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Microbial diseases of
skin and eyes
Lesson Objectives
– List the protective features of the skin and mucous membranes.
– Discuss the methods that pathogens use to invade the skin and
mucous membranes.
– State locations and examples of normal flora.
– Discuss selected bacterial infections of the skin and eyes; the
mode of transmission and clinical symptoms of each.
– List the mode of transmission, and clinical symptoms of
herpesvirus and papillomavirus.
– List the cutaneous fungal infections.
– Discuss microbial diseases of the eye and list the microbes that
cause them.
Skin—the First Line of Defense (remember???)
The important stuff:
1) epidermis:
Sebum is a food source
for some microbes, but
it produces toxic byproducts (toxic to
pathogens, harmless to
us!
stratum corneum (horned layer).
Layer of dead cells that are
continually sloughed off. This
removes microbes.
Sebaceous glands: produce oil
(sebum). Sebum has a low pH
(acid) which kills many
pathogens.
Perspiration—high salt, contains lysozyme (kills
bacteria).
“normal” microbes of the skin: what do we
expect to find?
Staphylococcus species:
Gram positive cocci in
clusters.
Streptococcus species,
especially S. pyogenes.
Dermatophytes: various
molds (fungi) of different
species.
• Although some of these species are
pathogens, most of the time, they don’t cause
disease (why?)
What parts of the skin would we
expect to find the most microbes?
• Hands___________________________________
• Face____________________________________
• Axillae__________________________________
• Anus___________________________________
• Genitalia________________________________
• Feet____________________________________
Culture of skin or tissue
• Collected on a culturette, or from skin
scrapings. If pus is generated, this is collected
with a syringe.
• Usually a Gram stain is performed. Plated on
blood agar, sometimes other agar if other
pathogens are suspected.
Diseases of skin—by pathogen
Staphylococcus aureus:
• Gram positive cocci in clusters.
• Gold colonies on most media.
• Beta hemolytic on blood agar
• Catalase positive (H2O2 fizzes—true of all
staph)
Coagulase positive (produces an exotoxin that
makes mammalian plasma clot.)
Virulence of Staphylococcus aureus
• Exotoxins: many contribute to S. aureus’s ability to cause
disease:
coagulase: described above
DNase: digests cellular DNA
lipase: digests fats, allows staph to colonize skin.
Hemolysins (many): These are enzymes that lyse blood
cells.
Hyaluronidase: digests the material that holds cells in
tissues together.
Staph. aureus is a notorious pathogen because…
• High tolerance to environmental stress (salt tolerant, heat
tolerant, facultative anaerobe.
• Produces a large variety of toxins
• Generally is present as normal skin bacteria
• When S. aureus breeches the First Line of Defense, it can
cause many types of disease (boils, impetigo, pneumonia,
food poisoning, septicemia, etc.)
• Although it is usually sensitive to penicillin and related
antibiotics, resistance to antibiotics is possible. MRSA.
How S. aureus invades tissue:
invasiveness
1. Pathogen enters skin through a pore, sebaceous
gland, a cut, or other portal. Fimbriae enable
attachment.
2. Pathogen excretes exotoxins that kill or exclude
host cells. The dead cell products may be a food
source for the pathogen.
3. The pathogen reproduces, and continues to
produce exotoxins that kill/exclude host cells.
Diseases of skin/tissue related to S.
aureus invasive infection:
• Impetigo: p. 438. Flaking “crusty” skin.
• Cellulitis: p. 440. This usually involves the
tissues. Sometimes occurs post-surgery. Usually
uncomplicated if caught early.
• Boils: infected hair follicles. Usually fluid filled
skin eruptions, cause mild-severe pain. These can
develop into an abscess (extend to subcutaneous
tissue, and invasive).
Next pathogen: Streptococcus
pyogenes (Group A streptococcus)
• Gram positive cocci in chains (~ 20 cocci per
chain)
• Beta hemolytic on blood agar (complete
hemolysis). Smaller colonies than S. aureus.
• Catalase negative.
Sensitive to bacitracin:
Many of the toxins produced by S. pyogenes
are similar to those produced by S. aureus.
Both organisms can be invasive.
Necrotizing fasciitis (“flesh eating bacteria”). A very
rapid invasive infection. Any invasive infection can
lead to
• Septicemia (bacteria in the blood. Life
threatening situation)
• Osteomyelitis (bacteria in the bone marrow).
Scarlet Fever
• Caused by S. pyogenes that contains a
bacterial virus.
• Erythrogenic toxin: causes skin to become
very red and rough (“sandpaper feel”)
• Usually the portal of entry for scarlet fever is
the respiratory tract.
Other bacteria that can enter through the
skin and cause invasive infection:
• Clostridium perfringens obligate anaerobe,
endospore former. Causes gangrene.
• Bacillus anthracis obligate aerobe, endospore
former. Causes cutaneous anthrax (p. 447)
• Propionibacter acnes causes acne, an
infection of the sebaceous glands. Much
more mild than boils.
Treatment of skin and tissue infections
• Antibiotic therapy: S. aureus must always be
tested for antibiotic sensitivity.
• Debridement: surgical removal of necrotic
and/or infected tissue.
• Extreme cases (necrotizing fasciitis):
amputation of affected parts.
Viral infections of the skin
• Maculopapular infections (red rashes) pp.
434-438
• These are usually red, blotchy, sometimes
raised, but not open.
• Portal of entry is usually respiratory system.
Other symptoms include fever, sore throat,
and flu-like symptoms
• All maculopapillary infections (except scarlet
fever) are viral. They are self-limiting (they “go
away”) and generally confer natural active
immunity.
- Measles
- Rubella (a danger to pregnant women for fetus)
- “fifth” disease
- Coxsackie Virus
- Scarlet fever
Herpesviruses and papilloma virus
• Chicken pox: portal of entry: respiratory system
• Begins as macular rash, develops into fluid filled
vesicles.
• End of infection, vesicles (pox) which open and
crust over. Infection is generally self-limiting.
However…
• Herpesvirus (Varicella Zoster) that causes chicken
pox can also cause shingles later in life.
Shingles: infection of Varicella Zoster virus on
nerve tissue. P. 443.
Papilloma virus: warts
Portal of entry: skin. Can spread from one part of the
body to another through direct contact (autoinoculation). Raised irregular growth.
Plantar warts: on soles of the feet. Can be painful
during walking.
Genital warts: may appear on vulva, penis, or anus.
Sexually transmitted, may be painful. In some cases,
the human papilloma virus can lead to cervical or
penile cancers.
Fungal infections of the skin
Tinea: caused by a variety of molds called
dermatophytes. Usually localized, can cause
itching, redness (“ringworm.” This is not a
worm—it is a fungus!)
Because dermatophytes do
not penetrate past the
epidermis, diagnosis is done
through observation of
symptoms. Treatments are
usually topical.
Infections of the eye
• Conjunctivitis (“pink eye”): infection of the
conjunctiva of the eye. Heavy purulent (pus)
discharge, very painful.
Caused by a variety of bacteria (mostly
respiratory) and viruses, primarily Hemophilis
influenzae.
• Treated with antibiotics. In Delaware, children
are allowed in school/day care after 24 hours of
antibiotic treatment for conjunctivitis.
• Keratitis: infection of the cornea.
Portal of entry: traumatic event (scratched
cornea, sometimes contact lenses)
Can be caused by many bacteria (S. aureus, S.
pyogenes, Pseudomonas aeruginosa) and can
become invasive. In this case, diagnosis and
treatment must be immediate to prevent
permanent damage to/loss of the eye.