Streptococcus anginosus is a bacterium that is normally part of the human microflora, living harmlessly on and within the body. This organism, however, is opportunistic and can cause severe, pus-forming infections when it breaches natural barriers. Because it can cause deep-seated and sometimes life-threatening diseases, understanding its potential for harm is important.
The Streptococcus Anginosus Group and Its Usual Habitat
S. anginosus is classified as a member of the Streptococcus anginosus Group (SAG), historically known as the Streptococcus milleri Group. This group includes two other species, S. constellatus and S. intermedius, which share similar clinical tendencies. When grown in a laboratory, their colonies often produce a distinct, recognizable butterscotch or caramel-like odor.
The natural habitat of S. anginosus is widespread across the human body, where it exists as a commensal organism. It is found in the oral cavity, including dental plaque and the throat. It also colonizes the entire gastrointestinal tract and is a common inhabitant of the genitourinary tract.
Most infections caused by the bacterium are considered endogenous, meaning they originate from the person’s own flora. When a mucosal barrier is disrupted—such as through surgery, a dental procedure, inflammatory bowel disease, or a perforation—S. anginosus can enter sterile tissues and the bloodstream. The location of the infection often correlates with its origin; for instance, abdominal abscesses frequently arise from organisms migrating from the gastrointestinal tract.
Infections Associated with S. Anginosus
The primary pathology associated with S. anginosus and the SAG is its propensity for causing deep-seated, pyogenic (pus-forming) abscesses. Unlike many other streptococci, this group is strongly associated with the formation of these walled-off collections of immune cells and bacteria. The bacterium possesses specific virulence factors that contribute to tissue invasion and the formation of these localized lesions.
The most commonly reported sites for abscesses include the liver, where S. anginosus is a frequent cause of hepatic abscesses, and the abdominal cavity. Infections can also spread to the central nervous system, leading to brain abscesses, or to the chest cavity, causing empyema or lung abscesses. The organism’s source in these distant sites is often traced back to a breach in the mucosal lining of its normal habitat, allowing it to travel through the bloodstream.
S. anginosus can also cause systemic and focal infections in other sterile sites. Bacteremia (the presence of bacteria in the bloodstream) is a serious manifestation and is often found in conjunction with an occult (hidden) abscess somewhere in the body. The organism is also implicated in endocarditis, an infection of the heart valves, and osteomyelitis, an infection of the bone.
These infections often present as persistent, deep-seated disease that can be challenging to locate initially. Underlying conditions that compromise the immune system or disrupt mucosal integrity, such as diabetes, malignancy, or chronic alcoholism, frequently precede the onset of invasive disease. The severity of the infection is linked to the difficulty antibiotics have in penetrating the thick capsule surrounding an abscess, necessitating a combined treatment approach.
Identification and Treatment Strategies
Accurate identification of S. anginosus begins with culturing the organism from a sterile site, such as blood, cerebrospinal fluid, or abscess fluid. The bacteria are Gram-positive cocci that often grow in chains, forming minute, pinprick-sized colonies on blood agar plates. Their hemolytic pattern can vary significantly (non-hemolytic, alpha-hemolytic, or beta-hemolytic), which historically contributed to identification difficulties.
Initial identification relies on phenotypic characteristics, including small colony size and the characteristic odor. Serological testing classifies S. anginosus strains into Lancefield Group F, though Groups A, C, or G may also be present. Newer diagnostic methods, such as molecular techniques like Polymerase Chain Reaction (PCR) and automated identification systems, are becoming more common to distinguish S. anginosus from the other two species in the SAG.
The management of S. anginosus infection requires a dual approach: antibiotic therapy and surgical intervention. Penicillin remains the drug of choice, as most strains are susceptible to it, along with other beta-lactam antibiotics like ampicillin and cephalosporins. For patients with a penicillin allergy, alternative agents such as macrolides or vancomycin may be used.
The success of antibiotic treatment alone is often limited because the organism forms well-protected, deep-seated abscesses. These collections of pus are poorly penetrated by antibiotics, requiring a procedure known as source control. Source control involves the surgical incision and drainage of the abscess or the insertion of a catheter to drain the material. This is necessary to eliminate the bacterial burden and allow antibiotics to clear the remaining infection. Treatment courses are frequently prolonged, lasting several weeks, to ensure complete eradication and prevent relapse.