Study Guide: Pathogenic Gram-Positive Bacteria (Chapter 19)

Gram-Positive Bacteria

Classification and General Features

Gram-positive bacteria are characterized by their thick peptidoglycan cell wall, which retains the crystal violet stain and appears purple under the microscope. They are divided into two main groups based on their genomic G+C content:

• Low G+C Gram-Positive Bacteria: Includes genera such as Staphylococcus, Streptococcus, Enterococcus, Bacillus, Clostridium, Listeria, and Mycoplasma.

• High G+C Gram-Positive Bacteria: Includes genera such as Corynebacterium, Mycobacterium, Propionibacterium, Nocardia, and Actinomyces.

These bacteria are responsible for a wide range of diseases, from mild skin infections to life-threatening systemic illnesses.

Staphylococcus

Structure and Physiology

Staphylococcus species are Gram-positive, spherical, and often form clusters resembling grapes. They are facultative anaerobes, salt-tolerant, and can survive in harsh conditions such as high radiation, heat, and desiccation.

• S. aureus: More virulent, responsible for a variety of diseases.

• S. epidermidis: Part of normal skin microbiota, opportunistic in immunocompromised patients.

Pathogenicity

Pathogenicity is due to:

• Evading phagocytosis

• Production of enzymes

• Production of toxins

Structural Defenses Against Phagocytosis

• Protein A: Binds to Fc region of IgG, inhibiting opsonization and complement activation.

• Coagulase: Converts fibrinogen to fibrin, forming blood clots around bacteria.

• Capsule: Polysaccharide layer inhibits chemotaxis and phagocytosis.

Enzymes

• Coagulase: Only produced by S. aureus, triggers blood clotting.

• Hyaluronidase: Breaks down hyaluronic acid, facilitating tissue invasion.

• Staphylokinase: Dissolves fibrin clots, allowing spread.

• Lipase: Digests lipids, enables growth on skin and oil glands.

• Penicillinase: Breaks down penicillin, confers resistance to beta-lactam antibiotics.

Toxins

• Cytotoxic Toxins: Alpha, beta, gamma, delta toxins disrupt cell membranes; leukocidin lyses leukocytes.

• Exfoliative Toxins: Cause skin cell separation and sloughing.

• Toxic Shock Syndrome Toxin: Causes toxic shock syndrome.

• Enterotoxins: Heat-stable proteins causing food poisoning symptoms.

Epidemiology

• S. epidermidis is ubiquitous on skin; S. aureus is more common in skin folds.

• Both colonize upper respiratory, GI, and urogenital tracts.

• Transmission via direct contact, fomites, contaminated clothing.

• Handwashing is essential for prevention.

Diseases

• Non-Invasive: Food poisoning (N/V/D, headache, sweating).

• Cutaneous: Scalded skin syndrome, impetigo, folliculitis, furuncles, carbuncles.

• Systemic: Toxic shock syndrome, bacteremia, endocarditis, pneumonia, empyema, osteomyelitis.

Diagnosis, Treatment, and Prevention

• Diagnosis: Gram stain, coagulase test.

• Treatment: Vancomycin for MRSA; removal of pus and bacteria; long-term therapy for systemic infections.

• Prevention: Frequent handwashing; staph cannot be eliminated, only managed.

Streptococcus

Structure and Classification

Gram-positive cocci arranged in pairs or chains. Classified by:

• Serological (Lancefield) groups (A-H, K-V)

• Hemolysis type (alpha, beta, gamma)

• Cell arrangement and physiological properties

Group A: Streptococcus pyogenes (GAS)

Pathogenicity

• M Protein: Destabilizes complement, interferes with opsonization.

• Hyaluronic Acid Capsule: Camouflages bacteria from immune system.

• C5A Peptidase: Reduces chemotaxis of WBCs.

• Hyaluronidase: Facilitates tissue invasion.

• Pyrogenic Toxins: Cause fever, rash, shock (erythrogenic pathogens).

• Streptolysins: Lyse RBCs, WBCs, platelets.

Epidemiology

• Infects larynx and skin; spreads via respiratory droplets.

• More common in crowded conditions.

• Sensitive to penicillins.

Diseases

• Pharyngitis: Red, swollen throat, fever, purulent abscesses.

• Scarlet Fever: Rash, strawberry tongue, skin sloughing.

• Rheumatic Fever: Autoimmune damage to heart valves/muscle.

• Pyoderma/Impetigo: Pus lesions, contagious.

• Erysipelas: Inflammation of skin and lymphatics.

• Cellulitis: Deeper tissue infection, pain, inflammation.

• Streptococcal Toxic Shock Syndrome: Multisystem infection, shock, organ failure.

• Necrotizing Fasciitis: Flesh-eating disease, rapid tissue destruction.

• Glomerulonephritis: Immune complex deposition in kidneys, hypertension, low urine output.

Diagnosis, Treatment, and Prevention

• Rapid strep tests, ELISA for antigens.

• Penicillin, erythromycin, cephalosporin.

• Surgical removal for necrotizing fasciitis.

• Antibodies against M protein provide strain-specific immunity.

Group B: Streptococcus agalactiae (GBS)

Pathogenicity

• Capsules do not protect against immune system; pathogenic in newborns.

• Produces proteases, hemolysins, deoxyribonuclease.

Epidemiology

• Colonizes lower GI, genital, urinary tracts.

• Newborns at risk for early and late onset disease.

Diseases

• Puerperal Fever: Neonatal bacteremia, meningitis, pneumonia.

• Permanent neurological damage possible.

Diagnosis, Treatment, and Prevention

• ELISA for GBS antigens.

• Penicillin/ampicillin; vancomycin for resistant strains.

• CDC recommends prophylactic penicillin for colonized mothers.

Other Streptococci

• Beta Hemolytic: S. equisimilis and S. anginosus (pharyngitis).

• Alpha Hemolytic (Viridans Group): Cause dental caries, biofilm formation, can cause endocarditis and meningitis if entering bloodstream.

Streptococcus pneumoniae

Structure and Pathogenesis

• Short chains/pairs, round, mucus colonies.

• Capsule protects from digestion after exocytosis.

• Phosphorylcholine in cell wall stimulates endocytosis but prevents digestion.

• Secretes adhesins, IgA protease, pneumolysin (lyses cells).

Diseases

• Pneumococcal Pneumonia: Fluid, RBCs, leukocytes in lungs; fever, chills, productive cough.

• Sinusitis/Otitis Media: Pus, inflammation, pain in sinuses/middle ear.

• Bacteremia/Endocarditis: Bloodstream and heart valve infection.

• Pneumococcal Meningitis: High mortality, especially after head trauma.

Diagnosis, Treatment, and Prevention

• Quellung reaction (capsule swelling), antibody agglutination, bile solubility test.

• Penicillin; cephalosporin, erythromycin, chloramphenicol for resistant strains.

• Vaccines available but less effective in elderly, children, AIDS patients.

Enterococcus

Structure and Physiology

• Spherical, short chains/pairs, encapsulated, non-hemolytic.

• Grow at high temperatures, pH, NaCl, and bile salts.

• E. faecalis and E. faecium are main species.

Pathogenesis and Disease

• Adhere to epithelial cells, secrete bacteriotoxins.

• Cause HAI, bacteremia, endocarditis, wound infections if introduced to other body sites.

Diagnosis, Treatment, and Prevention

• Lactams, aminoglycosides, vancomycin.

• Prevention: Hygiene and aseptic techniques.

Bacillus

Structure and Physiology

• Large, rod-shaped, endospore-forming, anaerobic.

• Resistant to environmental extremes.

• Plasmid coding for anthrax toxins (three polypeptides).

Pathogenesis and Disease

• Primarily affects herbivores; humans contract via animals.

• Anthrax: GI (hemorrhage), inhalation (toxemia, shock), cutaneous (eschar formation).

Diagnosis, Treatment, and Prevention

• Antimicrobial drugs do not neutralize accumulated anthrax toxin.

Clostridium

Structure and Physiology

• Anaerobic, endospore-forming bacillus.

• Ubiquitous in soil, water, GI tracts.

• Produces potent exotoxins (Toxin A: diarrhea; Toxin B: cytotoxic).

Pathogenesis and Disease

• Opportunistic, especially after antibiotic overuse.

• Minor: self-limiting diarrhea; severe: pseudomembranous colitis.

Diagnosis, Treatment, and Prevention

• Isolation of organism.

• Discontinue causative antibiotics; metronidazole or vancomycin PO.

• Prevention: Hand hygiene, judicious antibiotic use.

Listeria

Structure and Pathogenesis

• Contaminates food/drink; causes listeriosis.

• Tolerant of cold; grows on refrigerated foods.

• Rarely pathogenic in healthy adults; can cause meningitis in immunocompromised.

Corynebacterium

Structure and Physiology

• High G+C, non-endospore forming, V-shaped, divides by snapping division.

• Ubiquitous on plants, animals, humans.

Pathogenesis and Disease

• Spread via respiratory droplets or skin contact.

• Diphtheria: Toxin inhibits polypeptide synthesis, causes cell death.

• Pseudomembrane formation can occlude airway, causing suffocation.

Diagnosis, Treatment, and Prevention

• Elek test for toxin detection.

• Antitoxin administration, penicillin, erythromycin.

• Immunization (DTaP vaccine) is best prevention.

Propionibacterium

Structure and Pathogenesis

• Small, anaerobic rods; cause acne.

• Grow in oil glands; excess sebum triggers inflammation.

• Dead bacteria and leukocytes form pus; blackheads from blocked glands.

• Cystic acne can cause scarring.

Treatment

• Usually self-limiting; clindamycin, erythromycin, retinoids for severe cases.

Nocardia and Actinomyces

Structure and Pathogenesis

• Elongated, filamentous cells resembling fungal hyphae.

• Nocardia: Difficult to stain; Actinomyces: Stain purple.

Diagnosis, Treatment, and Prevention

• Microscopic examination; antimicrobial drugs (6 weeks for Nocardia).

• Actinomyces: Surgical removal, penicillin (4-12 months).

• Prevention: Good oral hygiene, avoid soil exposure, prophylactic antimicrobials after trauma/surgery.

Summary Table: Major Gram-Positive Pathogens

Bacterium	Structure	Key Virulence Factors	Main Diseases	Treatment
Staphylococcus aureus	Clusters, Gram+, coagulase+	Protein A, coagulase, toxins	Food poisoning, skin/systemic infections	Vancomycin (MRSA), hygiene
Streptococcus pyogenes	Chains, Gram+, beta hemolytic	M protein, capsule, toxins	Pharyngitis, scarlet fever, rheumatic fever	Penicillin, surgery (severe)
Streptococcus agalactiae	Chains, Gram+, beta hemolytic	Capsule, enzymes	Neonatal meningitis, pneumonia	Penicillin, prophylaxis
Streptococcus pneumoniae	Pairs/chains, Gram+, alpha hemolytic	Capsule, phosphorylcholine	Pneumonia, meningitis, otitis media	Penicillin, vaccine
Enterococcus	Pairs/chains, Gram+, non-hemolytic	Adhesion, bacteriotoxins	HAI, endocarditis, wound infections	Vancomycin, hygiene
Bacillus anthracis	Rods, Gram+, endospore-forming	Anthrax toxins, capsule	Anthrax (cutaneous, GI, inhalation)	Antimicrobials (limited efficacy)
Clostridium difficile	Rods, Gram+, endospore-forming	Toxins A & B	Diarrhea, colitis	Metronidazole, vancomycin
Corynebacterium diphtheriae	V-shaped rods, Gram+, non-endospore	Diphtheria toxin	Diphtheria	Antitoxin, antibiotics, vaccine
Propionibacterium acnes	Rods, Gram+, anaerobic	Biofilm, sebum metabolism	Acne	Clindamycin, retinoids
Nocardia/Actinomyces	Filamentous, Gram+	Adhesion, tissue invasion	Skin, oral, systemic infections	Antimicrobials, surgery

Additional info: Some details about Mycoplasma and Mycobacterium were not provided in the original notes and are omitted here. For a complete study guide, refer to textbook sections on these genera.