Normal flora
The microbiome of the skin is complex, and has a thriving community of bacterial flora with a few commensal fungi. These microbiota comprise 103-104 organisms per square centimetre of skin. These bacteria may be:
■ normal or resident flora: a stable population of organisms in terms of numbers and composition
■ transient flora: essentially 'in transit' but may multiply for a short period; are quickly eliminated because of competition from the normal flora.
The main resident flora of the skin includes staphylococci, principally Staphylococcus epidermidis (asymptomatic carriage of Staphylococcus aureus is common in specific niches such as the anterior nares and axillae, and in hospital personnel), propionibacteria, micrococci and diphtheroids. Most of them are located superficially in the stratum corneum, but some are found in the hair follicles and act as a reservoir, replenishing the superficial flora, for example, after handwashing. The composition of the normal microbiota in specific anatomical niches of the body such as the scalp, axillae and pubic area differs considerably because of ecological differences in the pH, temperature and nutrients (e.g., sebum, fatty acids, urea).
Continuous desquamation of the stratum corneum and the impervious nature of the epithelium are major barriers for invading organisms. Other antimicrobial defences include lysozyme (in sweat, sebum and tears), bacteriocins produced by commensals and fatty acids produced from hydrolysis of sebum triglycerides.
Skin infections
The major forms of skin infections and the agents involved are shown in Table 28.1.
Bacterial skin infections
Staphylococcal infections
Boils, styes, carbuncles, sycosis barbae and angular cheilitis are all caused by staphylococci. A boil is a common, circumscribed infection of the hair follicle with central suppuration; pus eventually discharges and the boil heals, leaving no scar. Carbuncles, now rare, are large abscesses, which occur at the back of the neck, especially in people with diabetes. They are associated with constitutional upset and malaise. Sycosis barbae is a staphylococcal skin infection involving the shaving area of the face.
Streptococcal infections
In contrast to staphylococcal infections, which generally remain localized, streptococcal infections of the skin tend to spread subcutaneously and may lead to the following conditions.
Cellulitis
Streptococcus pyogenes group A is the most common offender, although Staphylococcus aureus may be involved in some. Cellulitis is a serious disease as subcutaneous spread of infection may carry the pathogen to lymphatic and blood vessels, resulting in marked constitutional upset and septicaemia.
Erysipelas
A distinctive type of cellulitis caused by Streptococcus pyogenes is usually seen in elderly adults. Lesions are typically on the face and limbs; the lesion distribution on the face is often butterfly-like with a characteristic 'orange-peel' texture of the skin and induration; the patient may be acutely ill with high fever and toxaemia.
Impetigo
A disease of young children: vesicles appear on the skin around the mouth and later become purulent, with characteristic honey-coloured crusts; both Streptococcus pyogenes and Staphylococcus aureus are involved.
Table 28.1 Agents of some important skin infectionsa
Aetiological agent |
Skin infection |
Bacteria |
|
Staphylococcus aureus |
Abscesses (boils), impetigo, pustules, carbuncles, toxic epidermal necrolysis (Ritter’s disease), omphalitis, angular cheilitis, sycosis barbae |
β-Haemolytic streptococci |
Cellulitis, impetigo, erysipelas |
Propionibacterium acnes |
Acne |
Mycobacterium tuberculosis |
Lupus vulgaris |
Mycobacterium ulcerans |
Swimming pool granuloma |
Mycobacterium leprae |
Leprosy |
Actinomyces israelii |
Actinomycosis (cervicofacial) |
Treponema pallidum |
Syphilis |
Haemophilus ducreyi |
Chancroid |
Viruses |
|
Herpes simplex virus |
Cold sore, herpetic whitlow |
Varicella-zoster virus |
Chickenpox, shingles |
Papovaviruses |
Papillomas, warts |
Coxsackievirus A |
Hand, foot and mouth disease |
Fungi |
|
Candida spp. |
Chronic mucocutaneous candidiasis Angular cheilitis |
Various dermatophytes |
Ringworm, etc. |
infections caused by protozoa and insects are not given. |
Necrotizing fasciitis
Necrotizing fasciitis is a rapidly progressing infection involving the full thickness of the skin down to the fascial planes, causing extensive necrosis and tissue loss. The skin looks initially normal, but the infection spreads surreptitiously along the fascial planes, destroying the blood supply to the skin, which discolours and becomes necrotic within hours (hence the tabloid term 'flesh-eating bacteria'). The patient is severely ill with toxaemia and shock, and may die within 24 h. Formerly called 'streptococcal gangrene', it can be caused by mixed flora comprising staphylococci, strict anaerobes and Enterobacteriaceae; the major offending organism is Streptococcus pyogenes. Management entails prompt excision of skin, antibiotics and supportive therapy.
Angular cheilitis (synonym: angular stomatitis)
Inflammation of one or both angles of the mouth, especially in denture-wearing elderly people, may be related to Staphylococcus aureus and/or Candida infection. However, many other predisposing factors are involved, and the dentist should be aware of the management of this condition (see Chapter 35).
Acne
Caused by Propionibacterium acnes, acne is a common and disfiguring facial infection of adolescents. The disease is a disorder of the pilosebaceous system and is believed to occur as a result of the production of fatty acids and lipases by bacteria, which initiates an inflammatory response and blocks the ducts, which drain the sebum from the gland to the skin surface. Hormonal imbalances also play a role. Long-term, low-dose antibiotic therapy may alleviate acne in chronic cases.
Leprosy
Caused by Mycobacterium leprae. The organism lives in human skin and nerves and is transmitted by prolonged contact to cause a chronic granulomatous disease. There are two types: the lepromatous and the tuberculoid forms (see Chapter 19).
Gram-negative infections
Gram-negative infections, less frequent than Gram-positive infections, are mostly associated with the moist areas of the skin such as the groin, axillae and perineum. Organisms involved include Pseudomonas aeruginosa and Bacteroides spp.
Diagnosis of bacterial skin infections
Swabs and smears of pus and exudate from the lesions are adequate; Gram-stained smears will generally indicate whether staphylococci or streptococci are involved. Swabs inoculated on blood agar (both aerobically and anaerobically) demonstrate the nature of haemolysis produced by streptococci (a-, β- or no haemolysis); subsequent confirmation of the identity of isolates is by appropriate tests (e.g., coagulase test, API tests).
Viral skin infections
Herpes simplex viruses (human herpesviruses 1 and 2) cause recurrent cold sores and genital lesions; herpetic whitlow may
be an occupational disease of dentists and nursing staff (see Fig. 21.2). Varicella-zoster virus (human herpesvirus 3) may cause chickenpox (primary lesion) and shingles of the skin (either in the facial dermatomes or others). Human herpesvirus 6 and human parvovirus B19 cause exanthem subitum and the 'slapped-cheek' syndrome, respectively; both are innocuous self-limiting diseases that cause facial rash and redness, mainly in children (see Chapter 21). Papovaviruses cause the common wart, and coxsackievirus A16 infection may result in hand, foot and mouth disease (Table 28.1).
Note that many infectious diseases such as rubella, chicken- pox, measles and glandular fever manifest as macules (spots) or papules (pimples) on the skin.
Diagnosis of viral skin infections
Diagnostic methods include serology for antibody studies; swab or vesicular fluid for tissue culture; and electron microscopy (see Chapter 6).
Fungal skin infections
Fungal skin infections are mainly caused by dermatophytes and the yeast Candida. As their name implies, dermatophytes (which include Microsporum, Epidermophyton and Trichophyton) live in keratinized tissues, especially hair, nails and the skin squames. Candida species are common opportunistic pathogens that may cause both skin and mucosal infections (see Chapter 35).
Wound infections
Surgical wound infection
Surgical wound infection accounts for approximately a quarter of hospital-acquired (nosocomial) infections. It is a significant cause of morbidity, prolonging the hospital stay of surgical patients, and frequently results in death.
Aetiology
Staphylococcus aureus and Escherichia coli are the major pathogens, but other coliforms such as Pseudomonas aeruginosa and Klebsiella spp. may be involved. If the wound is contaminated (e.g., large bowel), anaerobes, Clostridium spp. and Bacteroides spp. may also be involved. Most wound infections are polymicrobial in nature.
Clinical features
Wound edges become reddened, with or without pus formation; sometimes a wound abscess may form unnoticed in the deeper layers and eventually discharge through the suture line. Patients may or may not be pyrexial, depending on the degree of infection. Surgical wound infection may result in:
■ spread of infection either to adjacent tissues or into the blood, causing septicaemia (see below)
■ wound dehiscence (breakdown of the wound), necessitating resuture.
Pathogenesis and epidemiology
The infection could be either endogenous or exogenous. The source of an exogenous infection could be an infected person in an adjoining bed, or a carrier, who might be a member of staff. Reservoirs of infection include human skin, environmental dust and inanimate objects (fomites) such as bed linen. The mode of cross infection could be direct or indirect contact, or the airborne route. Many factors affect the incidence of wound infection; these include:
■ type of wound: clean (i.e., no incision through respiratory, gastrointestinal or genitourinary tract), contaminated (e.g., following surgery in a site with a normal flora) or infected (e.g., drainage of an abscess)
■ overcrowded wards
■ length of stay in the hospital (shorter hospital stay carries a lesser risk of infection)
■ length of the operation (longer operation carries a greater infectious risk)
■ presence of foreign bodies and drains
■ general health of the patient.
Prevention
Infection may be avoided by:
■ rigid observation of aseptic and antiseptic techniques during both patient preparation and the operation itself
■ rigid observation and implementation of infection control theatre protocols
■ appropriate theatre clothing, as transmission of infection from humans is the single most important cause of wound infection
■ positive-pressure ventilation within the operating room to prevent ingress of contaminated air and dust from the external hospital environment
■ isolation of patients with discharging wounds to prevent the dissemination of pathogens, that is, source isolation, where the patient is the source of infection (compare protective isolation of susceptible patients, for instance, a bone marrow transplant patient, from infectious agents)
■ carefully chosen preoperative antibiotic prophylaxis in specific situations (e.g., colonic surgery).
Infections of burns
Major burns create large, moist, exposed surfaces that are ideal for bacterial growth because the protective skin cover has been lost.
Aetiology
Common organisms that infect burns are Streptococcus pyogenes, Pseudomonas aeruginosa and Staphylococcus aureus; infection is usually polymicrobial.
Pathogenesis and epidemiology
Bacteria colonize burn wounds within 24 h if appropriate prophylaxis is not given, with eventual cellulitis of adjacent tissues and septicaemia. Streptococcus pyogenes, in particular, is a frequent cause of septicaemia; Pseudomonas aeruginosa has a special ability for surviving in burnt tissue and in burns wards, but it is not as virulent as Streptococcus pyogenes.
Diagnosis of wound infections
Swabs of exudate, tissue or pus are cultured on conventional media (blood agar, MacConkey's agar, Robertson's medium); the smears of the tissue or exudate are Gram-stained and examined for organisms.
Clostridial wound infections
Wound infections described earlier, which are suppurative, differ clinically from those caused by clostridia (Gram-positive, anaerobic, spore-forming rods; Chapter 13). These infections are severe, but fortunately rare. The two major clostridial wound infections are tetanus, caused by Clostridium tetani, and gas gangrene, due to three different but related organisms: Clostridium welchii, Clostridium novyi and Clostridium septicum.
Tetanus
See Chapter 25.
Gas gangrene
Gas gangrene is caused by Clostridium welchii (60%-65%), Clostridium novyi (20%-40%) and Clostridium septicum (10%-20%).
Clinical features
Spreading gangrene of the muscles is accompanied by toxaemia and shock. The involved tissues are black and oedematous with a foul-smelling serous exudate; they exhibit the sign of crepitus (palpable crackling on pressure due to subcutaneous movement of gas bubbles) as a result of the production of gaseous metabolites by the multiplying clostridia.
Pathogenesis and epidemiology
A serious disease with a high mortality rate, very often requiring the excision or amputation of the affected area or limb, gas gangrene is a result of the toxins and enzymes produced by clostridia thriving on damaged and devitalized tissues, which provide ideal conditions for anaerobic growth. The organisms produce a variety of toxins, one of which is a lecithinase that damages cell membranes; other enzymes produce gaseous byproducts within tissue compartments, helping further spread of infection.
Clostridia can be commonly isolated from faeces, and their spores are ubiquitous in nature.
Laboratory diagnosis
See Chapter 13.
Treatment
Gas gangrene is treated with:
■ surgical debridement, including wide excision or even amputation of affected areas
■ antibiotics: large doses of penicillin, with or without metronidazole
■ hyperbaric oxygen may be given, if available, to reduce anaerobiosis of affected tissues.
Prevention
Debridement and amputation should be performed as appropriate. Prophylactic penicillin should be administered for surgical procedures in the area of the thigh, perineum and buttocks (as clostridia are commensals in these regions).
Key facts
• The skin has a thriving microbiome of resident and transient flora; there are about 103—1 04 organisms per square centimetre of skin.
• The principal resident flora of the skin are Staphylococcus epidermidis, propionibacteria, micrococci and diphtheroids.
• Asymptomatic carriage of Staphylococcus aureus is common in sites such as the anterior nares and axillae, and in hospital personnel.
• Boils, styes, carbuncles, sycosis barbae and angular cheilitis may be all due to staphylococcal infection.
• Subcutaneous spread of infection or cellulitis is caused by Streptococcus pyogenes (group A), sometimes with Staphylococcus aureus.
• Necrotizing fasciitis is the term given to rapidly progressing infection involving the full thickness of the skin, including the fascial planes, causing extensive necrosis, tissue loss, toxaemia and shock.
• Angular cheilitis or stomatitis is mainly caused by Staphylococcus aureus and/or Candida infection; but other predisposing factors are involved.
Acne, a common, disfiguring facial infection of adolescents, is caused by Propionibacterium acnes.
Mycobacterium leprae, the agent of leprosy, lives in human skin and nerves and is transmitted by prolonged contact to cause two types of chronic granulomatous disease: the lepromatous and the tuberculoid forms.
Surgical wound infections account for approximately a quarter of hospital-acquired (nosocomial) infections.
Staphylococcus aureus and Escherichia coli are the major agents of surgical infection.
Factors affecting the incidence of wound infection include the type of wound (clean, contaminated or infected), overcrowded wards, length of stay in hospital, length of the operation, foreign bodies and drains, and the general health of the patient. Common organisms that infect burns are Streptococcus pyogenes, Pseudomonas aeruginosa and Staphylococcus aureus; infection is usually polymicrobial.
The two major clostridial wound infections are tetanus, caused by Clostridium tetani, and gas gangrene, due to Clostridium welchii, Clostridium novyi or Clostridium septicum.
Review questions (answers on p. 366)
Please indicate which answers are true, and which are false.
28.1 Which of the following statements on human skin are true?
A. a stable population of microorganisms is found
B. hair follicles act as reservoirs of pathogenic bacteria
C. bacteriocins act as a major inhibitory factor for invading organisms
D. sebum has antibacterial properties as it contains lysozyme
E. Gram-negative infections are more common than Gram-positive infections
28.2 With regard to skin infections, which of the following statements are true?
A. staphylococcal skin infections usually remain localized
B. cellulitis is predominantly caused by Staphylococcus aureus
C. necrotizing fasciitis may have a polymicrobial aetiology
D. angular cheilitis could present as a mixed bacterial and fungal infection
E. infections by dermatophytes can affect hair and nails
28.3 Which of the following statements on post-operative wound infections are true?
A. they are a major cause of nosocomial infections
B. coliforms are thought to be major pathogens
C. they can lead to wound dehiscence and septicaemia
D. prolonged operation time is not considered a risk factor
E. incidence may be reduced by preoperative antibiotic prophylaxis
28.4 Gas gangrene:
A. is exclusively caused by Clostridium welchii
B. often affects the lower limbs
C. classically exhibits crepitus in affected tissues
D. often necessitates amputation of the affected limb
E. hyperbaric oxygen has a place in treatment
28.5 Identify and match the major aetiological agent responsible for the skin conditions given below:
A. acne
B. folliculitis
C. cellulitis
D. impetigo
E. slapped-cheek syndrome
1. Propionibacterium acnes
2. Staphylococcus aureus
3. Streptococcus pyogenes
4. Staphylococcus epidermidis
5. parvovirus B19
Further reading
Mims, C., Playfair, J., Roitt, I., et al. (1998). Infections of the skin, muscle, joints, bone and hemopoietic system (Chapter 23). In Medical microbiology (2nd ed.). London: Mosby.
Murray, P. R., Rosenthal, K. S., Kobayashi, G. S., et al. (1998).
Superficial, cutaneous and subcutaneous mycoses (Chapter 69). In Medical microbiology (3rd ed.). St Louis: Mosby.
Shanson, D. C. (1999). Skin infections and infestations (Chapter 17). In Microbiology in clinical practice (3rd ed.). Oxford: Butterworth- Heinemann.