Streptococcus dysgalactiae ssp. equisimilis, often abbreviated as SDSE, is a bacterium gaining recognition for its role in human health. It is a notable cause of a wide spectrum of infections. The incidence of severe infections caused by SDSE has been increasing, highlighting its significance as a pathogen.
Microbiological Profile and Habitat
Streptococcus dysgalactiae ssp. equisimilis is a Gram-positive bacterium. Microscopically, these bacteria are cocci, or spherical cells, that typically arrange themselves in chains. A key characteristic used for identification is its hemolytic activity when grown on blood agar plates. SDSE is predominantly beta-hemolytic, meaning it produces toxins that break down red blood cells, creating clear zones around its colonies.
This bacterium is classified using the Lancefield system, a method that categorizes streptococci based on specific carbohydrate antigens in their cell walls. SDSE strains are the primary cause of infections attributed to Lancefield groups C and G in humans. SDSE is also a commensal organism, meaning it can live on the human body without causing harm. Its natural habitats include the upper respiratory tract, gastrointestinal tract, female genital tract, and the skin, from where it can gain access to normally sterile parts of the body and cause infection.
Clinical Manifestations of Infection
The range of diseases caused by Streptococcus dysgalactiae ssp. equisimilis is broad, extending from mild superficial infections to severe, life-threatening conditions. The clinical signs of these infections often mirror those caused by Streptococcus pyogenes, making laboratory identification important for a definitive diagnosis. The specific illness depends on the site of the infection and the health status of the individual.
Among the more common infections is pharyngitis, or a sore throat, which is clinically indistinguishable from typical “strep throat.” SDSE is also a frequent cause of skin and soft-tissue infections. These can manifest as impetigo, characterized by sores and blisters; cellulitis, a deeper infection of the skin that causes redness and pain; or erysipelas, a type of cellulitis involving the upper layers of the skin.
When SDSE enters sterile sites, it can lead to invasive diseases. Bacteremia, the presence of bacteria in the bloodstream, is a common form of invasive disease and can lead to sepsis. The bacterium can also seed other parts of the body from the bloodstream, causing conditions like septic arthritis, a painful joint infection, or osteomyelitis, a bone infection. In some cases, it can lead to endocarditis, an infection of the inner lining of the heart chambers and valves.
Although less common than with Streptococcus pyogenes, SDSE is capable of causing severe, rapidly progressing syndromes. These include streptococcal toxic shock syndrome (STSS), a condition characterized by a sudden drop in blood pressure and organ failure. It can also cause necrotizing fasciitis, a destructive infection of muscle and fat tissue often referred to as “flesh-eating disease.”
Virulence and Associated Risk Factors
The ability of SDSE to cause disease is dependent on its virulence factors, molecules produced by the bacterium that enable it to infect a host and evade the immune system. One prominent example is the M protein, a surface protein that helps the bacterium adhere to host cells and prevents it from being engulfed by immune cells. Another set of virulence factors are streptolysins S and O, toxins that create pores in the membranes of host cells, including red and white blood cells, causing them to rupture.
To spread through the body, SDSE utilizes enzymes that break down host tissues. Hyaluronidase is an enzyme that degrades hyaluronic acid, a component of connective tissue, allowing the bacteria to move more freely. Another enzyme, streptokinase, works by breaking down blood clots, which can help the infection disseminate from a localized site.
While anyone can become infected with SDSE, certain populations are at a higher risk for developing severe, invasive disease. Advanced age is a primary risk factor. Individuals with underlying chronic health conditions are also more vulnerable, including those with diabetes, chronic heart or lung disease, cancer, and any state of immunosuppression. Breaks in the skin, such as from wounds, surgical incisions, ulcers, or chronic skin conditions like lymphedema, provide a direct entry point for the bacterium.
Diagnosis and Treatment Protocols
Diagnosing an infection caused by SDSE requires isolating the bacterium from the site of infection for laboratory analysis. A clinical sample is collected, such as a throat swab for pharyngitis, a blood sample for bacteremia, or a tissue sample from a skin lesion. This sample is then cultured on a medium like blood agar, where the bacterium can grow and form visible colonies.
Once the bacterium is cultured, laboratory technicians perform further tests for definitive identification. Traditional methods involve a series of biochemical tests to observe the bacterium’s metabolic properties. More rapid techniques, such as MALDI-TOF mass spectrometry, can identify the specific subspecies by analyzing its unique protein profile, which is important to differentiate it from other streptococci.
The primary treatment for infections caused by SDSE is penicillin or related beta-lactam antibiotics like amoxicillin. This bacterium has remained highly susceptible to penicillin, which is considered the drug of choice. For patients who have a severe allergy to penicillin, alternative antibiotics are available. These may include clindamycin or vancomycin, depending on the severity and location of the infection.
While resistance to penicillin is rare in SDSE, some strains have shown resistance to other classes of antibiotics, such as macrolides. In cases of severe infection or if a patient is not responding to initial therapy, laboratories may perform antibiotic susceptibility testing. This testing determines which antibiotics will be effective against the specific strain causing the infection.