Aerococcus sanguinicola is a Gram-positive coccus recognized as a cause of human infection. Defined as a distinct species in 2001, it belongs to the genus Aerococcus. It is notable for being a non-spore-forming, catalase-negative organism. Advancements in laboratory technology have led to a better understanding of its role as a true pathogen, despite being previously overlooked or misidentified.
Fundamental Biological Characteristics
A. sanguinicola is spherical and aggregates in clusters or tetrads, visually resembling staphylococci. However, it is catalase-negative, distinguishing it from staphylococci and aligning it with certain streptococci. When grown on blood agar, it typically exhibits alpha-hemolysis, contributing to its resemblance to other alpha-hemolytic organisms.
The bacterium is facultatively anaerobic, allowing it to survive in both oxygen-rich and oxygen-poor environments. This adaptability enables it to exist as part of the indigenous microbiota, often associated with the urinary or digestive systems, from where it can cause infection. Historically, accurate identification was challenging because commercial biochemical test systems frequently misidentified it, often reporting it as Aerococcus viridans or a type of streptococcus.
This misidentification led to an underestimation of its prevalence and clinical importance. Modern identification relies on precise methods, such as 16S rRNA gene sequencing or matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS). These advanced techniques provide a quick and reliable way to differentiate A. sanguinicola from closely related species. Phenotypic tests also help, as A. sanguinicola strains are uniquely positive for both leucine aminopeptidase and pyrrolidonylarylamidase among the aerococci.
Clinical Manifestations and Disease Causation
A. sanguinicola can transition from a harmless organism in the body’s flora into an aggressive pathogen, especially when host defenses are compromised. Its ability to cause severe disease involves virulence factors, including the capacity to form biofilms. Biofilms are communities of bacteria encased in a matrix, making them highly resistant to the host immune system and antibiotic treatment.
The most common infections caused by this species are Urinary Tract Infections (UTIs). A. sanguinicola is frequently isolated from urine cultures and is recognized as a uropathogen, particularly in older individuals with underlying urological issues. If the infection is not contained, the bacteria can enter the bloodstream, leading to bacteremia or urogenic sepsis.
The most serious clinical manifestation is Infective Endocarditis (IE), an infection of the heart’s inner lining or valves. This condition is a severe complication of bacteremia and requires intensive, prolonged treatment. The organism’s ability to induce platelet aggregation is a potential virulence mechanism contributing to the formation of vegetations on heart valves, a hallmark of endocarditis.
Patients who develop invasive infections are typically older adults. Specific risk factors increase susceptibility, including underlying structural abnormalities of the urinary tract, such as prostatic disease in men. Immunocompromised status, the presence of indwelling urinary catheters, and pre-existing heart valve damage also predispose individuals to severe disease caused by A. sanguinicola. Invasive aerococcal infections often show a higher incidence in elderly men with concurrent urinary tract issues.
Antimicrobial Susceptibility and Treatment Challenges
Treatment for A. sanguinicola infections is complicated by its unique susceptibility profile and the difficulty of accurate identification. Fortunately, the organism generally remains sensitive to beta-lactam antibiotics, such as penicillin and ampicillin, which are often the first-line agents. It also demonstrates susceptibility to potent antibiotics, including vancomycin and third-generation cephalosporins like cefotaxime.
However, the therapeutic landscape is complex due to observed resistance patterns. A significant challenge is resistance to fluoroquinolone antibiotics, such as ciprofloxacin and levofloxacin, which are commonly used for empirical UTI treatment. Studies show that many isolates exhibit elevated Minimum Inhibitory Concentrations (MICs) to levofloxacin, limiting its utility.
Resistance to other common agents has also been reported, including high intrinsic resistance to nitroxoline, which is used for uncomplicated UTIs in some regions. High-level resistance to trimethoprim-sulfamethoxazole and, rarely, meropenem has been documented in certain strains. This variability underscores the need for specific antimicrobial susceptibility testing to guide treatment.
For severe, invasive infections like infective endocarditis, an aggressive approach is required. The standard regimen often involves combination therapy, pairing a beta-lactam antibiotic (penicillin or ampicillin) with an aminoglycoside. This combination achieves a synergistic bactericidal effect necessary for clearing infection from heart valve vegetations. The success of treatment relies heavily on the laboratory’s ability to correctly identify the species and perform timely susceptibility testing to avoid treatment failure.