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Microbiology

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Here is a thorough clinical reference on Gram-Positive Bacteria, sourced from Medical Microbiology 9e and Jawetz, Melnick & Adelberg's Medical Microbiology 28e.

Gram-Positive Bacteria - Clinical Reference

Cell Wall Structure

Gram-positive bacteria have a thick, multilayered peptidoglycan cell wall (150-500 Å) surrounding the cytoplasmic membrane. Key structural components include:

Structure	Components	Function
Peptidoglycan	Multiple layers of GlcNAc and MurNAc glycan chains, cross-linked by peptide bridges	Cell shape & structure; protection from complement killing
Teichoic acid	Polyribitol/glycerol phosphate cross-linked to peptidoglycan	Strengthens wall; calcium ion sequestration
Lipoteichoic acid	Lipid-linked teichoic acid	Activates innate host immune responses
Surface proteins	Bound to peptidoglycan or teichoic acid	Immune evasion, adhesion

The peptidoglycan is susceptible to lysozyme (found in tears and mucus), which cleaves the glycan backbone and destroys the cell wall.

Major Gram-Positive Pathogens

1. Staphylococcus aureus

Morphology: Catalase-positive, gram-positive cocci in clusters. Coagulase-positive; produces Protein A.

Key Virulence Factors:

Structural: Protein A (immune evasion), capsule (anti-phagocytic), biofilm formation
Toxins: Coagulase, cytotoxins, exfoliative toxins (scalded skin syndrome), enterotoxins (food poisoning), toxic shock syndrome toxin-1 (TSST-1)
Enzymes: Hyaluronidase, lipase, nuclease

Epidemiology:

Normal flora on skin and mucosal surfaces
Survives on dry surfaces for long periods (thick peptidoglycan, no outer membrane)
Spreads by direct contact or contaminated fomites
Risk factors: foreign body (catheter, prosthesis), surgery, prior antibiotic use
MRSA is now the most common cause of community-acquired skin and soft-tissue infections

Diseases:

Toxin-mediated: food poisoning, toxic shock syndrome, scalded skin syndrome
Pyogenic: impetigo, folliculitis, furuncles, carbuncles, wound infections
Systemic: bacteremia, endocarditis, pneumonia, osteomyelitis, meningitis (via shunts)

Diagnosis:

Gram stain: clusters of cocci (useful for pyogenic infections)
Culture: grows rapidly on non-selective media; mannitol-salt agar or chromogenic agar for selective recovery
Identified by: coagulase test, molecular probes, or mass spectrometry (MALDI-TOF)
NAAT screening for MSSA and MRSA carriage

Treatment:

Localized infections: incision and drainage
Systemic infections: empirical therapy must cover MRSA
- Oral: TMP-SMX, doxycycline/minocycline, clindamycin, linezolid
- IV: Vancomycin (drug of choice); alternatives: daptomycin, tigecycline, linezolid

2. Streptococcus pneumoniae (Pneumococcus)

Morphology: Elongated gram-positive cocci in pairs (diplococci) and short chains. Catalase-negative, optochin-sensitive, bile-soluble.

Key Virulence Factors:

Polysaccharide capsule (anti-phagocytic - primary virulence factor)
Pneumolysin (cytotoxin, activates complement)
IgA protease (colonization of mucosal surfaces)
Teichoic acid / peptidoglycan fragments (trigger local inflammation)
Surface adhesins (colonize oropharynx)

Epidemiology:

Infections arise from endogenous spread from nasopharynx/oropharynx
Highest colonization in young children
Risk groups: children and elderly (meningitis), patients with sickle cell disease or asplenia (fulminant sepsis), those with antecedent viral respiratory illness
More common in cooler months

Diseases: Pneumonia, sinusitis, otitis media, meningitis, bacteremia

Diagnosis:

Gram stain and culture (sheep blood agar); may be negative if antibiotics given
Antigen test (C polysaccharide): sensitive in CSF (meningitis), not reliable in urine
NAAT: preferred for meningitis, especially in partially treated patients

Treatment:

Penicillin for susceptible strains (resistance increasingly common)
Empirical therapy for meningitis: vancomycin + ceftriaxone
For susceptible isolates: cephalosporin, fluoroquinolone, or vancomycin monotherapy
Vaccines: 13-valent conjugated (PCV13) for children <2 years; 23-valent polysaccharide (PPSV23) for at-risk adults

3. Streptococcus pyogenes (Group A Streptococcus, GAS)

Morphology: Spherical cocci 1-2 µm, arranged in short chains in specimens, longer chains in liquid media. Beta-hemolytic on blood agar. PYR-positive.

Key Virulence Factors:

M protein (primary virulence factor): anti-phagocytic; Class I M proteins associated with rheumatic fever; Class II with glomerulonephritis
Hyaluronic acid capsule (anti-phagocytic, antigenically identical to human connective tissue)
Lipoteichoic acid + F protein: mediate adherence via fibronectin
Toxins: streptolysin O and S, pyrogenic exotoxins (cause scarlet fever and TSS-like syndrome), streptokinase, hyaluronidase

Diseases:

Suppurative: pharyngitis (most common bacterial cause), impetigo, necrotizing fasciitis ("flesh-eating bacteria"), cellulitis, erysipelas, scarlet fever
Nonsuppurative (post-infectious): acute rheumatic fever, post-streptococcal glomerulonephritis

Diagnosis:

Rapid antigen test (throat swab): high specificity; culture if negative
Antistreptolysin O (ASO) titre for post-infectious complications
Classification by emm gene sequencing (M protein type)

Treatment: Penicillin remains the drug of choice; amoxicillin for pharyngitis; clindamycin added for severe invasive disease

4. Enterococcus (faecalis / faecium)

Morphology: Gram-positive cocci in pairs and short chains (similar to S. pneumoniae but catalase-negative, PYR-positive, bile-resistant, optochin-resistant).

Virulence: Primarily through biofilm formation and intrinsic antibiotic resistance (naturally resistant to cephalosporins).

Epidemiology:

Normal GI flora; spreads to urinary tract, wounds, or blood when normal flora disrupted by broad-spectrum antibiotics
Risk: prolonged hospitalization, broad-spectrum antibiotic use
Most infections are endogenous; some nosocomial spread

Diseases: UTI, peritonitis (polymicrobial), wound infections, bacteremia, endocarditis

Diagnosis: Grows readily on non-selective media; bile-resistant, PYR-positive, optochin-resistant

Treatment:

Serious infections: aminoglycoside + cell wall-active agent (penicillin, ampicillin, or vancomycin)
VRE (vancomycin-resistant Enterococcus): linezolid, daptomycin, tigecycline, quinupristin/dalfopristin
E. faecium is increasingly resistant to all available agents

Quick Comparison Table

Organism	Morphology	Key Test	Key Disease	Drug of Choice
S. aureus	Clusters	Coagulase +	SSTI, endocarditis	Vancomycin (MRSA)
S. pneumoniae	Diplococci	Optochin sensitive	Pneumonia, meningitis	Vancomycin + ceftriaxone (empirical)
S. pyogenes (GAS)	Chains	PYR +, beta-hemolytic	Pharyngitis, necrotizing fasciitis, RF	Penicillin
Enterococcus	Pairs/chains	Bile resistant, PYR +	UTI, endocarditis	Ampicillin + aminoglycoside

Source: Medical Microbiology 9e (Murray et al.), Chapters 18-19

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