|Year : 2022 | Volume
| Issue : 1 | Page : 42-44
Escherichia coli urosepsis leading to native valve endocarditis
Sandeep Kamat1, V V. S.S. Sagar2, Chitturi Venkata Sai Akhil3, Sourya Acharya2, Samarth Shukla4, Sunil Kumar2
1 Department of Cardiology, Topiwala National Medical College and B.Y.L Nair Charitable Hospital, Mumbai, Maharashtra, India
2 Department of General Medicine, Jawaharlal Nehru Medical College and Acharya Vinoba Bhave Rural Hospital, Wardha, Maharashtra, India
3 Department of Pediatrics, Jawaharlal Nehru Medical College and Acharya Vinoba Bhave Rural Hospital, Wardha, Maharashtra, India
4 Department of Pathology, Jawaharlal Nehru Medical College and Acharya Vinoba Bhave Rural Hospital, Wardha, Maharashtra, India
|Date of Submission||05-Feb-2022|
|Date of Decision||15-Mar-2022|
|Date of Acceptance||19-Mar-2022|
|Date of Web Publication||26-Apr-2022|
V V. S.S. Sagar
Department of Medicine, Jawaharlal Nehru Medical College, Datta Meghe Institute of Medical Sciences (DU), Wardha, Maharashtra
Source of Support: None, Conflict of Interest: None
Escherichia coli, a Gram-negative facultative anaerobe, is the common causative organism leading to urinary tract infection. However, the involvement of endocardium by E. coli has been reported to be very rare in spite of the septicemia caused by this organism. However, the mortality rate due to infective endocarditis caused by E. coli was reported to be higher than due to other organisms like HACEK group of organisms. Conventional risk factors leading to infective endocarditis include cirrhosis of the liver, prosthetic heart valves, and other sources of infection like urosepsis. Here, we report the case of a 60-year-old diabetic male who presented with obstructive uropathy-induced urinary tract infection leading to infective endocarditis.
Keywords: Escherichia coli, Gram-negative bacteria, infective endocarditis, urinary tract infection
|How to cite this article:|
Kamat S, Sagar V V, Akhil CV, Acharya S, Shukla S, Kumar S. Escherichia coli urosepsis leading to native valve endocarditis. J Pract Cardiovasc Sci 2022;8:42-4
|How to cite this URL:|
Kamat S, Sagar V V, Akhil CV, Acharya S, Shukla S, Kumar S. Escherichia coli urosepsis leading to native valve endocarditis. J Pract Cardiovasc Sci [serial online] 2022 [cited 2022 May 25];8:42-4. Available from: https://www.j-pcs.org/text.asp?2022/8/1/42/344138
| Introduction|| |
Infectious endocarditis (IE) due to Escherichia More Details coli (E. coli) is rare, although it is a common organism leading to septicemia. The incidence of 0.51% was reported in endocarditis due to E. coli. Increased incidence has been reported in >70-year-old patients, particularly in older women. However, studies reported the incidence in younger patients also. Several risk factors can be attributed to the occurrence of infective endocarditis like hepatic cirrhosis, prosthetic cardiac valves, and any focus of infection like bacteremia, urosepsis. In addition to these risk factors, other comorbidities such as diabetes, excessive intake of alcohol, malignancy can be predisposing factors for the E. coli-induced infective endocarditis. Mitral valve has been reported more commonly affected in such cases. The low incidence of E. coli IE can be explained by the inability of E. coli to adhere to endocardium and circulating antibodies in the serum. There is an increased incidence of in-hospital mortality due to infective endocarditis caused by non-HACEK organisms, particularly E. coli. Hence, close attention is needed in E. coli IE during the hospital stay. Notably, the incidence of E. coli infective endocarditis has been recently increased both in immunocompetent and immunocompromised hosts leading to increased morbidity and mortality.
| Case Report|| |
A 60-year-old diabetic female came with complaints of left loin pain radiating to groin, lower abdominal pain, multiple episodes of high-grade fever associated with chills, burning micturition, increased frequency and urgency of urination, nausea, vomiting of three episodes, fatigue, and breathlessness which was of New York Heart Association grade 3 for 5 days.
On admission, the patient was febrile having pulse rate of 116/min, blood pressure of 130/80mm Hg, SpO2 on ambient air was 90%; hence, started on 2 L oxygen therapy with nasal mask after which saturation improved to 96%. On auscultation, bilateral basal crepitations and grade 2 pansystolic murmur best heard in mitral and tricuspid areas radiating to axilla during expiration. Per abdomen on examination revealed left loin tenderness.
Laboratory parameters- urine examination was found albumin trace, 30-40 pus cells and RBCs, haemoglobin 12g/dl, elevated Total leukocyte count 21,532 cells/cumm, platelet count 1.8lakh/cumm, raised serum creatinine 2.1mg/dl and serum urea 96mg/dl, reduced serum albumin 2.3g/dl. Urine culture was showed pink lactose fermenting translucent colonies of E. coli seen on MacConkey agar as shown in [Figure 1]. Ultrasound (USG) abdomen revealed left renal calculi with hydroureteronephrosis. Repeat blood investigations were suggestive of persistent leukocytosis. Repeat USG abdomen and pelvis have been done to rule out any focal renal and prostatic abscess which was normal. X-ray chest revealed opacities in bilateral perihilar and parenchymal lung fields with mild pleural effusion and a wedge-shaped peripheral opacity in the right lung field. Two-dimensional echocardiography revealed a small echogenic mass on anterior leaflets of mitral and tricuspid valves with prolapse causing moderate mitral and tricuspid regurgitation most likely vegetations, left ventricular ejection fraction 60% as shown in [Figure 2] and Video 1.
|Figure 1: Urine sample showing pink lactose fermenting translucent colonies of Escherichia coli seen on MacConkey agar|
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|Figure 2: (a and b) Small echogenic mass on anterior leaflets of mitral and tricuspid valves with prolapse causing mitral and tricuspid regurgitation most likely vegetations|
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Suspecting infective endocarditis, three blood cultures were drawn from three different sites 2 h apart revealed E. coli, inflammatory markers such as erythrocyte sedimentation rate 80mm/h, C-reactive protein 20mg/dl were grossly elevated. Antibiotic sensitivity testing was done on Mueller‒Hinton agar using disc diffusion method and found to be sensitive to nitrofurantoin, ceftriaxone, amikacin, gentamicin, and cotrimoxazole.
She was started initially on piperacillin-tazobactam 2.25g intravenous (IV) thrice a day, levofloxacin 500mg alternate day in renal doses, phenazopyridine 200mg twice a day, syrup disodium hydrogen citrate 15ml in 100ml water thrice a day, paracetamol 650mg thrice a day, and perinorm 10mg thrice a day. Insulin in divided doses was given to control hyperglycemia. Double J stenting was done on the left kidney.
Later, after getting the antibiotic sensitivity report, the patient was shifted to ceftriaxone 2gm IV twice a day, amikacin 500mg alternate day, lasix 40 mg twice a day, and carvedilol 3.125 mg half dose twice a day. After 4 weeks of treatment, the patient gradually improved symptomatically and two-dimensional echocardiography revealed no vegetations.
| Discussion|| |
Native valve endocarditis due to E. coli was reported to be extremely rare. Very few studies revealed the occurrence of infective endocarditis following urosepsis, especially in diabetics, immunocompromised hosts, and females. Noureddine et al. had reported increased affection of Gram-negative bacteria in people with comorbidities compared to other organisms. Infective endocarditis following urinary tract infection can be attributable to consequences of immunologic and embolic phenomena. Low incidence of endocarditis due to E. coli was due to the fact that poor adherence to endocardium and lack of surface proteins that help in binding to host matrix molecules but possess extraintestinal virulence factors such as toxins adhesins, host defense avoidance systems, and iron acquisition systems which make them potentially pathogenic in extraintestinal sites.
Gram-negative infective endocarditis leads to increased morbidity and mortality necessitating aggressive management. IE complications caused by Gram-negative organisms are renal failure, central nervous system involvement, and cardiac dysfunction. Pseudomonas infection superadded with E. coli frequently leads to annular abscesses, systemic embolization, and heart failure.
Very few guidelines are available in treating Gram-negative causative infective endocarditis. A combination of parenteral cephalosporin and an aminoglycoside is sensitive. However, extended spectrum beta lactamase ESBL-producing E. coli strains require carbapenem +/-aminoglycoside. Judicious antibiotic dosage after antibiotic sensitivity testing has been recommended with accurate monitoring of adverse drug reactions.
A similar case was reported by Lauridsen et al in a 67 year old patient who developed infective endocarditis affecting mitral valve. Rangarajan et al. had reported a case of an old individual with urinary infection and septicemia due to Gram-negative organisms who had later developed endocarditis affecting mitral valve with a preexisting coronary artery disease, contributing to declining left ventricular function and heart failure, finally, necessitating surgical intervention.
In our case, one major (vegetation over anterior mitral and tricuspid leaflets and mitral valve regurgitation on 2D echo) and three minor (fever, vascular phenomena such as pulmonary infarct and blood culture revealed E. coli) criteria fulfilled for modified Duke Criteria. Here, the patient had primary urinary tract infection which later led to infective endocarditis even without known history of cardiac disease. The patient was managed with intravenous antibiotics with good response to treatment without the necessity of surgical intervention.
| Conclusion|| |
Urosepsis has to be considered as an important risk factor for E. coli endocarditis that had no previous cardiac history. Prolonged fever in urinary tract infection in spite of appropriate antibiotic therapy should be evaluated further to rule out endocarditis that helps to reduce associated morbidity and mortality.
Appropriate consent was taken from the relatives of the patient before making the case report. As this is a case report the university's guideline does not require an ethical committee and/or Institutional Review Board (IRB) clearance for its scientific publication.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that her name and initials will not be published and due efforts will be made to conceal her identity, but anonymity cannot be guaranteed.
We thank microbiologists for providing pictures of E. coli on urine and blood cultures.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2]