Abigail C.

Co, MD, FPDS

 There are 2 distinct clinical situations regarding the nature of
skin changes:

The skin changes are incidental findings in well people noted

during the routine general physical examination
Bumps and Blemishes every general physician should be able to
recognize each of these diseases and disorders
Important skin lesions not noted by patient but cannot be overlooked by
the physician
(dysplastic nevi, melanoma, xanthomatoses, BCC, SCC, caf-au-lait
macules)

The skin changes are the chief complaint of the patient

Minor problems localized itchy rash, warts, moles, seborrheic keratosis,
etc
4S serious skin signs in sick patients
 Generalized Red Rash: with Fever
Measles, rubella, RMSF, viral
examthem
Generalized Red Rash: with Bullae
and Prominent Mouth Lesions
EM, TEN, Pemphigus vulgaris,
bullous pemphigoid, drug
eryptions
Generalized Red Rash: with Pustules
Pustular psoriasis, drug eruptions
Generalized Vesicular Lesions
Disseminated herpes simplex,
generalized herpes zoster,
varicella, drug eruptions
Multiple Bullous Lesions with Mouth
Lesions
Pemphigus, drug eruptions
Generalized Pustules
Drug eruptions, pustular psoriasis
Generalized Urticaria and
Angioedema
Drug Eruptions
Generalized Dermatitis
Erythroderma
Facial Inflammatory Edema with Fever
Erysipelas, Lupus erythematosus
Generalized Purpura
Thrombocytopenia, purpura
fulminans, drug eruptions
Palpable Purpura
Vasculitis, bacterial endocarditis
Multiple Skin Infarcts
Meningococcemia, Gonococcemia,
DIC
 Epidemiology Past Medical History
Operations
Age, race, sex, etiology,
Illnesses
occupation Allergies
History Medications
Constitutional Symptoms Habits
Atopic history
Acute illness syndrome
Chronic illness syndrome Family Medical History
History of skin lesions (7 key Social History (occupation,
ques) hobbies, exposure, travel)
When (onset) Sexual History
Where (site of onset)
Symptoms (itch/hurt)
Evolution (pattern of spread)
How have individual lesions changed
Provocative factors
Previous treatments
HPI
Review of Systems
 Physical Examination
Appearance
Vital signs
Skin (4 major skin signs)
1.Type of lesions
Flat macule, petechiae,
ecchymosis, infarct, sclerosis,
telangiectasia
Elevated papule, plaque, nodule,
wheal, vegetation, papilloma,
vesicle, bulla, pustule, abscess, cyst,
crust, scales, hypertrophies,
lichenification
Depressed atrophy, sclerosis,
erosion, excoriation, fissure, ulcer,
sinus, gangrene, sphacelus
Color of lesions
Palpation consistency, deviation in temp,
mobility, presence of tenderness, depth
Margination ill or well defined
2.Shape
Round, oval, polygonal,
polycyclic, annular, iris,
serpiginous, umbilicated
3.Arrangement
Grouped herpetiform,
zosteriform, arciform, annular,
reticulated, linear, serpiginous
Disseminated scattered
discrete lesions or diffuse
involvement
4.Distribution
Extent isolated, localized,
regional, generalized, universal
Pattern symmetrical, exposed
areas, sites of pressure,
intertriginous area, follicular
localization, random, Blaschkos
lines
 Hair and Nails Laboratory examination of
Mucous Membranes blood
General Physical Examination Blood culture
Laboratory Examinations Serology ANA
Hematologic
Dermatopathology Chemistry
Light microscopy
Imaging (CT, MRI, UTZ, X-ray)
Immunofluorescence
Special techniques Urinalysis
Microbiologic Exam of skin Stool exam
material Woods lamp
Direct microscopic examination
of skin Epiluminescence microscopy
10% KOH (yeast and fungi) (dermatoscopy) pigmented
Grams stain (bacteria) lesions
Tzanck smear (virus) Patch testing
Dark-Field Exam (spirochetes) Acetowhitening (5% acetic
Burrows (scabies) acid)
Culture (bacterial, viral,
mycologic, parasitic, granuloms
minced tissue)
 PRIMARY LESION

SECONDARY LESION
 Macule
Patch
Papule
Plaque
Nodule
Tumor
Wheal
Vesicle
Bulla
Pustule
 Scale
Crust
Excoriation
Fissure
Erosion
Ulcer
Scar
Abigail C. Co, MD, FPDS
 Dermatophytosis superficial infection caused by a
dermatophyte

Dermatophytes group of taxonomically related fungi

whose ability to form molecular attachments to keratin and
use it as a source of nutrients allows them to colonize
keratinized tissues

3 Genera Epidermophyton, Microsporum, Trichophyton

 Hair
Woods lamp examination
Microscopic examination
Ectothrix small or large
arthroconidia forming a
sheath around the hair shaft
Endothrix arthroconidia
within the hair shaft
Favic hyphae arranged in
parallel within and around the
hair shaft
Skin and Nails
KOH examination (fungal
hyphae septate,
branching structures)
Note
Hairs must be plucked not
cut for examination
Skin samples should be
taken by scraping with
dull edge of a scalpel
outward from the
advancing margins of the
lesion
Nail specimens must
include clippings of the
entire thickness of the
dystrophic areas of nail,
as proximal from the
distal edge as possible
 Culture Procedures PDA (Potato Dextrose Agar)
stimulates the production of
Speciation of superficial fungi is
based on macroscopic,
conidia and pigment
microscopic and metabolic
characteristics of the organism
SDA (Sabourauds Dextrose Agar)
most commonly used isolation
medium, serves as the basis for
most morphologic description
Mycosel and Mycobiotic Agar
contains cycloheximide &
chloramphenicol to inhibit
saprobes and bacteria, highly
selective medium for
dermatophytes
DTM (Dermatophyte Test
Medium) contains phenol red,
yellow (saprophytes), red
(dermatophyte)
 Tinea Capitis
Dermatophytosis Tinea Favosa
Tinea
DSO Barbae
(Distal Subungual
Tinea Corporis
Onychomycosis Onychomycosis)
Tinea Cruris
PSO (Proximal Subungual
Tinea Pedis and Manuum
Onychomycosis)
Tinea Nigra WSO (White Superficial
Onychomycosis)
Piedra Black PiedraCandidal Onychomycosis

White Piedra
 Dermatophytosis of the
scalp and associated hair
Microsporum canis most
common cause worldwide
Epidemiology
Children 3-14 years old
Decreased personal hygiene,
overcrowding, low
socioeconomic status
Fomites comb, caps,
pillowcases, theater seats
Clinical Manifestations
Noninflammatory, human or
epidemic type anthropophilic
ectothrix, begins as erythematous
papule surrounding a single hair
shaft and spreads centrifugally,
scaling, gray and lusterless hair,
hair breaks off just above scalp
level
Inflammatory type zoophilic or
geophilic pathogens, pustular
folliculitis or kerion (boggy mass
studded with broken hairs and
follicular orifices oozing with pus)
Black Dot Tinea Capitis
anthropophilic endothrix, with or
without hair loss, hairs broken at
level of scalp leaving grouped
black dots
 Inflammatory Noninflammatory
M. audouinii M. audouinii
M. canis M. canis
M. gypseum M. ferrugineum
M. nanum T. tonsurans
T. mentagrophytes
T. schoenleinii Black Dot
T. tonsurans T. tonsurans
T. verrucosum T. violaceum
 Griseofulvin gold standard Terbinafine
1g/day microcrystalline 3-6mkd x 2-4wks
0.5g/day ultramicrosize (Trichophyton)
10-20mkd ultramicrosize 3-6mkd x 4-8wks
(pediatric) (Microsporum)
Fatty meal (absorption)
6-8 weeks Adjuvant
Photosensitive, GI side effects Prednisone 1mkd x 10-15
days
Fluconazole Reduce incidence of scarring
6mkd x 20 days Relieves pain and swelling
8mk, 1x/wk , 8-16wks

Itraconazole
3-5mkd x 4-6wks
 Favus
Chronic dermatophyte
infection of the scalp,
glabrous skin, nails
Thick yellow crust (scutula)
within hair follicles
Scarring Alopecia
Epidemiology before
adolescence, associated
with malnutrition and poor
hygiene
T. schoenleinii most
common cause of human
favus
Clinical Manifestations
Early Favus (1st 3 weeks)
patchy follicular erythema of
the scalp with slight
perifollicular scaling and mild
matting of the hair
Hyphal invasion distends
follicle producing yellowish red
papules then yellow concave
crust centered about a single
dull, dry hair
Scutulum may reach 1cm
coalescing with other scutula
forming large adherent mats
with unpleasant cheese-like or
musky odor
 Griseofulvin gold
standard
1g/day microcrystalline
0.5g/day ultramicrosize
6-8 weeks
Concomittant nail infection (6-
12 months)
 Tinea sycosis, Barbers itch
Dermatophytosis of the
facial terminal hair of men
Tinea faciale
dermatophytosis of the
same area in females or
prepubertal males
involving glabrous skin
Epidemiology
contaminated barbers
razors, direct exposure to
cattle, horses, dogs
Zoophilic T.
mentagrophytes, T.
verrucosum, M. canis
Anthropophilic T. megninii,
T. schoenleinii, T. violaceum
Clinical Manifestations
unilateral, beard area >
moustache
Inflammatory/ Kerion-like
nodular and boggy with
crusting seropurulent
discharge, lusterless, brittle,
easily epilated hair
Superficial / Sycosiform less
inflammation, diffuse erythema
& perifollicular papules &
pustules
Circinate / Spreading active,
spreading vesiculopustular
border with central scaling,
relative hair sparing
 Griseofulvin
1g/day microcrystalline
2-3 weeks after clinical
resolution
Topical Antifungals
 Dermatophytosis of the Topical Antifungal
glabrous skin except the BID x 2-4 weeks
palms, soles and groin
Oral Antifungal
Epidemiology humans or Fluconazole 150mg/wk x 4-6
animals, fomites, wks
Itraconazole 100mg OD x 15
autoinoculation, occlusive
days
clothing, warm, humid
Terbinafine 250mg OD x 2 wks
climate Griseofulvin 500mg OD x 2-6
wks
Clinical Manifestations
annular, scaling across the
erythematous border,
advances centrifugally
 Dermatophytosis of the
groin, genitalia, pubic
area, perineal & perianal
skin

Multiple erythematous
papulovesicles with well-
marginated, raised border

Topical antifungals
Powder or cream
Minimize occlusion &
moisture
 Dermatophytosis of the
feet / palmar & interdigital
areas of the hand
Tinea pedis clinical
manifestations
Chronic intertriginous type
most common, scaling,
erosion, and erythema of
interdigital & subdigital skin of
the feet, lateral 3 toes
Tinea manuum
Chronic hyperkeratotic type
bilateral, patchy or diffuse
scaling limited to the thick
skin of the feet (moccasin-
type)
Vesiculobullous type tense
vesicles, >3mm ,
vesicopustules or bullae on thin
skin of the soles
Acute ulcerative type
rampant bacterial coinfection,
gram negative,
vesiculopustules and areas of
purulent ulceration on plantar
surface, cellulitis, lymphangitis,
lymphadenopathy, fever
hyperkaratotic type
crescentic, exfoliating,
vesicular, folliculopapular,
dorsal erythematous forms
 Topical Terbinafine (1wk), others
4-6 wks

Terbinafine 250mg OD x 2 wks

Itraconazole 200mg BID x 1 wk
Fluconazole 150mg/wk x 3-4 wks
 Infection of the nail
caused by dermatophytes
fungi, nondermatophyte
fungi, yeast
Tinea ungium
dermatophyte infection of
the nail plate
Clinical Manifestations
Distal Subungual
Onychomycosis (DSO) most
common, whitish to brownish-
yellow opacification at the
distal edge of the nail or near
the lateral nail fold
Proximal Subungual
Onychomycosis (PSO) white
to beige opacity on the
proximal nail plate
White Superficial
Onychomycosis (WSO) white
to dull yellow sharply bordered
patches anywhere on the
surface of the nail, rough and
friable
Candical Onychomycosis
rare, like DSO, thick, rough,
opaque or darkened
 Ciclopirox 8% lacquer OD x 48
wks only effective topical agent
for tinea ungium

Terbinafine 250mg OD x 6 wks

(fingernails) 12 wks (toenails)

Itraconazole 200mg BID x

1wk/month for 2 months
(fingernails) 3 months (toenails)

Fluconazole 150mg-300mg
1x/wk x 3-12 months
 Palmar stratum corneum
Phaeoannellomyces werneckii

Asymptomatic, mottled brown

to greenish black macule with
minimal to no scale, macule
darkest at advancing border,
plantar involvement is
possible

Keratolytics (Whitfields
ointment, 2% salicylic acid)
Azole antifungal or terbinafine
2-4 wks after clinical
resolution
 Asymptomatic fungal
infection of the hair shaft
Piedra hortae (black
piedra) scalp hair most
commonly affected, firmly
attached, hard, brown-
black nodules on the hair
shaft, broken hairs
Trichosporon beigelii (white
piedra) facial, axillary,
genital hairs, softer, less
adherent whitish to beige
nodules, discrete or
coalesce into sleeve-like
structures
Shaving infected hair,
topical azole antifungal
 Oral Candidiasis
Candidiasis Vaginal & Vulvovaginal Candidiasis
Balanitis or Balanoposthitis
Cutaneous Candidiasis
Pityrosporum Chronic Mucocutaneous
Candidiasis
Infections
 Acute pseudomembranous
candidiasis - most common,
Discrete white patches may become
confluent on buccal mucosa,
tongue, palate, gingivae, oral thrush
Acute Atrophic Candidiasis
(Erythematous Candidiasis) after
sloughing of thrush
pseudomembrane, asso. With
broad-spectrum antibiotics,
glucocorticoids, HIV, dorsal surface
of the tongue, patchy depapillated
areas with minimal
pseudomembrane formation
Chronic Atrophic Candidiasis
(Denture Stomatitis) chronic
erythema and edema of palatal
mucosa
Candidal Cheilosis (Angular Cheilitis)
or Perleche erythema, fissuring,
maceration, soreness at the angles
of the mouth, habitual lip lickers and
sagging skin at oral commissures,
riboflavin deficiency
Chronic Hyperplastic Candidiasis or
Candidal Leukoplakia adherent,
firm plaques, on buccal mucosa or
tongue, translucent to white color
with surrounding erythema
Median Rhomboid Glossitis central
papillary atrophy of the dorsal
surface of the tongue, exophytic
lobulated masses on midline portion
of tongue
Black Hairy Tongue - alteration of
the normal flora allows overgrowth of
fungi and bacteria, filiform papillae
and tongue surface cannot undergo
normal desquamation (Tx physical
debridement and good hygiene)
 Thick vaginal discharge,
burning, itching, dysuria,
whitish plaques on vaginal
wall with underlying
erythema and surrounding
edema

Topical imidazoles both

creams and suppositories
3-7 days

Oral fluconazole,
itraconazole, ketoconazole
 Small papules or fragile
papulopustules on the
glans or in the coronal
sulcus

Predisposing factors
include candidal vaginal
infection in sexual
partners, DM,
uncircumcised state

Clotrimazole cream
Fluconazole 150mg single
dose
 Candida albicans
predilection for moist,
macerated folds of the
skin
Intertrigo most common
clinical presentation on
glabrous skin
Pruritic, erythematous,
macerated skin, in
intertriginous areas with
satellite vesicopustules
Topical antifungals
 Chronic, treatment-resistant,
superficial candidal infections of
the skin, nails, and oropharynx
Childhood lesions are detected
before 3 y/o
Oral lesions or diaper dermatitis
appear 1st followed by angular
cheilitis, lip fissures, nail and
paronychial involvement,
vulvovaginitis and cutaneous
involvement
Chronic localized
mucocutaneous candidiasis
markedly hyperkeratotic,
hornlike, or granulomatous
lesions on face, eyelids, scalp,
lips or acral areas
Chronic diffuse candidiasis
erythematous, serpiginous
border or areas of brownish
desquamation on a
background of mild erythema
Esophagitis, laryngitis,
endocrinopathies, circulating
ANA, DM, vitiligo, iron def,
chronic active hepatitis,
pernicious anemia,
malabsorption, alopecia
totalis, enamel dysplasia,
keratoconjunctivitis,
pulmonary fibrosis, KID
syndrome
Antifungal + immune
deficiency correction
 Malassezia
Part of the normal flora,
particularly in sebum-rich
areas of the skin
Clinical Features
Papulosquamous
Folliculitis
Inverse Tinea Versicolor
Papulosquamous
Scaly hypo or hyperpigmented
macules
Dustlike or furfuraceous scales
White to reddish brown or
fawn-colored
Mild or absent pruritus
Pityrosporum Folliculitis
Back, chest, extremities
Pruritus is more common
Perifollicular, erythematous, 2-
3 mm papule or pustule
Inverse Tinea Versicolor
Flexural areas
 2.5% Selenium Sulfide
10 mins OD x 2 wks
Ketoconazole 2%
shampoo 5 mins x 3
days
Terbinafine 1% Solution
BID x 1 wk

Ketoconazole 200mg OD x
1 wk
Itraconazole 200-400mg
OD x 3-7 days
Fluconazole 400mg single
dose
Abigail C. Co, MD, FPDS
 Chronic granulomatous infection
Skin and nerves
Mycobacterium leprae gram +, noncultivable, obligate
intracellular, AFB
Genetic and environmental factors are important in
determining disease susceptibility and disease expression
(MHC II)
 Granulomatous Spectrum
Reactional State
Ridleys Granulomatous
Spectrum (high low
resistance)
TT (polar tuberculoid)
BT (borderline tuberculoid)
BB (borderline)
BL (borderline lepromatous)
LLs (subpolar lepromatous)
LLp (polar lepromatous)
TT and LLp are clinically
stable
Between the poles the host
granulomatous structure may
either
Upgrade to a posture of higher
resistance often with devastating
inflammation
Downgrade to a posture of lower
resistance, usually silent but
occasionally inflammatory
In virtually all TT patients and
most BT cases, AFB cannot
be found (paucibacillary)
BB-LLp, bacilli are
demonstrable with ease
(multibacillary)
 Nerve enlargement
(asymmetry) particularly
those close to the skin
such as great auricular,
ulnar, radial, superficial
peroneal, sural and
posterior tibial
Sensory loss in skin
lesions
Nerve trunk palsies s/sx
of inflammation, silent
neuropathy, sensory or
motor loss
(weakness/atrophy),
contracture
Acral distal symmetric
anesthesia withering
away of type C fibers, heat
and cold discrimination
before loss of pain or light
touch beginning in acral
areas and over time
extending centrally but
sparing the palms for a
while
 Polar Tuberculoid Leprosy
(TT)
Immunity is strong (spontaneous
cure), absence of downgrading

Primary skin lesion plaque,

annular, central clearing, sharply
marginated border, firm,
indurated, elevated,
erythematous, scaly, dry,
hairless, hypopigmented, nearby
sensory nerve +/- enlarge,
anesthetic, anhidrotic, solitary
 Borderline Tuberculoid
Leprosy (BT)
Immunity is strong enough to
restrain infection (disease is
limited and bacillary growth
retarded) but host response is
insufficient to self cure

Primary skin lesion plaques &

papules, annular sharply
marginated border may have
satellite papules, little or no
scaling, less erythema, induration
& elevation, multiple , asymmetric
lesions, loss of sensation and
nerve trunk involvement,
enlargement or palsies
 Borderline Leprosy (BB)
Immunologic midpoint, most
unstable, patient quickly up or
downgrade

Primary skin lesion annular

lesions with sharply marginated
interior and exterior margins,
large plaques with islands of
clinically normal skin within
plaque (Swiss cheese) or the
classic dimorphic lesion
 Borderline Lepromatous
Leprosy (BL)
Resistance is too low but still
sufficient to induce tissue
destructive inflammation (worst of
both worlds)

The classic dimorphic lesion is the

most characteristic, annular
configuration with poorly
marginated outer border
(lepromatous-like), sharply
marginated inner border
(tuberculoid-like), poorly or sharply
marginated plaques with punched
out or Swiss cheese marginated
areas of normal skin in the interior
plaque, nerve trunk palsies highest
 Lepromatous Leprosy (LL)
Lack of CMI permits unrestricted
bacillary replication and widely
disseminated, multiorgan
disease

Poorly defined, skin-colored

nodules symmetrically
distributed, leonine facies
Hair loss n eyebrows proceed
laterally to medially, loss of
eccrine sweating, nerve trunk
palsies occur but less common
than BL
May develop ENL
 Distinctive, tissue destructive, Erythema Nodosum Leprosum
inflammatory processes, (Joplings Type II Reaction)
immunologically driven LL patients
Superimposed upon Crops of painful & tender, bright
granulomatous reaction but pink, dermal and subcutaneous
usually dominates nodules, fever, anorexia and
malaise, arthralgias and arthritis,
neutrophilic leukocytosis, abrupt
Delayed-Type Hypersensitivity
fall in hematocrit (5g/dl)
Reaction (Joplings Type I
Reaction)
Abrupt conversion of previously
torpid plaques to tumid lesions,
purplish color, iritis and
lymphedema
Most common in the 1st year of
treatment
BL patients most common
 Logarithmic scale as to the
numbers of bacilli per oil
immersion field

6 >= 1000/OIF
5 100-1000/OIF
4 10-100/OIF
3 1-10/OIF
2 1 bacillus/ 1-10 OIF
1 1/ 10-100 OIF
0 no bacilli in 100 OIF
 Multi-drug approach is utilized to
treat leprosy, with a high success
rate for cure.

However, patient compliance is

essential, and treatment can be
extremely long; 12-24 months. (In
1997, the World Health
Organization reduced the
duration of therapy for
multibacillary leprosy to 12
months; however, in the United
States, treatment continues to be
done for 24 months for severe
cases.)

The WHO provides MDT in blister

packs, freely available throughout
the world.
Enjoy your weekend !