxacin, Piperacillin + Tazobactam, cefoxitin and sulfamethoxazole-trimethoprim.
Based on these findings, the patient was diagnosed with IE due to E. coli in accordance with the modified Duke criteria [5].
The patient was treated with intravenous infusion of ceftriaxone 2 g twice daily for six weeks and amikacin 160 mg once daily for ten days. He responded well to treatment and was afebrile within 72 h after initiation of therapy. Antibiotic treatment was continued for sex weeks. Repeat blood cultures were sterile.
Discussion
E. coli has emerged in recent years as an increasingly important cause of morbidity and mortality in both immunocompetent and immunosuppressed persons [6]. Nevertheless it remains an extremely uncommon cause of IE [7]. The increase in the numbers of immunocompromised patients has led to a change in the spectrum of organisms causing native valve endocarditis. E. coli is a common cause of urinary tract infections [6]. The low incidence of endocarditis caused by this organism has been attributed to its inability to adhere to endocardium, and also to the fact that normal serum often has antibodies to E. coli [8]. Gram-negative bacteria are less sensitive to complement-mediated lysis and other humoral innate immune defences; they lack surface proteins that specifically bind host matrix molecules and prosthetic material which make them rare causative agents of IE [6]. However, they possess virulence factors such as adhesins, iron acquisition systems, and toxins which make them serious pathogens once they gain entry into a normally sterile extra intestinal site [9]. IE caused by Gram-negative organisms is associated with high mortality and significant morbidity and necessitates aggressive medical management and early surgical intervention. This patient had no history of cardiac disease and the source of the infection was likely to be the urinary tract. He responded well to antibiotic therapy and did not require surgical intervention.
Conclusion
Urinary tract infection appears to be an important predisposing factor in the development of E. coli endocarditis in this young woman who had no specific cardiac risk factors. Persistent fever even in an immunocompetent individual with a urinary tract infection despite specific antibiotic treatment should be investigated to rule out serious infections such as endocarditis.
Author statement
All authors have seen and agreed to the submitted version of the paper, and bear responsibility for it.
Ethical approval
This study was conducted in accordance with the Declaration of Helsinki and was approved by the ethics committee of the Mohammed V Military University Hospital in Rabat.
Consent
The patient agreed to sign a bilingual consent to participate in our study. This signed consent was archived in the bacteriology department of the Mohammed V Military University Hospital in Rabat.
Author contributions
BE, YB have been involved in drafting in the manuscript, CM, MA ha revising the manuscript and ELM have given final approval of the version to be published.
Declaration of Competing Interest
The authors report no declarations of interest.
Contributor Information
E. Benaissa, Email: benaissaelmostafa2@gmail.com.
Ben Lahlou Yasssine, Email: benlahlouyassine@gmail.com.
M. Chadli, Email: mariamachadli@gmail.com.
A. Maleb, Email: maleb.adil@gmail.com.
M. Elouennass, Email: elouennassm@yahoo.fr.
References
- 1.Morpeth S., Murdoch D., Cabell C.H., Karchmer A.W., Pappas P., Levine D. International collaboration on endocarditis prospective cohort study (ICE-PCS) investigators. Non-HACEK gram-negative bacillus endocarditis. Ann Intern Med. 2007;147:829–835. doi: 10.7326/0003-4819-147-12-200712180-00002. [DOI] [PubMed] [Google Scholar]
- 2.Micol R., Lortholary O., Jaureguy F., Bonacorsi S., Bingen E., Lefort A. Escherichia coli native valve endocarditis. Clin Microbiol Infect. 2006;12:401–403. doi: 10.1111/j.1469-0691.2006.01375.x. [DOI] [PubMed] [Google Scholar]
- 3.Watanakunakorn C., Burket T. Infective endocarditis in a large community teaching hospital, 1980-1990. A review of 210 episodes. Medicine. 2013;72:90–102. doi: 10.1097/00005792-199303000-00003. [DOI] [PubMed] [Google Scholar]
- 4.Chambers S.T., Murdoch D., Morris A., Holland D., Pappas P., Almela M. International collaboration on endocarditis prospective cohort study investigators. HACEK infective endocarditis: characteristics and outcomes from a large, multinational cohort. PLoS One. 2013 8. [Google Scholar]
- 5.Baddour L.M., Wilson W.R., Bayer A.S., Fowler V.G., Tleyjeh I.M., Rybak M.J. Infective endocarditis in adults: diagnosis, antimicrobial therapy, and management of complications. Circulation. 2015;132:1435–1486. doi: 10.1161/CIR.0000000000000296. [DOI] [PubMed] [Google Scholar]
- 6.Menon T., Balakrishnan N., Somasundaram S., Dhandapani P. Native valve endocarditis caused by Escherichia coli. J Clin Diagn Res. 2017;11(6):DD05–DD06. doi: 10.7860/JCDR/2017/27201.10046. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 7.Johannes S. Escherichia coli endocarditis of the aortic valve with formation of a paravalvular abscess cavity. Echocardiography. 2005;22:126. doi: 10.1111/j.0742-2822.2005.03178.x. [DOI] [PubMed] [Google Scholar]
- 8.Watanakunakorn C., Burket T. Infective endocarditis in a large community teaching hospital 1980-1990. A review of 210 episodes. Medicine. 2013;72:90–102. doi: 10.1097/00005792-199303000-00003. [DOI] [PubMed] [Google Scholar]
- 9.Russo T.A., Johnson J.R. Proposal for a new inclusive definition for extraintestinal pathogenic isolates of Escherichia coli: ExPEC. J Infect Dis. 2000;181:1753–1754. doi: 10.1086/315418. [DOI] [PubMed] [Google Scholar]

