21.2 Bacterial Infections of the Skin and Eyes

Bacterial Pathogens and Infections of the Skin and Eyes

Bacterial infections of the skin and eyes range from superficial nuisances like acne to sight-threatening conditions like trachoma. Many of these infections share a handful of common causative organisms, so learning the key pathogens and how they behave gives you a framework for understanding diagnosis, treatment, and prevention across a wide range of conditions.

Common Bacterial Skin and Eye Pathogens

Staphylococcus species are among the most frequent causes of skin and eye infections.

• S. aureus causes impetigo, folliculitis, cellulitis, conjunctivitis, and keratitis. It's versatile and virulent, producing a variety of toxins and enzymes that help it invade tissue.
• S. epidermidis is part of the normal skin flora and typically harmless. It becomes a problem as an opportunistic pathogen, particularly on medical devices like catheters and prosthetics, where it readily forms biofilms.

Streptococcus species overlap with Staphylococcus in several skin infections but tend to cause more spreading, diffuse infections.

• S. pyogenes (Group A Streptococcus, or GAS) causes impetigo, erysipelas, cellulitis, and necrotizing fasciitis. It can also trigger post-infection immune complications like rheumatic fever and glomerulonephritis.
• S. pneumoniae can cause bacterial conjunctivitis and keratitis, though it's more commonly associated with respiratory infections.

Pseudomonas aeruginosa is an opportunistic gram-negative pathogen especially dangerous in burn wounds and for contact lens wearers. It causes keratitis and corneal ulcers that can progress rapidly, sometimes within 24 hours.

Other notable pathogens:

• Cutibacterium acnes (formerly Propionibacterium acnes) colonizes hair follicles and sebaceous glands. It contributes to acne vulgaris by triggering inflammation when it metabolizes sebum and produces fatty acids.
• Chlamydia trachomatis is an obligate intracellular pathogen that causes trachoma, the leading infectious cause of blindness worldwide. Repeated infections cause progressive scarring of the inner eyelid, which eventually turns the eyelashes inward (trichiasis), abrading the cornea.
• Moraxella spp. and Haemophilus influenzae are common causes of bacterial conjunctivitis, particularly in children.

Symptoms and Treatments of Infections

Impetigo

• Symptoms: Red sores (usually around the nose and mouth) that rupture, ooze, and form characteristic honey-colored crusts.
• Transmission: Direct contact with lesions or contaminated items like towels. Highly contagious, especially among young children.
• Treatment: Topical mupirocin for localized cases; oral antibiotics like cephalexin for widespread infection.

Cellulitis

• Symptoms: An area of skin that's red, swollen, warm, and painful, often with poorly defined borders. Systemic signs like fever and chills indicate the infection is spreading.
• Transmission: Bacteria (usually S. aureus or S. pyogenes) enter through breaks in the skin such as cuts, insect bites, or surgical wounds.
• Treatment: Oral antibiotics (cephalexin, dicloxacillin) for mild cases. IV antibiotics (vancomycin, linezolid) for severe cases or suspected MRSA.

Conjunctivitis (Pink Eye)

• Symptoms: Redness, itching, tearing, and a discharge that can be purulent (bacterial) or watery (viral/allergic). Bacterial conjunctivitis often produces a thick, yellow-green discharge that may crust the eyelids shut overnight.
• Transmission: Contact with infected secretions or contaminated objects (hands, towels, shared eye makeup).
• Treatment: Antibiotic eye drops or ointments such as erythromycin or fluoroquinolones (ciprofloxacin). Many mild cases are self-limiting, but treatment shortens the course and reduces transmission.

Trachoma

• Symptoms: Starts with inflammation and irritation of the conjunctiva. Repeated infections lead to eyelid scarring, trichiasis (inward-turning lashes), and eventually corneal opacity and blindness.
• Transmission: Direct contact with eye or nasal secretions from infected individuals, or mechanical transfer by flies. Strongly associated with overcrowding and poor sanitation.
• Treatment: The WHO promotes the SAFE strategy: Surgery for trichiasis, Antibiotics (oral azithromycin as a single dose, or tetracycline eye ointment), Facial cleanliness, and Environmental improvement.

Prevention Strategies

1. Wash hands frequently and avoid touching your eyes or open skin lesions.
2. Clean and cover wounds promptly to prevent bacterial entry.
3. Don't share personal items like towels, razors, or eye makeup.
4. Disinfect contact lenses and cases according to manufacturer instructions. Never wear lenses while swimming or sleeping (unless specifically designed for extended wear).

Challenges in Treatment

• Antibiotic resistance is a growing obstacle. Methicillin-resistant S. aureus (MRSA) is resistant to beta-lactam antibiotics (methicillin, oxacillin, and most cephalosporins), limiting treatment options to drugs like vancomycin, daptomycin, or linezolid.
• Misuse and overuse of antibiotics, both in medicine and agriculture, selects for resistant strains over time.
• Nosocomial (hospital-acquired) infections are particularly dangerous because hospital strains are often multi-drug resistant and patients may already be immunocompromised.

Biofilms in Antibiotic Resistance

A biofilm is a structured community of bacteria embedded in a self-produced extracellular matrix made of polysaccharides, proteins, and DNA. Biofilms are clinically important because they make infections dramatically harder to treat.

Why biofilms resist antibiotics:

• The extracellular matrix acts as a physical barrier, preventing antibiotics and immune cells from reaching bacteria deep within the biofilm.
• Bacteria within biofilms shift to slow-growing or dormant metabolic states. Since most antibiotics target actively growing cells (cell wall synthesis, protein synthesis, DNA replication), dormant cells are far less susceptible.
• The close proximity of bacteria within a biofilm facilitates horizontal gene transfer, spreading antibiotic resistance genes through conjugation, transformation, or transduction.

Clinically relevant biofilm infections in skin and eyes:

• P. aeruginosa biofilms on contact lenses and in chronic wound infections
• S. aureus biofilms in chronic wounds and on implanted medical devices
• S. epidermidis biofilms on catheters and prosthetics

Strategies to combat biofilms:

1. Combination antibiotic therapy using drugs with different mechanisms of action to target bacteria in various metabolic states.
2. Anti-biofilm agents that disrupt the matrix or interfere with bacterial communication. These include enzymes (DNase, dispersin B), chelators, and quorum sensing inhibitors that block the signaling bacteria use to coordinate biofilm formation.
3. Physical removal through wound debridement or removal of colonized medical devices.
4. Novel approaches under development, including bacteriophage therapy, antimicrobial peptides, and surface coatings that prevent bacterial adhesion.

Bacterial Virulence Factors and Host Immune Response

Virulence factors are the molecular tools bacteria use to establish infection and evade host defenses. For skin and eye pathogens, the most relevant categories are:

• Adhesins: Surface proteins that allow bacteria to attach to host cells and tissues. Without attachment, bacteria get washed away by tears, skin shedding, or fluid flow.
• Toxins: S. aureus alone produces a range of toxins including hemolysins (lyse red blood cells), leukocidins (kill white blood cells like Panton-Valentine leukocidin/PVL), and exfoliative toxins (cause the skin peeling seen in scalded skin syndrome). S. pyogenes produces streptolysins and pyrogenic exotoxins.
• Enzymes: Coagulase (clots plasma to shield bacteria), hyaluronidase (breaks down connective tissue to aid spread), and proteases (degrade host proteins and antibodies).

Host immune response operates on two levels:

• Innate immunity provides the first line of defense: the physical barrier of intact skin and mucous membranes, inflammation that recruits neutrophils and macrophages, phagocytosis of bacteria, and complement activation that opsonizes pathogens and forms membrane attack complexes.
• Adaptive immunity develops over days and provides specificity: B cells produce antibodies that neutralize toxins and opsonize bacteria, while T cells coordinate the immune response and directly kill infected cells.

Antibiotic resistance mechanisms in skin and eye pathogens include:

• Enzymatic inactivation: Beta-lactamases break down penicillins and cephalosporins. This is the primary mechanism behind MRSA resistance (encoded by the mecA gene, which produces an altered penicillin-binding protein, PBP2a).
• Target modification: Bacteria alter the molecular target of the antibiotic so it no longer binds effectively.
• Efflux pumps: Membrane proteins actively pump antibiotics out of the bacterial cell before they can reach their target. These pumps can confer resistance to multiple drug classes simultaneously.