What is Streptococcus parasanguinis?
Streptococcus parasanguinis is an atypical member of the viridans group streptococci, originally isolated from human throats, blood, and urine, and recognized as a distinct species based on molecular taxonomic studies. 1
Microbiological Classification
- S. parasanguinis belongs to the viridans group streptococci (VGS), which are gram-positive, alpha-hemolytic bacteria that form colonies on sheep blood agar 2
- It was established as a separate species in 1990 through DNA-DNA hybridization and 16S ribosomal RNA sequencing, which confirmed its genealogical distinctiveness from all other recognized oral and viridans streptococcal species 1
- The organism is classified within the broader sanguinis group of viridans streptococci 3
Normal Flora and Colonization Sites
- Like other viridans streptococci, S. parasanguinis can reside as normal flora in the oral cavity, respiratory tract, gastrointestinal tract, urogenital tract, and on skin 2
- The oral mucosa serves as the most common portal of entry for invasive infections caused by viridans group streptococci 4
Clinical Significance and Disease Associations
S. parasanguinis causes invasive diseases, though the exact mechanisms of pathogenesis remain incompletely understood. 5
Documented Infections
- Endocarditis: S. parasanguinis is recognized as a causative pathogen for infective endocarditis, similar to other viridans streptococci 3
- Respiratory infections: Case reports document S. parasanguinis causing pulmonary infections, including wedge-shaped nodular lesions in the lungs 3
- Acute exacerbations of COPD: The organism has been isolated from patients with acute exacerbations of chronic obstructive pulmonary disease 5
- Bacteremia and sepsis: Like other viridans streptococci, it can cause bacteremia following dental procedures or in immunocompromised hosts 2, 4
High-Risk Populations
- Neutropenic patients are particularly vulnerable to viridans streptococcal sepsis, with predisposing factors including profound neutropenia, mucositis (especially oral), cytarabine therapy, young age, and prophylactic antibiotic use 4
- Neonates are at risk for sepsis and meningitis from viridans group streptococci 4
Clinical Presentation Patterns
- Viridans streptococcal infections typically present with fever exceeding 39°C that persists for several days, even when blood cultures become negative after 24 hours of appropriate therapy 4
- Most patients recover uneventfully with early appropriate treatment, though fulminant septic shock can occur at onset or develop 2-3 days after presentation despite effective antibiotics 4
- Adult respiratory distress syndrome may manifest 2-3 days after initial bacteremia in severe cases 4
- The median mortality rate for viridans streptococcal sepsis is approximately 10% 4
Laboratory Diagnosis
- Cultivation begins with inoculation of clinical specimens onto sheep blood agar, looking for alpha-hemolytic colonies 2
- Key diagnostic features include gram-positive cocci on microscopy, optochin resistance, and bile insolubility (with few exceptions) 2
- Species-level identification requires biochemical reactions, automated diagnostic systems, or molecular methods 2
- Antibiotic susceptibility testing is critical, as penicillin and erythromycin resistance are increasing among viridans streptococci 2
Antibiotic Resistance Considerations
- Some isolates of viridans streptococci demonstrate resistance to penicillins and cephalosporins, necessitating vancomycin therapy 4
- Local susceptibility patterns should guide initial empiric therapy for suspected viridans streptococcal infections 4
- Genetic exchange between S. parasanguinis and related species (S. mitis, S. oralis, S. pneumoniae) can occur through transformation and lysis mechanisms, potentially facilitating transfer of antibiotic resistance genes 2
Important Clinical Pitfalls
- S. parasanguinis pulmonary infections are rarely reported and may be underrecognized 3
- Recurrence during subsequent neutropenic episodes is common and should be anticipated 4
- The organism's unusual genomic features suggest pathogenic mechanisms that remain incompletely characterized, warranting careful clinical monitoring 5