• Wounds
Micropara lec :)
Microbial Diseases of the Skin and Wounds
STRUCTURE OF THE SKIN
• Skin is also called the “Cutaneous
membrane”
- Efficient significant barrier or
protection
- 1st line of external defense
• Skin infection result from
- Break in the skin
- Systemic infection
- Toxin mediated skin damage
- Other condition
Functions of the Skin
- Prevents excessive water loss
- Regulates temperature
- Involved in sensory phenomena
- Assists in vit. D formation
- Barrier against microbial invaders
- Limits infection and disease (unless burned,
broken, or cut)
• Adult skin covers about 2 sq. meters making
it one of the largest organs of the body.
• Thickness of human skin is 0.05mm on the
lips to 4.0mm thick on the soles of the feet
and in calluses, which cover areas of
greatest wear and tear.
2 Main Layers of the Skin
- Dermis- tough leathery structure composed
of loosely packed cells, connecting protein
fibers, small muscles, sweat glands,
sebaceous glands, blood vessels, nerve
endings, and hair follicles, produce hairs that
grow up through the dermis and epidermis.
- Provide strength and flexibility
- Epidermis- bloodless. Consists of 4-5
layers.
- Basal cells- divides continuously pushing
their offspring towards the surface
- Melanin- pigment that gives skin its color
- Keratin- waterproofing protein. The
hardened keratin forms nails and hair
- Dendritic cells- defensive cells that
phagocytize microbes that penetrate into the
deeper layers of epidermis
- Sebum- oily lipid secreted by oil/sebaceous
glands. Prevent growth of many
microorganisms
- Hypodermis- layer of fat cells and fibers
lying beneath the dermis. Not technically
part of the skin; it’s subcutaneous.
- Trauma to any tissue of the body
- Cuts, scrapes, surgery, burns, bites, etc.
- Allow microbes to infect the warm, moist,
deeper tissues of the body.
- Dirty wounds provide platforms for growth
of microbes and development of biofilms.
- w/in a wound, microbes can multiply,
producing enzymes and toxins that enhance
their growth.
- Heal a wound by forming a blood clot
- Neighboring connective and epithelial cells
multiply and grow into the clot to restore
skin’s integrity
- In most cases, other body defenses inc.
phagocytosis, complement, and
inflammation, eliminate a wound infection
- Some infections overwhelm body’s
defenses, resulting in severe, even fatal
diseases.
NORMAL MICROBIOTA
OF THE SKIN
• Microbiome-
- normally harmless microbes present on the
skin
- compete with potential pathogens for
nutrients and space
- produce chemicals that interfere with the
growth of other microbes providing defense
against infection
- cannot be completely removed through
cleansing
- typically grown in moist areas of the skin
like in armpit and between the legs
- waste products cause body odor.
Made up of various microbes
• Yeast
- Malassezia- digest sebum, rarely pathogenic.
Can cause disease in immunosuppressed
patients
• Bacteria
- Staphylococcus and Micrococcus- Aerobic,
gram-positive bacteria in the genera. Grown
on the skin of all individuals; can tolerate
salt conc. Of 5-10%
- most common species is staphylococcus
epidermidis
- Diptheroids- gram+
- Corynebacterium diptheriae
- Propionibacterium acnes- a troublesome
diptheroid that causes acne. Also provides
protection by competing with pathogenic
microbes
 BACTERIAL DISEASES OF
THE SKIN AND WOUNDS
FOLLICULITIS
Signs and Symptoms
- Infections of the hair follicles in which the
base of the follicle becomes red, swollen,
and pus filled
- Often called a pimple
- Called a sty when it occurs at the eyelid base
- Spread of infection into surrounding tissues
can produce furuncles
- Furuncle- or boil is a large, painful, raised
nodular extension of folliculitis
- Carbuncle- forms when multiple furuncles
join together. More frequently in the thick
areas such as back of the neck
Pathogen and virulence factors
- Staphylococcus- most common cause of
folliculitis and associated infections of the
skin.
- A genus facultatively anaerobic, gram+
bacteria
- Spherical cells (cocci) are typically clustered
in grape-like arrangements
- Salt tolerant. Can grow to 10% NaCl
- Staphylococci are tolerant of drying out,
solar radiation, and heat.
• 2 species commonly found on the skin
- Staphylococcus Epidermidis- major member
of microbiome. 90% of bacteria on the skin.
- Staphylococcus Aureus- more virulent.
Often grows in nasal passages that produces
variety of disease conditions and symptoms
- Staphylococci have 3 categories of virulence
factors that allows them to produce diseases.
Enzymes, Structures, that enable them to evade
phagocytosis, and toxins.
• Coagulase- clots blood. Hide the bacterium
from phagocytes
Enzymes
• Hyaluronidase- breaks down hyaluronic acid
• Staphylokinase- dissolves blood clots
• Lipases- present in S. epidermidis as well.
Digests lipids, inc. sebum, providing
staphylococci w/ food on the surface of the
skin, hair follicles, and in sebaceous glands
• B-lactamase- plays no role in inhibiting the
natural defenses of the body. Covey
resistance to many beta-lactam antimicrobial
drugs such as penicillin and cephalosporin.
Structural
• S. aureus and S. epidermidis evade the
body’s defenses by synthesizing loosely
organized polysaccharide slime layers
(capsules)
• Opsonins- antibodies that enhance
phagocytosis
• Preotein A- complement cascade
Toxins
• Staphylococcus aureus- possesses several
toxins that contribute to virulence
• Cytolytic toxins- disrupt the cytoplasmic
membranes of a variety of cells.
• Leukocidin- kills leukocytes providing
staphylococcus with additional protection
• Epidermal cell differentiation inhibitor-
protein that induces large holes in the linings
of blood vessels allowing access for the
bacterium to invade body tissues
• Strains of S. aureus produce exfoliative
toxin or toxic shock syndrome toxin-
proteins that cause staphylococcal scalded
skin syndrome
Pathogenesis
• Staphylococcus transmitted via direct
contact or by fomites
- On the surface of the skin grows into the
hair follicles and invades sebaceous glands.
- Triggers fever and inflammation
- Infection can spread into the blood and
move to organs beyond the skin
• S. aureus transiently colonizes the skin or
mucous membranes of most people.
- May also spread into the blood- a condition
called bacteremia
Epidemiology
• S. epidermidis lacks virulence factors and
rarely causes disease
- Seldom cause disease.
• S. aureus- not a permanent resident but does
grow on the skin or mucous membranes of
most people particularly in the nostrils.

Diagnosis
• Isolation of gram+ bacteria in grapelike
clusters from pus
• Coagulase-negative staphylococcus is
usually S. epidermidis- normal part of the
microbiome of the skin
Treatment
• Physicians treat staphylococcal infections
with Topical Mupirocin
• Dicloxacillin (Semisynthetic penicillin)- a
semisynthetic oral form of penicillin not
inactivated by B-lactamase
• B-lactamase- another drug of choice for
staphylococcal infections
• Vancomycin is used to treat resistant strains
• Methicillin-resistant S. aureus (MRSA)-
more common in hospitals, imperative that
health care workers take precautions against
introducing such bacteria to patients.
Prevention
• Proper antiseptic, particularly correct hand
antisepsis
• Proper procedures in hospitals to minimize
MRSA infections
• Immunization
STAPHYLOCOCCAL SCALDED SKIN
SYNDROME(SSSS)
Signs and Symptoms
- In SSSS, cells of the outer epidermis
separate from one another and from the
underlying tissue
- Skin becomes red and wrinkled and form
blisters
- Followed by large blisters that contain clear
fluid lacking bacteria or wbc
- Outer epidermis peels off in sheets
Pathogen and Virulence Factors
- 5% (some) of strains of Staphylococcus
aureus secrete one or two distinct exfoliative
toxins
- Each toxin causes the dissolution of
epidermal desmosomes
- one or two different exfoliative toxins cause
SSSS
Pathogenesis
- blood carries exfoliative toxins from sites of
infection throughout the body
- body restores the lost epidermis in 7-10 days
- Toxemia- circulation of toxins in the blood
- No scarring because dermis is unaffected
- Death is rare but may be due to secondary
infections by yeasts such as candida
albicans or bacteria such as pseudomonas
aeruginosa
Epidemiology
- Disease primarily in infants and children
under 5 yrs old
- Antibodies protect people with well-
developed immune systems
- Transmitted by person-to-person spread of
bacteria
Diagnosis, Treatment, and Prevention
- Diagnosed by characteristic sloughing of
skin
- Fluid in the blisters doesn’t contain S.
aureus
- B-lactamase- deactivates many drugs in the
penicillin class
- Treated by administration of antimicrobial
drugs
- Little can be done to prevent SSSS because
S. aureus is normally on the skin and
susceptible patients lacks sufficient
immunity
- Widespread presence of S. aureus makes
prevention difficult
IMPETIGO (PYODERMA) AND
ERYSIPELAS
- Aka. “pyoderma”
Signs and Symptoms
- Characterized by small, flattened, red
patches
- Appear primarily on the face and limbs
- Particularly children whose immune systems
are incompletely developed
- Patched develop into oozing, pus-filled
vesicles on a red base
- Erysipelas- such infection of the skin
spreads into surrounding lymph nodes and
triggers pain and inflammation
- Reddening of the skin on the face, arms, or
legs.
- Swollen local lymph nodes, pain, fever,
chills, leukocytosis
- Leukocytosis- abnormally large number of
leukocytes in the blood
- Death ranging from 2-17%. Very young,
very old, and immunocompromised
Pathogens and Virulence Factors
 - S. aureus alone causes 80% of impetigo
cases
- 20% cases involve Streptococcus pyogenes
alone or in conjunction with S. aureus. Also
the cause of erysipelas
- Most cases are caused by S. aureus
- Some are S. pyogenes
- Gram+ occurs, arranged in chains
Virulence factors that contribute to impetigo
- M Protein- cytoplasmic membrane
component that destabilizes complement and
interferes with phagocytosis and lysis of the
bacterium
- Hyaluronic Acid capsule- serves to
camouflage the bacterium, hiding it from
phagocytes
- Pyrogenic Toxins- called erythrogenic
toxins’ proteins that stimulate macrophages
and helper T lymphocytes to release
cytokines that in turn stimulate a fever, rash,
and shock
Pathogenesis
- The bacteria invade where the skin is
compromised
- Children are often infected below the nose
where frequent wiping away of mucus
abrades the skin
- S. pyogenes may spread from a site of
impetigo or erysipelas
- Acute glomerulonephritis can result, if
infection spreads to the kidneys
Epidemiology
- Transmitted by person-to-person contact or
via fomites
- Impetigo occurs most in children 2-5 yrs
- Erysipelas can also occur in the elderly
Diagnosis, Treatment, and Prevention
- The presence of vesicle is diagnostic or
impetigo
- Impetigo is treated with oral and topical
antimicrobials and careful cleaning of
infected areas
- Erysipelas is treated with penicillin
- Prevent with proper hygiene and cleanliness
NECROTIZING FASCIITIS
- Bacteria can destroy soft body tissues
- “flesh-eating bacteria”
Signs and Symptoms
- Hot, intensely painful, sunburn-like rash at
the site of infection
- Develop fever, tiredness, and muscle aches
- As tissue is destroyed, the bp drops and
patients become mentally confused and
ultimately comatose
Pathogen and Virulence Factors
- Most cases are caused by S. pyogenes also
known as group A streptococcus
- Have factors that allow the bacterium to
invade body tissues, resist phagocytosis, and
damage cells and tissues
- Various enzymes facilitate invasion of
tissues
- Exotoxin A and streptolysis S- damage cells
and tissues
Pathogenesis and Epidemiology
- S. pyogenes enters through breaks in the
skin
- Usually spread person-to-person
Diagnosis, Treatment, and Prevention
- Early diagnosis is difficult because
symptoms are nonspecific
- Treat with clindamycin and penicillin. Used
together had a cure rate of 83%. Penicillin
alone has a rate of 41%
ACNE
Pathogen
- Commonly caused by Propionibacterium
acnes
- Causes acne 85%
- Gram+, rod-shaped diptheroids
- Commonly found on the skin
- Named after propionic acid- by-product of
their fermentation of carbohydrates
- S. aureus can also cause acne
Pathogenesis
- Propionibacterium typically grown on
sebum w/in the sebaceous glands of the skin
- Excessive production of oil triggered by
hormones stimulates growth of bacteria
- Blackhead is formed when a plug of dead
and dying bacteria blocks the pore.
- In cystic acne- severe form; bacteria forms
inflamed pustules (cysts)
- Rupture triggering the scar tissue
- Develops where sebaceous glands are more
numerous such as face, scalp, neck, chest,
back, upper arms, and shoulders
 Epidemiology
- Propionibacteria are normal microbiota
- Typically begins in adolescence but can
occur later in life
- Not a reportable disease
- Severe cystic acne is much more rare
Diagnosis, Treatment, and Prevention
- Diagnose by visual examination of the skin
- Treated w/antimicrobial drugs and drugs that
cause exfoliation of dead skin cells
- Accutane is used to treat severe acne
- Also prescribe benzoyl peroxide- causes
exfoliation of dead skin cells. Kills
Propionibacterium and reduces the amount
of lipid on the skin’s surface
- Retinoic acid- derivative of vit. A. inhibits
the formation of sebum. Prescribe only on
severe cases because it can cause intestinal
bleeding and birth defects
- UV Light- also used in killing bacteria.
15mins. exposure/week
- Foods do not affect sebum production
CAT SCRATCH DISEASE
Signs and Symptoms
- Fever, malaise, localized swelling at
infection site, nearby lymph nodes for
several months
Pathogen and Virulence Factors
- Caused by Bartonella henselae (Gram-neg.
bacillus)
- Can grow and reproduce inside rbc and in
cells lining the blood vessel walls
- Endotoxin (Lipid A) is the primary virulence
factor
Pathogenesis and Epidemiology
- Transmitted by cat bites or scratches and by
blood-sucking arthropods
- Fleas may transmit the bacterium from the
cats to people
- Bartonella- releases endotoxin when in dies,
w/c can trigger fever, blood clotting,
inflammation, and possibly shock
- Only causes disease in people
Diagnosis, Treatment, and Prevention
- Diagnosed with serological testing
- Treated with antimicrobials
- Azithromycin- antimicrobials physicians
prescribe for cat scratch disease
- Avoid cat-inflicted wounds and adequate
cleansing of bites or scratches
PSEUDMONAS INFECTION
Signs and Symtoms
- Pseudomonas aeruginosa- invades the
bloodstream causing;
- Blood infection causes fever, chills, and
shock
- Blue-green color from the bacterial pigment,
pyocyanin, occurs in massive infections
Pathogen and Virulence Factors
- Pseudomonas aeruginosa is the causative
agent
- Gram-neg. bacillus
- Found in soil, decaying matter, moist
environments
Numerous virulence factors of P.
aeruginosa
- Fimbriae and adhesins- attach to host cells
and enable biofilm formation
- Capsule- composed of mucoid
polysaccharide, plays a role in bacterial
attachment and biofilm formation. Shields
bacterium for phagocytosis
- Neuraminidase- modifies host cell receptor
molecules to make bacterial attachment to
the cells more likely
- Elastase- breaks down elastic fiber,
degrades complement components and
cleaves IgA and IgG
- Endotoxin- trigger fever, blood clotting,
inflammation, or possibly shock
- Exotoxin A and exoenzyme S- inhibit
eukaryotic protein synthesis, lead to host cell
death
- Pyocyanin- blue-green pigment of
pseudomonas, triggers the formation of
reactive forms of oxygen that damage host
cells
- Rarely causes disease despite virulence
factors
- P. aeruginosa cannot penetrate the intact
structure cells
Pathogenesis
- Infection can occur in burn victims
- Thick, scablike crust forms over the surface
of a severe burn
- Bacteria grow under the surface of the burn
 - The bacteria kill cells, destroys tissue, and
triggers shock
- Debridement of burn is required for topical
antimicrobials to be effective
Epidemiology
- P. aeruginosa is inhabitant of water and soil
- Bacterium is rarely part of the human
microbiota
- Can infect almost any organ or system once
in a body
- Besides skin infections, can be involved in
bacteremia, endocarditis, urinary, ear, eye,
nervous system, GI, muscular and skeletal
infections.
- Swimmers can develop otitis externa also
called as swimmer’s ear- painful
pseudomonas infection of the external ear
canal.
Diagnosis, Treatment, and Prevention
- Diagnosis can be difficult
- Pyocyanin discoloration indicates massive
infection
- Infections are treated with combination of
antimicrobials
- Treatment is difficult because of multi-drug
resistance of P. aeruginosa
- P. aeruginosa is widespread, but infections
typically don’t occur in healthy individuals
- Pseudomonas has been reported to live in
solutions of some antimicrobial drugs and
disinfectants
SPOTTED FEVER RICKETTSIOSIS
- A number of arthropod-borne rickettsias
cause rashes in humans
- Rocket mountain spotted fever is the most
severe.
- RMS and Emerging Disease case study: a
new cause of spots considers a newly
recognized spotted fever rickettsiosis
Signs and Symptoms
- Nonitchy spotted rash on trunk and
appendages
- Organ failure (Respi., CNS, GI, Renal) can
occur in severe cases
- The rash develops into subcutaneous
hemorrhages called petechiae
Pathogen and Virulence Factors
- Gram-neg. intracellular parasite
- Rickettsias do not use glucose as a nutrient
- Obliged to live inside other cells
- Pathogen avoids digestion in phagosome
Rocket Mountain Spotted Fever
Pathogenesis
- R. rickettsia does not secrete any toxins
- Disease occurs from damage to blood
vessels
Epidemiology
- Transmitted via bite of an infected tick
Diagnosis, Treatment, and Prevention
- Diagnosed with serological testing
- Treated with various antimicrobials
- Removing the tick and prescribing
doxycycline for most adults
- Chloramphenicol for children and pregnant
women
- Prevented with the use of tick repellents
and avoidance of tick-infested areas esp. in
the spring and summer where they are most
voracious
- Wear tight-fitting clothing
CUTANEOUS ANTHRAX
- Has 3 distinct clinical manifestations: GI,
Inhalation, and Cutaneous.
- Gastrointestinal are rare in humans
- Caused by Bacillus anthracis
- Endospores often shed by an infected animal
enter a wound in the skin producing a solid
skin nodule
- The nodule spreads to form a painless,
swollen black, crusty ulcer called eschar
- Anthrax means charcoal in Greek
- Treat with oral antimicrobial drugs such as
doxycycline or ciprofloxacin for 7-14 days
- Prevention requires control of the disease in
animals
- Farmers must vaccine their stock and bury
or burn the carcasses of dead animals
- Anthrax vaccine is effective and safe for
humans. Requires 16 doses for 18 mons.
GAS GANGRENE
Signs and Symptoms
- Ischemia- develops when a blood supply to
a tissue is interrupted, for example by a
wound
 - Clostridium produces toxins that kill
surrounding tissues, providing the bacterium
with more nutrients
- Death of muscle and connective tissue
- Intense pain at the initial site of infection
followed by gas gangrene which involves
blackening of the infected muscle and skin
- Bubbles can be felt under the skin with
palpation
Pathogens and Virulence Factors
- Clostridium is an anaerobic, gram+,
endospore-forming bacillus. Ubiquitous in
soil, water, sewage and GI tracts of animals
and humans. Grows in vagina of 1-9%
healthy women
- Gram-neg. endospore-forming bacilli
- Several species of clostridium cause gas
gangrene
- Ability of endospores to survive in harsh
conditions and to the vegetative cells that
secrete 11 toxins.
- C. perfringens is most often isolated from
patients
Pathogenesis and Epidemiology
- Does not affect healthy tissues and is not
invasive
- Traumatic event must introduce endospores
into dead tissue (surgical incision, puncture
wound, gunshot wound, abortion, fracture)
- In anaerobic environment, they germinate
and grow on nutrients released by dead cells
- Mortality rate exceeds 40%
Diagnosis, Treatment, and Prevention
- Appearance is usually diagnostic
- Rapid treatment is crucial
- Surgical removal of dead tissue
- Administration of antitoxin and
antimicrobials
- Prevented with proper cleaning of wounds
- Difficult to prevent infections of C.
perfringens because the organism is
common is soil
VIRAL DISEASES OF THE
SKIN AND WOUNDS
- Many viral diseases are systemic
- Spread by respi. and oral routes
- These diseases can result in signs and
symptoms of the skin.
DISEASES OF POXVIRUSES
- Poxviruses that cause human diseases
- Small pox
- Orf(sheep and goat), cowpox and
monkeypox (rare in humans)
- Chickenpox is not caused by poxvirus
- Small pox is the first human disease to be
eradicated
- Edward Jenner- first demonstrated
immunization using relatively cowpox virus
to protect against smallpox
Signs and Symptoms
- Produce lesions that progress through a
series of stages
- Begin as flat, reddened, macules which then
become raised sores called vesicles, which
then progress to pus-filled pustules which
are also known as pox or pocks
- Poxvirus dry to form crusts
- Lesions penetrate the dermis. May result in
scars particularly on the face
- Fever as high as 42 deg,c.
- Malaise, delirium, prostration. Infection of
the eye may induce blindness
Pathogens and virulence factors
- Poxviruses are DNA viruses
- Carry genes for transcription enzyme,
allowing them to replicate entirely
- Produce various proteins that interfere with
the immune response
- Orthopoxvirus (variola virus) causes
smallpox. Attaches only to humans
- Transmission of these poxviruses to humans
requires prolonged close contact with
infected animals
Pathogenesis
- Close contact is necessary for infection
- Occurs by inhalation of viruses in droplets
or dried crusts
- Crusts can remain ineffective for two years
- Viruses spread from the respiratory tract
throughout the body
- Other poxviruses are spread by direct
contact
Epidemiology
- Exists in two strains: variola major
(mortality rate of 20-40% or higher) and
variola minor(mortality rate of less than 1%)
- Variola virus stocks are maintained in U.S.
and Russian labs for research
- Monkeypox cases have increased over the
past decade
Diagnosis, Treatment, and Prevention
 - Treatment requires immediate vaccination - Health care workers can wear gloves to limit
- Vaccination discontinued in 1980s exposure
- Smallpox vaccinations ended in 1972 in - Can be controlled with nucleoside analogs
most locales of the U.S. such as acyclovir or penciclovir

HERPES INFECTION

Signs and Symptoms

- Herpes is derived from the Greek word
meaning “to creep”. Slowly spreading skin
lesions that are seen with herpes viruses.
- Produces painful, itchy skin lesions on the
lips (fever blisters or cold sores) or
genitalia (genital herpes).
- Herpetic gingivostomatitis(oral cavity),
whitlow(inflamed blister. May occur in
finger), herpes gladiatorum(athletes. Contact
with herpes lesion during sports)
- Recurrence of lesions is common
Pathogens and Virulence Factors
- Caused by human herpesviruses 1(above-
the-waist herpes) and 2 (below-the-waist
herpes)
- Produce various proteins that act as
virulence factors
Pathogenesis
- Often spread between mucous membranes of
the mouth or genitals
- Painful lesions caused by inflammation and
cell death
- Active lesions are the usual source of WARTS
infection
- Fusion of infected cells forms syncytia Signs and Symptoms
- Syncytium- structure formed by HHV-1 and - Benign epithelial growths on the skin or
HHV-2. A multinucleate cytoplasmic mass mucous membranes
allowing the viruses to spread - Can form on many body surfaces
Epidemiology Pathogens and Virulence Factors
- Spread between mucous membranes of - Various papillomaviruses cause warts
mouth and genitalia - Some strains trigger oncogenes in host
- chromosome
- Initial infections with herpesvirus are Pathogenesis
usually age specific - Warts develop several months after infection
- Herpes infections in adults are not life - Most warts are harmless
threatening - Papillomaviruses may precipitate some
- Neonatal infections can be fatal cancers
- Fetus can be infected in the utero when the
virus crosses the placental barrier
- Whitlow is a hazard for children who suck
their thumbs
Diagnosis, Treatment, and prevention
- Diagnosis is made by presence of
characteristic lesions
- Immunoassay reveals presence of viral
antigens
- Chemotherapeutic drugs help control the
disease but do not cure it

Epidemiology
- Transmitted via direct contact and fomites
- Individuals can spread viruses among
locations on their own body
Diagnosis, Treatment, and Prevention
- Diagnosed by observation
- Various techniques to remove warts
- New warts can develop as a result of latent
viruses
CHICKENPOX AND SHINGLES
Signs and Symptoms
• Chickenpox
- Medically termed as varicella
- “Teardrop on rose petals” thin walled fluid-
filled vesicles on red bases
- Highly contagious infectious disease
- Characterized by lesions on the back and
trunk that spread across body
- Virus becomes latent within sensory nerves
• Shingles
- Aka. Herpes zoster
- Forms in the band of the skin associated
with the nerve or in the eye
- Occurs following reactivation of the virus
- Lesions are localized to skin along an
infected nerve
- Pain may last after lesions have healed
Pathogen
- Varicella-zoster virus (VZV) causes both
diseases
Pathogenesis
- Infection spreads from the respiratory tract
to the skin via blood and lymph
- Infected dermal cells cause characteristic
rash of chickenpox
- Chickenpox is usually a mild disease
- Virus becomes latent in nerve ganglia
- Reactivated VZV causes shingles
Epidemiology
- Chickenpox occurs mostly in children
- VZV infected 90% of children prior to
immunization
- Disease is more severe in adults. Can lead to
fatal pneumonia
- ~20% of people who have had chickenpox
develop shingles
- Risk of shingles increase with age
- Only 15-20% of adults who had chickenpox
as children will develop shingles
Diagnosis, Treatment, and Prevention
- Diagnosis based on characteristic lesions
- More difficult to distinguish shingles
- Reye’s Syndrome- condition which the liver
and brain cease to function. Associated with
aspirin usage
- Treatment based on relief of symptoms
- Vaccine available against chickenpox
- Treatment of shingles involves management
of the symptoms, bedrest, oral acyclovir.
Loose-fitting clothing and non-adherent
dressing
RUBELLA
- Another childhood diseases
- Produce skin lesions. First distinguished as a
separate disease from measles by German
physicians
- Known in the US as German Measles or
three-day measles
Signs and Symptoms
- Children develop a mild rash
- Adults may develop arthritis and
encephalitis
- Congenital infection can result in birth
defects or death of fetus
Pathogen and Pathogenesis
- Caused by rubella virus (RNA virus)
- Infection spreads from the respiratory tract
throughout the body via the blood
- The immune response to infected cells
contributes to the disease severity in adults
Epidemiology
- Spread by respiratory secretions
- Infect only humans
Diagnosis, Treatment, Prevention
- Diagnosis made by observation of rash and
serological testing
- Vaccine is available
- Aimed at preventing rubella infections in
pregnant women
MEASLES (RUBEOLA)
Signs and Symptoms
- Characterized by Koplik’s sports
- Subacute sclerosing panencephalitis is rare
complication
Pathogen and Virulence Factors
- Caused by measles virus
- Adhesion and fusin proteins help virus avoid
immune recognition
Pathogenesis
- Immune response to infected cells causes
most symptoms
- Disease can be fatal in children

Epidemiology
- Measles is highly contagious
- Spread via respiratory droplets
- Humans are the only host
- Vaccination has reduced spread of the
disease
Diagnosis, Treatment, and Prevention
- Diagnosis is based on signs of measles
- Treatment involves administration of vit.A,
antibodies against measles, and ribavirin
- MMR vaccine protects against measles
Other Viral Rashes
• Erythema Infectiosum
- Also referred to as fifth disease
- Caused by B19 virus
- Respiratory disease that manifests as a rash
- Adults may also develop anemia and joint
pain
• Roseola
- Endemic disease of children
- Caused by human herpesvirus 6 (HHV-6)
- Characterized by a rose-colored rash
MYCOSES OF THE HAIR, NAILS, AND SKIN
- Mycoses are diseases caused by fungi
- Most are opportunistic pathogens
- Mycoses are classified by infection location
• Superficial
- Occur on the outer surfaces
• Cutaneous
- Occur in the skin
• Systemic
- Affect numerous systems
SUPERFICIAL MYCOSES
- Most common fungal infections
- Occur on the hair, nails, and the outer skin
layers
Signs and Symptoms
- Pityriasis versicolor
- Hypo- or hyperpigmented patches of scaly
skin
Pathogens and virulence factors
- Caused by Malassezia furfur
- Normal inhabitant of human skin
Pathogenesis and Epidemiology
- Fungi produce keratinase, which dissolves
keratin
- Fungi are often transmitted via shared hair
brushes and comb
- Disease occurs most often in adolescents
Diagnosis, Treatment, and Prevention
- Infected skin is pale green under UV light
- Definitive diagnosis requires microscopic
examination
- Treated with topical or oral drugs
CUTANEOUS MYCOSES
• Dermatophytoses
- Cutaneous lesions caused by some fungi that
grow in the skin
- Caused by dermatophytes
- Cell-mediated immune responses damage
deeper tissues

Pathogens
- Three genera cause most dermatophytoses
• Microsporum
• Trichophyton
• Epidermophyton floccosum
Pathogenesis
- Dermatophytes colonize skin, nails, and hair
- Use keratin as nutrient source
- Infection is rare
- Fungi must invade living layers of skin
Epidemiology
- Dermatophytes are among the few
contagious fungi
- Dermatophytes classifies by natural habitat
• Anthropophilic- associated with humans
• Zoophilic- associated with animals
• Geophilic- soil fungi
Diagnosis, Treatment, and Prevention
- Diagnosed by clinical observation
- KOH preparation of skin or nail samples
confirms diagnosis
- Limited infections treated with topical
agents
- Widespread infections treated with oral
drugs
WOUND MYCOSES
- Some fungi grow in deep tissues but do not
become systemic
- Fungi eventually grow into the epidermis
produce skin lesions
• Chromoblastomycosis
- Caused by four species of ascomycete fungi
- Painless lesions form that progressively
worsen
- Presence of golden brown bodies in skin
sample is diagnostic
• Treatment requires removal of infected
tissues and administration of antifungal
drugs
- People who work barefoot in the soil are at
risk
- Wearing shoes reduces number of infections
• Phaeohyphomycosis
- Caused by over 30 genera of fungi
- Acquired when spores enter wounds
- Disease is variable in presentation
- Depends on site of fungal colonization
- Diagnosed by observation of hyphae in skin
sample, biopsy material, or cerebrospinal
fluid
- Some cases can be treated with itraconazole
- Disease is permanently destructive to tissues
• Mycetomas
- Caused by several genera of soil or fungi
- Pricks and scrapes introduce fungi into
people
- People who work barefoot in soil most at
risk
- Tumorlike lesions form on skin, fascia, and
bones
- Infections are prevalent in countries near the
equator
- Diagnosis based on symptoms and presence
of fungi in clinical samples
- Treatment involves surgical removal of
mycetoma and antifungal therapy
• Sporotrichosis
- Caused by Sporothrix schenckii
- Resides in the soil
- Pricks and splinters introduce fungi into
humans
- Occurs most often in gardeners and farmers
- Subcutaneous infection usually limited to
the arms and legs
- Fixed sporotrichosis remains localized
- Lymphocutaneous sporotrichosis occurs
when the fungus enters the lymphatic system

- Diagnosed based on patient’s history,

clinical signs, and observation of fungi in
clinical samples
- Cutaneous lesions are treated with antifungal
drugs
- Prevention requires wearing proper attire to
avoid inoculation of the fungus