Staphylococcus
Gram-positive cocci can be classified into: Micrococcaceae and Streptococcaceae Family
Table of Contents
Read And Learn More: Micro Biology And Immunology Notes
Staphylococcus Aureus
Staphylococcus aureus is catalase positive, coagulase-positive, facultative anaerobe, non-motile,non-sporing and occasionally capsulated.
In Greek, Staphyle means bunch of grapes.
- Staphylococcus was discovered by Sir Alexander Ogston and S.aureus was named by Rosenbach.
Virulence Factors of S. aureus
Pathogenesis
Laboratory Diagnosis
- Direct smear microscopy: Pus cells with gram-positive cocci in cluster
- Culture:
- Nutrient agar: Golden yellow-pigmented colonies (pigments made up of beta carotene)
- Blood agar: Colonies with narrow zone OF β-hemolysis
- Selective media:
- Mannitol salt agar (yellow colonies due to mannitol fermentation)
- Salt milk agar
- Ludlam’s medium
- Culture smear microscopy: Gram-positive cocci in clusters
- Biochemical identification
- Catalase test-positive
- Tests differentiating staphylococci from micrococci- OF test (shows fermentative pattern)
- Tests differentiating S. aureus (positive) from CoNs (negative)
- Coagulase test (slide and tube)—positive
- Heat stable thermo nuclease test—positive
- DNase test—positive
- Phosphatase test—positive
- Mannitol sugar is fermented
- Black colored colonies on potassium tellurite agar
- Gelatin liquefaction—positive
- Protein A detection
Typing of S.aureus:
- MC method for typing of S. aureus – Phage typing (pattern method)
- National reference centre for phage typing—in Maulana Azad Medical College, Delhi.
- Epidemic strain of S. aureus is Phage type 80/81. It causes outbreaks in hospitals.
Treatment of Staphylococcus aureus Infections
Since S. aureus rapidly develops drug resistance, antibiotics should be cautiously chosen.
Drug Resistance in S. aureus
Resistance in S. aureus to β lactam antibiotics
S. aureus shows resistance to β lactam antibiotics in various ways:
- Production of β lactamase enzyme: β lactamase or penicillinse enzymes cleave the β lactam ring:
- This resistance is plasmid coded, can be transferred between S.aureus strains by transduction.
- It is produced by > 90% of strains of S.aureus.
- This resistance can be overcome by addition of β lactamase inhibitors such as clavulanic acid or sulbactam.
- By alterations of PBP: It is shown by MRSA strains (see below)
Methicillin-Resistant Staphylococcus aureus (MRSA)
MRSA is mediated by mecA gene; which is a chromosomally coded. It alters penicillin-binding protein (PBP) present on the S.aureus cell membrane to PBP-2a:
- PBP is an essential protein needed for cell wall synthesis of bacteria. β lactam drugs bind and inhibit this protein, thereby inhibiting cell wall synthesis.
- The altered PBP2a of MRSA strains has less affinity for β lactam antibiotics; hence MRSA strains are resistant to all β lactam antibiotics.
- BORSA strains (Borderline Oxacillin resistant S.aureus): Occasionally a non-mecA gene-mediated low-level resistance to oxacillin is observed in some strains of S.aureus, which is due to hyperproduction of β lactamase.
- MRSA infection rate has been increasing over last few decades, though it varies from place to place. MRSA rates are higher (>50%) in America, some Asian and European countries and Malta. Countries with lowest MRSA rates are Netherlands and Scandinavia (<1%).
- In India, the MRSA rate is around 30–40% (varies between years and place)
Types of MRSA: MRSA are either community or hospital associated.
Resistance to Vancomycin (VRSA and VISA)
Erroneous and overuse of vancomycin may lead to emergence of resistance to vancomycin,which may be of two types:
- VRSA (Vancomycin Resistant S. aureus): High grade resistance with MIC >8 μg/mL
- VISA (Vancomycin Intermediate S. aureus): Low grade resistance with MIC 4-8 µg/ml
- MIC creep: Vancomycin MIC for susceptible strains of S. aureus has been gradually increasing over time (known as MIC creep); which indicates that the frequency of VISA and VRSA is likely to increase in future. Current guidelines recommend consideration of alternative drugs if vancomycin MIC is >1 μg/mL, as treatment failure has been frequently observed beyond this MIC level.
- Epidemiology: VRSA is very rare. In India, it is reported from few places such as Hyderabad,Kolkata and Lucknow. However, VISA is more frequently reported. Mechanisms:
- VRSA is mediated by van A gene. The van A gene is believed to be acquired from a vancomycin-resistant strain of Enterococcus fecalis by horizontal conjugal transfer.
- VISA is due to increase in cell wall thickness of S. aureus.
- Treatment of VRSA/VISA: Linezolid, telavancin, daptomycin, and quinupristin/dalfopristin are the effective drugs. Vancomycin and Teicoplanin are not effective.
S. aureus carriers
- About 25–50% of healthy population are carriers of S. aureus.
- MC site of colonization: Anterior nares and Skin, (perineum, axilla, groins)
- MC way of spread of infection in hospital- through the hands of hospital staff
- Most effective way to prevent the hospital infection – handwashing
- DOC for nasal carriers of MRSA: Mupirocin 2% ointment.
Control Measures
Prevention of spread of S. aureus infections in hospitals involves:
- Screening of MRSA carriers among hospital staff should be done when there is an outbreak.
- Mannitol oxacillin agar is the preferred media for this purpose
- Treatment of carriers is done by use of topical mupirocin (for nasal carriers) and chlorhexidine (for skin carriers)
- Stoppage of antibiotic misuse in hospitals
- Hand hygiene (most efficient way to prevent hospital spread),
- Isolation of the patients and all other measures of contact precautions.
Coagulase Negative Staphylococcus (Cons)
They are mostly the normal flora of skin.
Staphylococcus Epidermidis
- MC CoNS—Accounts for 60–70% of CoNS
- Produces polysaccharide glycocalyx (slime) (Biofilm production)
- Adhere to any implanted foreign bodies like valvular shunts, prosthetic devices
- Infections:
- Endocarditis with insertion of valvular prosthesis
- Ventricular shunt infections and Stitch abscess.
Staphylococcus saprophyticus
- It causes UTI in young sexually active females.
- It is resistant to novobiocin.
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