Bacterial Infection

Involving the Skin

Nicole.Cyril.Dash.Sheena.Leigh.Tracy.Myolaine
Cutaneous Bacterial
Infections
Introduction
• Pyodermas are infections in the epidermis, just
below stratum corneum or in hair follicles
• Pathogens involved:
• Staph aureus
• Most common cause of superficial pyodermas, especially in
industrialized nations.
• Group A strep
• Common cause of pyoderma in developing countries
• If untreated, it can extend to the dermis, resulting
in ecthyma and funcuncle formation
Impetigo
• 2 Clinical Patterns
• BULLOUS
• Staph aureus

• NON BULLOUS
• S. aureus ( developed)
• Group A strep
(developing)
Nonbullous Impetigo
• Accounts for >70% of cases
• Occurs in children of all ages as well as in
adults
• Bacteriocins by certain S. aureus strains
(phage group 71)
• Highly bactericidal to group A Strep
• May be responsible for isolation of only S. aures
from some lesions initially caused by
Streptococci
Nonbullous Impetigo
• S. aureus spreads from nose to normal skin
(approx. 11 days later), and then develop
into skin lesions ( after another 11 days)
Nonbullous Impetigo
• Lesions commonly arise on the skin of the face
(especially around the nares) or extremities after
trauma
• Nasal carriers can present with a very localized type
confimed to the anterior nares and adjacent lip area
• Pruritus and soreness of the area is a common
complaint
Nonbullous Impetigo
• Conditions that disrupt the integrity of the
epidermis, providing a portal of entry of
impetiginization:
• Insect bites
• Epidermal dermatophytoses
• Herpes simplex
• Varicella
• Abrasions
• Lacerations
• Thermal burns
Nonbullous Impetigo
• The initial lesion is a transient vesicle or pustule
that quickly evolves into a honey-colored
crusted plaque that can enlarge
to greater than 2 cm in diameter
• Surrounding erythema may be present.
Constitutional symptoms are absent.
• Regional lymphadenopathy may be present in
up to 90% of patients with prolonged, untreated
infection.
Nonbullous Impetigo
• If untreated, the lesions may slowly enlarge
and involve new sites over several weeks.
• In some individuals, lesions resolve
spontaneously
• in others, the lesions extend into the
dermis, forming an ulcer
Bullous Impetigo
• Occurs more commonly in the
newborn and in older infants
• Rapid progression of vesicles to
flaccid bullae
• Bullae usually arise on areas of
grossly normal skin.
• The Nikolsky sign (sheet-like
removal of epidermis by
shearing pressure) is not
present.
Bullous Impetigo
• Bullae initially contain clear yellow fluid that
subsequently becomes dark yellow and turbid and
their margins are sharply demarcated without an
erythematous halo.
• Bullae are superficial, and within a day or two, they
rupture and collapse, at times forming thin, light-
brown to golden-yellow crusts.
Bullous Impetigo
• Laboratory Tests.
• Gram stain of exudates from bullous impetigo
• Gram-positive cocci in clusters.
Bullous Impetigo
• Prognosis and Clinical Course
• If untreated, invasive infection can complicate S.
aureus impetigo with cellulitis, lymphangitis, and
bacteremia, resulting in
• Osteomyelitis
• Septic arthritis
• Pneumonitis,
• Septicemia.
• Exfoliatin production can lead to SSSS in infants and
in adults who are immunocompromised or have
impaired renal function.
Bullous Impetigo
• Treatment
• Mild to moderate
• Mupirocin ointment or cream
• Removal of crusts
• Good hygien
• Retapamulin 1% ointment is also effective for
localized impetigo and secondarily impetiginized
dermatitis as well, although decreased effiacy
against MRSA was noted in some trials
• Fusidic acid is an equally effective topical agent for
localized impetigo and has
very few adverse effects topically.
Impetigo
• Extensive Cases
• Staph : dicloxacillin, erythromycin ( if penicillin-
allergic), azithromycin
• Erythromycin-resistant S. aureus : amoxicillin plus
clavulanic acid, cephalexin ,cefaclor, cefprozil or
clindamycin
• CA-MRSA :TMP-SMX, rifampin, clindamycin, and
tetracycline.

• NO role for geneal disinfectant treatment or

bacitracin
Ecthyma
• Cutaneous pyoderma characterized by thickly crusted
erosions or ulcerations.
• Usually a consequence of neglected impetigo and classically
evolves in impetigo occluded by footwear and clothing.
• Lesion, typically occurring in the homeless and soldiers
in combat on maneuver in a humid and hot climate
• S. aureus and/or group A Streptococcus can be isolated on
culture
Ecthyma
• Untreated staphylococcal or streptococcal
impetigo can extend more deeply,
penetrating the epidermis, producing a
shallow crusted ulcer
• Ecthymatous lesions can evolve from a
primary pyoderma or within a preexisting
dermatosis or site of trauma
Ecthyma
• Ecthyma gangrenosum is a cutaneous ulcer
caused by P. aeruginosa and resembles
staphylococcal or streptococcal ecthyma
Ecthyma
• Ecthyma occurs most commonly on the lower
extremities
• children
• neglected elderly patient
• individuals with diabetes

• Poor hygiene and neglect are key elements in

pathogenesis.
Ecthyma
• The ulcer has a “punched-out” appearance when the dirty
grayish-yellow crust and purulent material are debrided.
• The margin of the ulcer is indurated, raised, and violaceous
and the granulating base extends deeply into the dermis.
• Untreated ecthymatous lesions enlarge over weeks to
months to
a diameter of 2–3 cm or more.
Ecthyma
• Management
• Systemic
• Same agent used for Staph impetigo
Furuncle and Carbuncle
Furuncle
• Boil
• Deep-seated inflmmatory
nodule that develops
around a hair follicle,
usually from a preceding,
more superfiial folliculitis
and often evolving into
an
abscess.
Carbuncle
• More extensive,
deeper,
communicating, and
infitrated lesion that
develops when
suppuration occurs in
thick inelastic skin
when multiple, closely
set furuncles coalesce.
Furuncle
• Furuncles arise in hair-bearing sites,
particularly in regions subject to friction,
occlusion, and perspiration
• Neck
• Face
• Axillae
• Buttocks
• They may complicate preexisting lesions such
as
• Atopic dermatitis
• Excoriations
• Abrasions
• Scabies
• Pediculosis
Furuncle
• Associated with a variety of host factors
• obesity,
• blood dyscrasias,
• defects
in neutrophil function
• Treatment with glucocorticoids and cytotoxic agents
• Immunoglobulin defiiency states.

• The process is often more extensive in patients

with diabetes. The majority of patients with
problems of furunculosis appear to be
otherwise healthy.
Furuncle
• Starts as a hard, tender, red folliculocentric
nodule in hair-bearing
skin that enlarges and becomes painful and
fluctuant
after several days
• Rupture occurs with discharge of pus, and
often a core of necrotic material.
• The pain surrounding the lesion then
subsides, and the redness and edema diminish
over several days to several weeks
• May occur as solitary lesions or as multiple
lesions in
sites such as the buttocks
 Carbuncle
• Larger, more serious
inflammatory lesion with a
deeper base, characteristically
occurring as an extremely
painful lesion at
the
• Nape of the neck
• Back
• Thighs
• Fever and malaise are often
present, and the patient
may appear quite ill.
Carbuncle
• Involved area is red and indurated, and multiple pustules
soon appear on the surface, draining externally around
multiple hair follicles.
• Lesion soon develops a yellow–gray irregular crater at the
center, which may then heal slowly by granulating,
although the area may remain deeply violaceous for a
prolonged period.
• The resulting permanent scar is often dense and readily
evident
Furuncle and Carbuncle-
Laboratory Tests
• Extensive furunculosis or a carbuncle may be
associated with leukocytosis.
• S. aureus is almost always the cause with CA-MRSA
being more than likely in most geographic locations.
• The diagnosis is made on the basis of the clinical
appearance.
• Gram stain of pus, clusters of Gram-positive cocci,
or isolation of S. aureus
on culture confims the diagnosis.
Furuncle and Carbuncle-
Prognosis and Clinical Course
• Major Problems
• Bacteremic spread of infections
• Recurrence
Furuncle and Carbuncle-
Treatment
• Simple Furunculosis
• Local application of moist heat
• Carbuncle or Furuncle with surrounding cellulitis, or if with
associated fever
• Systemic antibiotiv
• Severe infections or infections in dangerous area
• Maximal antibiotic dosage by the parental route
• CA-MRSA should be suspected in all serious infections
• Vancomycin (1.0–2.0 g intravenously daily
in divided doses) or other systemic parenteral agents
that have anti-CA-MRSA activity are indicated for
these patients.
• Antibiotic treatment should be continued for at least 1 week.
Furuncle and Carbuncle-
Treatment
• Large, painful and fluctuant lesions
• Incision and drainage :most important
• Culture If the infection is recurrent or
complicated by comorbidities
• Antimicrobial therapy should be continued until
all evidence of inflammation has regressed and
altered appropriately as culture results become
available.
• Draining lesions should be covered to prevent
autoinoculation
• Diligent hand washing
Abscess

• Commonly occur in folliculocentric

infections—that is, folliculitis, furuncles, and
carbuncles
• can also occur at sites of
• trauma,
• foreign bodies,
• burns, or
• sites of insertion of intravenous catheters.
Abscess- Treatment

• Incision and drainage :most important

treatment
Abscess
• Antibiotic usage after incision and drainage is
only recommended if
• Lesion is severe or associated with cellulitis,
• Signs of systemic illness,
• Comorbid factors or immune suppression,
• Patient is very young or very old,
• Abscess is in a body location that is diffiult
to drain,
• Associated septic phlebitis,
• No response to incision and drainage alone
SOFT TISSUE INFECTION
 Introduction
• Cellulitis and erysipelas are usually caused by
S. aureus or β-hemolytic Streptococci [primarily
group A Streptococcus (GAS)]
• Factors that increase the likelihood of SSTI
• exposure to pathogenic organisms
• local breach of the skin barrier function
• immunocompromised (including acquired immunodeficiency
syndrome [AIDS], diabetes, end-stage renal disease/dialysis,
neutropenia, cancer, and immunosuppressive medications),
• obesity
• circulatory compromise
 Introduction
• Skin and soft tissue infections (SSTI) are
characterized by clinical findings:

acute, tender, spreading, edematous, suppurative

inflammation of the skin, subcutaneous fat, or
muscle
 associated with systemic symptoms of
malaise, fever, chills, and local pain
 Introduction
• Cellulitis - infection of the dermis and
subcutaneous fat
• Erysipelas - more superficial variant affecting
the superficial dermal lymphatics and
adjacent tissue

• Along with the pyodermas, cellulitis and

erysipelas are the predominant form of non-
necrotizing SSTI
 Cellulitis
• Cellulitis presents with erythema, pain, firm
and tender induration, and less commonly,
fluctuance
• The erythema may rapidly intensify and
spread
• margins are generally indistinct
 Cellulitis
• In some cases of cellulitis,
the overlying epidermis
undergoes bulla formation
or necrosis, resulting in
extensive areas of
epidermal sloughing and
superficial erosion
• Regional lymphadenopathy
may be associated with Cellulitis with swelling, erythema, and
cellulitis on an extremity tenderness. A. Note the blistering and
crusting on the lower extremity.
B. The cellulitis is emanating from an
upper extremity abscess.
 Cellulitis
• Systemic symptoms, such as fever,
chills, and malaise are variable, and
sometimes may antedate localizing
complaints and signs of SSTI
• infection may also cause deeper
necrosis, resulting in dermal and
subcutaneous abscess formation,
fasciitis, and myonecrosis

 Pain in the absence of erythema, or out

of proportion to the appearance of the
local area, should raise suspicion for an
early deep-seated infection
 Crepitus is a rare sign that signifies a
gas-forming pathogen
 Cellulitis
• usually presents at the site of an antecedent
lesion
• acute and chronic ulcers
• Traumatic wounds (abrasions, lacerations, animal and
human bites)
• surgical procedure sites
• Dermatoses
• Percutaneous catheters
 Erysipelas
• shares many clinical features
with classical cellulitis
• Pain
• Ternderness
• Erythema and edema

• the plaque-like edema has a

more sharply defined margin to
normal tissue, and the erythema
is classically bright red

• The surface findings are often

described as peau d’orange (skin
of an orange) in appearance
 Erysipelas
• Fever may precede local signs, and occasionally
before distal extremity findings, patients
complain of groin pain caused by swelling of
femoral lymph nodes

• Lymphangitis and abscess are not common, but

the process may spread rapidly from the initial
lesion

• Infrequently, bullae or epidermal sloughing may

occur in the involved area.
 Erysipelas
• 75% to 90% of cases involve the
lower extremities, while the face is
affected in 2.5%–10% of cases

• Facial erysipelas
 begins unilaterally but may spread
by contiguity over the nasal
prominence to involve the face
symmetrically
 Oropharynx is a common portal of
entry, and throat culture may show
GAS
 Inflammatory edema can extend to
the eyelids, but orbital
complications are rare.
 SSTI – Prognosis and Clinical course
• Acute cellulitis, with or without abscess
formation, has a tendency to spread through the
lymphatics and bloodstream and may be a
serious disease, if not treated early.

• Uncomplicated erysipelas remains confined

primarily to the lymphatics and subcutaneous
tissues.

• often a self-limited process, subsiding over 7–10

days
SSTI – Prognosis and Clinical course
• often a self-limited process, subsiding over 7–10
days. Occasionally, untreated erysipelas or
cellulitis may be complicated by:
• bulla formation,
• Abscess
• necrotizingfasciitis
• bacteremia with sepsis
• Metastatic infection in various organs
• Prompt diagnosis and treatment prevents both
suppurative and nonsuppurative complications
SSTI – Prognosis and Clinical course
• Rapid progression that can lead to fatal
outcome in
• Young infant and elderly debilitated patients
• Individual receiving glucocorticoid
SSTI – Prognosis and Clinical course
• Both classical cellulitis and erysipelas tend to
recur in the same area, probably as a result of
chronic lymphatic obstruction and persistent
edema.

• Recurrent erysipelas may produce persistent

swelling of the lips (macrocheilia), cheeks
(particularly the lax tissues beneath the eyes),
abdomen, and lower extremities, sometimes
resulting in elephantiasis nostra verrucosa
 SSTI- Diagnostic Studies
• Cultures and stains from swabs, aspirates,
tissue biopsies, and blood may provide
valuable microbiologic data in select situations
SSTI- Treatment
 SSTI- Adjunct Therapies
• bed rest
• elevation of the involved area to reduce local edema
• Cool, sterile saline dressings decrease the local pain
and are particularly indicated in the presence of
bullous lesions
• application of moist heat may aid in the localization of
an abscess in association with cellulitis
• Surgery is not generally
• needed for erysipelas or cellulitis unless an abscess or
• necrotizing infection is suspected
Gram positive infections
associated with toxin
production
Staphylococcal scalded skin syndrome
(SSSS)
• Generalized exanthematous disease consisting
of cutaneous denudation
 SSSS- Etiology & pathogenesis
• Exfoliative toxins (ET) made by certain strains
of S. Aureus (usually group 2)
– Exfoliatin A and B
– Serine protease that bind to the cell adhesion
molecule desmoglein 1 and cleave it, resulting in a
loss of cell-cell adhesion
– Epidermolysis take place usually between the
stratum spinosum and granulosum very thin-
walled, flaccid blister that is easily disrupted (+)
Nikolsky sign
 SSSS- Etiology & pathogenesis
• 2 forms of ET-mediated disease
1. Localized bullous impetigo
2. Systemic SSSS
 Localized form (bullous empitigo)
• Infection of the upper part of the skin (epidermis)
by S. Aureus or S. Pyogenes results in Impetigo
contagiosa
• Usually disease of children
• Early lesion: cloudy vesicles or bullae surrounded
by an erythematous rim
• Blisters often rupture, leaving superficial erosions
• Lesions at various stages can often be seen
• Lesions tend to be found around exposed parts of
the body and around orifices
 Localized form (bullous impetigo)
• Diagnosis: based on clinical appearance
• Confirmation of diagnosis can be easily
obtained by aspiration of blister fluid for gram
stain and cultures will reveal S. aureus
 Generalized form (SSSS)
• Outbreaks tend to occur in clusters as a
consequence of cross infection
• Typically neonatal or maternal hospital staff
colonized or infected with ET-producing Staph
are the source of these outbreaks
• More commonly seen in infants/children, but
can also be seen in adults
 Generalized form (SSSS)
• Risk factors for adult
– Compromised immune response
– Impaired amounts of toxin-neutralizing antibodies
– Renal insufficiency
 Generalized form (SSSS)
• Faint, orange-red macular exanthem or
uniform erythema sparing mocusal surfaces in
association with a purulent conjunctivitis,
otitis media, nasopharyngeal infection, or
occasionally, pyogenic skin infection (staph
foci from which the toxin is released)
• Periorificial and flexural accentuation of the
exanthema is often noted
 Generalized form (SSSS)
• Early rash is not distinctive in appearance, the
concomitant cutaneous tenderness is usually present
at this early stage.
– Tenderness can often be so severe that infants will refuse
to lie down or allow anyone to hold them.
• Within 1–2 days the rash progresses from an
exanthematous scarlatiniform to a blistering eruption.
• Very, superficial tissue paperlike wrinkling of the
epidermis which is characteristic, progresses to large
flaccid bullae in flexural and periorificial surfaces.
 Generalized form (SSSS)
• A positive Nikolsky sign can be elicited by
stroking the skin, which results in a superficial
blister
• Large sheets of the epidermal surface are
typically shed, revealing a moist underlying
erythematous base. At this stage, the disease
looks very worrisome, resembling a generalized
scalding burn.
• Although fevers are often present and outwardly
the signs of SSSS may look serious, the infants
and children do not usually appear toxic unless
they have developed complications such as
septicemia or pneumonia.
 Generalized form (SSSS)
• The cutaneous process usually resolves
spontaneously or faster with antibiotics and
superficial desquamation, with healing
completed within 5–7 days
• Cultures obtained from an intact blister are
usually sterile, consistent with the
pathogenesis of a hematogenously
disseminated toxin originating from a distant
focus of infection.
 SSSS- Treatment and prognosis
• Bullous impetigo
– Topical mupirocin ointment therapy alone and/or oral antibiotics.
– Prognosis for recovery: excellent

• SSSS
– Treatment should be directed toward eradication of S. aureus, which
generally requires hospitalization and intravenous antistaphylococcal
antibiotics.
– For uncomplicated cases, oral antibiotics can usually be substituted
after several days.
– The use of suitable antibiotics, combined with supportive skin care
and management of potential fluid, and electrolyte abnormalities due
to the widespread disruption of barrier function, will usually be
sufficient to ensure rapid recovery.
 SSSS- Treatment and prognosis
• Neonates benefit from incubators to maintain
body temperature and humidity.
• The use of nonadherent dressings, including
petrolatum-impregnated gauze, to the
widespread areas of superficial blistering are
helpful.
• Antibiotic mupirocin ointment applied several
times per day to clearly impetiginized areas,
including the original source, is often a helpful
adjunct to systemic antibiotic therapy.
 SSSS- Treatment and prognosis
• Major compliaction
– Serious fluid and electrolyte disturbances
• The mortality in uncomplicated pediatric SSSS
is very low (2%) and is not usually associated
with sepsis.
• Adult mortality is higher (approximately 10%)
due to concomitant morbidity factors and
increased likelihood of sepsis.
 Toxic Shock Syndrome
• An inflammatory response characterized by:
– Fever
– Rash
– Hypotension
– Multiorgan involvement
Representing the severed end of the spectrum of
superantigen-mediated diseases
 Staphylococcal TSS
• TSST-1
– most common staphylococcal toxin associated with TSS
– Predominant toxin associated with menstrual-associated
cases
– unique among superantigens in its ability to cross-mucosal
surfaces

• Non-menstrual TSS
– Associated with postsurgical wounds, sinusitiws,
osteomyelitis, influenza, IV drug use, burn wounds and
gynecologic infection
– staphylococcal enterotoxins B and C (SEB and SEC)
comprise
• 50% of nonmenstrual TSS
 Staphylococcal TSS
• Symptoms of TSS begin with the acute onset of
fever, sore throat, and myalgia.
• Diarrhea is common, and vomiting may also
occur.
• Rash is most often a macular erythema but a
scarlatiniform type can also sometimes be seen.
• Eruption usually begins on the trunk and spreads
to extremities and can involve palmsand soles
• If the patient is hypotensive, the eruption tends
to be more prominent on the trunk than
extremities.
 Staphylococcal TSS
• Symptoms of hypotension
– Orthostatic dizziness
– Fainting
– Overt shock
• Nonpurulent conjunctival hyperemia, pharyngeal
inflammation, and strawberry tongue are invariably present
• Signs of decreased mentation can also occur
• Rash will desquamate within 1-2 weeks after it appears
• In cases associated with postoperative infections, the
classic signs of a localized infection such as erythema, pain,
and purulence can be absent. This is often in contrast to
streptococcal TSS.
 Streptococcal TSS
• The majority of cases are due to streptococcal
pyrogenic exotoxin A (SPEA)
• Can result from nearly any type of group A
streptococcal infection
• Most common types of infections: wounds
• In many cases, the route of infection cannot
be determined
• In contrast to Staph TSS, disease induced by
GAS is from skin in 80% of cases
 Streptococcal TSS
• Initial presentation: skin pain that is localized
to an extremity in many cases
• Localized pain often progresses over several
days to localized erythema and edema
• Then cellulitis associated with necrotizing
fasciitis and myositis with concomitant
streptococcal invasion of the bloodstream
develops
 Streptococcal TSS
• Blood cultures are positive in more than 1/2 of
patients with streptococcal TSS, in contrast to
only 1/10 of patients with staph TSS
• Majority of cases have occurred in otherwise
healthy adults
 TSS-Treatment
Staph TSS
– Supportive; and focused on eradicating the offending
S. aureus
– Clindamycin
– Vancomycin(if MRSA is suspected)
– IVIG : for severe or recalcitrant cases
• Strep TSS
– Similar to staph
– If associated with necrotizing fascitis/ myositis: rapid
recognition and surgical debridement are imperative
– IVIG
 Scarlet Fever
• A syndrome characterized by:
– Exudative pharyngitis
– Fever
– Scarlatiniform rash
• Most commonly due to pyogenic exotoxin-
producing group A strep
• Exact mechanism by which toxins produce the
symptom complex is unclear
 Scarlet Fever
• Streptococcal SF
– A childhood disease that occurs most commonly in
winter and early spring
– 10% of childhood group A streptococcal (GAS)
pharyngitis patients develop scarlet fever
– Approximately 12 hours to 5 days after exposure, an
abrupt prodrome develops, consisting of:
• pharyngitis
• Headache
• Vomiting
• abdominal pain
• fever
 Scarlet Fever
• The rash appears 1–2 days after onset of the
illness, first on the neck and then extending to
the trunk and extremities, although it spares
the palms and soles.
• The exanthem texture: coarse, like fine-grade
sandpaper
• Erythema blanches with pressure
 Scarlet Fever
• Skin can be is not painful
• A few days after generalization of the
exanthem, the rash becomes more intense
around skin folds and lines of confluent
petechiae, due to increased capillary fragility
(Pastia’s sign), can be seen
 Scarlet Fever
• Oral Findings
• edematous, erythematous tonsils sometimes
covered with a yellow, gray, or white exudate
• Petechiae and punctate red macules are seen
on the soft palate and uvula (Forchheimer’s
spots)
 Scarlet Fever
• Tongue changes
• First 2 days: has a white coat through which
the red and edematous papillae project (white
strawberry tongue)
• After 2 days: desquamation occurs, resulting
in a red tongue with prominent papillae (red
strawberry tongue)
 Scarlet Fever
• Tender anterior cervical lymphadenopathy is
common
• Flushed face with circumoral pallor is also
commonly noted
 Scarlet Fever
• Diagnosis:
– characteristic clinical signs and confirmed by the rapid streptococcal
test or throat culture
• Usually follows a benign course
• Complications
• Suppurative
– Peritonsillar abscess
– Sinusitis
– Pneumonia
– Meningitis
• Nonsuppurative complications
– immune-related rheumatic fever
– glomerulonephritis
 Scarlet Fever
• Treatment
• Antibiotics (penicillin or erythromycin for a 10-
day course)
• Supportive care
• Fever usually abates within 12–24 hours after
initiation of antibiotic therapy
• Recurrences are common
Fungal Infection of
the Skin and Hair

Superficial Fungal Infections

Dermatophytes
 What are dermatophytes?
• Group of toxonomically related fungi represented by 40
species and divides among 3 genera:
– Epidermophyton
– Microsporum
– Trochophyton

Classified further accdg to their natural habitats – humans, animals or

soil

Ability to attach to and invade keratinized tissue of animals and

humans and to utilize degradation products as nutritional sources

Superficial fungal infections of skin, hair and nails(“dermatophytoses”)

 Geophilic Zoophilic Anthropophilic
“Earth-loving” “Animal-loving” “Man-loving”
Habitat Soil Domestic animals Humans
and pets
Pattern of infection Direct contact with Direct contact with Direct contact or
the soil; infection a specific animal fomites (infected
spread by spores species; skin or hair retained
Indirect contact in clothing, combs,
when infected caps, socks, towels,
animal hair is etc)
carried on clothing
or present in
buildings or feeds;
Type of infection Potential for Acute and intense Epidemic in nature
epidemic spread inflammatory Elicit a mild to
(higher responses inflammatory host
virulence;ability to response
form long-lived
spores) intense
inflammatory
responses
 Tinea Capitis
• Tinea capitis describes dermatophyte infection of hair and scalp, typically
caused by Trichophyton and Microsporum species, with exception of
Trichophyton concentricum

• most commonly observed in children between 3 and 14 years of age.

More common among children of African descent for unknown reasons

• Transmission is increased with:

• decreased personal hygiene
• Overcrowding
• low socioeconomic status

• Even after shedding, hairs may harbor infectious organisms for more than
1 year.
• Infection of hair by dermatophytes follows 3
main patterns:
• Ectothrix
• Endothrix
• Favus
 Ectothrix infections
• only the arthroconidia on the surface of the
hair shaft may be visualized, although hyphae
are also present within the hair shaft
• cuticle is destroyed
• Wood’s lamp examination, a yellow–green
fluorescence may be detected, depending on
the causative organism
 Ectothrix infections
• arthroconidia and hyphae remain within the
hair shaft and leave the cortex and cuticle
intact
• associated with the appearance of “black
dots” which represent broken hairs at the
surface of the scalp
• do not show fluorescence on Woods lamp
exam
 Favus
• Longitudinally arranged hyphae and air spaces
within the hair shaft
• Arthroconidia are not usually noted in infected
hairs
 Clinical Findings
• depends on the causative species as well as
other factors such as the host immune
response
• Infection of the scalp results in:
• hair loss,
• scaling
• Varying degrees of an inflammatory response
**
 Noninflammatory Type
• Seborrheic form of tinea capitis
since scale is the predominant
feature
• Arthroconidia may form a sheath
around affected hairs turning them
gray and causing them to break off
just above the level of the scalp
• Alopecia may be imperceptible or in
• more inflammatory cases there may
be circumscribed
• erythematous scaly patches of
nonscarring alopecia
• with breakage of hairs (“gray patch”
type)
 “Black Dot” Tinea Capitis
• “black dot” form of tinea capitis is typically caused
by the anthropophilic endothrix organisms T.
tonsurans and T. violaceum

• Hairs broken off at the level of the scalp leave

behind grouped black dots within patches of
polygonal shaped alopecia with finger-like margins

• Normal hairs also remain within patches of broken

hairs

• Diffuse scaling is also often present

• minimally inflammatory, some patients may

develop follicular pustules, furuncle-like nodules,
or in rare cases kerion—a boggy, inflammatory
mass studded with broken hairs and follicular
orifices oozing with pus
 Inflammatory Type
• Zoophilic or geophilic pathogens, such
as M. canis, M. gypseum, and T.
verrucosum

• Inflammation, which is the result of a

hypersensitivity reaction to the
infection, in this setting ranges from
follicular pustules to furunculosis

• scalp is usually pruritic or tender

• Associated with posterior cervical

lymphadenopathy, which serves as a
clinical pearl in differentiating tinea
capitis from other inflammatory
disorders involving the scalp
 Tinea Corporis
• refers to any dermatophytosis of glabrous skin except
palms, soles, and the groin
• Transmission
• infected humans or animals
• via fomite
• via autoinoculation from reservoirs of dermatophyte colonization
on the feet

• Aggrevating factor
• Occlusive clothing
• humid climate are associated with more frequent and severe
eruption
• Freq skin to skin contact
 Etiologic agents - Tinea Corporis

• T. rubrum is also the most likely candidate in cases

with concomitant follicular involvement
• Epidermophyton floccosum
• T. interdigitale (anthropophilic and zoophilic strains)
• M. canis
• T. tonsurans
 Classic presentation- Tinea Corporis
• annular (“ring-worm”-like) or serpiginous
plaque with scale across the entire active
erythematous border
• border, which may be vesicular, advances
centrifugally
• center of the plaque is usually scaly but it may
exhibit complete clearing
Tinea Corporis
• Majocchi’s granuloma is a superficial
and subcutaneous dermatophytic
infection involving deeper portions of
the hair follicles that presents as scaly
follicular papules and nodules that
coalesce in an annular arrangement

• most commonly by T. rubrum, T.

interdigitale, and M. canis

• observed on the legs in women who

become inoculated after shaving or
who apply topical corticosteroids to
the involved area, which facilitates
infection

• observed increasingly among

immunocompromised patients
 Tinea Cruris
• Common dermatophytosis of
the groin, genitalia, pubic area,
and perineal and perianal skin
• 2nd most common type of
dermatophytosis worldwide
• Transmission
• direct contact
• Fomites
• Autoinfection (distant reservoirs
of T. rubrum or T. interdigitale on
the feet, for example, is common
• Exacerbating factors
» occlusion
»Warm, moist climates
 Tinea Cruris

• 3x more common in men than in women

• Adults more commonly affected than children

• Etiologic agents
• T. rubrum
• Epidermophyton floccosum (responsible for epidemics)
• well-marginated annular plaque with a scaly raised border
which extends from the inguinal fold on to the inner thigh,
often bilaterally

• Pruritus is common, as is pain when plaques are macerated

or secondarily infected

• E. floccosum
• central clearing, and are more often limited to the genitocrural crease
and the medial upper thigh

• T. rubrum
• coalesce with extension to the pubic, perianal, buttock, and lower
abdominal areas

• Genitalia including the scrotum are infrequently affected


Tinea Pedis & Tinea Mannum
Tinea pedis
• Dermatophytosis of the
feet
• High incidence
associated with:
- Modern occlusive footwear
- Use of communal baths,
showers or pool
Most common dermatophytoses,
10% prevalence rate
Tinea mannum
• Dermatophytosis of the palmar and
interdigital areas of the hands
• Acquired through:
- Direct contact
- Soil
- Autoinnoculation
• Most commonly, only 1 hand is involved,
concommitant with infection of the feet
and toenails (“two feet-one hand”
syndrome)
• Secondary infection of the hand acquired
from excoriating and picking infected feet &
toenails
• Suspect in individuals who have fine dry
scaling of the palm or palms, often
accentuated in the creases
• Etiology
– T.rubrum (most common)
– T. interdigitale
– E. floccosum
Tinea Pedis
• 4 clinical forms:
• Interdigital type
• Most common presentation
• Begins as scaling, erythema & maceration of the interdigital and
subdigital skin of the feet, particularly between the lateral 3rd and 4th
toes
• Infection spreads to the adjacent scale or instep, rarely involving the
dorsum
• Occlusion an bacterial co-infection interdigital erosions with
pruritus & malodor characteristic of the dermatophytosis complex
(“athlete’s foot)
• Chronic hyperkeratotic (Mocassin) type
• Patchy or diffuse scaling on the soles and the lateral &
medial aspects of the feet, in a distribution similar to a
mocassin on a foot
• Degree of erythema is variable, and there may exist few
minute vesicle that heal with collarets of scale <2 mm in
diameter
• Etiologic agents:
• T. rubrum (most common)
• E. floccosum, T. interdigitale
• Vesiculobullous type
• Caused by zoophilic stains of T. interdigitale
• Tense vesicles >3 mm in diameter, vesiculopustules, or
bullae on the soles and periplantar areas
• Uncommon in childhood
• Acute ulcerative type
• Co-infection between T. interdigitale and bacteria (often
gram negatives)
• Vesicles, pustules and purulent ulcers on the plantar
surface
• Associated symptoms:
• Cellulitis
• Lymphangitis
• Lymphadenopathy
• Fever
Onychomycosis
• Fungal infection of the nail caused by dermatophytes,
nondermatophyte molds or yeasts
• Tinea unguium: dermatophyte infection of the nail
• Most prevalent nail disease (~50% of all onychodystrophy)
• Most often caused by dermatophytes
• T. rubrum & T. interdigitale = ~90% of all cases
Clinical types:

• Distolateral subungal type (DLSO)

• Most common form of onychomycosis
• Begins with invasion of the stratum corneum of the hyponychium and
distal bed, forming a whitish to brownish-yellow opacification at the
distal edge of the nail
• Infection spreads proximally up the nail bed to the ventral nail plate
• Hyperproliferation or altered differentiation of the nail bed in response
to infection subungal keratosis
• Progressive invasion of the nail plate increasingly dystrophic nail
• Proximal subungal type (PSO)
• From infection of the proximal nail fold primarily with T. rubrum & T. megninii
• White to beige opacity on the proximal nail plate
• Opacity gradually enlarges to affect the entire nail subungal hyperkeratosis,
leukonychia, proximal onycholysis and destruction of the entire nail unit
• Patients should be screened for HIV (marker for this disease
• White superficial type (WSO)
• Direct invasion of the dorsal nail plate resulting in white to
dull yellow sharply bordered patches anywhere on the
surface of the toenail
• T. interdigitale
Treatment
• Tinea capitis
• Infections involving hair-bearing skin usually necessitate
oral antifungal treatment since dermatophytes penetrating
the follicle are usually out of reach for topically applied
agents
• Griseofulvin, along with allylamine (terbinafine) and oral
triazoles (itraconazole and fluconazole) are considered safe
& effective in the treatment of tinea capitis
Griseofulvin: (together with terbinafine)approved by the
USFDA for patients older than 4 yrs
• For 8 wks
• 20-25 mkday (microsize form)
• 15 mkday (ultramicrosize form)
Fluconazole
• 6 mkday x 20 days
• 6 mg/kg once weekly dosing for 8-12 weeks
Itraconazole
• 5 mkday for 2-4 wks
• 5 mkday for 1 week/month for 1-3 pulses
Terbanifine
• 3-6 mkday for 2-4 wks (Trichophyton), 4-8 wks (Microsporum)
• Adjuvant therapy
• Selenium sulfide
• Zinc pyrithione
• Povidone iodine
• Ketaconazole
• Shampoo 2-4x/week for 2-4 weeks
• Tinea corporis/Tinea cruris
• Isolated lesions
• Topical agents: allylamines, imidazoles, tolnaftate,
butenafine or ciclopirox: BID x 2-4 wks
• Widespread or more inflammatory lesions
• Oral antifungals:
• Fluconazole 150-300 mg weekly for 4-6 weeks
• Itraconazole 200 mg OD x 1 wk
• Terbinafine 250 mg OD x 2-4 weeks
• Griseofulvin 500 mg OD x 2-6 weeks
 Tinea pedis & Tinea mannum
• Mild interdigital tinea pedis without bacterial involvement
• Topical antifungals: allylamine, azole, benzylamine, tolnaftate or
undecenoic acid: terbinafine
• Severe or refractory tinea pedis accompanied by onychomycosis
• Oral antifungals
• Terbinafine 250 mg x 2wks
• Itraconazole 200 mg BID x 1 wk, 200 mg OD x 3 wks or 100 mg OD x 4 wks
• Fluconazole 150 mg weekly for 3 to 4 weeks or 50 mg daily for 30 days
• Treatment of coexisting onychomycosis, bacterial infection
(antibiotics) and immune reaction (corticosteroids)
Onychomycosis
• Without matrix area involvement
• Topical treatment
• Ciclopirox daily for 48 weeks
• Amorolfine once a week
• With matrix involvement
• Oral and combination treatments
• Terbinafine 250 mg OD x 6 weeks
• Itraconazole 400 mg daily for 1 week per month, or continuous
dose of 200 mg daily
• Fluconazole 150-300 mg once per week for 3-12 months
 CANDIDIASIS
 Diverse group of infections caused by Candida albicans or by
other members of the genus Candida
 Skin,nails,mucous membranes and GI tract may also cause
systemic disease

Candida albicans
 Dimorphic yeast responsible for 60-70% of all candida
infections
 Most common cause of superficial and systemic candidiasis
Candidal intertrigo
 C.albicans has a predilection for colonizing skin
folds,
intertriginous zones in which the local
environment is moist
& warm
Usual Locations
Genitocrural
Gluteal
Interdigital
Inframammary
Beneath the pannus and axillary areas
Predisposing Conditions
Obesity
Wearing of occlusive clothing
Diabetes mellitus
Occupational factors
 Pruritic eruption appears as macerated red
erythematous patches & thin plaques with satellite
vesicopustules.
 Pustules enlarge & rupture, leaving an erythematous
base with a collarette of easily detachable scale that
contributes to further maceration & fissuring.
Candidal diaper dermatitis
 Results from yeast colonization of the
gastrointestinal tract and chronic occlusion with
wet diapers.
 Lesions appear first in the perianal area, and spread
to the perineum and inguinal creases, which show
pronounced erythema
Treatment
 Topical antifungals
Nystatin
Imidazole creams
 Powder preparations
Miconazole powder – keep moist environment dry
 Systemic antifungal theraphy for extensive
cutaneous infections, follicular involvement or
infections in immunocompromised patients.
 Malassezia
• Includes species of lipophilic basidiomycetous yeast
• Cause a wide spectrum of superficial cutaneous
disease, including tinea versicolor and seborrheic
dermatitis, while contributing to atopic dermatitis
and psoriasis
Tinea versicolor
• Opportunistic infection of the skin
• Occurs more frequently in regions with higher
temperatures and relative humidity
• Incidence is same in all races
• Eruption is more apparent in darker-skinned individuals
due to resulting alteration in skin pigmentation
• No sex predominance
• Most common among adolescents and young adults, in
whom lipid-producing sebaceous glands are more
active
Clinical manifestations:
• Scaly oval to round macules scattered over characteristic
areas of the body, including the upper trunk, neck, and
upper arms
• Macules often coalesce irregular shaped patches of
pigmentary alteration
• Color: varies from almost white to pink to reddish brown
or fawn colored
• Scale: dust-like or furfuraceous
• Patches may have a wrinkled surface appearance: useful
clinical pearl for the diagnosis
• Presenting complaint: cosmetic  lesions often fail to tan
with sun exposure
• Pruritus: mild or absent
Treatment:
 Local lesions: Topical Antifungals
• 2.5% Selenium sulfide lotion daily for 2 wks, left on
for 10 mins, and rinsed
• Azoles: Ketoconazole 2% shampoo- 5 minutes x 3 days
• Terbinaline 1% solution BID x 7days
 Extensive disease or frequent recurrences: Oral
treatment
• Ketoconazole 200 mg daily x 7days
• Itraconazole 200-400 mg daily x 3-7days, or 400 mg
single dose
• Fluconazole 400 mg single dose
Thank You!!! 