Streptococcus dysgalactiae subspecies equisimilis (SDSE) is a bacterium increasingly recognized as a source of human infection. This organism belongs to the large genus Streptococcus, which includes species that reside harmlessly in the body or cause disease. While SDSE was historically considered a pathogen primarily associated with animals, human-adapted strains are now a significant cause of illness in people. Infections range from common, self-limiting conditions to life-threatening invasive diseases.
Classification and Identity of SDSE
SDSE is a Gram-positive, spherical bacterium that typically grows in chains, a characteristic reflected in the genus name Streptococcus. When grown on blood agar plates, it exhibits complete red blood cell destruction, known as beta-hemolysis, and forms large colonies. This places it within the group of pyogenic, or pus-forming, streptococci.
The most widely used classification system is the Lancefield grouping, based on carbohydrate antigens found on the bacterial cell wall. SDSE is defined primarily by its possession of the Lancefield Group C and Group G antigens. Almost all human infections involving large-colony, beta-hemolytic streptococci of these groups are caused by SDSE.
The natural habitat of SDSE in humans is the mucosal surfaces, particularly the pharynx and the skin. While it can exist as a commensal organism, human-adapted strains possess virulence factors that enable them to cause disease. These human-adapted strains are genetically distinct from the animal isolates that cause veterinary disease.
Clinical Manifestations in Humans
Infections caused by SDSE span a broad clinical range, from superficial conditions to severe systemic disease. Non-invasive infections are common and frequently involve the skin and soft tissues. Examples include cellulitis, a deep skin infection causing redness and swelling, and erysipelas, a more superficial skin infection. SDSE is also recognized as a cause of pharyngitis, commonly known as strep throat.
The most concerning manifestations are invasive infections, where the bacterium enters normally sterile sites, such as the bloodstream. Bacteremia, the presence of SDSE in the blood, is a common invasive presentation often originating from a skin or soft tissue source. More severe, deep-seated infections include necrotizing fasciitis, a rapidly progressing and destructive infection of the underlying fascia and muscle.
The bacterium can also cause streptococcal toxic shock syndrome (STSS), a life-threatening condition characterized by shock and organ failure. Invasive SDSE infections, including bacteremia and STSS, are increasingly reported, particularly in older adults and individuals with underlying health conditions like diabetes or malignancy. The case fatality rate for SDSE bacteremia can reach 15% to 18%.
Distinguishing SDSE from Common Strep
SDSE is often compared to Streptococcus pyogenes, commonly known as Group A Streptococcus (GAS), because they share many similarities in their capacity to cause disease. Both organisms occupy the same ecological niches in the human throat and skin, causing the same acute illnesses, such as pharyngitis and severe invasive infections like necrotizing fasciitis. This overlap in clinical presentation can make initial diagnosis challenging.
Genomic studies show that SDSE and S. pyogenes share many virulence factors, explaining their overlapping ability to cause serious illnesses. Both possess genes that encode for toxins, facilitating the development of severe conditions like STSS. The incidence of invasive SDSE disease in some regions now approaches, or even exceeds, that of invasive S. pyogenes disease.
A key difference lies in the post-infectious sequelae. S. pyogenes is the established cause of Acute Rheumatic Fever (ARF) and post-streptococcal glomerulonephritis (PSGN). SDSE is generally not associated with ARF, though a link to PSGN has been suggested. The primary threat from SDSE is its propensity for severe, acute invasive disease, rather than the immune-mediated long-term complications typical of GAS.
Management and Treatment Protocols
The management of SDSE infections relies on prompt diagnosis and the administration of appropriate antibiotics. SDSE remains highly susceptible to beta-lactam antibiotics, which interfere with bacterial cell wall synthesis. Penicillin is considered the standard and preferred treatment for both non-invasive and invasive SDSE infections.
For non-invasive infections, a standard course of oral penicillin is typically effective. For severe, invasive infections like necrotizing fasciitis or STSS, treatment is more aggressive and often involves high-dose intravenous penicillin. In these serious cases, a second drug, such as clindamycin, is often added to the regimen. Clindamycin works by inhibiting bacterial toxin production, which is thought to improve outcomes in life-threatening streptococcal infections.
Timely intervention is necessary, especially for invasive disease, to improve the prognosis. While non-invasive infections generally resolve completely with treatment, the higher mortality associated with SDSE bacteremia underscores the importance of rapid diagnosis and effective antibiotic therapy.