To the best of our knowledge, this is the third reported case in the English literature and the first reported case in Australia of aortic root abscess caused by Aerococcus urinae.
Although infective endocarditis is a rare manifestation of Aerococcus urinae, a high index of suspicion of deep-seated infection is required if a patient is bacteraemic, even in the absence of clinical findings such as a new heart murmur, clinical signs of heart failure, or other peripheral stigmata of infective endocarditis, as described in this case. Due to the high clinical index of suspicion given the prolonged bacteraemia, with appropriate investigations, the diagnosis was established leading to appropriate therapy.
Aerococcus urinae belongs to the group of organisms called Aerococcus-like organisms (ALO). Along with Aerococcus viridans and Aerococcus sanguinicola, Aerococcus urinae is increasingly being recognized as a causative pathogen in many human infections [5]. A. urinae most commonly causes urinary tract infections, however invasive infections such as endocarditis can occur. There are also occasional reports of spondylodiscitis and spontaneous bacterial peritonitis caused by A. urinae [6, 7]. Risk factors for A. urinae infection are male gender, age greater than 65 years, and underlying urinary tract abnormalities [8]. The virulence mechanisms displayed by A. urinae are the formation of biofilm on plastic surfaces and the aggregation of human platelets, which can result in the formation of heart valve vegetations [1].
Early identification of A. urinae in cultures can be challenging due to the following reasons. Firstly, A. urinae is alpha-haemolytic, producing semi-transparent colonies, hence can be misidentified as Streptococcus on culture. Additionally, on Gram stain, Aerococcus and Staphylococcus share similar appearance, as Gram-positive cocci in clusters. However, unlike staphylococci, Aerococcus is catalase negative. Due to these challenges, there are often in delays in accurate diagnosis. However, due to improved diagnostic techniques identification of A. urinae has improved [5, 9]. A. urinae can reliably be identified with 16s rRNA-gene sequence (the gold standard) and mass spectrometry, but less so with VITEK 2 [9]. In addition, routine urine cultures may not isolate A. urinae, because A. urinae optimally requires prolonged incubation in 5% carbon dioxide in anaerobic conditions to be isolated in urine culture [6]. In a review by Senneby et al. [1], out of 42 patients who had A. urinae bacteraemia, only 6 patients had urine culture that were positive for A. urinae. 15 others had sterile urine, while the rest had urine culture that grew other organisms. In a large number of patients, A. urinae was not isolated from the urine samples despite having obvious UTI symptoms [1].
Aerococcus urinae displays in-vitro susceptibilities to penicillin, amoxicillin, cefotaxime, ceftriaxone, doxycycline, linezolid, and vancomycin. There is variable resistance to clindamycin, fluoroquinolones, and erythromycin. A. urinae is resistant to sulphamethoxazole, while sensitivities to trimethoprim and trimethoprim–sulphamethoxazole are poorly defined and variable depending on methodology [1, 10, 11]. Hence, clinicians need to be aware that the commonly used antibiotics for empirical treatment of urinary tract infections when isolate on culture is pending may be ineffective for treatment of Aerococcus urinae infections. In a study of 30 A. urinae isolates, 97% of isolates had a ceftriaxone MIC ≤ 0.5 µg/mL. 100% had penicillin MIC ≤ 0.06 µg/mL and vancomycin MIC ≤ 1 µg/mL. High erythromycin and levofloxacin MICs were identified in 17% and 33% of the A. urinae isolates respectively [12]. Two older studies have showed a synergistic killing effect when there is combination therapy of penicillin and an aminoglycoside. A recent larger study identified this synergy in only 7 of 15 isolates [13]. Both the Clinical and Laboratory Standards Institute (CLSI) and the European Committee on Antimicrobial Susceptibility Testing (EUCAST) have published recommended clinical breakpoint MICs for A. urinae [14, 15].
The incidence of infective endocarditis among patients with A. urinae bacteraemia is unclear. A population-based study reports that of 16 patients with A. urinae bacteraemia, 3 patients had infective endocarditis [1]. In a review of 46 cases of A. urinae infective endocarditis, mortality was reported as 28.2%, similar to overall endocarditis mortality reported. Of patients who underwent surgery, 80% survived. On review of the patients who had a good outcome, 80% of them received antibiotic therapy for 4–6 weeks. While a majority of individuals with A. urinae infective endocarditis had urologic abnormalities, underlying valvular conditions were less frequent [8].
Duration of antibiotics for A. urinae infective endocarditis is currently guided by expert opinion. However, the outcomes of previous cases in the literature would suggest the need for further research regarding extended intravenous antibiotic therapy for uncomplicated bacteraemia. Two case reports described patients who failed therapy after a short course (≤ 10 days) of intravenous antibiotics [2, 16].