21 Microbial Diseases of the Ski

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					21: Microbial Diseases of the Skin and

Learning Objectives
1. Describe the structure of the skin and mucous membranes and the ways pathogens can
   invade the skin.
2. Provide examples of normal skin microbiota, and state their locations and ecological roles of
   its members.
3. Differentiate staphylococci from streptococci, and name several skin infections caused by
4. List the causative agent, method of transmission, and clinical symptoms of Pseudomonas,
   dermatitis, otitis externa, acne.
5. List the causative agent, method of transmission, and clinical symptoms of these skin
   infections: warts, smallpox, chickenpox, shingles, cold sores, measles, rubella, fifth disease,
6. Differentiate cutaneous from subcutaneous mycoses, and provide an example of each.
7. List the causative agent of and predisposing factors for candidiasis.
8. List the causative agent, method of transmission, clinical symptoms, and treatment for scabies
   and pediculosis.
9. Define conjunctivitis.
10. List the causative agent, method of transmission, and clinical symptoms of these eye
    infections: neonatal gonorrheal ophthalmia, inclusion conjunctivitis, trachoma.
11. List the causative agent, method of transmission, and clinical symptoms of these eye
    infections: herpetic keratitis, Acanthamoeba keratitis.

New in this Edition
•   The new discussion of the causes of toxic shock syndrome makes a clear distinction between
    staphylococci and streptococci.
•   The new Clinical Problem Solving box describes infections in the gym.

Chapter Summary
Introduction (p. 613)
 1. The skin is a physical barrier against microorganisms.
 2. Moist areas of the skin (such as the armpit) support larger populations of bacteria than dry
    areas (such as the scalp).
 3. Human skin produces antibiotics called defensins.

Structure and Function of the Skin (pp. 614–615)
 1. The outer portion of the skin (epidermis) contains keratin, a waterproof coating.
 2. The inner portion of the skin, the dermis, contains hair follicles, sweat ducts, and oil glands
    that provide passageways for microorganisms.
 3. Sebum and perspiration are secretions of the skin that can inhibit the growth of
 4. Sebum and perspiration provide nutrients for some microorganisms.
 5. Body cavities are lined with epithelial cells. When these cells secrete mucus, they constitute
    the mucous membrane.

Normal Microbiota of the Skin (pp. 615–634)
 1. Microorganisms that live on skin are resistant to desiccation and high concentrations of salt.
 2. Gram-positive cocci predominate on the skin.
 3. The normal skin microbiota are not completely removed by washing.
 4. Members of the genus Propionibacterium metabolize oil from the oil glands and colonize hair
 5. Malassezia furfur yeast grows on oily secretions and may be the cause of dandruff.

Microbial Diseases of the Skin (p. 615)
 1. Vesicles are small fluid-filled lesions; bullae are vesicles larger than 1 cm; macules are flat,
    reddened lesions; papules are raised lesions; and pustules are raised lesions containing pus.

Bacterial Diseases of the Skin (pp. 615–623)
Staphylococcal Skin Infections (pp. 615–620)
 2. Staphylococci are gram-positive bacteria that often grow in clusters.
 3. The majority of skin microbiota consist of coagulase-negative Staphylococcus epidermidis.
 4. Almost all pathogenic strains of S. aureus produce coagulase.
 5. Pathogenic S. aureus can produce enterotoxins, leukocidins, and exfoliative toxin.
 6. Many strains of S. aureus produce penicillinase; these are treated with vancomycin.
 7. Localized infections (sties, pimples, and carbuncles) result from S. aureus entering openings in
    the skin.
 8. Impetigo of the newborn is a highly contagious superficial skin infection caused by S. aureus.
 9. Toxemia occurs when toxins enter the bloodstream; staphylococcal toxemias include scalded
    skin syndrome and toxic shock syndrome.

Streptococcal Skin Infections (pp. 620–622)
10. Streptococci are gram-positive cocci that often grow in chains.
11. Streptococci are classified according to their hemolytic enzymes and cell wall antigens.
12. Group A beta-hemolytic streptococci (including Streptococcus pyogenes) are the pathogens
    most important to humans.
13. Group A beta-hemolytic streptococci produce a number of virulence factors: M protein,
    erythrogenic toxin, deoxyribonuclease, streptokinases, and hyaluronidase.
14. Erysipelas (reddish patches) and impetigo (isolated pustules) are skin infections caused by S.
15. Invasive group A beta-hemolytic streptococci cause severe and rapid tissue destruction.

Infections by Pseudomonads (p. 622)
16. Pseudomonads are gram-negative rods. They are aerobes found primarily in soil and water
    that are resistant to many disinfectants and antibiotics.
17. Pseudomonas aeruginosa produces an endotoxin and several exotoxins.
18. Diseases caused by P. aeruginosa include otitis externa, respiratory infections, burn infections,
    and dermatitis.
19. Infections have a characteristic blue-green pus caused by the pigment pyocyanin.
20. Quinolones are useful in treating P. aeruginosa infections.

Acne (pp. 622–623)
21. Propionibacterium acnes can metabolize sebum trapped in hair follicles.
22. Metabolic end-products (fatty acids) cause inflammatory acne.
23. Tretinoin, benzoyl peroxide, erythromycin, and Accutane are used to treat acne.

Viral Diseases of the Skin (pp. 623–629)
Warts (p. 623)
24. Papillomaviruses cause skin cells to proliferate and produce a benign growth called a wart or
25. Warts are spread by direct contact.
26. Warts may regress spontaneously or be removed chemically or physically.

Smallpox (Variola) (pp. 623–624)
27. Variola virus causes two types of skin infections: variola major and variola minor.
28. Smallpox is transmitted by the respiratory route, and the virus is moved to the skin via the
29. The only host for smallpox is humans.
30. Smallpox has been eradicated as a result of a vaccination effort by the WHO.

Chickenpox (Varicella) and Shingles (Herpes Zoster) (pp. 624–626)
31. Varicella-zoster virus is transmitted by the respiratory route and is localized in skin cells,
    causing a vesicular rash.
32. Complications of chickenpox include encephalitis and Reye’s syndrome.
33. After chickenpox, the virus can remain latent in nerve cells and subsequently activate as
34. Shingles (herpes zoster) is characterized by a vesicular rash along the affected cutaneous
    sensory nerves.
35. The virus can be treated with acyclovir. An attenuated live vaccine is available.
Herpes Simplex (pp. 626–627)
36. Herpes simplex infection of mucosal cells results in cold sores and occasionally encephalitis.
37. The virus remains latent in nerve cells, and cold sores can recur when the virus is activated.
38. HSV-1 is transmitted primarily by oral and respiratory routes.
39. Herpes encephalitis occurs when herpes simplex viruses infect the brain.
40. Acyclovir has proven successful in treating herpes encephalitis.

Measles (Rubeola) (p. 627)
41. Measles is caused by measles virus and transmitted by the respiratory route.
42. Vaccination provides effective long-term immunity.
43. After the virus has incubated in the upper respiratory tract, macular lesions appear on the
    skin, and Koplik’s spots appear on the oral mucosa.
44. Complications of measles include middle ear infections, pneumonia, encephalitis, and
    secondary bacterial infections.

Rubella (pp. 627–628)
45. The rubella virus is transmitted by the respiratory route.
46. A red rash and light fever might occur in an infected individual; the disease can be
47. Congenital rubella syndrome can affect a fetus when a woman contracts rubella during the
    first trimester of her pregnancy.
48. Damage from congenital rubella syndrome includes stillbirth, deafness, eye cataracts, heart
    defects, and mental retardation.
49. Vaccination with live rubella virus provides immunity of unknown duration.

Other Viral Rashes (pp. 628–629)
50. Human parvovirus B19 causes fifth disease, and HHV-6 causes roseola.

Fungal Diseases of the Skin and Nails (pp. 629–631)
Cutaneous Mycoses (pp. 629–630)
51. Fungi that colonize the outer layer of the epidermis cause dermatomycoses.
52. Microsporum, Trichophyton, and Epidermophyton cause dermatomycoses called ringworm, or
53. These fungi grow on keratin-containing epidermis, such as hair, skin, and nails.
54. Ringworm and athlete’s foot are usually treated with topical antifungal chemicals.
55. Diagnosis is based on the microscopic examination of skin scrapings or fungal culture.

Subcutaneous Mycoses (p. 630)
56. Sporotrichosis results from a soil fungus that penetrates the skin through a wound.
57. The fungi grow and produce subcutaneous nodules along the lymphatic vessels.

Candidiasis (pp. 630–631)
58. Candida albicans causes infections of mucous membranes and is a common cause of thrush (in
    oral mucosa) and vaginitis.
59. C. albicans is an opportunistic pathogen that may proliferate when the normal bacterial
    microbiota are suppressed.
60. Topical antifungal chemicals may be used to treat candidiasis.

Parasitic Infestation of the Skin (pp. 631–634)
61. Scabies is caused by a mite burrowing and laying eggs in the skin.
62. Pediculosis is an infestation by Pediculus humanus.

Microbial Diseases of the Eye (pp. 634–637)
 1. The mucous membrane lining the eyelid and covering the eyeball is the conjunctiva.

Inflammation of the Eye Membranes: Conjunctivitis (pp. 634–
 2. Conjunctivitis is caused by several bacteria and can be transmitted by improperly disinfected
    contact lenses.

Bacterial Diseases of the Eye (pp. 635–636)
 3. Bacterial microbiota of the eye usually originate from the skin and upper respiratory tract.
 4. Neonatal gonorrheal ophthalmia is caused by the transmission of Neisseria gonorrhoeae from
    an infected mother to an infant during its passage through the birth canal.
 5. All newborn infants are treated with an antibiotic to prevent Neisseria and Chlamydia
 6. Inclusion conjunctivitis is an infection of the conjunctiva caused by Chlamydia trachomatis. It is
    transmitted to infants during birth and is transmitted in unchlorinated swimming water.
 7. In trachoma, which is caused by C. trachomatis, scar tissue forms on the cornea.
 8. Trachoma is transmitted by hands, fomites, and perhaps flies.

Other Infectious Diseases of the Eye (pp. 636–637)
 9. Inflammation of the cornea is called keratitis.
10. Herpetic keratitis causes corneal ulcers. The etiology is HSV-1 that invades the central
    nervous system and can recur.
11. Acanthamoeba protozoa, transmitted via water, can cause a serious form of keratitis.

The Loop
For a taxonomic approach, pages can be assigned as follows:
Bacterial diseases of the skin                     pp. 615–623
Bacterial diseases of the eye                      pp. 634–635
Viral diseases of the skin                         pp. 623–629, 633
Viral disease of the eye                           p. 637
Fungal diseases of the skin                        pp. 629–631
Protozoan disease of the eye                            p. 637
Arthropod infestations of the skin                      pp. 631–633

1. Bacteria usually enter through inapparent openings in the skin. Fungal pathogens (except
   subcutaneous) often grow on the skin itself. Viral infections of the skin (except warts and
   herpes simplex) most often gain access to the body through the respiratory tract.
2. Staphylococcus aureus; Streptococcus pyogenes.
      Disease      Etiology                     Symptoms           Treatment           Notes

      Impetigo     Staphylococcus aureus        Vesicles that      Hexachlorophene     May be
                                                rupture and                            epidemic
                                                crust over
      Erysipelas   Streptococcus pyogenes       Thickened red      Penicillin          May be
                                                patches, swollen                       endogenous
                                                at margins

                        Etiological                                                  Method of
      Disease           Agent               Clinical Symptoms                        Transmission

      Acne              P. acnes            Infected oil glands                      Direct contact
      Pimples           S. aureus           Infected hair follicles                  Direct contact
      Warts             Papovavirus         Benign tumor                             Direct contact
      Chickenpox        Herpesvirus         Vesicular rash                           Respiratory route
      Fever blisters Herpesvirus            Recurrent ―blisters‖                     Direct contact
      Measles           Paramyxovirus       Papular rash, Koplik’s spots             Respiratory route
      Rubella           Togavirus           Macular rash                             Respiratory route

5. Both are fungal infections. Sporotrichosis is a subcutaneous mycosis; athlete’s foot is a
   cutaneous mycosis.
6. a.     Conjunctivitis is inflammation of the conjunctiva, and keratitis is inflammation of the
     b.   Table 21.2.
7. Candidiasis is caused by Candida albicans. The yeast is able to grow when the normal
   microbiota are suppressed or when the immune system is suppressed. The yeast can be
   transferred from another person or be transient microbiota. White patches in the mouth or
   bright red areas of the skin and mucous membranes are signs of infection. Antifungal agents
   such as miconazole are used to treat candidiasis. Systemic infections are treated with oral
8. The test determines the woman’s susceptibility to rubella. If the test is negative, she is
   susceptible to the disease. If she acquires the disease during pregnancy the fetus could
   become infected. A susceptible woman should be vaccinated.
9.    Symptoms                        Disease
      Koplik’s spots                  Measles
      Macular rash                    Measles
      Vesicular rash              Chickenpox
      Small, spotted rash         German measles
      ―Blisters‖                  Cold sore
      Corneal ulcer               Keratoconjunctivitis
10. The central nervous system can be invaded following keratoconjunctivitis; this results in
11. Attenuated measles, mumps, and rubella viruses.
12. Varicella-zoster virus appears to remain latent in nerve cells following recovery from a
    childhood infection of chickenpox. Later, the virus may be activated and cause a vesicular
    rash (shingles) in the area of the nerve.
13. To prevent neonatal gonorrheal ophthalmia. This is caused by N. gonorrhoeae contracted by
    the newborn during passage through the birth canal.
14. Trachoma.
15. Scabies is an infestation of mites in the skin. It is treated with permethrin insecticide or
    gamma benzene hexachloride. The presence of a six-legged arthropod (insect) indicates
    pediculosis (lice).

Critical Thinking
1.   S. aureus is adapted for surviving on the human skin, which has a high concentration of NaCl.
     Microorganisms that are not adapted to this hypertonic environment will not be able to
     tolerate the 7.5% NaCl in mannitol salt agar.
2.   Most warts regress spontaneously. Removal of warts is usually for cosmetic reasons.
     Occasionally warts are painful when they are located where pressure is placed on them (e.g.,
     plantar warts on the sole of the foot).
3.   The infections were transmitted by the contact lenses or cosmetics. Cosmetics are inoculated
     with microbes each time they are used. Some of the microbes grow, resulting in large
     inoculations of the eyes. Contact lenses can be improperly cleaned (i.e., not using an
     antiseptic) or contaminated by fingers.
4.   The virus had one host—humans. It was not found in soil, water, or nonhuman organisms.
     Polio and measles meet this criterion.

Clinical Applications
1.   Pseudomonas aeruginosa. This bacterium is common in soil and is resistant to many antibiotics.
2.   Toxic shock syndrome due to growth of Staphylococcus at the injection site.
3.   The symptoms of toxic shock syndrome were caused by toxins produced from the secondary
     infection (S. aureus).

Case History: Wrestling with Skin Infections
A wrestling camp held July 2 through July 28 was attended by 175 male high school wrestlers
from throughout the United States. On July 19, seven wrestlers were referred to a local urgent
care facility because of complaints of painful vesicles on various parts of their bodies [head or
neck (3), extremities (2), trunk (1)] and conjunctiva (1). Bacterial and fungal cultures from the skin
lesions were negative.
    A questionnaire was administered to wrestlers by telephone following the conclusion of
camp. Sixty-one wrestlers met the case definition of the presence of cutaneous vesicles. The
athletes had onset during the camp session or within one week after leaving camp (see the
    Athletes who reported wrestling with a participant with a rash were more likely to have the
infection. Thirty-eight wrestlers interviewed reported a past history of oral cold sores. The attack
rate was 24% for wrestlers who reported a past history of oral cold sores and 38% for wrestlers
without a history of oral cold sores.

1.   What diseases do you suspect?
2.   How was this disease transmitted?
3.   How is this disease treated?
4.   Provide a possible explanation of the lower attack rate in wrestlers with a history of oral cold
5.   How can such outbreaks be prevented?

The Solution
1.   Herpes gladiatorum
2.   Direct contact
3.   Acyclovir
4.   Individuals with a history of oral herpes may have circulating antibodies that will prevent a
     new infection or recurrence.
5.   Control methods should include education of athletes and trainers regarding herpes
     gladiatorum, routine skin examinations before wrestling contact, and exclusion of wrestlers
     with suspicious skin lesions. This outbreak might have been prevented if athletes with such
     lesions had been promptly excluded from contact competition.