Bacterial Disease of the

Skin
Dr. Salma Elnour
Anatomy
Microbiome
 microbes living deep in the hair follicles and sweat
ducts soon recolonize the skin’s surface. Organisms of
the microbiome typically grow in small clusters,
particularly in the armpits and between the legs, where
conditions are moister. Their waste products produce
body odor.
 Significant members of the microbiome include small
lipophilic yeasts such as Malassezia, which digest
keratin. Such yeasts are rarely pathogenic, though they
can cause disease in immunosuppressed patients.
 Aerobic, Gram- positive bacteria in the genera
Staphylococcus and Micrococcus also grow on the skin
of all individuals. These bacteria can tolerate salt
concentrations of 5–10%. The most common species is
Staphylococcus epidermidis.
Microbiome
 Diphtheroids are another common type of Gram-
positive bacteria living on the skin. These
pleomorphic bacilli are named for the similarity of
their appearance to the pathogen Corynebacterium
diphtheriae, though diphtheroids of the microbiome
are generally non- pathogenic. A common
troublesome diphtheroid is Propionibacterium acnes
 Propionibacteria reside in hair follicles, where they
ferment car- bohydrates to form propionic acid,
which lowers the pH of the skin, acting as a further
defense against additional infection.
Folliculitis
 Folliculitis is an infection of a hair follicle in which the base of
the follicle becomes red, swollen, and pus filled. This condition
is often called a pimple.
 When it occurs at the base of an eyelid, it is called a sty.
 A furuncle , or boil, is a large, painful, raised nodular extension
of folliculitis resulting from spread of the infection into
surrounding tissues.
 When several furuncles join together more frequently in areas
where the skin is thick, such as at the back of the neck they form
a carbuncle.
 In severe cases, the body responds to folliculitis by triggering
fever.
What is the difference between
Folliculitis, sty, furuncle , carbuncle
Pathogen and Virulence Factors
 Causative agent is S. aureus and S.
epidermidis
 Staphylococci have at least three categories

of virulence factors that allow them to

produce disease: enzymes, structures that
enable them to evade phagocytosis, and
toxins.
Pathogenesis
 Humans transmit both species of Staphylococcus via direct contact
between individuals as well as via fomites
 Staphylococcus on the surface of the skin grows into hair follicles
and invades sebaceous glands. This triggers fever and inflammation,
which are natural responses against infection, and causes the follicle
to enlarge and fill with pus composed of leukocytes, dead cells, and
bacteria.
 The infection may spread into the hypodermis to form a furuncle or
into neighboring hair follicles to form a carbuncle. S. aureus (and
infrequently S. epidermidis) may also spread into the blood causing
bacteremia and be carried to the lining of the heart, lungs, and bones,
causing endocarditis, pneumonia, and osteomylitis respectively
Diagnosis
 Isolation of the organism
 HOW?!!
Staphylococcal Scalded Skin
Syndrome
 In staphylococcal scalded skin syndrome (SSSS), cells
of the outer epidermis separate from one another and
from the underlying tissue.
 SSSS involves a reddening and wrinkling of the skin

that typically begins near the mouth, spreads over the

entire body, and is followed by large blisters that
contain clear fluid lacking bacteria or white blood cells.
Within two days, the affected outer epidermis peels off
in sheets, as though the flesh had been dipped into
boiling water.
SSSS
Pathogen and Virulence Factors
 Five percent of strains of Staphylococcus aureus
secrete one or two distinct exfoliative toxins that cause
SSSS.
 Each toxin causes the dissolution of epidermal

desmosomes, which are intercellular bridge proteins

that hold together cytoplasmic membranes of adjoining
cells. Both toxins affect keratinized cells of the
epidermis.
Pathogenesis
 The blood carries exfoliative toxins from sites of infection
throughout the body. Such circulation of toxins in the blood
is called toxemia.
 The body restores the lost epidermis within 7 to 10 days
after protective antibodies circulate in the blood.
 Though 100% of the skin surface may be afflicted, scarring
does not occur because the toxin does not affect the dermis.
 Mortality is rare; death, if it occurs, is most often due to
secondary infections of skinless areas by yeasts such as
Candida albicans or bacteria such as Pseudomonas
aeruginosa.
Diagnosis
 Diagnosis is made on the basis of the distinctive
sloughing of the skin.
 Fluid in the blisters of SSSS does not contain S. aureus,

since the disease is mediated by toxins released from a

site of infection that may be elsewhere in the body.
Impetigo (Pyoderma) and Erysipelas
 Impetigo also called pyoderma appear primarily on the
face and limbs particularly of children whose immune
systems are incompletely developed. The patches
develop into oozing, pus-filled vesicles on a red base.
Such vesicles eventually break and form a thick,
honey-colored, sticky crust that is attached firmly to
the skin and may cause intense itching.
 Numerous vesicles at various stages of development

characterize impetigo because bacteria from a vesicle

spread to adjacent sites on the skin.
 Erysipelas When such an infection of the skin spreads
into surrounding lymph nodes and triggers pain and
inflammation, the condition is called erysipelas
manifests as reddening of the skin on the face, arms, or
legs. The red area has a distinct margin, almost as if it
were painted onto the skin. Swollen local lymph nodes,
pain, fever, chills, and leukocytosis—an abnormally large
number of leukocytes in the blood— are also seen.
Without treatment, erysipelas may be fatal, with
mortality ranging from 2% to 17%. The very young, very
old, and immunocompromised are more likely to die.
Pathogens and Virulence Factors
 S. aureus acting alone causes about 80% of impetigo
cases, and about 20% of cases involve Streptococcus
pyogenes alone or in conjunction with S. aureus. S.
pyogenes, causing 20% of impetigo cases,
Streptococcus pyogenes is also the cause of erysipelas.
 What are Streptococcus pyogenes virulence factors?!!
Pathogenesis
 The bacteria of impetigo and erysipelas occasionally
colonize the skin and then invade through scratches,
abrasions, cold sores, or other wounds where the skin’s
integrity is compromised.
 Children are often infected just below the nose, where

frequent wiping away of mucus abrades the skin. Some

strains of S. pyogenes may spread from a site of
impetigo or erysipelas into the blood (bacteremia) and
then into the kidneys, where they cause a disease of the
kidneys known as acute glomerulonephritis.
Diagnosis
 Isolation of the organism
Necrotizing Fasciitis
 Necrotizing fasciitis also known as “flesh-eating bacteria”
inflammation of the soft tissues surrounding the muscles
 Causative agent is S. pyogenes
 Necrotizing fasciitis is usually characterized by redness, intense
pain, and swelling at the site of infection.
 Initially, the pain does not seem proportionate to the appearance
of the infected area. As the bacterium digests muscle fascia the
connective tissue surrounding muscles and fat tissue, the
overlying skin becomes distended and discolored.
 Patients develop fever, nausea, and malaise, and they may
become mentally confused as their blood pressure drops severely.
Pathogenesis
Pathogenesis
 S.pyogenes spread from person to person
and enters the body through breaks in the
skin. It spreads rapidly along muscle fascia.
 S. pyogenes secretes enyzmes that allow the

bacterium to invade body tissues

◦ Streptokinases dissolve blood clots
◦ Hyaluronidase breaks down hyaluronic acid
between cells.
◦ Deoxyribonucleases break down DNA released from
damaged host cells.
Pathogenesis
 Other virulence factors include M protein
◦ M protein on the surface of streptococcal cells helps the
bacterium attach to nose and throat cells, and after entry into
the body, M protein allows S. pyogenes to survive
phagocytosis
 S. pyogenes also secretes toxins that damage tissue.
◦ Streptolysin S can kill many types of human cells, including
neutrophils and erythrocytes.
◦ Exotoxin A triggers an overactive immune response that
further damages healthy tissue.
Diagnosis
 Diagnosis is difficult because early symptoms are general and
flulike. Extreme pain that seems out of proportion to an injury
should be treated as a possible case of necrotizing fasciitis or
infection with S. pyogenes.
 Affected tissues must be removed completely to prevent the
spread of bacteria.
 Intravenous broad-spectrum antimicro bial drugs help curb the
severity of the disease. It is difficult to prevent necrotizing
fasciitis because S. pyogenes is commonly found on humans.
 Patients with diabetes, cancer, or chickenpox are at a greater
risk for necrotizing fasciitis.
 Any opening in the skin, even a minor cut, is a potential site of
invasion by the bacterium; therefore, such openings should be
washed thoroughly.
Buruli Ulcer
 Buruli ulcer, an emerging disease that affects more
and more people each year as a result of human
encroachment into the swamps where
Mycobacterium ulcerans lives
 Causative agent: Mycobacterium ulcerans
 the infection starts with a small, painless nodule.
 When ignored the site of the infection will swell to
twice its normal size; it was painless.
 But if further ignored the bacterium will produce a
potent toxin known as mycolactone that destroys
cells below the skin, especially fat and muscle cells.
Buruli Ulcer
 Though the infected site continues to swell,
making it difficult to work normally, it
remained pain free.
 six weeks of this condition, pain begins

suddenly and excruciatingly.

 The swollen part will rupture, releasing a

foul-smelling fluid.
 .Treatment: Surgery to remove dead tissue
and bacteria, several skin grafts, and two
months of treatment with the antimicrobial
drugs rifampicin and streptomycin.
Acne
 The most common causes of acne are
Propionibacterium acnes
Pathogeneses
Cat Scratch Disease
 Cat scratch disease involves fever for a few
days, prolonged malaise, and localized
swelling at the site of infection and nearby
lymphnodes for sevral month.
 Causative agent is Bartonella henselae
Pathogenesis
 Cat scratches or bites, particularly wounds by kittens, introduce
the bacterium into the skin.
 Blood-sucking arthropods such as fleas may also transmit the
bacterium from cats to people.
 In the skin, the bacterium grows intracellularly inside the RBCs.
 Bartonella releases endotoxin when it dies, which can trigger
fever, blood clotting, inflammation, and possibly shock
 Though carried by cats, Bartonella apparently causes disease
only in people; it is not known to cause disease in animals.
 Cat scratch disease has emerged as a relatively common and
occasionally serious infection of children and adults.
Diagnosis
 A positive indirect fluorescent antibody test against
Bartonella antigens confirms a diagnosis of cat scratch
disease in individuals who exhibit the characteristic
signs and symptoms following exposure to cats.
Pseudomonas Infection
 patients whose skin has been burned away by
a fire or exposure to steam, opportunistic
pathogens gain access to the moist, nutrient-
rich environment of the fascia and deeper
tissues. The most common microorganism
seen in burn victims is Pseudomonas
aeruginosa.
 What are the other diseases caused by this

organism?
Signs and symptoms
 When Pseudomonas aeruginosa invades the
bloodstream, it causes fever, chills, and
shock. Massive infections are often readily
diagnosed because the bacterium typically
produces a blue-green pigment, pyocyanin,
that colors such infections
Pathogen
 Pseudomonas aeruginosa is a Gram-negative, aerobic
bacillus that metabolizes a wide range of organic
carbon and nitrogen sources. It is almost everywhere
in soil, in decaying organic matter, and in almost
every moist environment, including swimming pools,
hot tubs, sponges, washcloths, and contact lens
solutions. In hospitals, it grows in sinks, moist foods,
vases of cut flowers, sponges, toilets, floor mops,
dialysis machines respirators, and humidifiers. Some
strains can even grow using small amounts of
nutrients left in distilled water.
Virulence Factors
 Fimbriae
 Capsule
 Nuraminidase
 Elastase
 Endotoxin lipid A
 Exotoxin A
 Exoenzyme A
 Pigments
Pathogenesis
 The surface of a burned area provides a warm, moist
environment that is quickly colonized by this ubiquitous
opportunist. A thick, scablike crust naturally forms over the
surface of a severe burn. Pseudomonas growing beneath the
crust can move into the blood. Once inside the body, it kills
cells and destroys tissues, and endotoxin mediates fever,
vasodilation, inflammation, shock, and other symptoms.
Microbes on the burned area are not readily accessible to
medical workers because the crust is generally impermeable
to antimicrobial drugs, and blood vessels are absent. Health
care workers must remove the crust in a medical procedure
termed debridement so that antimicrobial drugs can be
effective.
Diagnosis
 Write full account about the Pseudomonas
burn infection Diagnosis?
Cutaneous Anthrax
 Causative agent Bacillus anthracis
 Virulence factors endospore, capsule, three

anthrax toxins.
 Portal of entry Direct contact of endospores

with wounded skin, infected animals, or

contaminated animal products. (Two other
forms of anthrax—gastrointestinal and
inhalation—have routes of entry via the
gastrointestinal tract and respiratory tract,
respectively.
 igns and symptoms Localized itching
followed by a raised lesion that eventually
forms a painless, black eschar (see photo)
within 7 to 10 days.
 Incubation period Immediate response, within

one day.
 Treatment Doxycycline or ciprofloxacin are

the preferred antimicrobials. There is no

treatment for the toxin.
Anthrax
Gas Gangrene
 When blood supply to a tissue is interrupted,
for example by a wound, a condition known
as ischemia develops. The tissue becomes
anaerobic, and necrosis (death) sets in. If the
wound is infected with endospores of
anaerobic Clostridium, then gas gangrene
develops in the dead tissue.
Signs and Symptoms
 Clostridium produces toxins that kill surrounding tissues,
providing the bacterium with more nutrients and increasing
the size of the anaerobic environment necessary for
Clostridium to grow. The rapidly growing bacteria then spread
into the surrounding tissue, causing the death of muscle and
connective tissues.
 The immediate result is intense pain at the initial site of
infection (often in a foot), followed by gas gangrene, which
involves blackening of the infected muscle and skin and the
production of bubbles of hydrogen and carbon dioxide gases
that may break out with a frothy brownish fluid The bubbles
can be felt under the skin by palpation. Shock, kidney failure,
and death can follow, often within a week of infection.
Pathogens and Virulence Factors
 Clostridium is an anaerobic, Gram-positive, endospore
forming bacillus that is ubiquitous in soil, water, sewage, and
the gastrointestinal tracts of animals and humans. It also
grows in the vaginas of 1–9% of healthy women.
 Several species of Clostridium cause gas gangrene.
Pathogenicity is due in great part to the ability of endospores
to survive harsh conditions and to the vegetative cells’
secretion of 11 toxins that lyse erythrocytes and leukocytes,
increase vascular permeability, reduce blood pressure, and kill
cells, resulting in irreversible damage.
 C. perfringens, the species most frequently isolated from
patients, is a large, almost rectangular cell. Although it is
nonmotile, its rapid growth and reproduc- tion (cell divisions
every 12 minutes) enable it to rapidly colo- nize wounds.
Pathogenesis
 Clostridium does not affect healthy tissues and is not
invasive.
 A traumatic event, such as a surgical incision, puncture
wound, gunshot wound, crushing trauma, abortion, or
compound fracture, must introduce endospores into dead
tissue.
 There, in the anaerobic environment of dead tissue, they
germinate and grow on nutrients released by the dead
cells.
 Despite therapeutic care, the mortality rate for gas
gangrene exceeds 40%. Clostridial toxins kill neighboring
cells, and the bacterium spreads into the dead tissue.
Diagnosis, Treatment, and Prevention
 The appearance of gas gangrene is usually diagnostic by itself,
though the detection of large Gram-positive bacilli is confirmatory.
 The condition is often a medical emergency, and a physician must
intervene quickly and aggressively to stop the spread of necrosis by
surgically removing dead tissue and administering antitoxin and
large doses of intravenous penicillin and clindamycin.
 Oxygen applied under high pressure may also be effective.
 It is difficult to prevent infections of C. perfringens because the
organism is common in soil.
 Given that gas gangrene occurs following introduction of
endospores into tissues, proper cleaning of wounds can prevent
many cases of the disease.
Types and classification of wounds