Case Reports in Cardiology
Volume 2019 (2019), Article ID 5496851, 7 pages
https://doi.org/10.1155/2019/5496851

Case Report

Mitral Valve Endocarditis with Perforation from a Urinary Source: An Unusual Case and Literature Review

Fernando Figueroa Rodriguez, Antonio Faieta Lasarcina, and Francisco Davila Grijalva

Oakland University Beaumont Hospital, West 13 Mile Road, Royal Oak, MI 48073, USA

Correspondence should be addressed to Fernando Figueroa Rodriguez; fernando.figueroarodriguez@beaumont.org

Received 9 March 2019; Accepted 23 May 2019; Published 9 June 2019

Academic Editor: Ertugrul Ercan

Copyright © 2019 Fernando Figueroa Rodriguez et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract.

Aerococcus urinae (AU) is a rare pathogen, identified as gram-positive, catalase-negative coccus that grows in pairs and clusters which has been reported to mainly cause urinary tract infections (UTI), especially in elderly males. Treatment for this microorganism is usually with beta-lactams although cultures with antibiotic susceptibility testing are imperative. We present a case of AU endocarditis initially treated with IV antibiotics; nevertheless, the patient required emergent mitral valve replacement due to severe mitral insufficiency and perforation. We also present an analysis with high-yield points summarizing epidemiology, risk factors, microbiology, clinical features, diagnostic workup, and management of AU in general and AU endocarditis. Finally, we post a literature review of relevant cases and the impact of different variables associated with it.

1. Case Presentation

A 55-year-old male with no significant past medical history presented with a one-week history of nonproductive cough, dyspnea at rest, dysuria, and urinary frequency and urgency. He was diagnosed with a urinary tract infection (UTI) and a viral upper respiratory tract infection by his primary care physician two days prior and was prescribed ciprofloxacin. His symptoms did not improve so he decided to go to the emergency department (ED). Upon presentation, his oxygen saturation was noted to be 90%, with tachycardia and a low-grade fever. On exam, he had significant bibasilar crackles as well as a holosystolic apical murmur; additionally, he was found to have 2+ lower extremity edema and several punctuate macular lesions on his feet, highly suspicious for vascular emboli phenomena (Figure 1). His laboratory studies demonstrated leukocytosis with neutrophilia (14.7 bil/L and 11.3 bil/L, respectively) and evidence of acute kidney injury. The urinalysis bacteriuria and leukocytes. A chest X-ray (CXR) was unremarkable. Blood and urine cultures were obtained, and he was empirically started on ceftriaxone. A transthoracic echocardiogram revealed a mobile mass on the posterior leaflet of the mitral valve consistent with a vegetation. Ejection fraction was calculated to be 40% (Figure 2). Preliminary blood cultures reported gram-positive cocci in pairs and clusters. At day 3, AU was identified as the pathogen in both, blood and urine, cultures. The patient was then started on intravenous gentamicin and penicillin G with plans for a 6-week therapy. He was medically treated for acute heart failure with aggressive diuresis. At day 5, the patient received a transesophageal echocardiogram (TEE) which confirmed a “” vegetation attached to the posterior leaflet of mitral valve (Figure 3(a)), with severe mitral regurgitation and posterior leaflet perforation (Figure 3(b)). On day 8, the patient was acutely decompensated, and he was endotracheally intubated due to hypoxic respiratory failure and consequently underwent emergent prosthetic mitral valve replacement. He had a prolonged complicated postoperative period requiring mechanical ventilation, vasopressor support, and hemodialysis. Repeat blood cultures showed resolution of AU bacteremia. Finally, after 3 months, the patient was discharged to a subacute rehabilitation unit.

Figure 1: Right first toe with Janeway lesion (vascular emboli phenomena).

Figure 2: Arrowhead: TTE showing a mobile mass on the posterior leaflet of the mitral valve consistent with a vegetation.

(a)

(b)

Figure 3: (a) TEE image of vegetation on posterior leaflet of mitral valve, measuring “” (arrowhead). (b) TEE image with evidence of blood flow regurgitation with Doppler into the left atrium in the setting of the mitral valve posterior leaflet vegetation.

2. Discussion

AU is a rare pathogen, first isolated in 1953 found in lobsters and thought to be of no clinical significance. It was until 1967 when it was first described to cause infection in humans [1]. This organism is a gram-positive, catalase-negative growing coccus in clusters that belongs to a bacterial group referred to as Aerococcus-like organisms (ALO) [2]. It has been associated with UTI mainly, nevertheless there are reports that identify it as the culprit of blood stream infections and endocarditis. Due to difficulties in the biochemical identification, the incidence of infections with this microorganism has likely been underestimated. Currently, it is thought to be the cause of 0.15 to 0.54% of UTIs [1]; additionally, it is responsible for 0.03 to 0.05% of blood stream infections (BSI). There is not enough data regarding the incidence of AU endocarditis as there have been only 45 reports in English literature. Advanced age (>65 years) and underlying urologic conditions are the best-known risk factors for UTI and, potentially, BSI [3] and endocarditis. Both sexes are equally affected [4, 5].

The diagnosis is usually challenging due to the rarity of this pathogen. It is commonly mistaken with Staphylococcus sp. and even Streptococcus viridians; for this reason, molecular diagnostic techniques are often needed to identify it. Testing for leucine aminopeptidase, which is positive only for AU, can be used to differentiate it with Staphylococcus [6]. Secure identification also relies on genetic techniques like 16S ribosomal subunit sequencing or mass spectroscopic methods such as MALDI-TOF [7]. To date, there are no guidelines that recommend starting with any of these modalities, even in the presence of the above risk factors, as they are nonspecific, so the diagnostic algorithms remain the same as for the rest of the pathogens.

Due to the current lack of controlled scientific trials and lack of formalized treatment guidelines, therapy is often empiric and guided by expert opinion. In an effort to standardize a treatment, Yabes et al. in 2018 [8] compiled the reported cases and therapies in literature and found that treatment regimens for AU have largely relied on beta-lactams, with the possible addition of synergistic aminoglycosides for endocarditis. In vitro studies regarding the antibiotic susceptibilities of AU have shown susceptibility to amoxicillin, cefotaxime, ceftriaxone, doxycycline, linezolid, meropenem, penicillin, rifampin, and vancomycin. It had variable resistance to clindamycin, erythromycin, and levofloxacin [9–11]. It is, however, inherently resistant to sulfonamides and fluoroquinolones [10]. The duration of treatment vary from ten days for UTI and phlegmon to 14 to 28 days for BSI and 42 days (6 weeks) for endocarditis [8]. It is important to mention that treatment for the latter very commonly includes surgical intervention as well, but indications are the same as for other etiologies.

Overall mortality of AU infections, including UTI and BSI, has been shown to be equivalent to that of other etiologies. For endocarditis in particular, a higher rate of complications and mortality has been described, with 27% more when compared to other causes. It is thought that this could be associated with an older patient population with multiple other comorbidities, making their surgical profile highly unfavorable, and dependent on medical management only [8].

3. Literature Review

Between 2000 and 2012, the incidence of endocarditis in the United States increased from 11 per 100,000 population to 15 per 100,000 population [12, 13]. Nowadays, the precise incidence is difficult to ascertain because case definitions have varied over time between authors and between clinical centers. In addition, the presence of predisposing conditions such as rheumatic heart disease or injection drug use is variable over time and between regions and in low- and high-income countries [14, 15].

A literature search on PubMed, Web of Science, Cochrane, and Google Scholar databases revealed 45 cases of AU endocarditis in English literature (Table 1). We present a summary with a mathematical analysis and calculations involving all reports in an effort to identify patterns regarding risk factors, clinical course, treatment modalities, and prognosis.

Table 1: Summary of clinical characteristics of the forty-five AU endocarditis cases reported in English literature as well as our case.

Case
Age (years)
Gender
Comorbidities or risk factors
Affected valve
Surgery
Antibiotic regimen and duration
Survived?

1 [16]
69
M
Cystoscopy
Aortic
No
Beta-lactam and aminoglycoside for 6 weeks
Yes

2 [17]
54
M
Phimosis
Mitral
Yes
Beta-lactam for 6 weeks
Yes

3 [18]
43
M
Untreated hepatitis C
Aortic
No
Beta-lactam and aminoglycoside for 5 days
No

4 [19]
68
M
Indwelling urinary catheter
Aortic
Yes
Beta-lactam 6 weeks and aminoglycoside for 2 weeks
Yes

5 [20]
80
M
Nonurologic malignancy
Aortic
Yes
Beta-lactam for 2 weeks
Yes

6 [21]
77
M
Benign prostatic hypertrophy
Aortic
No
Beta-lactam and vancomycin; duration not reported
No

7 [22]
68
M
Benign prostatic hypertrophy
Mitral
No
Beta-lactam for 3 weeks; oral aminoglycoside duration not reported
Yes

8 [23]
75
M
Cystoscopy
Aortic
Yes
Beta-lactam and aminoglycoside for 6 weeks
Yes

9 [24]
89
M
Transurethral resection of prostate
Mitral
No
Beta-lactam and aminoglycoside for 7 days
No

10 [25]
81
M
Recurrent UTIs
Aortic
No
Beta-lactam 2 weeks and aminoglycoside for 8 days
No

11 [26]
42
M
None
Aortic
Yes
Beta-lactam and aminoglycoside for 6 weeks
Yes

12 [27]
49
M
Not reported
Aortic
Not reported
Beta-lactam and aminoglycoside; duration not reported
Yes

13 [28]
54
M
Urethral stricture
Tricuspid and aortic
No
Beta-lactam and aminoglycoside; duration not reported
No

14 [29]
69
M
Nonurologic malignancy
Aortic
Yes
Beta-lactam for 12 weeks
Yes

15 [30]
62
M
Benign prostatic hypertrophy
Mitral and aortic
Yes
Beta-lactam and rifampin for 6 weeks and aminoglycoside for 2 weeks
Yes

16 [31]
78
M
Aortic stenosis
Aortic
No
Beta-lactam and aminoglycoside for 10 days
No

17 [32]
74
M
Benign prostatic hypertrophy
Mitral
Yes
Beta-lactam and aminoglycoside for 4 weeks
No

18 [33]
81
M
Benign prostatic hypertrophy
Mitral
No
Beta-lactam and aminoglycoside for 6 weeks
Yes

19 [33]
78
M
Indwelling urinary catheter
Aortic
No
Beta-lactam; duration not reported
No

20 [33]
87
M
Benign prostatic hypertrophy
Mitral
No
Not reported
No

21 [33]
78
F
Ureteral stent
Aortic
No
Beta-lactam and vancomycin for 2 weeks
No

22 [34]
48
M
Atrial septal defect
Mitral
No
Beta-lactam and aminoglycoside; duration not reported
Yes

23 [34]
79
F
Recurrent UTIs
Aortic
No
Beta-lactam and aminoglycoside for 6 weeks
Yes

24 [35]
91
M
Indwelling urinary catheter
Mitral
Not reported
Beta-lactam for 4 weeks and aminoglycoside for 10 days
Yes

25 [35]
91
M
Benign prostatic hypertrophy
Mitral
Not reported
Beta-lactam 4 weeks and aminoglycoside for 10 days
Yes

26 [35]
89
F
Not reported
Mitral
Not reported
Beta-lactam 4 weeks and aminoglycoside for 10 days
Yes

27 [35]
86
M
Urethral stricture
Aortic
Not reported
Beta-lactam 4 weeks and aminoglycoside for 10 days
Yes

28 [35]
83
M
Urethral stricture
Mitral
Not reported
Beta-lactam 4 weeks and aminoglycoside for 10 days
Yes

29 [35]
80
F
Not reported
Mitral
Not reported
Beta-lactam 4 weeks and aminoglycoside for 10 days
Yes

30 [35]
77
M
Not reported
Aortic
Not reported
Beta-lactam for 4 weeks and aminoglycoside for 10 days
Yes

31 [35]
75
M
Benign prostatic hypertrophy
Mitral
Not reported
Beta-lactam for 4 weeks and aminoglycoside for 10 days
Yes

32 [35]
74
M
Suprapubic catheter
Not reported
Not reported
Beta-lactam for 4 weeks and aminoglycoside for 10 days
Yes

33 [35]
65
M
Indwelling urinary catheter
Mitral
Not reported
Beta-lactam for 4 weeks and aminoglycoside for 10 days
Yes

34 [35]
53
M
None
Aortic
Not reported
Beta-lactam 4 weeks and aminoglycoside for 10 days
Yes

35 [35]
49
F
Intermittent urinary catheter
Aortic
Not reported
Beta-lactam for 4 weeks and aminoglycoside for 10 days
Yes

36 [35]
81
M
Indwelling urinary catheter
Mitral
Not reported
Beta-lactam for 4 weeks and aminoglycoside for 10 days
Yes

37 [35]
74
F
Nonurologic malignancy
Not reported
Not reported
Beta-lactam for 4 weeks and aminoglycoside for 10 days
Yes

38 [36]
87
M
Nonurologic malignancy
Mitral
Not reported
Beta-lactam and aminoglycoside; duration not reported
No

39 [36]
77
M
Liver failure
Aortic
Not reported
Beta-lactam and aminoglycoside; duration not reported
Yes

40 [36]
83
M
Indwelling urinary catheter
Mitral
Not reported
Beta-lactam and aminoglycoside; duration not reported
Yes

41 [36]
73
M
Suprapubic catheter
Not reported
Not reported
Beta-lactam and aminoglycoside; duration not reported
No

42 [36]
88
F
Aortic stenosis
Aortic
Not reported
Beta-lactam and aminoglycoside; duration not reported
Yes

43 [8]
43
M
Indwelling urinary catheter
Mitral
Yes
Beta-lactam and aminoglycoside for 6 weeks
Yes

44 [37]
49
M
Phimosis and recurrent UTIs
Mitral
Yes
Beta-lactam and aminoglycoside for 5 days
No

45 [38]
84
M
Pacemaker and nonurologic malignancy
Pacemaker
Yes
Beta-lactam for 6 weeks
Yes

Present case
55
M
None
Mitral
Yes
Beta-lactam and aminoglycoside for 6 weeks
Yes

3.1. General Statistics

The general statistics are as follows:

(i)85% (39) of the patients were male and only 15% female (7)(ii)The average age was 72 years, with the youngest patient being 42 years and the oldest 91 years (2)(iii)Of the forty patients, only three had no reported associated risk factors or comorbidities (6.5%), 93.5% did have risk factors which are as follows:

(a)69% of the patients had urologic comorbidities while only four patients (9.5%) had an underlying known cardiac condition (one patient with aortic stenosis, one patient with atrial septal defect, and one patient with pacemaker(b)Five patients were also reported to have a nonurologic associated malignancy (11.9%)(c)Only two patients (4.6%) had a different risk factor other than the ones mentioned above, a case with untreated hepatitis C and other case with liver failure (2.3% each)

(iv)Regarding urologic risk factors:

(a)Current or recent presence of indwelling urinary catheter was seen in eight patients (19%), benign prostatic hypertrophy was also seen in eight patients (19%)(b)Recurrent UTIs were seen in three patients (6.9%), same goes for urethral strictures (three patients—6.9%)(c)History of cystoscopy was found in two patients (4.6%), phimosis was also reported in two patients only (4.6%)(d)Transurethral resection of the prostate, ureteral stent, and suprapubic catheter were seen with one patient each (2.3% per patient)

(v)In terms of affected valve: 43.4% (20 patients) had involvement of the mitral valve and the same percentage for aortic valve. One patient, 2.3%, had both valves affected; one patient had aortic and tricuspid valves affected. Finally, one patient (2.3%) had a pacemaker. Affected valves were not reported in 3 patients (6.5%)(vi)For surgical intervention, in 20 cases, it was not reported whether the patient had surgery or not; for the 26 cases, that it was. Statistics are as follows:

(a)14 patients (53.8%) did not have cardiac valve surgery(b)12 patients (46.2%) did have cardiac valve surgery(c)80% of the patients that received surgery survived

(vii)Regarding antibiotic treatment: 98% of the patients received antibiotics. In one patient (2%), treatment was not reported

(a)In 100% of the cases, a beta-lactam was used

(1)In 5 patients (11.1%), it was used as a single therapy(2)In the rest of the patients (91%), it was used in combination: in 38 patients (83%), it was combined with an aminoglycoside; in 2 patients (4.5%), it was used along vancomycin; and in 1 patient (2.2%), it was used in combination with aminoglycoside and rifampin

(b)In patients that survived, the duration of beta-lactam ranged from 2 to 12 weeks; meanwhile, aminoglycoside ranged from 1 to 6 weeks. Vancomycin was used for 2 weeks in 1 patient (in the other one duration was not reported), and finally rifampin was used for 6 weeks

3.2. Mortality Statistics

The mortality statistics are as follows:

(i)Overall mortality was 28.2% (13 patients)

(a)92.3% (12) were male and only 1 female(b)84.6% (11) were over 50 years old (average age: 71 years)

(ii)In terms of risk factors:

(a)69.2% (9) had an underlying urologic condition(b)1 patient (7.6%) had underlying aortic stenosis, and 1 patient (7.6%) had nonurologic malignancy(c)In 2 patients, the underlying comorbidities were not reported

(iii)Most patients that eventually died did not undergo surgical intervention, only 2 patients (15%) had it(iv)Regarding affected valve:

(a)46.8% (6 patients) had aortic valve endocarditis(b)38.4% (5 patients) had mitral valve endocarditis(c)1 patient (7.6%) had both aortic and tricuspid involvement(d)In 1 patient (7.6%), the affected valve was not reported

3.3. Analysis

As seen in previous reports, most of the patients were elderly males. The majority had underlying urologic comorbidities; baseline cardiac anomalies like valvular diseases were very seldom seen. Additionally, mitral and aortic valves were equally affected.

All of the patients received treatment with beta-lactam antibiotics. In most of them, aminoglycosides were used in combination; other less commonly used add-on therapies were vancomycin and rifampin. More than half of the patients did not undergo surgery, as they were deemed as poor surgical candidates or did not meet criteria for intervention. Interestingly enough, 100% of the patients that received beta-lactam as monotherapy in combination with surgery survived.

Aerococcus urinae endocarditis is associated with a 28% mortality from our calculations, deeming a high grade of aggressiveness to this microorganism. It is unclear at this time if this high mortality is due to the bacteria itself or the fact that most of the patients were elderly and had other comorbidities. Lack of surgical intervention in most patients possibly plays a role as 80% of the patients that underwent a surgical procedure survived. An underlying urologic condition was commonly seen in the patients that died, although it was recurrently seen in patients that survived as well. The affected valve does not seem to have an impact on mortality.

4. Conclusion

AU is an extremely unusual cause of human disease; it has been described to cause urinary tract infections, blood stream infections, and infective endocarditis. We do believe, however, that its actual incidence is higher than reported. Reliable data regarding clinical presentation, diagnosis, and potential treatments of AU are becoming more available to health-care workers making this a promising era in its management. With this case report and literature review, we aim to add critical data to the current medical literature regarding this rare pathogen. We urge health-care professionals to share related experiences in order to build up literature and treat patients in a more appropriate manner; at this time evidently, randomized studies are univariably defiant as with any rare disorder.

Conflicts of Interest

The authors declare that they have no conflict of interest

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