Staphylococcus Hominis Treatment: Effective Strategies for Today

Staphylococcus hominis, a coagulase-negative staphylococcus (CoNS), is commonly found on human skin and is usually harmless. However, in healthcare settings, it can become an opportunistic pathogen, particularly in immunocompromised patients or those with medical devices like catheters and prosthetic implants. Its increasing resistance to antibiotics has made treatment more challenging, requiring careful selection of antimicrobial therapies.

Managing S. hominis infections requires accurate detection, appropriate antibiotic use, and strategies to prevent its spread.

Classification And Habitat

Staphylococcus hominis belongs to the Staphylococcus genus, a diverse group of Gram-positive bacteria that thrive in aerobic and facultatively anaerobic conditions. As a coagulase-negative staphylococcus, it lacks the enzyme coagulase, distinguishing it from more virulent species like Staphylococcus aureus. It is classified within the Staphylococcus epidermidis group, which includes other skin-associated species such as S. epidermidis and S. haemolyticus. Phylogenetic analyses have identified two primary subspecies: S. hominis subsp. hominis and S. hominis subsp. novobiosepticus, the latter being more frequently associated with multidrug resistance and hospital-acquired infections.

S. hominis is a predominant member of the human skin microbiota, particularly in areas with high sweat gland density, such as the axillae, groin, and perineal region. It metabolizes components of human sweat, contributing to body odor by converting odorless precursors into volatile sulfur-containing compounds. It also produces antimicrobial peptides like epidermin, which inhibit the growth of other bacteria, including S. aureus.

In healthcare environments, S. hominis can colonize medical devices and frequently touched surfaces, forming biofilms that enhance its resistance to desiccation and disinfectants. This biofilm-forming ability allows it to evade host defenses and antimicrobial treatments. Whole-genome sequencing has identified biofilm-associated genes, such as icaADBC, which facilitate adherence to synthetic materials.

Laboratory Detection

Identifying S. hominis in clinical specimens is essential due to its dual role as a commensal organism and opportunistic pathogen. Since it is a coagulase-negative staphylococcus, distinguishing it from other skin-associated staphylococci, particularly S. epidermidis, requires microbiological and molecular techniques.

Initial detection involves culturing the organism from blood, wound exudates, or catheter tips on selective media like mannitol salt agar (MSA) or Columbia blood agar. Unlike S. aureus, S. hominis does not ferment mannitol, appearing as non-yellow colonies on MSA, while on blood agar, it forms small, white-to-cream-colored colonies with no significant hemolysis.

Further differentiation relies on biochemical tests. The catalase test confirms its classification within the Staphylococcus genus, while the coagulase test differentiates it from S. aureus. Additional tests, such as the oxidase test (negative) and urease activity (variable), provide further identification clues. Automated systems like VITEK 2 and BD Phoenix enhance accuracy, though misidentifications can occur.

Molecular diagnostics improve precision. PCR-based assays targeting the 16S rRNA gene or species-specific markers, such as tuf or rpoB, allow rapid identification. Whole-genome sequencing (WGS) has refined bacterial classification, revealing subspecies and antimicrobial resistance determinants. Matrix-assisted laser desorption/ionization-time of flight mass spectrometry (MALDI-TOF MS) has emerged as a rapid and reliable identification tool, with accuracy rates exceeding 95% for CoNS species.

Antimicrobial susceptibility testing (AST) is critical due to S. hominis’s multidrug resistance. The Clinical and Laboratory Standards Institute (CLSI) and the European Committee on Antimicrobial Susceptibility Testing (EUCAST) provide guidelines for determining minimum inhibitory concentrations (MICs) via broth microdilution, disk diffusion, or automated platforms. Methicillin resistance, conferred by the mecA gene, is detected using cefoxitin disk diffusion or PCR-based assays. Vancomycin-intermediate strains necessitate MIC testing via E-test or automated systems to guide therapy.

Antimicrobial Options

Treating S. hominis infections requires careful antibiotic selection due to its increasing resistance. Methicillin-resistant S. hominis (MRSH) strains carry the mecA gene, encoding an altered penicillin-binding protein (PBP2a) that reduces beta-lactam efficacy. Treatment depends on susceptibility testing, infection severity, and the presence of medical devices.

Beta Lactams

Beta-lactam antibiotics, including penicillins and cephalosporins, were once effective against S. hominis, but resistance is now widespread. MRSH strains render oxacillin and nafcillin ineffective. First-generation cephalosporins like cefazolin may still be used for methicillin-susceptible strains, though resistance rates vary.

Beta-lactam/beta-lactamase inhibitor combinations like piperacillin-tazobactam are generally ineffective against MRSH but may be used in polymicrobial infections. Carbapenems, such as meropenem, have limited utility due to intrinsic resistance in many CoNS species. Routine susceptibility testing is essential to determine beta-lactam viability.

Glycopeptides

Vancomycin remains the primary treatment for MRSH infections, inhibiting cell wall synthesis by binding to peptidoglycan precursors. However, reduced susceptibility has been reported, necessitating careful MIC monitoring.

Therapeutic drug monitoring (TDM) is recommended for vancomycin to maintain trough levels between 15-20 µg/mL in serious infections while minimizing nephrotoxicity. Teicoplanin, another glycopeptide, offers a longer half-life and lower nephrotoxicity but has variable pharmacokinetics. In cases of vancomycin failure or intolerance, alternatives like daptomycin or linezolid may be considered. Combination therapy with rifampin or fosfomycin is sometimes used for biofilm-associated infections.

Newer Agents

Newer antibiotics have expanded treatment options for multidrug-resistant S. hominis. Daptomycin, a lipopeptide, disrupts bacterial membrane potential and is effective for bloodstream infections and endocarditis, though inactivated by pulmonary surfactant.

Linezolid, an oxazolidinone, inhibits bacterial protein synthesis and is effective against vancomycin-resistant strains. Its oral bioavailability allows step-down therapy, though prolonged use can cause myelosuppression and neuropathy.

Ceftaroline, a fifth-generation cephalosporin, retains activity against MRSH due to its high PBP2a affinity, though clinical data on CoNS infections remain limited. Other agents, such as tedizolid and dalbavancin, provide additional options, particularly for complicated skin infections.

Local And Systemic Management

Managing S. hominis infections depends on infection site and bacterial dissemination. Localized infections, like catheter-associated infections, often respond to debridement and topical antimicrobials. When biofilms form on medical devices, removal may be necessary, as biofilm-associated bacteria exhibit significantly reduced antibiotic susceptibility.

Systemic infections, including bacteremia and endocarditis, require prompt intravenous antibiotics guided by susceptibility testing. Empiric treatment typically involves vancomycin, with adjustments based on MIC values and patient factors like renal function. Persistent infections may require combination therapy with rifampin or fosfomycin. Echocardiography is often recommended to assess cardiac involvement, as S. hominis has been implicated in prosthetic valve endocarditis.

Prevention Strategies

Preventing S. hominis infections requires infection control, antimicrobial stewardship, and reducing bacterial colonization on medical devices. Hospitals and long-term care facilities implement hygiene measures to limit bacterial spread.

Hand hygiene is essential. Alcohol-based sanitizers with at least 60% ethanol or isopropanol effectively reduce CoNS colonization on healthcare workers’ hands. Regular disinfection of high-touch surfaces, such as bed rails and medical equipment, further limits bacterial persistence. Antimicrobial-impregnated catheters and dressings coated with agents like chlorhexidine or silver sulfadiazine reduce bloodstream infections by inhibiting bacterial adhesion and biofilm formation.

Antimicrobial stewardship programs help prevent resistant S. hominis strains by curbing broad-spectrum antibiotic overuse. Surveillance programs monitoring local resistance patterns guide empirical treatment decisions. Research into novel preventive measures, such as bacteriophage therapy and quorum-sensing inhibitors, offers potential future interventions to disrupt S. hominis biofilms and reduce infection rates.