Dermatological Pathology

Leslie Solomonian, BSc., ND

BAS 206 Pathology
Module 2
Review of Normal Physiology
!
Diagram oI normal skin
!
Skin Functions:
!
Protection barrier Irom UV
!
Absorption
!
Temp regulation/thermoregulation
!
Antibacterial properties IgA
!
Sensation


Review of Normal Physiology
!
Layers Irom the TOP
1) Epidermis
!
Basal cell layer Irom bottom they multiply and
migrate up
!
Keratinocytes top dead layer
2) Dermis
!
Active skin Iunction
!
Sweat glands, hair Iollicles, sebaceous glands
(appendages)
!
Nerve endings, blood vessels
!
Damage more serious to dermis
3) Adipose
!
Insulation/padding
Naturopathic Concepts of
Dermatology
!
Skin is the maniIestation oI other conditions, Ior example gut
Iunction
!
Asian med: LI/LU maniIests on skin & Wei Qi
!
Herings Law: cure starts Irom the inside and moves out
!
II skin is unhealthy: elimination backed up OR skin is taking on
too much
!
Look at DIET 1
st
thing to do Ior lesions is elimination diet
Terminology

Flat lesions

Macule colour e.g. freckle

Elevated solid lesions

Papule less than 5mm

bump

Nodule greater than 5mm

domed

Plaque elevated, flat top

Elevated fluid-filled
lesions

Vesicle fluid filled blister

less than 5mm

Bulla fluid filled blister

greater than 5mm

Pustule pus instead of fluid

Change because of
nta eson (e.g.
scratchng)

Scae - mperfect cornfcaton

Lchenfcaton - skn
markngs (due to scratchng
usuay)

Excoraton - breakage n
epderms

Hyperkeratoss/Acan
thoss - hyperkeratoss ncreased
keratn n s. corneum and
acanthoss=spnosum.

Spongoss - fud n
derms
http://www.infoderm.com/scc/index.html
Disorders of Hair Follicles

Acne vulgaris

Acne rosacea

Folliculitis inflammation of the follicle.

Evolves to boils, cysts, cellulitis. Usually
staph aureus.

See the next few slides for summaries

Acne vulgaris

There is a danger zone on the face: drains

into the sinuses " bloodstream. Usually
not harmful

Open comedomes: blackheads sebum

is oxidized and turns black

Non-inflammatory

Follicular papules with black keratin plug

Closed comedomes: whiteheads

nflammatory

Trapped keratin plug " inflammation "

erythema, papules, nodules, pustules
Acne vulgaris
f you damage the follicle it has the tendency to be affected again (why squeezing
is bad)
Naturopathic Diet: Vitamin A very important (watch toxicity & pregnancy), topical
antimicrobials (tee tree oil), EFA's (anti-inflamm), Se (free radical scavenging)
Stress Decreases the immune system & digestive function
Summary:
Acne vulgaris is a common skin disorder
Chronic disease of sebaceous follicle, primarily affecting face, chest, and back
Onset typically occurs at puberty because of increased sebum production
triggered by increased androgen levels
nflammation is due in part to over-proliferation of Propionibacterium acnes, an
anaerobic Gram-positive organism that resides in follicles
Classified on basis of type of lesions (comedonal noninflammatory vs
inflammatory) and number of lesions present

Acne vulgaris
Androgens
Propionibacterium
acnes
Increased sebum
production
Keratin plug Iormation
Follicular obstruction
InIlammation
Closed comedome
Open comedome
FFA release
Hyperkeratinization oI
Iollicular canal

Acne Rosacea
Chronic facial skin disorder most commonly seen in individuals
between the ages of 30 and 60 years
More common in women than men, but often more severe in men
Features incIude erythema, teIangiectasia, papuIes, pustuIes, ocuIar Iesions
(conjunctivitis), and edema of midfaciaI skin
Frequently causes significant psychologic distress
Disease is progressive, commonly with periods of exacerbation and remission
Originally termed 'acne rosacea' because of the similarity in appearance to acne vulgaris
Often associated with easy flushing and blushing
Eye involvement is common
Rhinophyma
Common causes
Cause is largely unknown
Theories suggest underlying vasomotor instability, or infestation with the skin mite
Demodex follicularum, but there is little evidence for either
Contributory or predisposing factors
Genetic predisposition: 40% of sufferers have a family member with the disease
n sensitive individuals: sun exposure, stress, hot and cold weather, alcohol, spicy foods,
exercise, wind, hot baths, hot drinks, skin care products, certain drugs
Topical or oral steroid treatment

Folliculitis
nflammation of a hair follicle caused by bacteriaI and viraI
infections, chemicaI irritation, or physicaI injury
Lesions generally consist of asymptomatic erythematous
perifoIicuIar papuIes or pustuIes, but may be painful or itchy
pustules surrounded by erythema with a centraI hair present
The scalp, face, legs (thighs), inguinal area, axilla, and trunk are
most often affected
May be superficial or deep in the hair follicle; if deep may cause
scarring
Usually asymptomatic, but may be itchy
PostinfIammatory hyper- or hypopigmentation may occur
around resoIving Iesions
Scarring may result from scratching
Bullous Diseases

Pemphigus vulgaris

Bullous pemphigoid
Pemphigus vulgaris
Autoimmune
gG to intercellular adhesion molecules
Desmosomes connect epithelial cells
FRAGLE blisters. Risk of infection
Middle age and older
nvolves mucosa and skin on scalp, face, axilla, groin, trunk and
points of pressure.
Lysis oI epithelial intercellular adhesions
Fragile !"#$%&%!%' blister
Rupture oI blisters
Erosions and crusting
Bullous Pemphigoid

Elderly

Autoimmune

IgG to basement membrane (hemidesmosomes

connect basement mem & basal cells). Basal cells lift
off dermis. More tesnse bullous less fragile

Occur on inner aspects of the thighs, flexor surfaces

of the forearms, axillae, groin, and lower abdomen
Destruction oI connection between dermis and epidermis
Tense !"&(#)*($+%' blister
Urticaria (hives)
Antigen sensitization (IgE)
Mast cell degranulation releases histamines
Dermal vascular hyperpermeability
Dermal edema and pruritis
Papules " Plaques (Wheals)
!
gE associated with allergic reactions (hypersensitivity)
!
Mast cells (high # near small blood vessels in skin) contain histamines creates
itchiness
!
Spongiosis (WHEAL) is primary lesion
Urticaria
Urticaria is due to IocaIized capiIIary vasodiIatation, foIIowed by extravasation
of protein-rich fIuid into the surrounding tissues
t is characterized by the appearance of a transient, migratory pruritic rash with
raised, round, oval, or serpiginous patches that bIanch on pressure (wheals)
Lesions often have a pale center and are surrounded by an area of erythema
Lesions may vary in diameter from a few millimeters to the size of a hand or more
and may be confluent
Most common on trunk and limbs, but may affect any epidermal or mucosal surface
May be most prominent in areas of chafing (e.g. waistband or bra strap area)
Angioedema is due to the same process occurring at deeper levels. t presents as a
poorly-defined swelling that may be painful rather than pruritic and often occurs on
the face
GUT
FOOD
STRESS
TCM " wind-heat; wind-damp; ST/S-heat
nflammatory Conditions

Dermatitis (eczema)

Psoriasis

Pityriasis rosea

Lichen Planus
Eczematous Dermatitis atopic eczema
Allergic contact
Atopic
Drug-related
Photoeczematous
Primary irritant (immediate)
Antigen stimulation
InIlammatory inIiltrate into
dermis and epidermis
Fluid separates keratinocytes
Dermal edema and vesicle Iormation
Hyperkeratosis and acanthosis
Possible licheniIication and excoriation
Atopic is gE related priming immune system (hygiene hypothesis). Cascades and
dehydrates. Associated with allergies, Middle ear infections, asthma
Atopic dermatitis is an inflammatory skin
disorder
Characterized by erythema, edema,
intense pruritus, exudation, crusting,
xerosis, and lichenification
Many patients have a family history of
allergy or a personal history of asthma, hay
fever, or allergic rhinitis
This is the first of the allergic diathesis to
present. The child with atopic dermatitis
may go on to develop allergic asthma and
allergic rhinitis
Atopic Dermatitis

Viewed as a hypersensitivity reaction

Skin tends to be dry, hyperkeratotic and easily

lichenified

Risk factors:

Not breastfed

Urban environment

Hygiene

Diet

Poor digestive health

Histamine release*

"Emotional tension
Stratum cornium dead top layer
Granulosum is next if thin, you expose dermis more
readily = PNPONT bleeding = Auspitz sign
Higher than squamas cell carcinoma! (except no
mutations, no dysplasia/anaplasia)
Psoriasis

Multifactorial
T-cell inIiltrate into epidermis
Secretion oI cytokines and growth Iactors
,-.$(%!(*/0($%1)-2.31(/
$(#').%1)2-
Acanthosis and
extensive hyperkeratosis
Thinned stratum granulosum
'Auspitz sign
intrinsic (genetics) and
extrinsic (environment) factors
associated with it
*SiIvery scaIes on extensor surfaces. PIaques of dead skin ceIIs
Psoriasis

What stimulates the

T-cells????
ALWAYS ASK WHY!!! find etiology!
Autoimmune condition some sort of Ag attracting T-cells
Associated with gut conditions and chrone's when reacting to one part of the body
they may also react to other parts of the body
Pathogenic bacteria in the gut tend to break down proteins and produce toxic by-
products
These toxic metabolites may leave, go into bloodstream and NC cyclic GMP
CycIic GMP (seIf proIiferation) to AMP (maturation and proIiferaction decrease)
ratio increases = increased proIiferation (may want to down reg cycIic GMP)
Also people with psoriasis have decrease in vitamin D sunlight helps with tx

Pityriasis Rosea
nitial lesion is "herald patch, which is pink-salmon coloured patch/plaque with slightly
raised margin (on trunk, neck, proximal extremeties)
Cause unknown, resolves spontaneously in 6-8 weeks
Eruptions last hours/days/weeks of oval
annular lesions
Up to 100 lesions, 4-5 mm in diameter
Symmetrical lesions
Puritis occasionally
Symptoms mimicking viral infection

Lichen Planus
"Pruritic, purpIe, poIygonaI papuIes"
resolves spontaneously 1 to 2 years after onset, often
Ieaving zones of postinfIammatory hyperpigmentation
Oral lesions may persist for years. Malignant degeneration
has been noted to occur in chronic mucosal and paramucosal
lesions
Cutaneous Iesions consist of itchy, vioIaceous, fIat-
topped papuIes that may coalesce focally to form plaques.
These papules are often highlighted by white dots or lines
called Wickham striae, representing the clinical correlates of
zones of hypergranulosis that typify lesions histologically.
Multiple lesions are characteristic and are symmetrically
distributed, particularly on the extremities, often about the
wrists and eIbows, and on the gIans penis
n 70% of cases, oral lesions are present as white,
reticulated, or netlike areas involving the mucosa
t is plausible that lesions are caused by cell-mediated
immune reactions secondary to release of antigens at the
levels of the basal cell layer and the dermoepidermal junction.
characterized histologically by a dense, continuous infiltrate
of lymphocytes along the dermoepidermaI junction
nflammatory Reactions
Drug eruptions adverse reactions (Common). Hypersensitivity. Unintended
response to meds
Erythema multiforme hypersensitivity rxn
Many forms can be pustuIar, macuIar, buIIous
Tends to have characteristic "target Iesions"
Target lesions caused by the centrifugal spread of red
maculopapules with a purpuric, vesicular, or papular
center
Symmetric lesions
1-3cm in diameter
MainIy on hands, feet, and extensor surface of
forearms and Iegs
n severe form, can be on the trunk, in the oral cavity,
nasopharynx, conjunctiva, and urethra
Urticarial papules, vesicles, and bullae in severe disease
ndividual lesions heal without scarring in 1-2 weeks
Due to CD8 cytotoxic T ceIIs reacting with antigens
near basaI ceII Iayer of skin or mucosa
Erythema nodosum (next slide)

Erythema nodosum
Acute tender, erythematous, nodular skin
eruptions
Fever, arthralgia, and maIaise usually
precede the tender nodules
Nodules erupt without ulceration normally on
anterior aspects of Iegs
Other sites include the backs of legs, thighs,
neck, face, and forearms
Usually between five and 10 nodules, each up
to 4 inches (101.6mm) in diameter
Nodules may become fluctuant, but they
never suppurate
SIow regression over severaI weeks to
resembIe contusions
The nodules usually disappear within 6
weeks, but they may recur
Signs of the underlying disease may be
present, e.g. respiratory or gastrointestinal
illness

inflammatory reaction in the

subcutaneous fat
Pigmentary Conditions

Vitiligo autoimmune melanocytes destroyed by the body in epidermis. Common

disorder characterized by partiaI or compIete Ioss of pigment-producing meIanocytes
within the epidermis
Can be developed at the site of trauma (koebnerization). Asymptomatic, flat, well-demarcated macules
and patches of pigment loss; their size varies from few to many centimeters. VitiIigo often invoIves
the hands and wrists; axillae; and perioral, periorbital, and anogenital skin
Albinisim is different enzyme missing in melanocyte (all over the body) melanocytes present but not
working = NO MELANN
Associated with other autoimmune conitions
More frequent in darker individuals. May show up in lighter individuals after tanning

Lentigo one long flat line along basement membrane. Melanocytes proliferate move
along this membrane. Forms macule. The essential histologic feature of the lentigo is Iinear
(non-nested) meIanocytic hyperpIasia (hyperplasia restricted to the cell layer immediately
above the basement membrane) that produces a hyperpigmented basaI ceII Iayer***
benign localized hyperplasia of melanocytes occurring at all ages but often in infancy and childhood
Unlike freckles, lentigines do not darken when they are exposed to sunlight
Associated with age solar lentigo (due to skin damage) this is lentigo in older individuals after
prolonged sun exposure
Different than freckles due to increased proliferation of melanocytes
small (5 to 10 mm across), oval, tan-brown patches (macule)

Melasma look up (next slide)

Moles and freckles are different. Moles increase in prolif of melanocyte.
Freckle increase melanin

Melasma
Melasma produces dark brown patches
of pigmentation on sun-exposed areas,
usually the face.
Melasma tends to appear during pregnancy (mask of pregnancy) and in women who take oral
contraceptives, although it can occur in anyone. The disorder is most common in sunny
climates and in people of Latin or Asian origin.
poorly defined, blotchy, tan-brown macules and patches involving the
cheeks, temples, and forehead bilaterally. Sometimes people have the patches only
on the sides of the face. Rarely, melasma appears on the forearms.
The patches do not itch or hurt and are only of cosmetic significance.
Melasma usually fades after pregnancy or when an oral contraceptive is discontinued. People
with melasma can use sunscreens on the dark patches and avoid sun exposure to prevent the
condition from getting worse. Skin-bleaching creams containing hydroquinone and retinoic acid
can help lighten the dark patches.
The pathogenesis of meIasma appears to reIate to functionaI aIterations in meIanocytes
resuIting in enhanced pigment transfer to basaI keratinocytes or to dermaI macrophages
Benign and Premalignant
Lesions
Common usually not clinically relevant but psychological. Confused with malignancies.

Seborrheic Keratosis

Keratoacanthoma

Verrucae wart!

Melanocytic Nevi

Actinic Keratosis
Seborrheic Keratosis
Middle-age to older
Spontaneous; trunk
Exophytic neoplasm (exophytic = goes outward large and dark)
Proliferation of basal cells
Hyperkeratosis " keratin-filled cysts and invaginations may extend down into
the dermis
Large and unsightly
Sometimes in people who have a neoplasma somewhere else in the body.
Screen for cancer elsewhere
Lesions may give the impression that they are "stuck on" and may be
easily peeled off. nspection with a hand lens will usually reveal small,
round, porelike ostia impacted with keratin, a feature helpful in
differentiating these pigmented lesions from melanomas.
round, flat, coinlike, waxy plaques that vary in diameter from millimeters to
several centimeters
uniformly tan to dark brown and usually show a velvety to granular surface

Keratoacanthoma
a rapidly developing neoplasm that clinically and histologically may mimic weII-differentiated
squamous ceII carcinoma. Often it will heal spontaneously, without treatment! Men are more
often affected than women, and lesions most frequently affect sun-exposed skin of whites
older than age 50 years
Originate in piIosebacious gIands
flesh-colored, dome-shaped noduIes with a central, keratin-fiIIed pIug, imparting a crater-
like topography
predilection for facial skin, including the cheeks, nose, and ears, and the dorsa of the hands
(sunIight exposed areas)
There is growing belief that keratoacanthomas may represent a form of squamous cell
carcinoma that regresses as a consequence of interactions with host tissues that fail to
support inexorable growth
Like most squamous cell carcinomas, the majority of keratoacanthomas have mutations in the
p53 gene
PathophysioIogy: Both sunlight and chemical carcinogens have been implicated as
pathologic factors in growth of the tumor. Trauma, human papilloma virus, genetic factors,
and immunocompromised status also have been implicated as etiologic factors.

Verrucae
caused by human papiIIomaviruses (60 types) epitheIiaI tumors
HPV 16 linked to cancer
May be single or multiple. May be malignant. Exist in outer epithelium, not deep enough to
serve as antigens.
Many types. Verruca vulgaris is the most common and is characterized by gray-white to
tan, flat to convex, 0.1- to 1-cm papules with a rough, pebble-like surface
Transmission of disease usually involves direct contact between individuals or
autoinoculation.
Verrucae are generally seIf-Iimited, regressing spontaneously within 6 months to 2 years
Histologic features common to verrucae include epidermaI hyperpIasia that is often
undulant (wave-like) in character (so-called verrucous or papillomatous epidermal
hyperplasia) and cytoplasmic vacuolization (koilocytosis) that preferentially involves the
more superficial epidermal layers, producing halos of pallor surrounding infected nuclei.
Melanocytic Nevi = MOLES

Benign melanocytic neoplasm

Congenital

Blue

Spitz

Halo

Dysplastic
Aggregation oI melanocytes
at dermoepidermal junction
Growth into
dermis
Elevation above
epidermis
'Maturation
All similar in that there is an aggregation of melanocytes different shapes/configurations. t is
CONTROLLED growth just hyperplastic
Some people have sporatic nevi or Familial nevi (this group is more predisposed to dysplasia).
ncreased vulnerability to UV (both types)
Distinguises between
malignancy.
Hair = functional (mature) cells

Melanocytic Nevi
tan to brown, uniformly pigmented, small (usually <6 mm across),
solid regions of relatively flat (macules) to elevated skin (papules)
with well-defined, rounded borders
Melanocytic nevi are initially formed by melanocytes that have been
transformed from highly dendritic single cells normally interspersed
among basal keratinocytes to round cells that grow in aggregates,
or "nests," along the dermoepidermal junction
Progressive growth of nevus cells from the dermoepidermal junction
into the underlying dermis is accompanied by a process termed
maturation. Whereas less mature, more superficial nevus cells are
larger, tend to produce melanin, and grow in nests, more mature,
deeper nevus cells are smaller, produce little or no pigment, and
grow in cords.
This sequence of maturation of individuaI nevus ceIIs is of
diagnostic importance in distinguishing some benign nevi from
meIanomas, which usuaIIy show IittIe or no maturation.
Actinic Keratosis
PremaIignant dyspIasia - excessive sun exposure. Actinic = solar
usually less than 1 cm in diameter; are tan-brown, red, or skin-colored; and have a rough,
sandpaper-like consistency. lesions may produce so much keratin that a "cutaneous horn"
develops
Generally referred.
NucIei of keratinocytes retained (abnormaI)
Excessive sun exposure
Basal cell hyperplasia Fibroblast damage
(dermal layer)
Parakeratosis
(abnormal Iormation oI horn cells,
Persistance oI nuclei, incomplete Iormation oI
keratin observed as scaling)
Atypia and dyskeratosis
Abnormal
Iiber synthesis
Thickened dermis
Thickened
stratum corneum
(keratin layer oI the skin)

Actinic Keratosis
Leukoplakia

"White plaque
Atypia of squamous cells, hyperkeratosis

WHO definition: a white patch or plaque that cannot

be scraped off and cannot be characterized clinically
or pathologically as any other disease
Considered precancerous until proven otherwise
Risks " men 40-70yoa; tobacco use
Malignant Lesions
Skin is a common place for cancers. t's what we face the world with. 1
st
and
foremost interaction!

Squamous cell carcinoma

Basal cell carcinoma

Malignant melanoma

Kaposi's sarcoma
Squamous Cell Carcinoma
GeneraIIy smaII and removabIe; Iow invasive potentiaI
Dysplasia/anaplasia
Lack of control irregular relplication
Lack of differentiation of cells
Grows quickly. Asymmetrical.
Caused by: sun, industrial chemicals, old scars and trauma, tobacco (in the mouth)
COMPARE THIS WITH BASAL CARCINOMA - ceIIs, where??
In situ (in one place contained) carcinoma
In epidermal layer and not invading dermis
Hyperkeratosis and ulceration
Invasion through basement membrane

Squamous ceII carcinoma
The age-adjusted incidence among Caucasians is 1-1.5/1000 per year in the US
Clinical presentation varies from scaIy erythematous pIaques or cutaneous horn to
crusted uIcerated Iesions
Unlike basal cell carcinomas, squamous cell carcinomas are associated with a substantial
risk of metastasis
Second most common type of skin cancer
Chronic sun exposure is the strongest environmental risk factor
Precancerous lesions associated with sun damage are strong risk factors
Histology shows full-thickness pleomorphic, atypicaI keratinocytes in the epidermis.
nvasive squamous cell carcinomas also show dermal invasion
BasaI ceII carcinoma
Most common malignant skin tumor arising from the basaI ceIIs of the epidermis
There are four main subtypes: nodular, superficial, pigmented, and aggressive growth type
(morpheaform, infiltrative, or sclerosing)
These subtypes vary with respect to macroscopic appearance (and thus presentation),
histology, and biologic aggressiveness
Most common presentation is the noduIar type, with a papuIe that has a pearIy, shiny
border, and surface teIangiectasia. The Iesion may uIcerate in the center, thus causing
the characteristic bleeding and scabbing lesion that heals and recurs
Morpheaform basal cell carcinoma is the most biologically aggressive
They rareIy metastasize: their malignant potential lies in their ability to invade and destroy
local tissues, such as bone and brain
Main causative factor is accumulative exposure to sunlight
85% occur on the face and neck, as these areas are most exposed to the sun
Treatment depends on the site and size of the tumor, tumor margins, and histology

Malignant Melanoma
Malignant Melanoma
SUN!
Prevalence is increasing
Nevi are predisposing. most important clinical sign of the disease is change in
color, size, or shape in a pigmented lesion. Usually greater than 10mm
variations in pigmentation, appearing in shades of black, brown, red, dark
blue, and gray
clinical warning signs of melanoma are (1) enlargement of a pre-existing
mole, (2) itching or pain in a pre-existing mole, (3) development of a new
pigmented lesion during adult life, (4) irregularity of the borders of a pigmented
lesion, and (5) variegation of color within a pigmented lesion.
Radial growth (horizontal) " vertical growth (into deeper layers) no
maturation " metastasis (increases with vertical growth due to blood vessels
and movement throughout the body)
The nature and extent of the verticaI growth phase determine the
bioIogic behavior of maIignant meIanoma
ncreased mitoses

Kaposi's Sarcoma

Cancer that causes multiple flat, pink, brown or purple

patches or bumps on the skin

three stages can be identified: patch, plaque, and nodule

Caused by human herpes virus (HHV) type 8

Occurs in several distinct groups of pepople, acts

differently in each group
Older men
Mediterranean Jewish
People with ADS
mmunosuppressants after transplants
Childern and young men from Africa
Vasculitis

Manifest on skin. Covered in CV system (inflammation of

blood vessels)

Not tested here familiarize yourself

Hemangioma

Spider angioma

Telangiectasis

Cherry angioma
nfectious Conditions

Viruses needs a host & machinery

Herpes Zoster / Pox
Acute infection with VZV (varicella zostar virus) causes chickenpox; reactivation of latent VZV causes
shingles
VZV infects neurons and/or satellite cells around neurons in the dorsal root ganglia and may
recur many years after the primary infection, causing shingles
vesicular lesions, pruritis and PAN in shingles
Painful, unilateral dermatomal erupation, common in thoracic region
Human Papillomae (verrucae) warts (epidermal hyperplasia). Manifests differently
HPV Type 16 and 18 best known and mostly studied
nvolved in cervical dysplasia
So associated that HPV should be tested in pap smear!
Looking at vaccinating all girls for this

Bacteria
mpetigo, folliculitis, boils, cellulitis

Fungi
Ringworm (tinea), Candidiasis yeast affects mucous membranes (ubuqitous, seen in HV,
diaper rash likes warm, moist environment), tinea versicolour due to a yeast, manifests differently
Confined to stratum corneum
Dermatophyte all "tinea (fingi that are skin loving defined by where it occurs on
the body)
Bacteria gets in and infects the area leads to inflammation
Name based on area (e.g. capitis, pedis)
Herpes Simplex
80% have it! Manifest differently
Viral infection of epithelium " inflammatory reaction of the
epithelium (vesicles on an erythematous (inflammation - hyperemia)
base) " dormancy in a nerve ganglion (moves to spine and can be
transmitted by touch) f activated they are transmissible.
Herpes 1 AND 2 can be transferred

Aggravating factors: stress, sunlight, temperature changes, acidic

foods, illness, lack of sleep, menses
Lysine controIs the infection, Arginine increases infection (used in naturopathic
tx high lysine and low arg foods)
Oregano antiviral
Treat the predisposition!
Herpes Simplex

30-100% carrier rate; 20-40% recurrence

rate

WHY THE DISCREPANCY?

Dormancy

IndividuaI susceptibiIity (cancer, HIV

positive)

Decreased immunitiy
mpetigo superficial bacterial inflammation of the skin

Organism: staph aur.

Transmission: pus is
infectious. Contains the bacteria,
neutrophils and dead cells.
Neutrophilic inIiltrate
Pustule Iormation goes to epidermis here
4"#($5).)%' dermal inIlammation
Rupture oI pustules
Wet erosions
'Honey-coloured crust
Boils & folliculitis affect hair follicle.
mpetigo is the actual epidermis
Homeopathic remedy: graphities
strongly associated with impetigo