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. 2016 Jul 20;2016:bcr2016215421. doi: 10.1136/bcr-2016-215421

Aerococcus urinae, a rare cause of infective endocarditis

Stephen Melnick 1,2, Salik Nazir 3, Rittu Hingorani 3, Philip Wexler 3
PMCID: PMC4964113  PMID: 27440847

Abstract

We present the case of an elderly male who was initially seen in our hospital for a urinary tract infection that was treated with oral ciprofloxacin. He was admitted 2 weeks later with altered mental status and fever, and was found to have bacteraemia with Aerococcus urinae. Owing to altered mental status a brain MRI was performed which showed evidence of embolic stroke. Following this, a transesophageal echocardiogram showed severe mitral regurgitation and a vegetation >1 cm involving the mitral valve with associated destruction of posterior valve leaflets. The patient was started on antibiotics intravenous penicillin G and intravenous gentamicin for a total duration of 6 weeks. He underwent mitral valve replacement on day 4 of hospitalisation. The postoperative course was complicated by ventilator-dependent respiratory failure, requiring tracheostomy and eventual transfer to a skilled nursing facility. Unfortunately, he died after 2 weeks of stay at the facility.

Background

A frequently misidentified organism, Aerococcus, is an aerobic, α-hemolytic Gram-positive coccus that grows in pairs or clusters and is becoming an increasingly important pathogen in medicine. Aerococcus urinae is a rare cause of urinary tract infection (UTI) that can unusually be associated with infective endocarditis.1 Infection with this organism is usually seen in elderly males with underlying urinary tract abnormality where it can cause bacteraemia leading to infective endocarditis.2 Infective endocarditis due to A. urinae is associated with a significant fatality rate.3 Hence, timely recognition and early treatment of this fatal infection is essential in order to decrease morbidity and mortality.

Case presentation

A 74-year-old male with a history of benign prostatic hyperplasia presented to the emergency department (ED) of our hospital with fever and altered mental status that started 24 hours prior to presentation. His temperature was 39.3°C, heart rate of 100 bpm, respirations of 30/min and blood pressure of 128/73 mm Hg. Examination revealed normal heart sounds without a murmur. The patient was moving all his limbs but altered mental status precluded complete neurological examination. The rest of the examination was unremarkable.

Two weeks prior to the admission, the patient was evaluated in the ED of our hospital with symptoms of frequency and dysuria. His urinalysis was found to be positive for leucocytes, nitrite and bacteria suggesting a UTI. He was discharged from the ED on oral ciprofloxacin for 5 days, pending urine cultures which eventually were found to be negative. Despite completing antibiotic therapy, the patient continued to develop occasional fevers with fluctuations in cognition that worsened 24 hours prior to the present admission.

Investigations

Relevant laboratory testing on admission showed a sodium level of 129 mEq/L, glucose 158 mg/dL, white cell count 13.1×103/L and erythrocyte sedimentation rate 77 mm/hour. The rest of the laboratory investigation was unremarkable, including repeat urinalysis with culture, chest X-ray, blood alcohol levels and a urine drug screen. The initial head CT scan performed in the ED was unremarkable. Blood cultures at 24 hours grew Gram-positive cocci in clusters which were assumed to be of Staphylococcus spp and, hence, a transthoracic echocardiogram was performed, which showed annular calcification of the mitral valve. As a result of persistent altered mental status, MRI of the brain was performed on day 2 of hospitalisation which showed multifocal bilateral areas of acute/subacute infarction suggesting an embolic source. Following this, a transoesophageal echocardiogram was performed which showed a large mobile 1.7×1.9 cm cavitating vegetation suggesting an abscess and severe mitral regurgitation due to the destruction of the posterior mitral leaflet, as shown in figure 1. The final results of blood culture eventually showed A. urinae, on day 4 of hospitalisation.

Figure 1.

Figure 1

Transesophageal echocardiogram of infective endocarditis. Three-dimensional, short-axis view of the vegetation adherent to the mitral valve (A). Two-dimensional, long-axis view of the mitral valve showing vegetation measuring 1.7×1.9 cm (B). Two-dimensional, four-chamber view with amorphous vegetation of the mitral valve (C). Two-dimensional, four-chamber view of mitral valve with color flow Doppler demonstrating significant mitral regurgitation with suspicion of valve perforation (D).

Treatment

Hyponatraemia was thought to be secondary to hypovolaemia as it rapidly improved with normal saline (0.9%) administration. He required frequent doses of intravenous furosemide because of the new onset heart failure. The patient was started on empiric broad spectrum antibiotics in the ED including cefepime and vancomycin. Once the blood cultures returned positive for A. urinae, the antibiotics were switched to intravenous penicillin G and intravenous gentamicin. A decision to pursue mitral valve replacement was made based on the presence of new severe MR and a highly mobile vegetation >1 cm with associated valve destruction leading to heart failure. He underwent surgery on day 4 of hospitalisation. The mitral valve from surgery was cultured and was found to be positive for A. urinae. Repeated blood cultures after 48 hours of administration of intravenous penicillin G and intravenous gentamicin returned negative.

Outcome and follow-up

Post mitral valve replacement surgery, the patient's course was complicated by ventilator-dependent respiratory insufficiency requiring the placement of a tracheostomy and a gastrostomy tube. Following this, the family requested no further intervention and patient was transferred to a long-term skilled nursing facility on day 26 of hospitalisation. Unfortunately, he died shortly thereafter.

Discussion

A. urinae is a Gram-positive coccus that was recognised as a separate species in 1992.4 A. urinae is frequently misidentified as Staphylococcus (growing in clusters) or Streptococcus (α-haemolysis) or an Enterococcus (shares antibiotic resistance pattern).5 6 Owing to these reasons, correct identification of the species has been difficult. Identification of A. urinae with biochemical tests is possible, but sequencing of the gene encoding 16S ribosomal RNA remains the gold standard. This technique reliably distinguishes A. urinae from the other species within the Aerococcus genus and from other genera as well.7 8

A. urinae has been found to cause UTIs,9 10 invasive infections such as septicaemia,11 and infective endocarditis.12 These infections usually occur in elderly males with underlying urological abnormalities.3 11 The estimated prevalence of A. urinae UTI and endocarditis is 54 and 3/1 million, respectively.13 In a Swedish study by Senneby et al3 the case fatality rate for infective endocarditis caused by A. urinae was reported to be 50% and multiple cases have reported a similar high mortality.14

The patient described in this case was initially diagnosed with UTI and was treated with ciprofloxacin for 5 days. Treatment of this infection is challenging as Aerococci are often resistant to the typical antibiotics used for UTIs. A. urinae is intrinsically resistant to sulfamethoxazole.15 Trimethoprim resistance is also reported, which generally depends on which test medium is used.16 17 Resistance to ciprofloxacin has recently been reported as well,18 19 suggesting that in patients with positive urine cultures antibiotic susceptibility testing should be performed where treatment with ciprofloxacin is initiated. Since infection with this organism is so rare, no current recommendations exist about any alternative treatment options in patients who are at risk for A. urinae UTI.

The ideal treatment for infective endocarditis caused by A. urinae has not been determined, but in most instances a β-lactam such as penicillin G has been combined with an aminoglycoside like gentamicin. This combination is supported by in vitro study that showed synergistic effect when such a combination was used.20 We started our patient on intravenous penicillin G and intravenous gentamicin based on the limited evidence available in the literature.

The 2015 American Heart Association guideline on the management of infective endocarditis recommends early valve replacement surgery can be considered in the following cases: symptoms of congestive heart failure caused by severe valve dysfunction and severe valve regurgitation with a large mobile vegetation >1 cm.21 Our patient met these criteria and hence we proceeded with surgical mitral valve replacement. Unfortunately, our patient died despite the aggressive management which is consistent with many fatal cases reported so far in the literature.3 14

Learning points.

  • Aerococcus urinae is a rare cause of infective endocarditis that is associated with significant morbidity and mortality.

  • A. urinae can be misidentified as Staphylococcus, Streptococcus or Enterococcus.

  • Treatment options are limited but in most instances penicillin G and gentamicin in combination have been used effectively.

Footnotes

Contributors: SM wrote the case report, followed the patient and supervised the manuscript writing. SN was involved in writing the manuscript and literature search. RH was involved in writing the manuscript and following the patient. PW was the primary physician involved in patient care and also involved in the final editing. Moreover, all authors were involved in proofreading and revision of the manuscript. SM is the study guarantor. All the authors significantly contributed to the development of this manuscript.

Competing interests: None declared.

Patient consent: Obtained.

Provenance and peer review: Not commissioned; externally peer reviewed.

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