The skin, the largest organ of the body, is made up of several
layers of living and dead cells. The living layers include the
connective tissue layers called the hypodermis and the dermis with a
rich supply of blood and lymph as well as sensory receptors, sweat
glands, sebaceous glands and hair follicles.
Also alive are the lower layers of the epidermis (the stratum basale,
stratum spinosum, stratum granulosum and the stratum lucidum) the
squamous epithelial cells of which are constantly dividing and
synthesizing keratin.
Once keratinized, these cells undergo APOPTOSIS or "programmed
cell death" to form the outer surface layer of the epidermis (the
stratum corneum); a surface layer composed of multiple layers of
dead, keratinized squamous epithelial cells.
The skin's surface is typically a dry environment although
perspiration and sebum serve to moisten the skin with a cocktail of
salts, lipids, lysozyme and other proteins in water. These secretions
are inhibitory to many microorganisms but they are also nutritive and
growth promoting for many of the NORMAL FLORA organisms. These normal
flora tend to be resistant to drying and tolerant of high salt
concentrations. These organisms are highly adapted to this
environment, hanging on tenaciously, colonizing the deep layers and
spaces between the cells of the stratum corneum as well as the many
hair follicles, sebaceous gland ducts and sweat gland pores. Vigorous
washing may briefly reduce their numbers but the population will
rebound quickly.
The normal skin flora serves some useful purposes. Most notably
many of these organisms produce organic acids such as proprionic acid
which lowers the pH and makes the skin less hospitable to many of the
more harmful TRANSIENT FLORA. Perhaps another beneficial effect of
the normal flora would be the production of volatile, aromatic
compounds which each of us come to recognize as our own natural
scent.
The common skin organisms include: Staphylococcus
epidermidis, Staphylococcus aureus,
Corynebacterium xerosis and Proprionibacterium
acnes.
Numerous studies have shown that handwashing by health care
practitioners helps to reduce the spread of infection within the
hospital and clinic environment thereby reducing the incidence of
NOSOCOMIAL infections (1-5).
In spite of these studies and in spite of the fact that there are
many good handwashing agents available; it is often difficult to
establish rigorous handwashing habits even by people who have been
highly trained and should know better. Overall,
routine handwashing before, during and after general patient care
occurs in approximately half of the instances in which it is
indicated and usually is of shorter duration than recommended.
Additionally, hospital staff generally overestimate the frequency and
quality of their handwashing behavior
(6).
Washing with detergent or plain soap is usually sufficient for the removal of transient flora although repeated handwashings may be necessary if the hands are exceptionally soiled or if contamination has been rubbed in. On the other hand, washing with soap and water has been reported to increase the amount of shedding of normal flora organisms (7,8). (Keep this in mind when interpreting the results of our experiment.)
The purpose of the surgical hand scrub is to not only remove and destroy any transient flora but also to reduce the resident normal flora. A variety of antimicrobial soaps and lotions are used to achieve this in conjunction with vigorous handwashing and brushing. The most common antimicrobial ingredients include:
REFERENCES:
1. Steere, A.C. and Mallison, G.F., Ann Intern Med, 1975; 83:683
2. Garner, J.S. and Favero, M.S., Infect Control, 1986; 7:231
3. Khan, M.U., Trans R Soc Trop Med Hyg, 1982; 76:164
4. Black, R.E., et. al., Am J Epidemiol, 1981; 113:445
5. Ansari, S.A.,et. al., J Clin Microbiol, 1991; 29:2115
6. Larson, E.L., Am J Infect Control, 1994; 22:25A
7. Lilly, et. al., J Clin Pathol, 1979; 32:382
8. Larson, E., et. al., Infect Control, 1986; 7:59
9. Babb, J.R., et. al., J Hosp Infect, 1991; 18 (Suppl B):41
10. Nicoletti, G., et. al., J Hosp Infect 1990; 15:323
11. Webster, J., J Hosp Infect 1992; 21:137