EMBRYOLOGY: Skin begins to form in the first 20-30 days of embryonic life.  By 60 days skin formed.  Fetal growth and differentiation continues until birth

·       Epidermis: developed from the ectoderm.

·       Dermis:  developed from somitic dermatomes & somatopleuric layer of  the lateral plate mesoderm


·       The epidermis makes up the epithelium, and the dermis below is the connective tissue layer.

·       The dermis is separated from the epidermis by a connective tissue, the basal lamina.  The dermis is then further broken down into:

         o   Papillary layer:   composed of loose connective tissue and small capillaries. that supply blood to and carry waste away from the epidermis.

         o   Reticular layer:  more dense, irregular connective tissue

·       Layers of the epidermis in order from most deep to superficial:  B-before S-signing G-get L-legal C-counsel = STRATUM BSGLC -->

B-basale (aka stratum germinativum) - it sits directly on top of the basal lamina. Contains stem cells of keratinocytes, which divide and push the new cells up into the stratum spinosum.
S-spinosum- keratinocytes are maturing in this layer, though they still retain their mitotic ability. Desmososmes hold the cells together here.
G-granulosum- these cells accumulate (in their cytoplasm) membrane limited granules, or keratohyaline granules, that stain basophilically, giving the layer its bluish tinge.
L-lucidum- only found in thick skin.
C-corneum- by now, the cells have extruded their nuclei and most of their organelles.  Their cytoplasm packed full of keratin bundles. About a couple weeks after their division in the basale layer, keratinocytes are sloughed off

·       Layers of the epidermis in order from most deep to superficial:  B-before S-signing G-get L-legal C-counsel = STRATUM BSGLC -->

B _______________, _______________, _______________, _______________, _______________
S _______________, _______________, _______________, _______________, _______________
G _______________, _______________, _______________, _______________, _______________
L _______________, _______________, _______________, _______________, _______________
C _______________, _______________, _______________, _______________, _______________

·       4 cells in the epidermis: KLM (in alphabetical order) -->

K eratinocytes:  80-85% of all cells. These cells accumulate keratin and undergo apoptosis at the same time. They provide a cornified layer that protects from abrasion. The cells also accumulate a protein complex on the inside of the cell membrane, and a lipid coating along the outside of the membrane so that water can’t get into or out of the cell. Thus if the epidermis layer is destroyed (burn victims), the patient can no longer maintain his fluids and becomes severely dehydrated. Keratinocytes also have the ability to produce vitamin D.

L angerhans cells- Antigen presenting dendritic cells found in the s. spinosum. Important in contact dermatitis.

M elanocytes- Derive from neural crest and migrate into the epidermis. Their cell body are in the s. basale, with dendritic extensions that each makes contact with 30-100 keratinocytes in the s. spinosum. Melanocytes produce melanin (in response to UV radiation) and secrete it in vesicles, or melanosomes, into the extracellular matrix (cytocrine secretion). Keratinocytes then take up the melanin via phagocytosis. It is not the number of melanocytes in the epidermis that determines how dark ones skin is; it’s the half-life of melanin. Melanin in light-skinned individuals has a shorter half-life.
Ø  Tyrosinase converts: tyrosine --> DOPA --> melanin.

M erkel cells- mechanoreceptors in s. basale. Mostly found in palms and soles.  Unmyelinated nerve fibers.
4 cells in the epidermis: KLM (in alphagetical order) -->
Ø  K _______________, _______________, _______________, _______________, _______________

Ø  L _______________, _______________, _______________, _______________, _______________

Ø  M _______________, _______________, _______________, _______________, _______________

·       Appendages of the Skin:  1) Hair follicles (each hair follicle has an associated sebaceous gland) 2) Glands

GlandsSEA --> S-sebaceous gland (release sebum into the hair follicle), E-eccrine gland (typical sweat gland, cover most of the body), A-apocrine gland (in axilla, pubic region, mammary glands)
Ø  S _______________, _______________, _______________, _______________, _______________

Ø  E _______________, _______________, _______________, _______________, _______________

Ø  A _______________, _______________, _______________, _______________, _______________


·       Microscopic descriptions of skin anomaliesV-SHAPE -->

o   V-vacuolization:   Formation of vacuoles within or adjacent to cells. Usually occurs at the DE (dermoepidermal) junction.  It is indicative of an Ag-Ab reaction.  (Example à SLE).

o   S-spongiosis: Intercellular edema of the epidermis --> squamous epithelium keratinocytes are separated by a lot of clear space (edema).  This finding is not very specific & is usually due to an inflammatory process.

o   H-hyperkeratosis: ↑ thickness of the stratum corneum (the acellular part); frequently associated with acanthosis.

o   A-acanthosis: epidermal hyperplasia as a result of a fundamental reaction to many different insults. A cantholysis: loss of intracellular connections & discohesion; can be indicative of fairly serious conditions. Acanthocyte = another term for a squamous epithelial cell

o   P-parakeratosis: persistence of the nucleus in the keratinized squamous cells of the stratum corneum. Cells at the surface of the epithelium should be anucleate. This can be due to a process causing rapid proliferation/metabolic turn-over of the squamous cells (Example --> psoriasis).

o   E-exocytosis:  infiltration of the epidermis by leukocytes.

o   Microscopic descriptions of skin anomalies:  V-SHAPE

Ø  V _______________, _______________, _______________, _______________, _______________

Ø  S  _______________, _______________, _______________, _______________, _______________

Ø  H  _______________, _______________, _______________, _______________, _______________

Ø  A _______________, _______________, _______________, _______________, _______________

Ø  P  _______________, _______________, _______________, _______________, _______________

Ø  E  _______________, _______________, _______________, _______________, _______________



Hyperkeratosis - hyperplasia of the stratum corneum




·       Macroscopic descriptions of skin anomalies:

o  Macule/Patch: flat area of coloration </> 0.5 cm.

o   Papule/Plaque: elevated solid area </>0.5 cm

o   Nodule: solid area, deeper than papule, ≥ 0.5 cm

o   Wheal (aka hive): itchy, transiently elevated area with variable blanching & erythema. Appears rapidly.

o   Vesicle/ Bulla: Fluid-filled raised area </> 0.5cm

Pustule: Discrete, pus-filled raised area,_fissures,_and_erosions.svg

PHYSIOLOGY: Skin dual function in thermoregulation and protective barrier

•       Thermoregulation:  The generalized eccrine sweating is the physiologic response to ↑ body temperature.  It is the most effective means by which humans regulate temperature through evaporative heat loss.  2-4 million eccrine sweat glands on the body

•       Protective barrier:  1) Skins protects against H2O loss by lipids in the stratum corneum 2) Stratum corneum impedes absorption of toxic substances & invasion by micro-organisms (dried, cracked skin = problem) 4) Skin protects against UV radiation via protein barrier, stratum corneum & melanin dispersed thru-out the epidermis 5) Skin protects against mechanical damage via stratum corneum & dermis/subq fat

HYPERSENSITIVITY REACTION:  undesirable (damaging, discomfort-producing and sometimes fatal) reactions produced by the normal immune system. Require a pre-sensitized (immune) state of the host. The four-group classification was expounded by P. H. G. Gell and Robin Coombs in 1968.

•       ACID --> Anaphylactic (WHAT), Cytotoxic (BIGGER), Immune complex (RAGS), Delayed type (TC= T-cells).

Anaphylactic:  Ag cross-links IgE on sensitized mast cells & basophils --> release vasoactive amines (e.g. histamine).  Reaction develops rapidly after Ag exposure due to preformed Ab.  Examples:  WHAt --> Wheal & flare, Hive (urticaria), Allergy, Asthma, Anaphylactic, Angioedema
Ø  W  _______________, _______________, _______________, _______________, _______________

Ø  H _______________, _______________, _______________, _______________, _______________

Ø  A  _______________, _______________, _______________, _______________, _______________

Ø  T  _______________, _______________, _______________, _______________, _______________


Cytotoxic: IgM or IgG bind Ag on foreign cell --> lysis by complement (MAC-membrane attack complex) or phagocytosis.  Examples:  BIGGER --> Bullous pemphigoid, Immune hemolytic anemia, Goodpasture’s syndrome, Grave’s disease, Erythema multiforme, Rh disease, Rheumatic fever.
Ø  B  _______________, _______________, _______________, _______________, _______________

Ø  I  _______________, _______________, _______________, _______________, _______________

Ø  G _______________, _______________, _______________, _______________, _______________

Ø  G  _______________, _______________, _______________, _______________, _______________

Ø  E  _______________, _______________, _______________, _______________, _______________

Ø  R  _______________, _______________, _______________, _______________, _______________

Graves' Disease, proptosis and lid retraction

Erythema multiforme minor (note of make of the blanching centers of the lesion)

Rheumatic heart disease at autopsy with characteristic findings (thickened mitral valve, thickened chordae tendineae, hypertrophied left ventricular myocardium),_gross_pathology_20G0013_lores.jpg

Immune complex:  Ag-Ab complexes deposit in tissue --> attract neutrophils --> release lysosomal enzymes.  Examples: RAGS -->R-rheumatoid arthritis, A-arthus reaction (intradermal injection of Ag induces Ab --> Ag-Ab complexes in the skin --> NEC --> NECrosis, Edema, Complement activation; e.g. hypersensitivity pneumonitis & thermophilic actinomycetes, vaccination) , ADCC, G-glomerunephritis (PSGN), SLE, Serum sickness (most now caused by drugs and not serum; Abs to foreign proteins are produced --> form immune complexes --> deposited in membranes --> fix complement --> U FLAP = Urticaria, Fever, LAD, Arthralgias, Proteinuria 5-10 days after exposure)
Ø  R _______________, _______________, _______________, _______________, _______________

Ø  A  _______________, _______________, _______________, _______________, _______________

Ø  G  _______________, _______________, _______________, _______________, _______________

Ø  S  _______________, _______________, _______________, _______________, _______________

severe arthritis in hand which was not treated

Young woman with the typical "butterfly rash" found in lupus

D elayed type:  Sensitized T lymphocytes encounter Ag --> release lymphokines --> MØ activation.  Examples: TC (T-Cells are the players) --> T-tuberculin test, T-transplantation reaction, T-tumor-cell lysis, T-termporal arteritis, C-contact dermatitis, C-celiac disease.
Ø  T _______________, _______________, _______________, _______________, _______________

Ø  C  _______________, _______________, _______________, _______________, _______________

TB (Mantoux) test:  The size of induration is measured 48–72 hours later. Erythema (redness) should not be measured.

3-year-old girl with contact dermatitis, one day after contact with poison ivy

Dermatitis herpetiformis characteristic rash associated with celiac disease

GIVE CARD --> G-granulomatous diseases, G-genodermatoses (inherited Genetic skin conditions grouped into three categories: chromosomal, single gene, and polygeneAc.)• I-infections, I-infestations• V-vasculitis & other purpuric diseases, V-vesicular & pustular diseases (intraepidermal vs. subepidermal) • E-Eczematous & papulosquamous diseases • C-Connective tissue alterations • A-adnexal inflammatory diseases

G-granulomatous disease (non-infectious):  Granuloma annulare, necrobiosis lipoidica, rheumatoid nodule, sarcoidosis, xanthoma

Granuloma annulare:  Common idiopathic non-scaly annular plaques and erythematous papules. 

Ø  EPIDEMIOLOGY: Most common on hands, feet, elbows, mostly children and young adults, spontaneously resolve in several years

Ø  PATHOPHYSIOLOGY: Usually seen in otherwise healthy people. Occasionally, it may be associated with diabetes or thyroid disease, and auto-immune diseases (systemic lupus erythematosus, rheumatoid arthritis, and Addison's disease.

Ø  PRESENTATION:  Ring of small, firm bumps (papules) over the backs of the forearms, hands or feet, often centered on joints or knuckles. These papules enlarge and spread over time. New lesions continue to develop at the edges of the aging rings.

Ø  DIAGNOSTIC EVALUATION: History and physical Biospy/Histology: Palisaded granuloma with dermal epithelioid histiocytes surrounding a central zone of mucin and necrotic collagen.

Ø  DIFFERENTIAL DIAGNOSIS: Necrobiosis lipoidica, rheumatoid nodule, other granulomatous lesions.

Ø  TREATMENT: Steroids:  Initially topical steroid creams, followed by oral steroids and finally intradermal injections at the site of each ring.  

Ø  PROGNOSIS:  Most lesions of granuloma annulare disappear in pre-pubertal patients within two years even with no treatment, while older patients (50+) may have persistent disease. Recurrent of disease with formation of new rings years later is not uncommon.

Granuloma Annulare on hand

Palisaded granuloma in a case of granuloma annulare

Necrobiosis lipoidica:

Ø  EPIDEMIOLOGY: Usually occurs in patients with diabetes mellitus (0.3% of the diabetic population) but can also be associated with rheumatoid arthritis.  F:M ratio 3:1.  It is mostly found in younger patient with insulin-dependent diabetes, but is not directly correlated to the severity or control of diabetes.

Ø  PRESENTATION:  Occurs most commonly on the shins with early lesions appearring as red plaques, while older lesion are atrophic, yellow-brown. 

Ø  DIAGNOSTIC EVALUATION:  Skin biopsy:  Epidermis is normal or atrophic with underlying superficial and deep dermal perivascular and interstitial mixed inflammatory cell infiltrate (including lymphocytes, plasma cells, mononucleated and multinucleated histiocytes, and eosinophils).  There is dermal horizontal necrobiotic collagen, often with sclerosis, with palisading granulomas that often oriented parallel to the epidermis. Areas of necrobiosis are often more extensive and less well defined than in granuloma annulare.

Ø  TREATMENT:  No clearly defined treatment; PUVA therapy and improved diabetes control may help.  Low dose aspirin and steroid cream or injection into the affected area may be effective for only a small percentage of those treated.

Necrobiosis lipoidica lesion on leg of diabetic patient

By Warfieldian - Own work, CC BY-SA 3.0,

Necrobiosis lipoidica in a punch biopsy.By Nephron - Own work, CC BY-SA 3.0,

Rheumatoid nodule:  Characteristic palisading granuloma with a core consisting of necrotic collagen and fibrin.

By Nephron - Own work, CC BY-SA 3.0,

Rheumatoid nodule:

Ø  EPIDEMIOLOGY:  Occurs almost exclusively in association with rheumatoid arthritis, where the cumulative prevalence is about 25%, and also in 5% of patients with lupus erythematosus.  In the absence of autoimmune disease, they are called pseudorheumatoid nodules.

Ø  PRESENTATION: Firm lump or local swelling particularly  over bony prominences such as the olecranon or the interphalangeal joints. Less commonly they occur in the pleura and other internal organs. The occurrence of nodules in the lung of miners exposed to silica dust was known as Caplan's syndrome. In most cases, the nodules are not painful or disabling.

Ø  DIAGNOSTIC EVALUATION:  Biopsy:  Nodules in the deep dermis or subcutaneous tissue consisting of central degenerated connective tissue (necrobiosis) surrounded by palisading granuloma with radially arranged densely packed layer of histiocytes, lymphocytes, fibroblasts, and few mutinucleated giant cells.

Ø  TREATMENT: Surgical excision, but tend to recur.  May regress with anti-rheumatoid medications (e.g. rituximab).

Sarcoidosis:  An uncommon, multisystemic disease, most commonl involving the lung (fibrosis, hilar adenopathy) and eye (uveitis). 

Ø  PATHOPHYSIOLOGY: Unknown etiology and although is thought not to be infectious, some studies have demonstrated mycobacterial DNA in the lesions, while others have found foreign material in the lesions.

Ø  PRESENTATION: Skin lesions are highly variable (a great mimicker), including papules, nodules, annular plaques, and ulcers.  Lupus pernio refers to nose, cheek, and ear plaques resembling perniosis. 

Ø  DIAGNOSTIC EVALUATION:  SPEP: polyclonal gammopathy.  CMP: hypercalcemia.  Elevated serum ACE levels.  Skin biopsy: usually normal epidermis (sometimes parakeratosis, hyperkeratosis, acanthosis) with dermal to subcutaneous noncaseating well-demarcated granulomas that are “naked” (having few surrounding lymphoid cells).  Multinucleated cells within granulomas may exhibit Schaumann bodies (round, blue, calcified, laminated inclusions) and/or asteroid bodies (stellate, eosinophilic inclusions).

By Nowack et al. - Nowack et al. BMC Dermatology 2002 2:15 doi:10.1186/1471-5945-2-15, CC BY-SA 2.0,

Asteroid body in sarcoidal granuloma

By Ed Uthman, MD -, CC BY-SA 2.0,

Xanthoma: Deposition of yellowish cholesterol-rich material that can appear in various disease states associated with hyperlipidemias, both primary and secondary types.

Ø  PRESENTATION:  Variations:  Xanthoma tuberosum:  Nodules located over joints of elbows, knees, buttocks, or fingers, which contain cholesterol esters.  Xanthoma tendinosum: Similar to tuberous xanthoma, fixed to tendon (Achilles, fingers), associated with hypercholesterolemia. Xanthelesma: Eyelids, assoicated with hypercholesterolemia. Xanthoma planum: Macules or plaques in axilla, groin, or palms, associated with cholesterolemia.  Normolipemic plane xanthoma: Widespread macules and patches around face or periocular associaged with paraproteinemia or myeloma, usually without hyperlipdemia.  Tuberoeruptive xanthoma: Multiple reddish-yellow papules of rapid onset over trunk or thighs, contain mostly triglycerides, more lymphocytes and neutrophils, and most likely to spontaneously regress.

Ø  DIAGNOSTIC EVALUATION:  Skin biopsy: Foamy histiocytes in the dermis admixed with lymphocytes or neutrophils in youger lesions and fibrosis or cholesterol clefts in older lesions.  Touton-type giant cells are also found at times. Stain: Oil-red-O-positive.

Ø  TREATMENT: Treat underlying conditions.

xanthoma tuberosum

By Min.neel - Own work, CC BY-SA 3.0,

Xanthoma showing lipid-laden foam cells with large areas of cholesterol clefts

CC BY 2.0,


Exanthem:  widespread rash, usually of viral origin, and usually occurring in children. It represents either a reaction to a toxin produced by the organism, damage to the skin by the organism or an immune response. Exanthems may also be due to a drug, most commonly antibiotics.

·      Viral exanthem:  MERCHAnt --> Measels (rubeola), Erythema infectiosum (Fifth disease by parvovirus), Exanthem subitum (roseola by HHV-6/7), Rubella, Chickenpox (VZV), Hand, foot, and mouth disease (coxsackie A16), Herpes zoster, Asymmetric periflexural exanthem of childhood

o   M  _______________, _______________, _______________, _______________, _______________

o   E  _______________, _______________, _______________, _______________, _______________

o   R _______________, _______________, _______________, _______________, ________________

o   C _______________, _______________, _______________, _______________, _______________

o   H  _______________, _______________, _______________, _______________, _______________

o   A  _______________, _______________, _______________, _______________, _______________

o   N _______________, _______________, _______________, _______________, ________________

o   T  _______________, _______________, _______________, _______________, _______________

M easels (aka rubeola):  caused by a paramyxovirus of the genus Morbillivirus.  Spread through respiration and is highly contagious—90% of people without immunity sharing a house with an infected person will catch it. Airborne precautions should be taken for all suspected cases.  The incubation period usually lasts for 4–12 days.  Infected people remain contagious from the appearance of the first symptoms until 3–5 days after the rash appears.

Ø  Evaluation:  fever (up to 105°F) for at least three days, and the 3 C’s --> Cough, Coryza, Conjunctivitis.  Koplik's spots seen inside the mouth are pathognomonic for measles but are not often seen, even in real cases of measles, because they are transient and may disappear within a day of arising.  The characteristic measles rash is classically described as a generalized, maculopapular, erythematous rash that begins several days after the fever starts. It starts on the head & spreads to cover most of the body, often causing itching. The rash is said to "stain", changing colour from red to dark brown, before disappearing.  Labs:  (+) measles IgM antibodies or isolation of measles virus RNA from respiratory specimens. 

Ø  Treatment:  There is no specific treatment or antiviral therapy for uncomplicated measles. Most patients with uncomplicated measles will recover with rest and supportive treatment.  Complication:  from relatively common and less serious diarrhea,  MEP --> Myocarditis, Encephalitis (subacute sclerosing panencephalitis), Eye damage, Pneumonia.  Complications are usually more severe amongst adults who catch the virus.

v 4 C’s --> Cough, Coryza, Conjunctivitis, Coplik’s spot

§  C  _______________, _______________, _______________, _______________, _______________

§  C  _______________, _______________, _______________, _______________, _______________

§  C _______________, _______________, _______________, _______________, ________________

§  C _______________, _______________, _______________, _______________, _______________

v Complications:  MEasel’ MEP (vs. Mumps MOP --> Meningitis, Orchiditis, Parotitis; they are together in the MMR vaccine) -> Myocarditis, Encephalitis, Eye damage, Pneumonia.

§  M  _______________, _______________, _______________, _______________, _______________

§  E  _______________, _______________, _______________, _______________, _______________

§  P _______________, _______________, _______________, _______________, ________________

Child shows a classic day-4 rash with measles

By CDC/NIP/Barbara Rice - <a rel="nofollow" class="external free" href=""></a> (ID#: 132), Public Domain,

“Koplik's spots” on the third pre-eruptive day

By CDC -, Public Domain,

o   Erythema infectiosum (aka Fifth disease):  Caused by parvovirus B19.  Occurs at anny age may be affected although it is most common in children aged 5-14 y/o. About half the adult population will have become immune following infection at some time in their past. Outbreaks can arise especially in nurseries and schools. 

Ø  Evaluation:  Children:  slapped cheecks (bright red cheeks) are a defining symptom;  red, lacy rash on the rest of the body, with the upper arms and legs being the most common locations. The rash can last a couple of weeks (some cases lasting for several months) and may itch. Patients are usually no longer infectious once the rash has appeared.  Teenagers & adults: may present with a self-limited arthritis.  The disease is usually mild, but in certain risk groups it can have serious consequences:

v Pregnant women:  infection in the first trimester has been linked to hydrops fetalis, causing spontaneous abortion

v Sickle-cell disease or other forms of chronic hemolytic anemia:  infection can precipitate an aplastic crisis


Child with Fifth Disease (aka Slapped face, Parvovirus B19)

By Andrew Kerr - Own work, Public Domain,

o   E xanthem subitum (aka roseola infantum, sixth disease):  Caused by HHV-6 & 7.   

Ø  Evaluation:  Mostly affects a child between 6 months-3 years of age.  Begins with a sudden high fever of 102-104 degrees Fahrenheit (39-40 degrees Celsius). This can cause, in some cases, febrile convulsions (also known as febrile seizures or "fever fits") due to the sudden rise in body temperature, but in many cases the child appears and acts normal. After a few days the fever subsides, and just as the child appears to be recovering, a red rash appears. This usually begins on the trunk, spreading to the limbs but usually not affecting the face. It disappears again in a matter of hours to a day or so.

Roseola on a 21-month-old girl

By M Davis - Own work, Public Domain,

o   R ubella (also known as epidemic roseola, German measles, liberty measles or three-day measles):  Caused by rubella virus.   It is often mild and an attack can pass unnoticed. However, this can make the virus difficult to diagnose. The virus usually enters the body through the nose or throat. The disease can last 1-5 days. Children recover more quickly than adults. Like most viruses living along the respiratory tract, it is passed from person to person by tiny droplets in the air that are breathed out.   If the mother is infected within the first 20 weeks of pregnancy, the child may be born with CRS (congenital rubella syndrome), which includes a range of birth defects.  CRS --> Cardiovascular defect (PDA, septal defect), Cataracts,  Cephaly-micro, Retardation-mental, Radiolucent bone, Sensorineural deafness. 

Ø  C  _______________, _______________, _______________, _______________, _______________

Ø  R  _______________, _______________, _______________, _______________, _______________

Ø  S _______________, _______________, _______________, _______________, ________________

Ø  Evaluation:  Low grade fever (rarely > 100.4), swollen glands (persist upt to 1 week), joint pain, headache, conjunctivitis.  Rash:  apppears as pink dots under the skin --> first on the face and then spreads to the trunk and limbs.  It appears on the first or third day of the illness but it disappears after a few days with no staining or peeling of the skin).  Forchheimer's sign (in 20% of cases): small, red papules on the area of the soft palate,  flaking, dry skin, nerves become weak or numb (very rare). 

Ø  Treatment:  Symptoms are usually treated with paracetamol until the disease has run its course. There is no treatment available for congenital rubella.  MMR vaccine:  given to children at 12-15 months. A second dose is required before age 11. The vaccine may give lifelong protection against rubella. A side-effect of the vaccine can be transient arthritis

Rash of rubella on skin of child's back. Distribution is similar to that of measles but the lesions are less intensely red.

By CDC - crop of File:Rash of rubella on skin of child's back.JPG, Public Domain,

Characteristic maculopapular rash of rubella

By CDC -, Public Domain,

Cataracts due to congenital rubella syndrome

By, Public Domain,

o   C hickenpox:  Caused by the VZV (aka HHV-3).  10-14 day incubation period. Primary infection there --> lifelong protective immunity. Chickenpox is rarely fatal (usually from varicella pneumonia, but also meningoencephalitis and hepatitis), with pregnant women and those with a suppressed immune systems being more at risk. This is less of an issue after 20 weeks.  Later in life, viruses remaining dormant in the nerves can reactivate causing localised eruptions of shingles. This occurs particularly in people with compromised immune systems, such as the elderly, and perhaps even those suffering sunburn. Unlike chickenpox which normally fully settles, shingles may result in persisting post-herpetic neuralgia pain.  Chickenpox spreads by direct contact or through the air from coughing or sneezing or touching the fluid from a chickenpox blister.  A person with chickenpox is contagious from 1-2 days before the rash appears until all blisters have formed scabs. This may take 5-10 days. 

Ø  Evaluation:  Chickenpox blisters start as a 2–4 mm red papule which develops an irregular outline (rose petal). A thin-walled, clear vesicle (dew drop) develops on top of the area of redness. This "dew drop on a rose petal" lesion is very characteristic. After about 8–12 hours the fluid in the vesicle gets cloudy and the vesicle breaks leaving a crust, which falls off after 7 days sometimes leaving a crater-like scar.   Another hallmark of chickenpox that the lesions are in diffent stages of healing due to the fact that new lesions crop up every day for several days. Children are not to be sent back to school until all lesions have crusted over. Second infections with chickenpox occur in immunocompetent individuals, but are uncommon.

Congenital defects in babies occur if the child's mother was exposed to VZV during pregnancy à need urgent treatment with acyclovir IV. Effects on the fetus may be minimal in nature but physical deformities range in severity from under developed toes and fingers, to severe anal and bladder malformation. Possible problems include:

v  Damage to brain: encephalitis, microcephaly, hydrocephaly, aplasia of brain

v  Damage to the eye (optic stalk, optic cup, and lens vesicles), microphthalmia, cataracts, chorioretinitis, optic atrophy.

v  Other neurological disorder: damage to cervical and lumbosacral spinal cord, motor/sensory deficits, absent deep tendon reflexes, anisocoria/Horner's syndrome

v  Damage to body: hypoplasia of upper/lower extremities, anal and bladder sphincter dysfunction

v  Skin disorders: (cicatricial) skin lesions, hypopigmentation

Ø  Treatment:  Children (milder disease): symptomatic treatment, with a little sodium bicarbonate in baths or antihistamine medication to ease itching, and acetaminophen to reduce fever.   Maintain good hygiene and daily cleaning of skin with warm water to avoid secondary bacterial infection. Adults (more severe):  acyclovir is generally advised. Patients of any age with depressed immune systems or extensive eczema are at risk of more severe disease and should also be treated with antiviral medication. In the U.S., 55 percent of chickenpox deaths are in the over-20 age group.

Chickenpox (varicella) rash, early stage, with dew-drop appearance

Chickenpox (varicella) rash, day 5, with crusting

By F malan - Own work, CC BY-SA 3.0,

o   Hand, foot, and mouth disease (coxsackie A16 of enteroviruses in the family Picornaviridae):  Commonly affects infants and children. It is highly contagious and spreads through direct contact with mucus or feces. It typically occurs in small epidemics in nursery schools or kindergartens, usually during the summer and autumn months.

Ø  Evaluation:   fever, sores with blisters on palms of hands and soles of feet, mouth ulcers.  Sores or blisters may be present on the buttocks of small children and infants. 

Ø  Treatment: No specific treatment. Fever reducers & cool baths will help bring temperature down.  Only a very small minority require hospital admission, mainly as a result of neurological complications (encephalitis, meningitis or acute flaccid paralysis) or pulmonary edema/pulmonary hemorrhage.

Rash on the palms and soles

By KlatschmohnAcker - Own work, CC BY-SA 3.0,

Typical lesions around the mouth

By MidgleyDJ at en.wikipedia, CC BY-SA 3.0,

o   H erpangina:  Usually, herpangina is produced by one particular strain of coxsackievirus A, but it can also be caused by coxsackievirus B or echoviruses. It is most common in children.

Ø  Evaluation:  Can be asymptomatic.  Symptoms:  High fever and sore throat.   Small number of lesions (usually 2 - 6) forms in the back area of the mouth, particularly the soft palate or tonsillar pillars. The lesions progress initially from red macules to vesicles and lastly to ulcerations which can be 2 - 4 mm in size. The lesions heal in 7 - 10 days.  Histology:  epithelial cells show signs of intracelular and intercellular edema.

Ø  Treatment:  Minimizing the discomfort of symptoms. Aspirin is avoided.

Sores from herpangina

By Aphilosophicalmind - Own work, Public Domain,

o   Herpes zoster (shingles):  Reactivation (from the general area of the spinal cord) of VZV.  The blisters therefore only affect one area of the body and do not cross the midline.  VZV can be spread from a person with active shingles to a person who has never had chickenpox through direct contact with the rash. The person exposed would then develop chickenpox. 

Ø  Evaluation:  Prodrome:  HA, sensitivity to light, fever, and malaise, all of which may, within one to several days, be followed by itching, tingling, and extreme pain where the rash is developing. In addition, a general pain also develops in other areas of the body where affected nerves may run. During this phase, herpes zoster is frequently misdiagnosed as other diseases with similar symptoms, including heart attacks and renal colic. Some patients may have these symptoms without developing the characteristic rash. This situation, known as "zoster sine herpete," can delay diagnosis and treatment.  The initial phase is followed by development of the characteristic skin rashes of herpes zoster. The skin lesions begin as a rash, similar to hives, that follows a distribution near dermatomes. The rash evolves into vesicles or small blisters filled with serous fluid. The vesicles are generally painful, and their development is often associated with the occurrence of anxiety and further flu-like symptoms, such as fever, tiredness, and generalized pain. The vesicles eventually become hemorrhagic, or filled with blood, and crust over within seven to 10 days. As the crusts fall off, patients are generally left with scarring and pigmented skin.  They are most common on the torso, but can also appear on the face (where they are potentially hazardous to vision) or other parts of the body. 

Ø  Treatment:  acyclovir (Zovirax), or prodrugs such as famciclovir (Famvir), or valacyclovir (Valtrex).  Most effective if taken within 12 to 72 hours after th e appearance of the rash.

Herpes zoster:  Typical dermatomal distribution, in this case C8/T1

By James Heilman, MD - Own work, CC BY-SA 3.0,

Herpes zoster on the chest

By Fisle - Fisle, CC BY-SA 3.0,

Trigeminal herpes zoster with uveitis and keratitis

By Jonathan Trobe, M.D. - University of Michigan Kellogg Eye Center - The Eyes Have It, CC BY 3.0,

BACTERIAL SKIN INFECTIONS:  FICS --> Folliculitis, Furuncles, Impetigo, Carbuncles, Cellulitis, Scalded Skin Syndrome.

·      F  _______________, _______________, _______________, _______________, _______________

·      I  _______________, _______________, _______________, _______________, _______________

·      C _______________, _______________, _______________, _______________, ________________

·      S _______________, _______________, _______________, _______________, _______________

·      F olliculitis:  Inflammation of one or more hair follicles.   Most carbuncles and furuncles and other cases of folliculitis develop from Staphylococcus aureus.  Folliculitis starts when hair follicles are damaged by friction from clothing, blockage of the follicle, or shaving. Iron deficiency anemia is sometimes associated with chronic cases. 

o   Associated conditions:

Ø  Sycosis barbae or Barber's itch is a staph infection of the hair follicles in the bearded area of the face, usually the upper lip. Shaving aggravates the condition.  

Ø  Tinea barbae is similar to barber's itch, but the infection is caused by the fungus T. rubrum.  

Ø  Pseudofolliculitis barbae is a disorder occurring primarily in men of African descent. If curly beard hairs are cut too short, they may curve back into the skin and cause inflammation.  

Ø  Hot tub folliculitis is caused by the bacteria Pseudomonas aeruginosa often found in new hot tubs. The folliculitis usually occurs after sitting in a hot tub that was not properly cleaned before use. Symptoms are found around the body parts that sit in the hot tub -- typically the legs, hips and buttocks and surrounding areas. Symptoms are typically amplified around regions that were covered by wet clothing, such as bathing suits.

o   Evaluation:  rash (reddened skin area),  pimples or pustules located around a hair follicle, may crust over, typically occur on neck axilla, or groin area, may be present as genital lesions, itching skin  

Treatment:  Topical antibiotic such as mupirocin is adequate for most cases.  Some patients may benefit from systemic dicloxacillin.  Fungal folliculitis can  be treated with topical Econazole Nitrate or oral antifungal such as Fluconazole. 

Folliculitis, single lesion

By Jmarchn - Own work, CC BY-SA 3.0,

·      Furuncles (aka boils):  Inflammation of hair follicles --> localized accumulation of pus and dead tissues. Individual boils can cluster together and form an interconnected network of boils called carbuncles. In severe cases, boils may develop to form abscesses.  Boils are generally caused by an infection of the hair follicles by Staphylococcus aureus or staphylococcus epidermidis when tiny cuts of the skin allows this bacterium to enter the follicles and cause an infection. 

o   Evaluation:  red, pus-filled lumps that are tender, warm, and/or painful. A yellow or white point at the center of the lump can be seen when the boil is ready to drain or discharge pus. In a severe infection, multiple boils may develop and the patient may experience fever and swollen lymph nodes. A recurring boil is called chronic furunculosis. 

o   Treatment:  Most boils run their course within 4 to 10 days. For most, warm compress alleviates the pain and hasten draining of the pus.   For recurring cases, sufferers may benefit from diet supplements of Vitamin A and E.  In serious cases, prescription oral antibiotics such as dicloxacillin (Dynapen) or cephalexin (Keflex), or topical antibiotics, are commonly used.  Hidradenitis suppurativa causes frequent boils.

Ø  Hidradenitis suppurativa:  Skin disease that affects areas bearing apocrine sweat glands and hair follicles; such as the underarms, groin and buttocks, and under the breasts in women. 

v Evaluation:  Manifests as clusters of chronic abscesses or boils, sometimes as large as baseballs, that are extremely painful to the touch and may persist for years with occasional to frequent periods of inflammation, culminating in drainage of pus, often leaving open wounds that will not heal. Flare-ups may be triggered by stress, perspiration, hormonal changes, humid heat, and clothing friction. Persistent lesions may lead to scarring and the formation of sinus tracts, or tunnels connecting the abscesses under the skin. Bacterial infections and cellulitis may occur at these sites.

v Treatment:  changes in diet, warm compresses, intralesional corticosteroid injections, incision and drainage or lancing, oral antibiotics.


By The original uploader was Mahdouch at French Wikipedia - Transferred from fr.wikipedia to Commons., CC BY 1.0,

·      I mpetigo: Superficial skin infection caused by S. aureus or S. pyogenes.  Common among children age 2–6 years. People who play close contact sports such as rugby, American football and wrestling are also susceptible.  Two types:  Nonbullous and bullous impetigo.   Both forms of impetigo are primarily caused by S. aureus with Streptococcus usually being involved in the nonbullous form.  The infection is spread by direct contact with lesions or with nasal carriers. The incubation period is 1–3 days. 

o   Evaluation:  One or more pimple-like lesions surrounded by reddened skin. Lesions fill with pus, then break down over 4–6 days and form a thick crust. Impetigo is often associated with insect bites, cuts, and other forms of trauma to the skin. Itching is common. 

o   Treatment:  Washing with soap and water and letting the impetigo dry in the air.  Bactericidal ointment, such as fusidic acid (Fucidin) or mupirocin (Bactroban), but in more severe cases oral antibiotics such as flucloxacillin (e.g. Floxapen) or erythromycin (e.g. Erythrocin) or Dicloxacillin are necessary.  It is very important to remove the scabs before applying ointment, because the bacteria that cause the disease live underneath them.

Impetigo on the face

By James Heilman, MD - Own work, CC BY-SA 3.0,

Bullous impetigo

By US Gov - ID#: 5154 US Department of Health and Human Services, Public Domain,

·      C ellulitis:  Inflammation of the connective tissue underlying the skin.  Cellulitis can be caused by normal skin flora or by exogenous bacteria (most commonly S. aureus or S. pyogenes), and often occurs where the skin has previously been broken (cracks in the skin, cuts, burns, insect bites, surgical wounds, or sites of intravenous catheter insertion).  Cellulitis may be superficial but may also affect the tissues underlying the skin and can spread to the lymph nodes and bloodstream. 

o   Evaluation:  Early symptoms of fever, headache, nausea, and early signs on redness on the leg --> redness, swelling, warmth, and pain or tenderness --> red streaks may be seen traveling up the affected area. The swelling can spread rapidly.  The elderly and those with weakened immune systems are especially vulnerable to contracting cellulitis (e.g. diabetes, obesity, immunosuppressive drugs, HIV, chickenpox and shingles). 

Cellulitis of the leg with foot involvement

By Pshawnoah - Snapped a cell phone image., CC BY-SA 3.0,

Cellulitis following an abrasion: Note the red streaking up the arm from involvement of the lymphatic system

By James Heilman, MD - Own work, CC BY-SA 3.0,

·      S taphyloccus Scalded Skin Syndrome (aka Pemphigus neonatorum or Ritter's disease):  caused by Staphylococcus aureus. The syndrome is induced by 2 epidermolytic exotoxins A and B, which are released by S. aureus and cause the epidermis to detach from the underlying dermis. One of the exotoxins is produced by the bacterial chromosome, while the other is produced by a plasmid. 

o   Evaluation:  The symptoms somewhat mimic advanced arthritis and disorders of the nervous system, and can include severe and constant pain, loss of motor functions (such as severe stuttering when speaking) clinical depression and insomnia.

CUTANEOUS MYCOSIS (superficial fungal skin infection):  Tinea Nigra, Tinea Versicolor, Tinea Cruris/Corporis/Capitis -->Tinea North Viet Cong (North VC crawls in the jungle contracting some fungi) --> Tinea NVC.  Evaluation:  KOH examination of skin scrapings, Fungal culture (Sabouraud or Mycosel agar)

o   N  _______________, _______________, _______________, _______________, _______________

o   V  _______________, _______________, _______________, _______________, _______________

o   C _______________, _______________, _______________, _______________, ________________

·      Tinea Nigra:  superficial fungal infection that causes dark brown to black painless patches on the soles of the hands and feet. This infection is caused by the fungus Exophiala (cladosporium) werneckii. 

o   Treatment:  topical salicyclate

Tinea Nigra

·      Tinea Versicolor:  Caused by the yeast Malassezia furfur in warm and humid environment. 

o   Evaluation:  Oval or irregularly-shaped pale, dark tan, or pink in color spots of 1/4 to 1 inch in diameter with a sharp border, often merging together to form a larger patch.  These spots commonly affect the back, underarm, upper arm, chest, lower legs and neck, and cause an itch that can worsen with sweating or overheating.  Histology:  the yeasts can often be seen under the microscope within the lesions and typically have a so called "spaghetti and meat ball appearance" as the round yeasts produce filaments. 

o   Treatment:  Topical antifungal medications (2.5% selenium sulfide-Selsun® shampoo or 2% ketoconazole Nizoral® ointment and shampoo) applied to dry skin and washed off after 10 minutes, repeated daily for 2 weeks. Other topical antifungal agents such as clotrimazole, miconazole or terbinafine are less widely recommended.  Oral antifungal prescription only medications include 400 mg of ketoconazole or fluconazole in a single dose, or ketoconazole 200 mg daily for 7 days, or itraconazole 400 mg daily for 3-7 days.

Tinea versicolor

By Sarahrosenau on -, CC BY-SA 2.0,

Tinea versicolor fluorescence under Wood's lamp

By Warfieldian - Own work, CC BY-SA 3.0,

Malassezia furfur in skin scale from a patient with tinea versicolor

By, Public Domain,

·      Tinea Cruris/Corporis/Capitis:  Fungal infection of the groin/body/scalp, respectively.  Caused by MET --> Microsporidium, Epidermophyton, Trichophyton.

o   M  _______________, _______________, _______________, _______________, _______________

o   E  _______________, _______________, _______________, _______________, _______________

o   T _______________, _______________, _______________, _______________, ________________

o   Evaluation:  Tinea corporis with typical lesion begins as an erythematous, scaly plaque that may rapidly worsen and enlarge --> central clearing --> lesion may become annular in shape. 

o   Treatment:  Traditionally creams containing clotrimazole or miconazole have been used.  If the skin inflammation causes discomfort and itching, glucocorticoid may be combined with the anti-fungal drug to help prevent further irritation due to the patient scratching the area. However steroids, if used alone, for fungal infections may exacerbate the condition.

Tinea corporis due to Trichophyton mentagrophytes, Public Domain,

Tinea capitis

By myself - Own work, GFDL,

·      P ediculosis:  Infestation of lice -- which are parasitic insects. The condition is more commonly known as head lice, body lice or pubic lice.  Head lice and body lice (Pediculus humanus) are similar in appearance, although the head louse is often smaller. Pubic lice (Pthirus pubis), on the other hand, are quite distinctive. They have shorter bodies and pincer-like claws, making them look like crabs (hence, the nickname for pubic lice: "crabs"). 

o   Evaluation:  The most common symptom of lice infestation is itching. Excessive scratching of the infested areas can cause sores, which may become infected. In addition, body lice can be a vector for louse-borne typhus, louse-borne relapsing fever or trench fever. 

o   Treatment:  Lice on the hair and body are usually treated with medicated shampoos or cream rinses. Nit combs can be used to remove lice and nits from the hair. Laundering clothes using high heat can eliminate body lice. Efforts to treat should focus on the hair or body (or clothes), and not on the home environment.

Male human head louse, Pediculus humanus capitis.

By Gilles San Martin - originally posted to Flickr as Male human head louse, CC BY-SA 2.0,

Male head louse, adult

By KostaMumcuoglu at the English language Wikipedia, CC BY-SA 3.0,

Pubic lice in genital area.

By SOA-AIDS Amsterdam - SOA-AIDS Amsterdam, CC BY-SA 3.0,

INFESTATION:  PS --> Pediculosis, Scabies

·      S cabies:  Caused by the mite Sarcoptes scabiei.  It takes approximately 4-6 weeks to develop symptoms after initial infestation. Therefore, a person may have been contagious for at least a month before being diagnosed. 

o   Evaluation: Delayed hypersensitivity response resulting in a papular eruptions occurs 30-40 days after infestation. Generally diagnosis is made by finding burrows.   While there may be hundreds of papules, fewer than 10 burrows are typically found. The burrow appears as a fine, wavy and slightly scaly line a few millimeters to one centimeter long. A tiny mite (0.3 to 0.4 mm) may sometimes be seen at the end of the burrow.  Most burrows occur in the webs of fingers, flexing surfaces of the wrists, around elbows and armpits, the areolae of the breasts in females and on genitals of males, along the belt line, and on the lower buttocks. When a suspected burrow is found, diagnosis may be confirmed by microscopy of surface scrapings, which are placed on a slide in glycerol, mineral oil or immersion in oil and covered with a coverslip. Avoiding potassium hydroxide is necessary because it may dissolve fecal pellets. Positive diagnosis is made when the mite, ova, or fecal pellets are found.  The rash may become secondarily infected; scratching the rash may break the skin and make secondary infection more likely. In persons with severely reduced immunity, such as those with HIV infection, or people being treated with immunosuppressive drugs like steroids, a widespread rash with thick scaling may result. This variety of scabies is called crusted (Norwegian) scabies. 

o   Treatment (all household contacts must be treated simultaneously, even if asymptomatic):  The topical medication of choice is 5% permethrin because it is safe for all age groups: it should be applied for eight to twelve hours (overnight is the most convenient) then washed off. A second treatment of permethrin a week later may be recommended. Multiple applications of this cream is usually required to completely rid the body of the bugs.  Lindane has been used in the past to treat both scabies and lice. While infrequent, serious side effects have occurred when using lindane and is therefore considered a treatment option of last resort.  Although the mites are rapidly killed by treatment, itching can last for up to four weeks after treatment. A single dose of ivermectin (dosing: 200 µg/kg) has been reported to cure, but is an off-label use; some authorities recommend repeating treatment at 14 days. Additional topical treatments include 10% crotamiton (except to eyes, nose, mouth), 25% benzyl benzoate cream or lotion.

Burrowing trail of the scabies mite: The scaly patch on the left was caused by the scratching and marks the mite's entry point into the skin. The mite has burrowed to the top-right, where it can be seen as a dark spot at the end.

By Michael Geary - Own work, Public Domain,

Sarcoptes scabiei

By Kalumet - de.wikipedia, CC BY-SA 3.0,

Commonly involved sites of rashes of scabies

By Mikael Häggström - CDC web site > DPDx - Laboratory Identification of Parasites of Public Health Concern > Scabies [1], Public Domain,

Scabies of the hand

By Steschke - Own work, CC BY-SA 3.0,

STD:  Gay & HeteroSexual Contract These = GHSCT --> Gonorrhea, Hepatitis B + C, HSV, HPV, HIV, Hemophilus ducreyi, Chlamydia, Treponema pallidum.

·      G  _______________, _______________, _______________, _______________, _______________

·      H  _______________, _______________, _______________, _______________, _______________

·      S  _______________, _______________, _______________, _______________, ________________

·      C  _______________, _______________, _______________, _______________, _______________

·      T  _______________, _______________, _______________, _______________, _______________

·      G onorrhea:  Caused by Gram-negative bacterium Neisseria gonorrheae that spreads during sexual intercourse. Infected women also can pass gonorrhea to their newborn infants during delivery, causing conjunctivitis, which if left untreated, can cause blindness. This is prevented by applying small amounts of silver nitrate to the eyes of all newborns. 

o   Evaluation:  Between 30–60% of women with gonorrhea are asymptomatic.  Woman:  vaginal discharge, dysuria, off-cycle menstrual bleeding, or bleeding after sexual intercourse, cervicitis with pus & urethritis.  More advanced symptoms, which may indicate development of pelvic inflammatory disease (PID), include cramps and pain, bleeding between menstrual periods, vomiting, or fever.   Men:  dysuria, thick pussy discharge (also known as gleet), reddened external urethral meatus.  Gonococcal proctitis:  anal discharge, pain on defecating and rectal bleeding. Proctoscopy may show an inflamed mucous membrane with little mucus. It cannot be treated with penicillin because rectal commensal bacteria in the rectum produce β-lactamase that protects the gonococcus from penicillin.  Gonococcal pharyngitis:  sore throat.  Cotton swab and culture. 

Treatment:  A third-generation cephalosporin antibiotic such as ceftriaxone is recommended for use in most areas.  Areas such as Hawaii and California have very high levels of resistance to fluoroquinolone, they are no longer used empirically to treat infections originating in these areas.  Complication:  Men: epididymitis, prostatitis, urethritis.  Women:  bartholinitis, PID, Fitz-Hugh-Curtis syndrome, scarring of the fallopian tubes --> ↑ ectopic pregnancy, multiple distant sites of infection which can include the brain, heart and joints.  When joints become involved, gonococcal arthritis can develop. Gonococcal arthritis occurs after primary infection of the genitalia, anus, or throat. This occurs in about 1% of patients who are infected with gonorrhea and is more common in women than men. Typical symptoms include a 5–7 day history of fever, shaking, chills, multiple skin lesions, fleeting migratory polyarthralgias and tenosynovitis in fingers, wrists, toes or ankles. This should be evaluated promptly with a culture of the synovial fluid, blood, cervix, urethra, rectum, skin lesion fluid, or pharynx. The underlying gonorrhea should be treated; if this is done then usually a good prognosis will follow.

A patient with both gonorrhea (which is causing the pus to drip out the urethral orifice) and syphilis (note the chancre). 

Teaching file of Creighton University SOM

Gonococcal lesion on the skin of a patient’s arm. Gonorrhea, caused by Neisseria gonorrhoeae, if left untreated will enter the blood, thereby, spreading throughout the body. As is shown here, such full body dissemination may manifest itself as skin lesions in the form of gray pustules. Content Providers(s): CDC/Emory University, Dr. Thomas F. Sellers Creation Date: 1963 Copyright Restrictions: None - This image is in the public domain and thus free of any copyright restrictions. As a matter of courtesy we request that the content provider be credited and notified in any public or private usage of this image.

By This media comes from the Centers for Disease Control and Prevention's Public Health Image Library (PHIL), with identification number #2038.Note: Not all PHIL images are public domain; be sure to check copyright status and credit authors and content providers.English | Slovenščina | +/−, Public Domain,


If not treated gonococcal ophthalmia neonatorum will develop in 28% of infants born to women with gonorrhea.

By CDC/ J. Pledger - This media comes from the Centers for Disease Control and Prevention's Public Health Image Library (PHIL), with identification number #3766.Note: Not all PHIL images are public domain; be sure to check copyright status and credit authors and content providers.English | Slovenščina | +/−, Public Domain,

·      HSV (herpes simplex virus):  After an initial, or primary, infection, HSV establishes latency, during which the virus is present in the cell bodies of nerves which innervate the area of original outbreak. During reactivation, virus is produced in the cell and transported outwardly via the nerve cell's axon to the skin.  HSV is generally transmitted by direct contact of lips or genitals when the sores are present, or also when no sores are present (known as viral shedding). HSV can be present in semen, vaginal fluids, and saliva. In addition, herpes may be transmitted during childbirth, which can be fatal to the infant. The immature immune system of the child is unable to defend against the virus and even if treated, infection can result in brain damage. 

o   Evaluation:  painful, watery grouped vesicles in the skin or mucous membranes (such as the mouth or lips) or on the genitals.  Lesions heal with a crudescent scab, the hallmark of herpetic disease.  Tzank smear, culture, direct FL-Ab.

o   Treatment:  antiviral medications such as nucleoside analog, which reduce the duration of symptoms and accelerate healing.  Of these, Ganciclovir is known to have cytotoxic effects on infected cells, while Acyclovir is not known to have this effect

Herpes genitalis, female

By SOA-AIDS Amsterdam - SOA-AIDS Amsterdam, CC BY-SA 3.0,

Herpes labialis of the lower lip. Note the blisters in a group marked by an arrow.

Public Domain,

Herpes whitlow

By James Heilman, MD - Own work, CC BY-SA 3.0,

MR image shows high signal in the temporal lobes including hippocampal formations and parahippogampal gyrae, insulae, and right inferior frontal gyrus

·      H PV:  Papillomaviruses are a diverse group of DNA-based viruses that infect the skin and mucous membranes.  Some HPV types cause benign skin warts, or papillomas, for which the virus family is named. Some sexually transmitted HPVs, such as types 6 and 11, can cause genital warts. However, most HPV types that infect the genitals tend not to cause noticeable symptoms. Persistent infection with a subset of about 13 so-called "high-risk" sexually transmitted HPVs, including types 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, and 68 — different from the ones that cause warts — can lead to the development of cervical dyskaryosis, or precancerous lesions, which may in turn lead to cancer of the cervix.  Some of the HPV "early" genes, such as E6 and E7, are known to act as oncogenes that promote tumor growth and malignant transformation.  E6 inhibits p53, while E7 inhibits p53, p21, and RB. Genital HPV is the most common sexual transmitted infection in the United States à by the age of 50 more than 80% of American women will have contracted at least one strain of genital HPV. 

o   Evaluation:  Warts have a characteristic cauliflower-like surface and are typically slightly raised above the surrounding skin.  For detection of cervical cancer:

Ø  PAP smear: Women get a Pap test no later than 3 years after their first sexual encounter and no later than 21 years of age, then should have a Pap test every year until age 30.  After age 30, women should discuss risk factors with their health care provider to determine whether a Pap test should be done yearly. If risk factors are low and previous Pap tests have been negative, most women only need to have tests every 2-3 years until 65 years of age.

Ø  Detailed inspection of the cervix by colposcopy may be indicated if abnormal cells (koilocytes) are detected by routine Pap.

Ø  In March 2003, the US FDA approved a "hybrid-capture" test, marketed by Digene, as a primary screening tool for detecting the DNA of high-risk HPVs that may lead to cervical cancer. This test was also approved for use as an adjunct to Pap testing, and may be ordered in response to abnormal Pap smear results. The Digene test is the gold standard for the resolution of ASCUS pap results

Ø  On June 8, 2006, the FDA approved Gardasil, a prophylactic HPV vaccine which is marketed by Merck. The vaccine trial, conducted in adult women with a mean age of 23, showed protection against initial infection with HPV types 16 and 18, which together cause 70 percent of cervical cancers. HPV types 16 and 18 also cause anal cancer in men and women.  The trial also showed 100% efficacy against persistent infections, not just incident infections. The vaccine also protects against HPV types 6 and 11, which cause 90 percent of genital warts.

Ø  Food and Drug Administration FDA and CDC recommend that girls and women between the ages of 12 and 26 be vaccinated.

o   Treatment:  Warts:  podofilox, imiquinopod, cryotherapy, surgery.  Cervical dysplasia or cancer:  LEEP, ablation, conization, hysterectomy

Condylomata acuminata, penile

By SOA-AIDS Amsterdam - SOA-AIDS Amsterdam, CC BY-SA 3.0,

Condylomata acuminata, vaginal

By SOA-AIDS Amsterdam - SOA-AIDS Amsterdam, CC BY-SA 3.0,

Condylomata acuminata, anal

By SOA-AIDS Amsterdam - SOA-AIDS Amsterdam, CC BY-SA 3.0,

Main symptoms of acute HIV infection

By Mikael Häggström - All used images are in public domain., Public Domain,

·      H IV:  A retrovirus that causes AIDS.  Infection with HIV occurs by the transfer of blood, semen, vaginal fluid, pre-ejaculate, or breast milk.  AIDS has killed more than 25 million people since it was first recognized on December 1, 1981, making it one of the most destructive pandemics in recorded history.  HIV primarily infects vital cells in the human immune system such as helper T cells (specifically CD4+ T cells), macrophages and dendritic cells. HIV infection leads to low levels of CD4+ T cells through three main mechanisms: firstly, direct viral killing of infected cells; secondly, increased rates of apoptosis in infected cells; and thirdly, killing of infected CD4+ T cells by CD8 cytotoxic lymphocytes that recognize infected cells. When CD4+ T cell numbers decline below a critical level, cell-mediated immunity is lost, and the body becomes progressively more susceptible to opportunistic infections.  HIV was classified as a member of the genus Lentivirus, part of the family of Retroviridae. Lentiviruses are transmitted as single-stranded, positive-sense, enveloped RNA viruses. Upon entry of the target cell, the viral RNA genome is converted to double-stranded DNA by a virally encoded reverse transcriptase that is present in the virus particle. This viral DNA is then integrated into the cellular DNA by a virally encoded integrase so that the genome can be transcribed. Once the virus has infected the cell, two pathways are possible: either the virus becomes latent and the infected cell continues to function, or the virus becomes active and replicates, and a large number of virus particles are liberated that can then infect other cells.  Macrophage (M-tropic) strains of HIV-1, or non-syncitia-inducing strains (NSI) use the β-chemokine receptor CCR5 for entry and are thus able to replicate in macrophages and CD4+ T cells. Indeed, macrophages play a key role in several critical aspects of HIV infection. They appear to be the first cells infected by HIV and perhaps the source of HIV production when CD4+ cells become depleted in the patient. Macrophages and microglial cells are the cells infected by HIV in the central nervous system. In tonsils and adenoids of HIV-infected patients, macrophages fuse into multinucleated giant cells that produce huge amounts of virus.  T-tropic isolates, or syncitia-inducing (SI) strains replicate in primary CD4+ T cells as well as in macrophages and use the α-chemokine receptor, CXCR4, for entry. Dual-tropic HIV-1 strains are thought to be transitional strains of the HIV-1 virus and thus are able to use both CCR5 and LESTR as co-receptors for viral entry.  Some people are resistant to certain strains of HIV. One example of how this occurs is people with the CCR5-Δ32 mutation; these people are resistant to infection with R5 virus as the mutation stops HIV from binding to this coreceptor, reducing its ability to infect target cells.o  

Evaluation:  Primary infection (usually 2-4 weeks post-exposure):  most individuals (80 to 90%) develop an influenza or mononucleosis-like illness called acute HIV infection, the most common symptoms of which may include fever, lymphadenopathy, pharyngitis, rash, myalgia, malaise, mouth and esophagal sores, and may also include, but less commonly, headache, nausea and vomiting, enlarged liver/spleen, weight loss, thrush, and neurological symptoms. Infected individuals may experience all, some, or none of these symptoms. Symptoms have an average duration of 28 days and usually last at least a week although duration of symptoms may vary.  A strong immune defense reduces the number of viral particles in the blood stream, marking the start of the infection's clinical latency stage. Clinical latency:  vary between two weeks and 20 years. During this early phase of infection, HIV is active within lymphoid organs, where large amounts of virus become trapped in the follicular dendritic cells (FDC) network. The surrounding tissues that are rich in CD4+ T cells may also become infected, and viral particles accumulate both in infected cells and as free virus. Individuals who are in this phase are still infectious. During this time, CD4+ CD45RO+ T cells carry most of the proviral load.   When CD4+ T cell numbers decline below a critical level, cell-mediated immunity is lost, and infections with a variety of opportunistic microbes appear. The first symptoms often include moderate and unexplained weight loss, recurring respiratory tract infections (such as sinusitis, bronchitis, otitis media, pharyngitis), prostatitis, skin rashes, and oral ulcerations. Common opportunistic infections and tumors, most of which are normally controlled by robust CD4+ T cell-mediated immunity then start to affect the patient. Typically, resistance is lost early on to oral Candida species and to Mycobacterium tuberculosis, which leads to an increased susceptibilty to oral candidiasis and tuberculosis. Later, reactivation of latent herpes viruses may cause worsening recurrences of herpes simplex eruptions, shingles, Epstein-Barr virus-induced B-cell lymphomas, or Kaposi's sarcoma, a tumor of endothelial cells that occurs when HIV proteins such as Tat interact with Human Herpesvirus-8. Pneumonia caused by the fungus Pneumocystis jirovecii is common and often fatal. In the final stages of AIDS, infection with cytomegalovirus (another herpes virus) or Mycobacterium avium complex is more prominent. Not all patients with AIDS get all these infections or tumors, and there are other tumors and infections that are less prominent but still significant.  HIV-1 testing consists of initial screening with an enzyme-linked immunosorbent assay (ELISA) to detect antibodies to HIV-1. Specimens with a nonreactive result from the initial ELISA are considered HIV-negative unless new exposure to an infected partner or partner of unknown HIV status has occurred. Specimens with a reactive ELISA result are retested in duplicate.  If the result of either duplicate test is reactive, the specimen is reported as repeatedly reactive and undergoes confirmatory testing with a more specific supplemental test (e.g., Western blot or, less commonly, an immunofluorescence assay (IFA)). Only specimens that are repeatedly reactive by ELISA and positive by IFA or reactive by Western blot are considered HIV-positive and indicative of HIV infection.  

o   Treatment:  Current treatment for HIV infection consists of highly active antiretroviral therapy, or HAART. This has been highly beneficial to many HIV-infected individuals since its introduction in 1996, when the protease inhibitor-based HAART initially became available.  Current HAART options are combinations (or "cocktails") consisting of at least three drugs belonging to at least two types, or "classes," of anti-retroviral agents. Typically, these classes are two nucleoside analogue reverse transcriptase inhibitors (NARTIs or NRTIs) plus either a protease inhibitor or a non-nucleoside reverse transcriptase inhibitor (NNRTI). Because AIDS progression in children is more rapid and less predictable than in adults, particularly in young infants, more aggressive treatment is recommended for children than adults.  Most national guidelines say to start treatment once the CD4 count falls below 350.

Relationship between HIV copies (viral load) and CD4+ T cell counts over the average course of untreated HIV infection.

By Jurema Oliveira - Based on Figure 1 in Pantaleo, G et al. (February 1993). "New concepts in the immunopathogenesis of human immunodeficiency virus infection". New England Journal of Medicine 328 (5): 327-335. PMID 8093551.Also available via Figure 4 in The relationship between the human immunodeficiency virus and the acquired immunodeficiency syndrome. US National Institute of Allergy and Infectious Diseases Retrieved on November 3, 2009.Supporting data for this disease course is available in Piutak, M et al. (March 1993). "High levels of HIV-1 in plasma during all stages of infection determined by competitive PCR". Science 259 (510): 1749-54. PMID 8096089., CC BY-SA 3.0,

·      H emophilus ducreyi (Chanroid):  A fastidious Gram-negative streptobacillus.  Chancroid is known to be spread from one to another individual through sexual contact. Men can contract chancroid by practicing poor hygiene. 

o   Evaluation:  After an incubation period of one day to two weeks, chancroid begins with a small bump that becomes an ulcer within a day of its appearance. The ulcer characteristically:  1) Ranges in size dramatically from 1/8 inch to two inches (3 to 50 mm) across 2) Is painful 3) Has sharply defined, undermined borders 4) Has irregular or ragged borders 5) Has a base that is covered with a gray or yellowish-gray material 6) Has a base that bleeds easily if traumatized or scraped.  More specifically, the CDC's standard clinical definition for a probable case of chancroid includes all of the following: Patient has one or more painful genital ulcers. The combination of a painful ulcer with tender adenopathy is suggestive of chancroid; the presence of suppurative adenopathy is almost pathognomonic.  No evidence of Treponema pallidum is indicated by dark-field examination of ulcer or by a serologic test for.  Syphilis performed at least 7 days after the onset of ulcer.  The clinical presentation is not typical of disease caused by human herpesvirus 2 (Herpes Simplex Virus), or result of culture for HSV is negative.  About half of infected men have only a single ulcer. Women frequently have four or more ulcers, with fewer symptoms. The ulcers appear in specific locations, such as the coronal sulcus of the uncircumcised glans penis in men, or the fourchette and labia minora in women.  Approximately one third of the infected individuals will develop enlargements of the inguinal lymph nodes.  Half of those who develop swelling of the inguinal lymph nodes will progress to a point where the nodes rupture through the skin producing draining abscesses. The swollen lymph nodes and abscesses are often referred to as buboes. 

o   Treatment:  Single oral dose of Azythromicin or Single IM dose of Ceftriaxone or Oral Erythromycin for 7 days.

Penile chancroid lesion:  Begins as one or more sores surrounded by a narrow red border or raised bumps.   It becomes filled with pus, and eventually ruptures, leaving a painful open wound.

By CDC/Joe Miller - This media comes from the Centers for Disease Control and Prevention's Public Health Image Library (PHIL), with identification number #3728.Note: Not all PHIL images are public domain; be sure to check copyright status and credit authors and content providers.English | Slovenščina | +/−, Public Domain,

Buboes, Public Domain,

·      C hlamydia:  C. trachomatis is naturally found living only inside human cells and is one of the most common sexually transmitted infections in people worldwide — about four million cases of chlamydia infection occur in the United States each year. Not all infected people exhibit symptoms of infection. About ½  men and ¾  of all women who have chlamydia have no symptoms and do not know that they are infected. It can be serious but is easily cured with antibiotics if detected in time. Equally important, chlamydia infection of the eye is the most common cause of preventable blindness in the world. Blindness occurs as a complication of trachoma (chlamydia conjunctivitis). Chlamydia trachomatis can also cause PLUCA --> Pneumonia, Perihepatitis (Fitz-Hugh-Curtis syndrome), Proctitis, PID (pelvic inflammatory disease), LGV (lymphogranuloma venereum), Urethritis, Cervicitis, Arthritis (Reiter’s syndrome).

o   P  _______________, _______________, _______________, _______________, _______________

o   L  _______________, _______________, _______________, _______________, _______________

o   U  _______________, _______________, _______________, _______________, ________________

o   C  _______________, _______________, _______________, _______________, _______________

o   A  _______________, _______________, _______________, _______________, _______________

There are many other species of Chlamydiae that live in the cells of animals (including humans), insects, or protozoa. Two of these species cause lung infection in humans: Chlamydophila pneumoniae and Chlamydophila psittaci.  Mechanism:  Chlamydia: EB (elementary body) Enter via Endocytosis --> form RB (reticulate body) Replicates by binary fission & Reorg’ into EB --> Release--> infx cell.  C. trachomatis: 1) Type ABC: Africa, Blind, Chronic; 2) D-K: urethritis, PID; 3) L1-3: Lymphogranuloma venereum: draining lymphadenitis.  Neonate acq’ thru vagina tx w/ Erythromycin drops.

o   Evaluation:  Chlamydia is known as the "Silent Epidemic" because in women, it may not cause any symptoms and will linger for months or years before being discovered. Symptoms that may occur include: unusual vaginal bleeding or discharge, pain in the abdomen, painful sexual intercourse, fever, painful urination or the urge to urinate more frequently than usual.  Almost ½  women who get chlamydia and are not treated will get PID, a generic term for infection of the uterus, fallopian tubes, and/or ovaries. PID can cause scarring inside the reproductive organs, which can later cause serious complications, including chronic pelvic pain, difficulty becoming pregnant, ectopic pregnancy, and other dangerous complications of pregnancy. Men:  May not cause any symptoms, but symptoms that may occur include: a painful or burning sensation when urinating, an unusual discharge from the penis, swollen or tender testicles, or fever.  Male patients may develop a white, cloudy or watery discharge (shown) from the tip of the penis.  Chlamydia in men can spread to the testicles, causing epididymitis, which can cause sterility if not treated within 6 to 8 weeks. Chlamydia causes more than 250,000 cases of epididymitis in the USA each year.  Chlamydia may also cause reactive arthritis, especially in young men (Reiter's syndrome).  As many ½  infants born to mothers with chlamydia will be born with the disease. Chlamydia can affect infants by causing spontaneous abortion; premature birth; conjunctivitis, which may lead to blindness; and pneumonia. Conjunctivitis due to chlamydia typically occurs one week after birth (Compare with chemical causes [within hours] or gonorrhea [2-5 days]).  Nucleic acid amplification tests (NAAT), such as polymerase chain reaction (PCR), transcription mediated amplification (TMA), and the DNA strand displacement assay (SDA) now are the mainstays for detection. Lab: Cytoplasmic inclusion seen on Giemsa stain.   As of January 2007, the most commonly used and widely studied chlamydia NAATs in the US and many other industrialized countries are Aptima (Gen-Probe), Probe-Tec (Becton-Dickinson), and Amplicor (Roche). The Aptima Combo II assay tests simultaneously for C. trachomatis and Neisseria gonorrhoeae, the cause of gonorrhea. NAAT for chlamydia may be performed on swab specimens collected from the cervix (women) or urethra (men), on self-collected vaginal swabs, or on voided urine. Urine and self-collected swab testing facilitates the performance of screening tests in settings where genital examination is impractical. 

o   Treatment:  Azithromycin 1 gram oral as a single dose, or Doxycycline 100 milligrams twice daily for seven days.  Tetracycline, Erythromycin, Amoxicillin once a day until infection subsides.  Untested Treatments:  Ciprofloxacin 500 milligrams twice daily for 3 days.

Chlamydia cervicitis:  Mucoopurulent cervical discharge and redness

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Male patients may develop a white, cloudy or watery discharge (shown) from the tip of the penis.

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Chlamydial conjunctivitis

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·       Treponema pallidus (aka the "Great Pox"):  Causes syphilis.

o   Evaluation:  Different manifestations occur depending on the stage of the disease

Ø  Primary syphilis:  acquired via direct sexual contact with the infectious lesions.   Approximately 10-90 days after the initial exposure (average 21 days), a skin lesion may be seen on the genitalia. This lesion, called a chancre, is a firm, painless skin ulceration localized at the point of initial exposure to the spirochete, often on the penis, vagina or rectum. Rarely, there may be multiple lesions. The lesion may persist for 4 to 6 weeks and usually heals spontaneously.

Ø  Secondary syphilis:  approximately 1-6 months (commonly 6 to 8 weeks) after the primary infection. There are many different manifestations of secondary disease. There may be a symmetrical reddish-pink non-itchy rash on the trunk and extremities. The rash can involve the palms of the hands and the soles of the feet. In moist areas of the body, the rash becomes flat broad whitish lesions known as condylomata lata. Other symptoms common at this stage include fever, sore throat, malaise, weight loss, headache, meningismus, and enlarged lymph nodes. Rare manifestations include an acute meningitis that occurs in about 2% of patients, hepatitis, renal disease, hypertrophic gastritis, patchy proctitis, ulcerative colitis, rectosigmoid mass, arthritis, periostitis, optic neuritis, intersitial keratitis, iritis, and uveitis.

Ø  Latent syphilis is defined as having serologic proof of infection without signs or symptoms of disease. Latent syphilis is further described as either early or late. The distinction is important for both therapy and risk for transmission. In the real-world, the timing of infection is often not known and should be presumed to be late for the purpose of therapy.

v Early latent syphilis is defined as having syphilis for two years or less from the time of initial infection without signs or symptoms of disease.

v Late latent syphilis is infection for greater than two years but without clinical evidence of disease.

v Early latent syphilis may be treated with a single intramuscular injection of a long-acting penicillin. Late latent syphilis, however, requires three weekly injections. For infectiousness, however, late latent syphilis is not considered as contagious as early latent syphilis.

Ø  Tertiary syphilis usually occurs 1-10 years after the initial infection, though in some cases it can take up to 50 years. This stage is characterized by the formation of gummas which are soft, tumor-like balls of inflammation known as granulomas. The granulomas are chronic and represent an inability of the immune system to completely clear the organism. They may appear almost anywhere in the body including in the skeleton. Other characteristics of untreated tertiary syphilis include Charcot's joints which are a degeneration of joint surfaces resulting from loss of sensation and fine position sense (proprioception). Clutton's joints are bilateral knee effusions. The more severe manifestations include neurosyphilis and cardiovascular syphilis. In a study of untreated syphilis, 10% of patients developed cardiovascular syphils, 16% had gumma formation, and 7% had neurosyphilis.  Neurological complications at this stage can be diverse. In some patients, manifestations include generalized paresis of the insane which results in personality changes, changes in emotional affect, hyperactive reflexes, and Argyll-Robertson pupil. This is a diagnostic sign in which the small and irregular pupils constrict in response to focusing the eyes, but not to light. Tabes dorsalis, also known as locomotor ataxia, a disorder of the spinal cord, often results in a characteristic shuffling gait. Cardiovascular complications include syphilitic aortitis, aortic aneurysm, aneurysm of sinus of Valsalva, and aortic regurgitation. Syphilis infects the ascending aorta causing dilation and aortic regurgitation. This can be heard with a stethoscope as a heart murmur. The course can be insidious, and heart failure may be the presenting sign after years of disease. The infection can also occur in the coronary arteries and cause narrowing of the vessels. Syphilitic aortitis can cause de Musset's sign, a bobbing of the head that de Musset first noted in Parisian prostitutes.

v Summary of tertiary syphilis: PARESIS --> Personality change, Psychosis, Paresthesias, Posterior column dysfunction, Argyll-Roberson pupil, Reflex-hyper, Eyes damage, Sensorium damage, Intellect diminished, Infectious arteritis --> Stroke, Speech changes. 

§  P  _______________, _______________, _______________, _______________, _______________

§  A  _______________, _______________, _______________, _______________, _______________

§  R  _______________, _______________, _______________, _______________, ________________

§  E  _______________, _______________, _______________, _______________, _______________

§  S  _______________, _______________, _______________, _______________, _______________

§  I  _______________, _______________, _______________, _______________, _______________

§  S  _______________, _______________, _______________, _______________, _______________

v Summary of the stages of syphilis by manifestation:  CGAT (the four DNA bases) --> Chancre (primary) Condylomata lata (secondary), Gummas/Aortitis/Argyll-Robertson pupil/Tabes dorsalis (tertiary)

§  C  _______________, _______________, _______________, _______________, _______________

§  G  _______________, _______________, _______________, _______________, _______________

§  A  _______________, _______________, _______________, _______________, ________________

§  T  _______________, _______________, _______________, _______________, _______________

RPR & VDRL:  Cheap and fast but not specific  --> should always be followed up by a more specific treponemal test. VDRL False (+): VDRL --> Virus (EBV, hepatitis, varicella, measles), Drugs, Rheumatic fever (endocarditis), RA, Lupus & other CTD, Lyme disease, Leprosy.  More specific tests based on monoclonal antibodies and immunofluorescence, including Treponema pallidum hemagglutination assay (TPHA) and Fluorescent Treponemal Antibody Absorption (FTA-ABS) are more specific and more expensive.

Ø  V  _______________, _______________, _______________, _______________, _______________

Ø  D  _______________, _______________, _______________, _______________, _______________

Ø  R  _______________, _______________, _______________, _______________, ________________

Ø  L  _______________, _______________, _______________, _______________, _______________

FTA-ABS: Find The Abs ABSolutely; specific; turn (+) earliest & remains longest

o   Treatment:  The first-choice treatment for all manifestations of syphilis remains penicillin G. Parenteral penicillin G is the only therapy with documented effect during pregnancy. Early syphilis: 1 dose of penicillin is sufficient.  Ceftriaxone may be considered as an alternative therapy. If compliance and follow-up cannot be ensured, the CDC recommends desensitization with penicillin followed by penicillin treatment. All pregnant women with syphilis should be desensitized and treated with penicillin. Follow-up includes clinical evaluation at 1 to 2 weeks followed by clinical and serologic evaluation at 3, 6, 9, 12, and 24 months after treatment.  Late latent (latency for greater than one year) penicillin G is recommended as weekly doses for 3 weeks. If allergic, then tetracycline or doxycycline may be used but for 28 days instead of the normal 14.   Neurosyphilis:  aqueous crystalline penicillin G IV q4 hours or continuously for 10-14 days. If intravenous administration is not possible, then procaine penicillin is an alternative (administered daily with probenecid for two weeks).

o   Jarisch-Herxheimer reaction:  characterized by fever, fatigue, and transient worsening of any mucocutaneous symptoms, and usually subsides within 24 hours. These symptoms can be alleviated with acetaminophen and should not be mistaken for drug allergy.

Primary chancre of syphilis at the site of infection

By CDC/M. Rein, VD - This media comes from the Centers for Disease Control and Prevention's Public Health Image Library (PHIL), with identification number #6803.Note: Not all PHIL images are public domain; be sure to check copyright status and credit authors and content providers.English | Slovenščina | +/−, Public Domain,

Typical secondary syphilis with a rash on the palms of the hands

By CDC/ Robert Sumpter - This media comes from the Centers for Disease Control and Prevention's Public Health Image Library (PHIL), with identification number #6809.Note: Not all PHIL images are public domain; be sure to check copyright status and credit authors and content providers.English | Slovenščina | +/−, Public Domain,

Red papules and nodules over much of the body due to secondary syphilis

By Herbert L. Fred, MD, and Hendrik A. van Dijk, CC BY 2.0,

- V-vasculitis & other purpuric diseases: Leukocytoclastic vasculitis, granuloma faciale:

Treponema pallidum spirochetes using a modified Steiner silver stain

Public Domain,

-       V-vesicular & pustular diseases (intraepidermal vs. subepidermal):  Transient neonatal pustular melanosis, pemphigus vulgaris, bullous pemphigoid, dermatitis herpetiformis.

Molluscum Contagiosum:  By a DNA poxvirus called the molluscum contagiosum virus (MCV). The incidence of MC infections in young children is around 17% and peaks between 2-12 years of age. MC affects any area of the skin but is most common on the body, arms, and legs. It is spread through direct contact, saliva, or shared articles of clothing.  In adults, molluscum infections are often sexually transmitted and usually affect the genitals, lower abdomen, buttocks, and inner thighs. In rare cases, molluscum infections are also found on the lips, mouth and eyelids.  

·       Evaluation:  Molluscum contagiosum lesions are flesh-colored, dome-shaped, and pearly in appearance. They are often 1-5 millimeters in diameter, with a dimpled center. They are generally not painful, but they may itch or become irritated. Picking or scratching the bumps may lead to further infection or scarring. In about 10% of the cases, eczema develops around the lesions. They may occasionally be complicated by secondary bacterial infections.  The central waxy core contains the virus. In a process called autoinoculation, the virus may spread to neighboring skin areas. Children are particularly susceptible to auto-inoculation, and may have widespread clusters of lesions. 

·       Treatment:  Betadine,  trichloroacetic acid, Australian lemon myrtle, Over-the-counter substances (topical salicylic acid, tretinoin cream), Imiquimod, curettage, cryotherapy.

Molluscum contagiosum

By Evanherk from nl, CC BY-SA 3.0,

Wart:  Verrucous papules due to infection with the human papillomavirus (HPV), of which there are more than 60 subtypes. 

Ø  PRESENTATION:  Appearance on the skin resembles a cauliflower, with tiny black petechiae in the center representing thrombosed capillaries in the dermal papillae. Pinpoint bleeding may occur when these are scratched.  Common types of warts:

§  Verruca vulgaris (common wart):  Most common on acral skin of hands and fingers

§  Verruca plantaris (plantar wart): Located on plantar foot

§  Filiform wart: Mostly on the face

§  Verruca plana (flat wart):  Often on the face and legs of children and young adults (spread by shaving) with multiple papules less than 4mm in diameter with flat-topped smooth surface.

Ø  TREATMENT: Medications:  Salicylic acid: peeling away dead surface skin cells including along with the wart; immunotherapy:  Intralesional injection of antigens (mumps, candida or trichophytin antigens USP) to trigger a host immune response to the wart virus.  Surgery:  Liquid nitrogen, cauterization 

Plantar wart

By James Heilman, MD - Own work, CC BY-SA 4.0,

Filiform wart on the eyelid

By Schweintechnik - Own work, Public Domain,

Viral skin infection: Molluscum contagiosum, warts, viral exanthems




HYPERSENSITIVITY REACTION: ACID --> Anaphylactic (WHAT), Cytotoxic (BIGGER), Immune complex (RAGS), Delayed type (TC= T-cells)

MAJOR NON-CANCEROUS SKIN DISORDERSGIVE CARD --> G-granulomatous diseases: G-genodermatoses, • I-infections, I-infestations, V-vasculitis & other purpuric diseases, V-vesicular & pustular diseases (intraepidermal vs. subepidermal), E-Eczematous & papulosquamous diseases, C-Connective tissue alterations, A-adnexal inflammatory diseases, • R-reactive erythemas, • D-deposition & metabolic diseases

-       G-granulomatous diseases (non-infectious): Granuloma annulare, necrobiosis lipoidica, rheumatoid nodule, sarcoidosis, xanthoma

-       G-genodermatoses (inherited Genetic skin conditions grouped into three categories: chromosomal, single gene, and polygeneAc.):

-       I-infections/I-infestations: Viral (Molluscum congatiosum, warts (verruca), Viral exanthem:  MERCHAnt --> Measels (rubeola), Erythema infectiosum (Fifth disease by parvovirus), Exanthem subitum (roseola by HHV-6/7), Rubella, Chickenpox (VZV), Hand, foot, and mouth disease (coxsackie A16), Herpes zoster, Asymmetric periflexural exanthem of childhood), bacterial (BACTERIAL SKIN INFECTIONS:  FICS -->Folliculitis, Furuncles, Impetigo, Carbuncles, Cellulitis, Scalded Skin Syndrome), fungal (CUTANEOUS MYCOSIS (superficial fungal skin infection):  Tinea Nigra, Tinea Versicolor, Tinea Cruris/Corporis/Capitis), STD (Gay & HeteroSexual Contract These = GHSCT --> Gonorrhea, Hepatitis B + C, HSV, HPV, HIV, Hemophilus ducreyi, Chlamydia, Treponema pallidum); INFESTATION:  PS --> Pediculosis, Scabies

-       V-vasculitis & other purpuric diseases:  Leukocytoclastic vasculitis, granuloma faciale,

-       V-vesicular & pustular diseases (intraepidermal vs. subepidermal):  Transient neonatal pustular melanosis, pemphigus vulgaris, bullous pemphigoid, dermatitis herpetiformis,

-       E-Eczematous & papulosquamous diseases:  Eczema, contact dermatitis, lichen simplex chronicus (neurodermatitis), pityriasis rosea, psoriasis, lichen planus,

-       C-Connective tissue alterations:  scleroderma, lichen sclerosus,

-       A-adnexal inflammatory diseases: Acne, miliaria, alopecia areata,

-       R-reactive erythemas:  Urticaria, drug eruptions, erythema multiforme, pruritic urticarial papules and plaques of pregnancy (PUPPP), Sweet’s syndrome, livedo reticularis

-       D-deposition & metabolic diseases:  Amyloidosis, gout, pretibial myxedema, digital mucous cyst, mucocele, calcinosis cutis, argyria

 SKIN CANCERS: Bad Skin Malignancy = BSM --> B-BCC, S-SqCC, M-Melanoma, M-Mycosis fungoides (cutaneous T-cell lymphoma-CTCL)

-       Leukocytoclastic vasculitis:

Ø  PATHOPHYSIOLOGY: It is an inflammation of small blood vessels (usually post-capillary venules in the dermis).

Ø  PRESENTATION: Clinically characterized by palpable purpura, classically appearing on the legs. It is the most common vasculitis seen in clinical practice.  Systemic cases  may involve the kidneys, brain, or other organ and in some cases are associated with Henoch-Schonlein pupura (fever, arthralgias, abdominal pain, hematura); also associated with chronic idiopathic urticaria, hypocomplementemia, essential mixed cryoglobulinemia, drug reactions, connective tissue disorders.

Ø  DIAGNOSTIC EVALUATION: Skin biopsy: Neutrophilic inflammation with fibrinoid necrosis and fragmented neutrophilic nuclei (leukocytoclasis). 

Leukocytoclastic vasculitis  due to minocycline.

By James Heilman, MD - Own work, CC BY-SA 3.0,

Leukocytoclastic vasculitis

By James Heilman, MD - Own work, CC BY-SA 3.0,

Neutrophilic inflammation with fibrinoid necrosis and fragmented neutrophilic nuclei (leukocytoclasis)

Transient neonatal pustular melanosis:

Ø  EPIDEMIOLOGY: More common in dark skinned newborns (occur in 2 - 5% of black infants and less than 1% of white infants). They are more common in term infants and are almost always seen at birth or soon after birth.


Ø  PRESENTATION:  1- to 3-mm flaccid, superficial fragile pustules, some of which may have already resolved in utero, leaving pigmented macules. The pustules and vesicles are very superficial and resolve over a period of a few days. The hyperpigmented macules may last for weeks to months.

Ø  DIAGNOSTIC EVALUATION: Skin biopsy: Is not required but may show subcorneal pustule, sometimes with eosinophils as well as neutrophils, and perivascular neutrophils, lymphocytes, and eosinophils.

Transient neonatal pustular melanosis

By Gzzz - Own work, CC BY-SA 4.0,

•       P emphigus vulgaris:  AI disease that causes blistering and raw sores on skin and mucous membranes.  Fatal without immunosuppressant.  40-60 y/o.  Start in oral mucosa progressing from localized blister to generalized bullae.

Evaluation: Flaccid vesicles and bullae containing serous fluid.  Positive Nikolsky’s sign.  Pressure on bullae causes lateral extension.  Biopsy: Intraepidermal bullae and acantholysis.  Unlike in the related pemphigoid, pemphigus manifests as intra-epithelial clefting, meaning the spinous cells of the epithelium break apart, a phenomenon known as acantholysis. This is because the desmosomes are attacked. In pemphigoid, the epitheium remains intact, but is entirely "unzipped" from the underlying connective tissue bed, or lamina propria, because the hemidesmosomes are attacked. Also apparent in pemphigus is a "tombstone appearance" of the basal cell layer and Tzanck cells.  Direct IF: IgG & C3 deposit in intercellular epidermis.  Indirect IF: auto-Ab against desmoglein 3. 
Treatment:  SCAM --> Steroid taper, Cyclophosphamide, Azathioprine, MTX.
Ø  S  _______________, _______________, _______________, _______________, _______________

Ø  C  _______________, _______________, _______________, _______________, _______________

Ø  A _______________, _______________, _______________, _______________, ________________

Ø  M _______________, _______________, _______________, _______________, _______________

Pemphigus vulgaris with the characteristic "tombstoning"

By Nephron - Own work, CC BY-SA 3.0,

•       B ullous pemphigoid (IgG against hemidesmosome collagen XVII of BM):  patients are usually >60 y/o. 

Evaluation: Prodromal erythematous urticarial, popular lesion à large, tense pruritic bullae containing serous to blood fluid --> erosions & crusting.  Pressure on the bullae DO NOT lead to lateral extension.  Negative Nikolsky’s sign (skin separates after minor trauma).  Affects skin (groin, axillae, forearms, thighs, abdomen) & SPARE oral mucosa.  CBC: eosinophilia.  Biopsy:  Subepidermal bullae with characteristic lymphocytic & eosinophilic dermal infiltrate and neutrophils arranged in Indian file at the DE junction.
Treatment: Mild: topical steroids.  Severe: PO prednision or azathioprine or dapsone.

H erpetiform dermatitis:  Associated with Celiac’s disease.  Usually begin in age 20’s. 
Ø Evaluation:  breakouts are usually extremely itchy. In many people the vesicles or papules appear most commonly at pressure points like elbows, knees, back, and buttocks. It may also present as a patch of red skin with little water blisters scattered about. The unpredictable skin rash may appear or be exacerbated by any irritation such as dry skin, scratching or clothing that is rough or scratchy.  Skin and intestinal biopsy, and direct immunofluorescence test of the skin. 

Ø Treatment:  Dapsone and strict gluten-free diet.

Dermatitis herpetiformis characteristic rash

By Madhero88 -, CC BY-SA 3.0,

By Madhero88 -, CC BY-SA 3.0,

- E-Eczematous & papulosquamous diseases: Eczema, contact dermatitis, lichen simplex chronicus (neurodermatitis), pityriasis rosea, psoriasis, lichen planus

A topic dermatitis (eczema):  Hypersensitivity to allergens --> IgE crosslinking on mast cells & basophils à release of histamine, LT (leukotrienes), and chemoatrractants à late phase inflammatory cells infiltration in the skin.
Ø Evaluation: The skin of a patient with atopic dermatitis reacts abnormally and easily to irritants, food and environmental allergens and becomes red, flaky and very itchy. It also becomes vulnerable to surface infections caused by bacteria.  Atopic dermatitis in people often occurs together with other atopic diseases like hay fever, asthma and conjunctivitis.  Histology:  1) acute: spongiosis (epiderm intercell edema) w/ vesicles 2) chronic: HALL --> Hyperkeratosis, Acanthosis, Lichenification, Lymphocytic dermal infiltrate.   Likely locations of rash:

v Infant:  cheek, forehead, extensor surfaces

v Child-Adult:  flexural surfaces, neck, wrist, ankle

Ø Treatment:  SEA (it is thought that bathing in the sea improve atopic dermatitis) --> Steroids oinment, Emollient, Antibiotic (erythromycin, dicloxacillin, or cephazolin 250 mg QID) for infectious complications, Antithistamine (hydroxyzine, doxepin) for itching.

v S  _______________, _______________, _______________, _______________, _______________

v E  _______________, _______________, _______________, _______________, _______________

v A _______________, _______________, _______________, _______________, ________________

Eczematous dermatitis of the hands

By James Heilman, MD - Own work, CC BY-SA 4.0,

Eczematous dermatitis of the hands

By Jambula at English Wikipedia - Transferred from en.wikipedia to Commons., Public Domain,

C ontact dermatitis (Type IV delay type hypersensitivity):  Localized rash or irritation of the skin caused by contact with a foreign substances (e.g. poison ivy/oak, nickel, perfumes, soaps, cosmetics).  Only the superficial regions of the skin (epidermis & outer dermis) are affected in contact dermatitis. 
Ø  Evaluation:  Pruritic erythematous, weepy, crusted patches/plaques, papulovesicular rash aligned in specific patterns. 

Ø  Treatment:  Mild: cool compresses & topical steroids.  Severe: systemic steroids & antihistamine.

3-year-old girl with contact dermatitis, one day after contact with poison ivy

By Alborz Fallah - Own work, CC BY-SA 3.0,

Lichen simplex chronicus and prurigo nodularis:


Ø  PATHOPHYSIOLOGY: Both are end-stage lesions that start out as some kind of exzema, neurodermatitis, arthropod bite, folliculitis, that causes patient to pick and scratch.

Ø  PRESENTATION: Lichen simplex chronicus:  Scaly, erythematous plaque represents lichenified (thickened) skin due to chronic rubbing or irritation.  prurigo nodularis (picker’s nodule): same except that it is a localized nodule instead of a plaque.


Ø  TREATMENT:  Aimed at reducing itching and inflammation ( with a lotion or steroid cream (such as Betamethasone) applied to the affected area) to reduce rubbing and scratching, which exacerbate lichen simplex chronicus.

A plaque of lichen simplex chronicus

By kilbad (talk) - I (kilbad (talk)) created this work entirely by myself., CC BY 3.0,

Histologic features of LSC:

- Hyperkeratosis with focal parakeratosis

-Hypergranulosis with irregular acanthosis

-Vertical orientation of collagen in dermal papillae with perivascular lymphoid infiltrate, and, sometimes, prominent fibroblasts.

By Nephron - Own work, CC BY-SA 3.0,

•       P ityriasis rosea:  Associated with HHV-7. 

Evaluation: Diffuse pruritic oval erythematous plaques with white scale in a Christmas tree pattern.  Some preceded by the pathognomonic solitary 2-6 cm “herald patch”.  Skin biopsy: if does not resolve in 2 months.  VDRL: to r/o secondary syphilis. 
Treatment: Self Limited.  Sunlight/UVB hastens healing.  Pruritis: topical steroids/talc

Herald patch of pityriasis rosea which started before the rest of the lesion and was initially mistaken for a fungal infection

By James Heilman,MD - Own work, CC BY-SA 3.0,

Pityriasis rosea on human back

By James Heilman,MD - Own work, CC BY-SA 3.0,

•       P soriasis:  Affects both sexes equally and can occur at any age, although it most commonly appears for the first time between the ages of 15 and 25.  T-cell mediated inflammatory disorder --> epidermal hyperproliferation. 

Evaluation:  Red plaques with silvery scale and sharp margins over the extensor surface.  Auzpitz’s sign:  bleed on detachment.  Koebner’s sign: appear at site of trauma.  Psoriatic arthritis (15%):  pruritus, pain, joint stiffness.  Pustular psoriasis:  generalized toxicity, fever, malaise.  Biopsy: Thicken epidermis with an absent of granular layer.  Munro microabscesses: neutrophils in the stratum corneum.  Blood test: AEU --> Anemia, ESR ↑, Uric acid ↑. 
Ø  Psoriasis SPECK --> Silvery Scale on Scalp, Sacrum, Pelvis, Elbow, Knee, Parakeratosis, Extensor surface, Cytokine from T-cell (TNF-a) --> Keratinocytes hyperproliferation.

v S  _______________, _______________, _______________, _______________, _______________

v P  _______________, _______________, _______________, _______________, _______________

v E _______________, _______________, _______________, _______________, ________________

v C _______________, _______________, _______________, _______________, _______________

v K _______________, _______________, _______________, _______________, _______________

Treatment:  Mild (affect <3% of the body) – moderate (3-10%): topical steroids, coal tar.  Severe: PUVA/UVB, MTX, biologics

Psoriasis of the back

By Psoriasis_on_back.jpg: User:The Wednesday Island (of the English Wikipedia)derivative work: James Heilman, MD (talk) - Psoriasis_on_back.jpg, CC BY-SA 3.0,

Psoriatic plaque, showing a silvery center surrounded by a reddened border.

By James Heilman, MD - Own work, CC BY-SA 3.0,

•       L ichen planus:  Inflammation of the skin & mucus membrane often due to drug & Hep C.  There are cases of lichen planus-type rashes (known as lichenoid reactions) occurring as allergic reactions to medications for high blood pressure, heart disease and arthritis.

Evaluation:  5 P’s  --> Pruritic, Planar, Purple, Polygonal, Papules with white lines (Wickham’s striae) commonly on Penis, Eyelid, Wrist, Scalp, Shin.  Biopsy:  Inflammatory hyperkeratosis with band-like mononuclear infiltrate in the DE junction.  Sawtooth appearance of the rete pegs & necrotic basal cells in the papillary dermis (Civatte’s bodies). 
Treatment:  Mild: topical glucocorticoids.  Severe: Cyclosporine, PO prednisolone/retinoids, PUVA.  4 P’s -->
Ø  P  _______________, _______________, _______________, _______________, _______________

Ø  P  _______________, _______________, _______________, _______________, _______________

Ø  P _______________, _______________, _______________, _______________, ________________

Ø  P _______________, _______________, _______________, _______________, _______________

Lichen planus affecting the shins

By James Heilman, MD - Own work, CC BY-SA 3.0,

Lichen planus on the lips and the lateral border of the tongue

By Department of Dermatology, Mayo clinic, Rochester, Minnesota - Lehman report 2009, CC BY 3.0,

- C-Connective tissue alterations: scleroderma, lichen sclerosus

Morphea located on the back of a 16 year old caucasian woman

By Leith C Jones at English Wikipedia, CC BY 3.0,





-       Morphea: Localized sclerotic skin plaques often with a violaceous halo, usually on the trunk, and no systemic disease. 

-       Scleroderma:  Chronic systemic disease with indurated skin, especially of trunk, extremities, perioral, and fingers (sclerodactyly), associated with Raynaud’s phenomenon, hypertension, gastrointestinal disease (especially esophageal dysmotility), pulmonary fibrosis, and kidney disease.  A minority of patients have Scl-70 antibody.  ANA with a speckled or characteristic antinucleolar pattern.

-       CREST syndrome:  C-calcinosis, R-raynaud’s phenomenon, E-esophageal dysmotility, S-sclerodactyly, and T-telangiectasia with anticentromere antibody.  Better prognosis with regard to kidney disease than other forms of systemic scleroderma.


Ø  DIAGNOSTIC EVALUATION:  Skin biopsy: Epidermis is normal or atrophic, while the dermis and subcutaneous fat are hyalinized.  Sparse perivascular lymphocytes, sometimes plasma cells, are present in dermis or subcutaneous fat, more prominent in early lesions and in morphea than in systemic scleroderma.  Adnexal structures are decreased with eccrine glands entrapped by collagen and located higher up than usual because of increased colagen in subcutaneous fat.

CREST syndrome (calcinosis and sclerodactyly)

By James Heilman - Own work, CC BY-SA 4.0,

•       L ichen sclerosus et atrophicus:  40-50 y/o female.  It is an autoimmune disease and can be associated with hypothyroidism.  M > F, particularly around and after menopause, but girls may also get the disease.  Rare cases progresses to squamous cell carcinoma. 

Evaluation: Women: commonly occurs on the vulva and around the anus with ivory-white elevations that may be flat and glistening. There may be marked itching or the condition may be without any symptoms. There may also be thinning and shrinkage of the genital area that may make coitus painful.   Males:  whitish thickening of the foreskin, which cannot be retracted easily.  The lesion may also be found in the trunk, neck, and oral mucosa.  Waxing & waning course.  Biopsy:  Hyperkeratotic epidermis with follicular plugging & homogenous collage band in the dermis. 
Treatment: topical glucocorticoids, androgen; PO hydroxychoroquine.

Lichen sclerosus on an 82-year-old woman, showing an ivory white coloring in the vulva, and also stretching downward to the perineum

By Mikael Häggström - Own work, CC0,

Lichen sclerosus showing the characteristic subepithelial sclerosus

By Nephron - Own work, CC BY-SA 3.0,

A-adnexal inflammatory diseases: These are inflammatory diseases involving sweat glands or pilosabaceous units, and including acne, miliaria, alopecia areata

•       A cne vulgaris:  Androgen stimulates sebaceous gland --> hyperkeratosis & blockage of canal --> Propionibacterium acnes overgrowth behind the blockage --> lipase & chemotatic factors --> neutrophils migrate into area --> release hydrolases --> breakdown surround skin --> infiltrate deeper.

Ø  1) Comedonal:  white head (closed) & black heads (opened). 

Ø  2) Inflammatory: papules, nodule, cysts.

Evaluation: if suspected --> check serum TESTOSTERONE + DHEA
Ø  1) Mild non-inflammatory: topical tretinoin.  Skin seems to be worst within 3-4 weeks but most will see improvement after 6 weeks.

Ø  Mild inflammatory:  topical tretinoin + benzoyl peroxide + topical antibiotic (erythromycin, clindamycin)

Ø  Moderate inflammatory:  topical tretinoin + PO antibiotic (tetracycline, doxycycline, or minocycline)

Ø  Severe inflammatory:  above + Accutane (extremely teratogenic --> require 2 forms of birth controls 1 month prior, during, and 1 month after therapy).

Hair follicle anatomy

By BruceBlaus. When using this image in external sources it can be cited staff. "Blausen gallery 2014". Wikiversity Journal of Medicine. DOI:10.15347/wjm/2014.010. ISSN 20018762. - Own work, CC BY 3.0,

18-year-old male with moderate severity acne vulgaris demonstrating classic features of whiteheads and oily skin distributed over the forehead

By Roshu Bangal - Own work, CC BY-SA 4.0,

Nodular acne on the back

By James Heilman, MD - Own work, CC BY-SA 3.0,


Ø  PATHOPHYSIOLOGY: Most folliculitis is due to follicular occlusion with normal flora; some cases are due to staphylococcus, gram-negatives (especially in patients on chronic antibiotics), tinea, Candida, Pityrosprorum, or Demodex.


§  Folliculitis:  Papulopustular eruption, especially on the scalp, trunk, and legs of women from shaving .

§  Furuncle (boil):  Deep folliculitis most commonly caused by infection by Staphylococcus aureus.  It appears as a painful swollen pus-filled nodules.

§  Carbuncles:  Individual furuncle clustered together. 

Ø  DIAGNOSTIC EVALUATION: Skin biopsy: Peri- or intrafollicular mixed infiltrate of lymphocytes, histiocytes, or plasma cells.  Ruptured follicle are surrounded by neutrophils and multinucleated giant cells.  Perifollicular fibrosis in older lesions.

Ø  TREATMENT:  Topical antiseptic treatment is adequate for most cases.  Topical antibiotics such as mupirocin or Neomycin/polymyxin B/bacitracin ointment are required in more severe cases, while some cases may benefit from systemic narrow-spectrum penicillinase-resistant penicillins (such as dicloxacillin).  Fungal folliculitis may require topical antifungals such as Econazole Nitrate or an oral antifungal such as Fluconazole.


By Jmarchn - Own work, CC BY-SA 3.0,


By The original uploader was Mahdouch at French Wikipedia - Transferred from fr.wikipedia to Commons., CC BY 1.0,

Carbuncle on buttock of a diabetic person

By Drvgaikwad - Own work, CC BY 3.0,

Miliaria:  Common, but rarely biopsied “heat rash” or “prickly heat”

Ø  PATHOPHYSIOLOGY: Common ailment in hot and humid conditions, such as in the tropics and during the summer season. It is especially common in children and infants due to their underdeveloped sweat glands.  The sweat gland ducts get plugged due to dead skin cells or bacteria.

Ø  PRESENTATION:  Pruritic small red papules occurring most commonly on the upper chest, neck, elbow creases, under the breasts and under the scrotum.

§  Miliaria crystallina:  Hundreds of mostly clear small subcorneal vesicles over sweat ducts, which contain no inflamatory cells.

§  Miliaria rubra:  Red papules, spongiosis of intraepidermal sweat duct, sometimes producing intraepidermal vesicles, perivascular lymphocytes or neutrophils.

§  Miliaria profunda:  Red nodules or pustules, deeper and denser inflammation.

§  Fox-Fordyce disease (apocrine miliaria):  Rare, extremely pruritic eruption of papules in the axilla and anogenital area of women.  Skin biopsy: Spongiosis of vesicle in plugged follicle near connectin with aprocrine duct and perivascular or periadnexal lymphocytes or neutrophils.  Treatment:  Responds to estrogen therapy and/or topical antibiotic (clindamycin)

Ø  TREATMENT:  Primary remedy is to avoid overheating one's body by wearing lighter clothing or moving to a cooler climate.  Soothing ointment such as calamine lotion. In most cases the rash of miliaria will resolve without intervention. However, severe cases can last for weeks and cause significant disability, in which cases, the use of topical antibacterials (including antibacterial soaps) may shorten the duration of symptoms.

Ø  DIFFERENTIAL DIAGNOSIS:  Hidradenitis suppurativa: more impressive tender nodules or sinus tract rather than small pruritic papules. 

Typical red spots on chest, neck and shoulders, caused by miliaria rubra

By Sentient Planet - Own work, CC BY-SA 3.0,

Alopecia areata:  A common autoimmune non-scarring alopecia mostly in children.

Ø  PRESENTATION:  Smooth round patches of alopecia most commonly on scalp, but sometimes in the beard.  Spontaneous regrowth can occur, especially in localized forms.  Involvement of a continuous band from the temple to the occiput is called “ophiasis”, and has a poor prognosis for regrowth.

Ø  DIAGNOSTIC EVALUATION: Skin biopsy:  Lymphocytes around lower portion of follicle, resembling a “swarm of bee” in early lesion.  Increased miniature telogen and catagen follicles, or sometimes early anagen follicles, in superficial dermis.


§  Trichotillomania:  Traumatized follicular unit fom pulling at the hair or traction of braiding or straightening of hair that results in follicular degeration, scarring, and considerable alopecia.  Biopsy:  Presence of deformed hair shafts, pigmented casts in follicles, or empty follicles.  Perifollicular lymphocytes, plasma cells, or neutrophils usually sparse or absent.  Perifollicular fibrosis; if a follicle is destroyed, a vertical fibrous tract often remains.

§  Androgenetic alopecia: Common “pattern baldness” occurring in men on bitemporal areas and crown of the scalp.  Biopsy:  Increased telogen hairs and miniaturized vellus follicles in late stages.

Telogen effluvium:  Common acute molting of hair, usually from scalp, often presenting 3 months after stressful event (surgery, childbirth, febrile illness).  Due to cycling of growing anagen hairs into the telogen phase.  Biopsy:  Increased telogen hair count.

Alopecia areata

By Abbassyma at English Wikipedia - Transferred from en.wikipedia to Commons., Public Domain,

A pattern of incomplete hair loss on the scalp of a person with trichotillomania

By Robodoc (original uploader) -, Public Domain,

Male-pattern hair loss

R-reactive erythemas:  Reactions to infections, drugs, malignancies, etc.  These are generally more dermal, having less scale or epidermal changes (compare to eczematous and papulosquamous dieases).  The erythema blanches, and there is no purpura or vasculitis (compare o vasculitis and other purpuric diseases).  Acute lesions are bright red and edematous, often accompanied by palm and sole involvement or fever.  When erythemas make rings, they are annular, and are sometimes called gyrate erythemas.  They include urticaria, drug eruptions, erythema multiforme, pruritic urticarial papules and plaques of pregnancy (PUPPP), Sweet’s syndrome, livedo reticularis


Ø  EPIDEMIOLOGY: Common; occurs in 20% of the population in their lifetime

Ø  PATHOPHYSIOLOGY: IgE mediated type I hypersensitivity to foods, drugs, infection, or idiopathic.  Rare cases are due to cold exposure, sun exposure, pressure,  psychological stress, etc.

Ø  PRESENTATION: Pruritic evanescent wheals (hives) that move around

Ø  DIAGNOSTIC EVALUATION: Skin biopsy: Normal epidermal with underlying dermal edema with sparse perivascular and interstitial eosinophils, lymphocytes, neutrophils, &/or mast cells.


Ø  TREATMENT: Avoid triggers.  Antihistamines:  Blockade of the histamine H1 receptors is the first line of therapy. Systemic steroids:  Effective in controlling symptoms of chronic urticaria however use is limited by adverse effects such as adrenal suppression, weight gain, osteoporosis, hyperglycemia, etc. Leukotriene-receptor antagonists:  Montelukast and zafirlukast can be used as add on treatment or in isolation; may be more beneficial for patients with NSAID induced chronic urticarial.

Hives on the arm

By James Heilman, MD - Own work, CC BY-SA 3.0,

Drug eruptions:

Ø  PRESENTATION:  Can produce almost any clinical and histologic patterns

§  Maculopapular rashes:  Most common pattern with generalized small red papules and macules without scaling.  Biopsy: Perivascular lymphocytes, often with eosinophils, and sometimes interface changes.

§  Fixed drug eruption:  Clinically a bright red plaque, fixed in one place consistently when challenged with the drug, heals with hyperpigmentation.  Biopsy: Histology similar to erythema multiforme, but more likely to have eosinophils.

§  Lichenoid drug eruption: Histology similar to lichen planus, but more likely to have parakeratosis and eosinophils.

§  Bullous drug eruptions: Overlap clinically and histologically with erythema multiforme; immunofluorecence negative.

§  Acute generalized exanthematous pustulosis:  Similar to pustular psoriasis, but more likely to have papillary dermal edema, necrotic keratinocytes, and eosinophils.

§  Drug induced pseudolymphoma:

§  Drug induced hyperpigmentation: Argyria; minocycline (iron and melanin-positive brown dermal pigment), gold (chrisiasis pigment appers as black particles), bleomycin (increased melanin in basal layer), clofazimine (brown lipofuscin stains with PAS), amiodarone (brown pigment stains with PAS).

§  Neutrophilic eccrine hidradenitis:  Neutrophils around eccrine glands associated with chemotherapy.

Pruritic urticarial papules and plaques of pregnancy (PUPPP):

Ø  EPIDEMIOLOGY: Most common pregnancy rash usually occur in first pregnancies, in the third trimester and is more likely with twin pregnancies or rapid abdominal distension (lesions often first appear within stretch marks).

PRESENTATION: Very pruritic papular and urticarial rashes frequently begins on the abdomen striae and spreads to the legs, feet, arms, chest, and neck. 

Ø  DIAGNOSTIC EVALUATION:  Skin biopsy:  Mild focal parakeratosis and spongiosis with dermal edema and perivascular lymphocytes with eosinophils.  Negative direct immunofluorescence.


Ø  TREATMENT: Topical moisturising creams or aqueous/emollient ointments. Class I or II corticosteroid creams are used in more aggressive cases.  Antihistamines may provide relief from the itch.  Induction of labor:  In the majority of cases, PUPPP resolves spontaneously within a week of delivery.


By Heykerriann at English Wikipedia - Transferred from en.wikipedia to Commons by Jusses2 using CommonsHelper., Public Domain,

Erythema annulare centrifugum (EAC):

Ø  EPIDEMIOLOGY:  Uncommon, usually idiopathic, but sometimes a casuse such as tinea pedis is found.

Ø  PRESENTATION: Anular plaques (if rings are not present, then it is not EAC) usually of the trunk of adults, often with half-rings with a collarette of trailing scales.

Ø  DIAGNOSTIC EVALUATION: Skin biopsy: Focal spongiosis or parakeratosis with sharply demarcated “coat-sleeve” lymphocytes densely arranged around dilated superficial and deep blood vessels.

Ø  TREATMENT:  Topical corticosteroids may be helpful in reducing swelling and pruritus.  If caused by an underlying disease or malignancy, then treating and removing the disease or malignancy will stop the lesions.  Otherwise no treatment is usually needed as the condition is self-limited.

Erythema gyratum repens (EGR):

Ø  EPIDEMIOLOGY: Very rare and usually associated with underlying systemic malignancy, especially carcinomas of the lung.

Ø  PRESENTATION: Characteristic c clinical “wood-grain” pruritic, red, scaly, rash most commonly on trunk, and changing daily.

Ø  DIAGNOSTIC EVALUATION: Skin biopsy: Non-specific and resembles other diseases with perivascular dermatitis. 

•       Erythema multiforme:  Mediated by deposition of immune complex (mostly IgM) in the superficial microvasculature of the skin and oral mucous membrane that usually follows DIM --> Drug exposure (Barbiturates, Allopurinol, Penicillin, Phytoin, Sulfa drugs), Infection (HSV, mycoplasma, fungus), Malignancy.

Ø  Evaluation:  Flu-like prodrome: fever, sore throat, and headache, which may also be accompanied by photophobia and redness in the eyes, followed by the sudden development of multiforme mucocutaneous lesions that can cover the majority of the skin. These lesions begin as macules and can develop into papules, vesicles, blisters, or urticarial and target lesions.  Variants:

•       SJS (Stevens-Johnson syndrome):  when < 10% of body surface is involved.

•       TEN (toxic epidermal necrolysis): Extensive sloughing of full-thickness necrotic skin involving > 30% of body surface area. 

•       Necrolytic migratory erythema (glucagonoma syndrome): Crusted plaques around mouth, perioral, and acral skin with elevated serum glucagon level.  Skin biopsy:  Psoriasiform with tendency for only the upper epidermis to be necrotic and pale.

Ø  Treatment:  Discontinue all medications.  Treat similar to thermal burns, and continued care can only be supportive (e.g. IV fluids) and symptomatic (e.g. analgesic mouth rinse for mouth ulcer). Corticosteroids use is controversial since it might aggravate the condition or ↑ secondary infections. Other agents have been used, including cyclophosphamide and cyclosporine, but none have exhibited much therapeutic success. An ophthalmologist consult immediately, as SJS frequently causes the formation of scar tissue inside the eyelids leading to corneal vascularization and impaired vision, as well as a host of other ocular problems.  Erythema multiforme STEM --> EM includes SJS, TEN, it is a Type Two hypersensitivity reaction (cytotoxic) leading to Target lesion, Epidermal necrosis, and Multiforme (papules, vesicles, blisters, or urticaria) lesion.

Erythema Multiforme

By Nbrigham - Own work, CC BY-SA 3.0,

Target lesion

By kilbad (talk) - I (kilbad (talk)) created this work entirely by myself., CC BY-SA 3.0,

Erythema ab igne

Ø  PATHOPHYSIOLOGY:  Thermal radiation exposure can induce epidermal damage to superficial blood vessels that subsequently leads to vascular dilation.  The distribution of affected blood vessels — predominantly in the superficial subcutaneous plexus (found in the papillary dermis)— results in the net-like pattern of erythema ab igne skin lesions.  Red blood cell extravasion and deposition of hemosiderin that follows clinically appears as hyperpigmentation.

Ø  PRESENTATION:  Reticulated erythema, hyperpigmentation, scaling and telangiectasias.  Related to chronic heat exposure, especially from use of heating pads or sitting next to a fire.  Rarely occurs in females with hypothyroidism. 

Ø  DIAGNOSTIC EVALUATION: Primarily a clinical diagnosis.

Hot bottle rash in a person with chronic abdominal pain who found some relief from the application of heat.

By James Heilman, MD - Own work, CC BY-SA 3.0,

Sweet’s syndrome (acute febrile neutrophilic dermatosis):

Ø  PRESENTATION:  Acute onset of  painful, dark red or hemorrhagic crusted plaques or bullae, especially on the face or extremities.  About 50% of cases are associated with fever and leukocytosis, arthralgia, conjunctivitis or iridocyclitis, and oral apthous ulcer.  Although it may be idiopathic, Sweet’s syndrome is often associated with hematologic disease (including myelogenous leukemia), and immunologic disease (rheumatoid arthritis, inflammatory bowel disease, Behçet's syndrome), previous upper respiratory infection, or drugs. 

Ø  DIAGNOSTIC EVALUATION: Skin biopsy:  Variable epidermal changes, sometimes with necrosis.  Diffuse dermal neutrophils with fewer lymphocytes, histiocytes, and few eosinophils.  Superficial dermal edema, sometimes with extravasated red blood cells and subepidermal blister, but there is no true vasculitis. 

Ø  DIFFERENTIAL DIAGNOSIS:  Non-infectious neutrophilic dermatoses including pyoderma gangrenosum, rheumatoid neutrophilic dermatitis, and Behcet’s disease.  Vasculitis:  Neutrophils are vasocentric, with fibrin and inflammatory cells in vessel walls, and less diffuse in the dermis.

Ø  TREATMENT: Respond to systemic corticosteroids. 

Pustular lesions with central necrosis on the left leg of a patient with Sweet's syndrome associated with Crohn's disease.

By Nadia M Mustafa, Mark Lavizzo. - Sweet's syndrome in a patient with Crohn's disease: a case report. Journal of Medical Case Reports 2008, 2:221. doi:10.1186/1752-1947-2-221, CC BY 2.0,

Livedo reticularis:

Ø  PATHOPHYSIOLOGY: Often idiopathic, but may be associated with autoimmune diseases, drugs/toxins, calciphylaxis, dysproteinemia, or emboli.  In some cases, the discoloration is caused by swelling of the venules owing to obstruction of capillaries by small blood clots.

Ø  PRESENTATION:  Mottled reticulated vascular pattern that appears as a lace-like purplish discoloration of the skin.

Ø  DIAGNOSTIC EVALUATION: Skin biopsy:  Normal skin appearance to vascular dilation with sparse or no inflammation; not a true vasculitis.

Ø  TREATMENT:  Treat any underlying conditions in secondary livedo reticularis; idiopathic cases may improve with warming the area.

D-deposition & metabolic diseases:  Porphyria, amyloidosis, gout, pretibial myxedema, digital mucous cyst, mucocele, calcinosis cutis, argyria

Porphyria:  Rare group of porphyrin metabolism disorder presenting as photodermatitis (papules or vesicles on sun-exposed skin).  Some of the more common types:  Verocious APACHE = V APaCHE -->

Ø  V- variegate porphyria (VP): Autosomal dominant deficiency of protoporphyrinogen oxidase (PPOX).  PRESENTATION: Combined features of AIP and PCT (Photosensitivity, neurologic symptoms, developmental delay)

Ø  A-acute intermittent porphyria (AIP): Autosomal dominant deficiency of Hydroxymethylbilane synthase (HMBS) formerly porphobilinogen deaminase (PBGD) leading to the build up of porphobilinogen (PBG) in blood.  PRESENTATION:  Periodic abdominal pain, peripheral neuropathy, psychiatric disorders (psychosis), tachycardia, no skin lesion.

 Ø  Porphyria cutanea tarda (PCT):  Most common porphyria.  Autosomal dominant deficiency of uroporphyrinogen decarboxylase (UROD).  PRESENTATION: “Tarda” refers to “late” (adult) onset of photosensitivity with vesicles, papules, crusts, and milia in area of scarring, commonly on dorsum of hands, malar hypertrichosis.  May be associated with hepatitis C, alcoholism, and liver disease.  Elevated levels of plasma porphyrins, urinary uroporphyrin and heptacarboxyl porphyrin, and fecal isocoproporphyrin.  DIAGNOSTIC EVALUATION: Skin biopsy: Subepidermal blister with lateral festooning of dermal papillae and very little inflammation (cell poor).  Catepillar bodies (eosinophilic, linear, segmented basement membrane material) are sometimes found in the roof of the blister.  Sparse PAS-positive, diastase resistant material can be found around papillary dermal vessels.  Dermal sclerosis may be seen in late stages.  Immunofluorescent:  IgG and C3 around papillary dermal vessels, and to a lesser extent at the dermoepidermal junction.

 Ø  P-pseusoporphyria:  Associated with hemodialysis and certain drugs, especially NSAIDs, tetracycline, furosemide.  Histologically identical to PCT.

Ø  Congenital erythropoietic porphyria (CEP, Gunther’s disease):  Autosomal recessive deficiency of uroporphyrinogen III synthase (UROS). PRESENTATION: Severe congenital mutilating “werewolf” form with onset of in infancy with red fluorescent teeth, extensive hypertrichosis, hemolytic anemia, splenomegaly, and severe photosensitivity with erythema, swelling and blistering.  DIAGNOSTIC EVALUATION:  Skin biopsy:  More hyalinized material in dermis than other forms of porphyria.

Ø  H-hereditary coproporphria (HCP):  Autosomal dominant deficiency of coproporphyrinogen oxidase (CPOX).  PRESENTATION:  Combined features of AIP and PCT with photosensitivity, neurologic symptoms, and colic.

Ø  E-erythrocytic protoporphyria (EPP):  Autosomal dominant deficiency of ferrochelatase.  PRESENTATION:  Photosensitivity with dermatitis but with very few blisters begins in childhood, liver dysfunction (rarely fatal), and gallstons.  DIAGNOSTIC EVALUATION:  Elevation of free serum erythrocyte protoporphyrin.  Skin biopsy: Dermal deposits of hyalinizd material, less blistering.

Left figure is urine on the first day while the right figure is urine after 3 days of sun exposures showing the classic change in color to purple.

By Chen GL, Yang DH, Wu JY, Kuo CW, Hsu WH - Neuropathic pain in hereditary coproporphyria.Chen GL, Yang DH, Wu JY, Kuo CW, Hsu WH - Pak J Med Sci (2013)

A skin rash in a person with porphyria

By Chern, CC BY-SA 3.0,


Ø  PATHOPHYSIOLOGY:   Deposits of eosinophilic amyloid protein, due to systemic disease involving kidney, heart, or liver, or in rubbed or lichenified skin from degeneration of keratinocytes without systemic disease (macular or lichen amyloidosis):


§  Systemic amyloidosis: 1) Primary systemic amylodosis:  AL amyloid with immunoglobulin light chains (usually lambda) deposited as yellow, purpuric macules or plaques especially on the eyelids, mostly in elderly with myeloma. Skin biopsy: Diffuse deposit in demis &/or around blood vessels, sweat glands, and adipocytes, often with scattered lymphocytes, plasma cells, and extravasated RBCs. 2) Nodular amyloidosis: Diffuse light chain AL amyloid in the dermis with plasma cells presenting as large waxy nodule in the skin.  A minority of cases are ssociated with systemic amyloidosis or myeloma.  3) Secondary systemic amylodosis:  SAA amyloid deposits in organs, but no skin lesions in association with chronic systemic diseases such as rheumatoid arthritis or leprosy.  Clinicians may choose to biopsy lower abdomen skin to find subtle amyloid around vessels, sweat glands, or fat cells, obviating the need for rectal or internal organ biopsy. 3) Familial Mediterranean Fever:  Rare autosomal recessive condition in which patients present with cellulitis-like plaques of the legs, fever, peritonitis, pleurisy, arthritis, and SAA amyloid in kidney.

§  Non-sytemic amyloidosis:  1) Macular amyloidosis:  Present as brown macules with a rippled appearance, most commonly on upper back.  Skin biopsy:  Normal epidermis with subtle amyloid blobs in the papillary dermis in areas of melanin incontinence. 2) Lichen amyloidosis:  Present as peppled lichenified plaques, most commonly on the back or as scattered grouped papules in chronically rubbed areas.  Skin biopsy: deposits of amyloid limited to dermal papillae with melanin incontinece; may resemble lichen simplex chronicus

Ø  DIAGNOSTIC EVALUATION:  Skin biopsy: Deposits of amorphous, eosinophilic, fissured material that stains with Congo red, crystal violet, and PAS.  Lichen and macular amyloidosis may positively stain with cytokeratin.

Macular amyloidosis, located on the right lumbar region of the back

By Jmarchn - Own work, CC BY-SA 3.0,

Classic facial features of AL amyloidosis with purpura around the eyes

By Professor P N Hawkins -, CC BY-SA 3.0,

Top: Amyloid in lymph node; Bottom: Apple-green birefringence (Congo red stain, polarized)

By Ed Uthman, MD -, CC BY-SA 2.0,


Ø  PATHOPHYSIOLOGY: Associated with a metabolic defect causing uric acid accumulation

Ø  PRESENTATION: Whitish-red nodules on digits and over joints

Ø  DIAGNOSTIC EVALUATION: Skin biopsy: Seen as amorphous eosinophilic material in dermis and subcutaneous tissue with formalin fixed tissue, and as brownish doubly-refractive needle-shaped crystals with alcohol-fixed tissue. Deposits are surrounded by lymphocytes, histiocytes, and multinucleated giant cells.

Ø  DIFFERENTIAL DIAGNOSIS:  Other juxta-articular nodules including calcinosis cutis and rheumatoid nodules.

Tophus of the knee

By NickGorton - NickGorton, CC BY 2.5,

Rods of uric acid crystals from a synovial fluid sample 

By Bobjgalindo - Own work, GFDL,

Myxedema:  Deposition of mucopolysaccharide in the dermis

Ø  Generalized myxedema:  Uncommon skin changes seen in hypothyroidism.  PRESENTATION:  Skin may look normal, but often is edematous, especially periorbital, or eczematous.  DIAGNOSTIC EVALUATION:  Skin biopsy: Look almost normal; sometimes dermal collagen are slightly separated y clear spaces with slight increased acid mucopolysaccharide demonstrated between colagen bundles by special stains such as Alcian blue and colloidal iron.

Ø  Pretibial myxedema: Uncommon edematous swelling usually of lower extremities in patients with Grave’s disease who often have LATS (long-acting thyroid stimulating hormone) with initial hyperthyroidism.  DIAGNOSTIC EVALUATION:  Skin biopsy: Large spaces seen between collagen bundles occupied by abundant acid mucopolysaccharide stained with Alcian blue and colloidal iron.  Some cases have increased dermal fibroblasts &/or mast cells.

Ø  Lichen myxedematosus (papular mucinosis): PRESENTATION: Grouped papules usually on the face or arms; may be associated with monoclonal gammopathy.  DIAGNOSTIC EVALUATION:  Skin biopsy:  Circumscribed deposits of abundant acid mucopolysaccharide between collagen bundles with increased dermal fibrosis and mast cells.  Scleromyxedema:  A more severe condition with extensive induration of skin, internal organ involvement like scleroderma with biopsy showing more fibrosis than ordinary papular mucinosis.

Man with myxedema or severe hypothyroidism showing an expressionless face, puffiness around the eyes and pallor

By Herbert L. Fred, MD and Hendrik A. van Dijk -, CC BY 2.5,

Pretibial myxedema and thyroid acropachy accompanying hyperthyroidism

By Herbert L. Fred, MD and Hendrik A. van Dijk -, CC BY 2.0,

Digital mucous cyst: PRESENTATION: Translucet papule/nodule on dorsal proximal nail fold of a digit containing gelatinous material due to local synthesis of mucin by fibroblasts.  DIAGNOSTIC EVALUATION: Skin biopsy: Epidermal hyperplasia with dermal increased mucin in clefts between collagen or cystic space.  Some cases have mucin extruding into the epidermis.  These are not true cyst as there is no epithelial lining.  Some cases have a synovial lining, but most of the time the cell lining are flattened fibroblasts.  Stain: positve acid mucopolysacharides (PAS).

Digital mucous cyst in left index finger with nail depression

CC BY-SA 3.0,

Mucocele:  PRESENTATION: Common translucent papule or nodule especially on the mucosa of the lip, but may also be in paranasal sinuses, and is thought to be due to rupture of minor salivary glands.  DIAGNOSTIC EVALUATION: Skin biopsy: Ruptured salivary glands or ducts with ≥ 1 spaces filled containing PAS-Diastase-resistant+ sialomucin and lined by granulation tissue or mixutre of fibroblasts, lymphocytes, and histiocytes.  Stain: Sialomucin is positve for both neutral mucopolysacharides (PAS-D) and acid  mucopolysacharide (PAS).

Mucocele on the lower lip

By No machine-readable author provided. Dozenist assumed (based on copyright claims). - No machine-readable source provided. Own work assumed (based on copyright claims)., CC BY-SA 3.0,

Mucous retention cyst in maxillary sinus

By © Nevit Dilmen, CC BY-SA 3.0,

Histopathologic image of extravasation type mucocele of the lower lip. H & E stain.

By No machine-readable author provided. KGH assumed (based on copyright claims). - No machine-readable source provided. Own work assumed (based on copyright claims)., CC BY-SA 3.0,

Calcinosis cutis: PRESENTATION: Common, often whithish papules or nodules with erythema. DIAGNOSTIC EVALUATION: Skin biopsy: Dark, basphilic, brittle, fractured deposits, som surrounded by fibrosis or foreign body reaction. Stain: Positve von Kossa or alizarin red (more specific for calcium).

Calcinosis cutis

By Nephron - Own work, CC BY-SA 3.0,

By Department of Pathology, Calicut Medical College - Government Medical College, Kozhikode, CC BY-SA 4.0,

Argyria: PRESENTATION: Very rare, gray skin discoloration in photodistribution due to silver depositing in skin either from ingestion of silver medication or topical overuse of silver nitrate.  DIAGNOSTIC EVALUATION: Skin biopsy: Tiny black particles in dermis, around sweat glands, hair follicles, vessels, and elastic fibers.

For many years, this man had used nose drops containing silver. His skin biopsy showed silver deposits in the dermis, confirming the diagnosis of argyria.

SKIN CANCERSGenerally develops in the epidermis, the outermost layer of skin, so a tumor is usually clearly visible. This makes most skin cancers detectable in the early stages.  Three most common types of skin cancer, each of which is named after the type of skin cell from which it arises.  Bad Skin Malignancy = BSM --> BCC, SqCC, Melanoma

·       B  _______________, _______________, _______________, _______________, _______________

·       S  _______________, _______________, _______________, _______________, _______________

·       M  _______________, _______________, _______________, _______________, ________________

·       B CC:   Most common skin cancer. Risk is increased for individuals with a family history of the disease and a high cumulative exposure to UV light via sunlight or, in the past, carcinogenic chemicals especially arsenic.

o   Evaluation:  Raised, smooth, pearly bump on the sun-exposed skin of the head, neck or shoulders. Sometimes small blood vessels can be seen within the tumor. Crusting and bleeding in the center of the tumor frequently develops.  To diagnose, a biopsy is done using local anesthesia. In small lesions, the tumor is generally removed in its entiriety, while larger ones are biopsied first and surgically removed later if it is confirmed that it is malignant.  Histopathology: Basal cell carcinoma is a malignant epithelial tumor arising from the basal layer of the epidermis or of the pilosebaceous adnexa. Tumor is represented by compact areas, well delineated and invading the dermis, apparent with no connection with the epidermis. Tumor cells resemble normal basal cells (small, monomorphous) are disposed in palisade at the periphery of the tumor nests, but are spindle-shaped and irregular in the middle. Tumor clusters are separated by a reduced stroma (retraction artifact) with inflammatory infiltrate. 

Treatment:  Most basal cell carcinomas are removed surgically. "Electrodessication and curettage" (ED&C) is the most cost effective treatment.   Some superficial cancers respond to local therapy with 5-fluorouracil, a chemotherapy agent. Topical treatment with 5% IMIQUIMOD cream, with 5 applications per week for six weeks has a reported 70 - 90% success rate at reducing, even removing the BCC. Imiquimod may be used prior to surgery to reduce the size of the carcinoma.  Mohs micrographic surgery has the highest cure rate and is especially indicated for recurrent tumors or tumors in areas (eg. eyelid or nose) where minimal amounts of tissue removal are important. X-ray is still appropriate in older patients who are not candidates for surgery. Cryosurgery is another option, particularly for basal cell cancer invading cartilage, as the healthy cartilage is cryo-resistant. 

Ulcerated basal cell carcinoma

By James Heilman, MD - Own work, CC BY 3.0,

Basal-cell carcinoma, nodular type

By M. Sand, D. Sand, C. Thrandorf, V. Paech, P. Altmeyer, F. G. Bechara - M. Sand, D. Sand, C. Thrandorf, V. Paech, P. Altmeyer, F. G. Bechara: Cutaneous lesions of the nose. In: Head & face medicine Band 6, 2010, S. 7, ISSN 1746-160X. doi:10.1186/1746-160X-6-7. PMID 20525327. (Review). Open Access, CC BY 2.0,

·       S qCC:  Account for about 20% of non-melanoma skin cancers, (with basal cell carcinomas accounting for about 80%), but are clinically more significant because of their ability to metastasize.  Risk factors include sun exposure, radiation therapy, exposure to carcinogens, chronic skin irritation or inflammation, genetic diseases, and presence of premalignant lesions.  A carcinoma can be characterized as either in situ or invasive. 

o   Evaluation:  Characterized by red, scaling, thickened patch on sun-exposed skin. Ulceration and bleeding may occur. When SCC is not treated, it may develop into a large mass.  Biopsy: irregular anyplastic epidermal cell proliferating down into the dermis.  In dark people, it usually arise at site of chronic inflammation (osteomyelitis), at mucocutaneous junction (lip, vulva, penis), or old scar (Marjolin’s cancer). 

o   Treatment:  Surgery for large lesion.  Moh’s micrographic surgery. Radiation.

o    Summary:  PEARL --> Pearl-keratin, Epidermal cell proliferating down the dermis, Actinic keratosis, Arsenic exposure, Radiation exposure,  Rarely metastasize but is Locally invasive, Sun exposure.

Ø  P  _______________, _______________, _______________, _______________, _______________

Ø  E  _______________, _______________, _______________, _______________, _______________

Ø  A  _______________, _______________, _______________, _______________, ________________

Ø  R  _______________, _______________, _______________, _______________, _______________

Ø  L  _______________, _______________, _______________, _______________, _______________

Ø  S  _______________, _______________, _______________, _______________, _______________

o   Actinic Keratosis:  (also called solar keratosis, or AK) is a premalignant condition of SqCC of the skin. It is most common in fair-skinned people who are frequently exposed to the sun.

Ø  Evaluation:  When skin is exposed to the sun constantly, thick, scaly, or crusty bumps appear. The scaly or crusty part of the bump is dry and rough. The growths start out as flat scaly areas, and later grow into a tough, wart-like area.  An actinic keratosis site commonly ranges in between 2 to 6 millimeters, and can be dark or light, tan, pink, red, a combination of all these, or the same pigment of one's skin. It may appear on any sun-exposed area, such as the face, ears, neck, scalp, chest, back of hands, forearms, lips etc.  Biopsy (hyperkeratosis, loss of polarity, pleomorphism, hyperchromatic nuclei) may be necessary when the keratosis is large and/or thick, to make sure that the bump is a keratosis and not a skin cancer.

Ø  Treatment:   Cryosurgery,  topical 5-FU Electrocautery: burning off AKs.  Immunotherapy: topical treatment with imiquimod (Aldara™), an immune enhancing agent.  Different forms of surgery.

Squamous Cell Carcinoma. Tends to arise from pre-malignant lesions, actinic keratoses; surface is usually scaley and often ulcerates.

By Unknown photographer/artist -, Public Domain,

Well differentiated squamous cell carcinoma

By No machine-readable author provided. KGH assumed (based on copyright claims). - No machine-readable source provided. Own work assumed (based on copyright claims)., CC BY-SA 3.0,

·       M elanoma:  It is one of the rarer types of skin cancer but causes the majority of skin cancer related deaths.   Exposure to UVA and UVB is one of the major contributors to its development.  Fair and red-headed people, persons with multiple atypical nevi or dysplastic nevi and persons born with giant congenital melanocytic nevi are at increased risk.  A family history of melanoma greatly increases a person's risk because mutations in CDKN2A, CDK4 and several other genes have been found in melanoma-prone families. 

o   Evaluation:  Melanoma’s ABCDE --> Asymmetrical skin lesion, Border of the lesion is irregular, Color: melanomas usually have multiple colors, Diameter: moles greater than 5 mm are more likely to be melanomas than smaller moles,  Evolution: The evolution (ie change) of a mole or lesion may be a hint that the lesion is becoming malignant --or-- Elevation: The mole is raised or elevated above the skin.

Ø  A  _______________, _______________, _______________, _______________, _______________

Ø  B  _______________, _______________, _______________, _______________, _______________

Ø  C  _______________, _______________, _______________, _______________, ________________

Ø  D  _______________, _______________, _______________, _______________, _______________

Ø  E  _______________, _______________, _______________, _______________, _______________

Excisional biopsy is the management of choice, which reveal melanocyte with atypia (vacuolated cytoplasm, hyperchromatic nuclei with prominent nucleoli, pleomorphic) à invading into the epidermis.  The biopsy will include the epidermal, dermal, and subcutaneous layers of the skin, enabling the histopathologist to determine the depth of penetration of the melanoma by microscopic examination. This is described by Clark's level (involvement of skin structures) and Breslow's depth (measured in millimeters).  Lactate dehydrogenase (LDH) tests are often used to screen for metastases, although many patients with metastases (even end-stage) have a normal LDH; extraordinarily high LDH often indicates metastatic spread of the disease to the liver. It is common for patients diagnosed with melanoma to have chest X-rays and an LDH test, and in some cases CT, MRI, PET and/or PET/CT scans. Although controversial, sentinel lymph node biopsies and examination of the lymph nodes are also performed in patients to assess spread to the lymph nodes.

o   Clark’s staging:  Every Pigmented Junction Requires Formalin = EPJRF --> Epidermis, Papillary dermis, Junctional dermis, Reticular dermis, Fat tissue.

Ø  A  _______________, _______________, _______________, _______________, _______________

Ø  B  _______________, _______________, _______________, _______________, _______________

Ø  C  _______________, _______________, _______________, _______________, ________________

Ø  D  _______________, _______________, _______________, _______________, _______________

Ø  E  _______________, _______________, _______________, _______________, _______________

o   The most common types of Melanoma in the skin:

Ø  Lentigo maligna (60 y/o, white): Geographic shape/stain-like.  On sun-exposed area (head, neck, hands).

Ø  Acral lentiginous (60’s, M > F all other M = F, aka subungual melanoma).  Asian, Africans.  On palms & soles, mucus membrane, nail.

Ø  Nodular melanoma (50’s):   Most aggressive form of melanoma. It grows in vertical direction from the outset and grows very fast (months). Nodular melanoma has no known precursor. It is a small black (uniform, dark, blueberry), or if amelanotic, pink nodule that simply enlarges. The lesions tend to bleed.

Ø  Superficial spreading melanoma (SSM):   Most common form of cutaneous melanoma in Caucasians. The average age at diagnosis is in the fifth decade, and it tends to occur on sun-exposed skin, especially on the backs of males and lower limbs of females.  Often, this disease evolves from a precursor lesion, usually a dysplastic nevus. A prolonged radial growth phase, where the lesion remains thin, may eventually be followed by a vertical growth phase where the lesion becomes thick and nodular.

o   Treatment:  The sole effective cure is surgical resection of the primary tumor before it achieves a thickness > 1 mm.  Complete surgical excision with adequate margins and assessment for the presence of detectable metastatic disease along with short and long term follow up is standard. Often this is done by a "wide local excision" (WLE) with 1 to 2 cm margins. Mohs micrographic surgery is sometimes used in the treatment of melanoma. Melanomas which spread usually do so to the lymph nodes in the region of the tumour before spreading elsewhere. Attempts to improve survival by lymphadenectomy were associated with many complications but unfortunately no overall survival benefit. Recently the technique of sentinel lymph node biopsy has been developed to reduce the complications of lymph node surgery while allowing assessment of the involvement of nodes with tumour.  If the disease is completely resected the patient will be considered for adjuvant therapy.  Chemotherapy & immunotherapy.  Radiation.

o   Summary for melanoma: MELANomaS = MELANS --> arises from MElanocytes & Nevus cells; types Lentigo maligna, Acral lentiginous, Nodular, Superficial Spreading

Ø  ME  _______________, _______________, _______________, _______________, _______________

Ø  L  _______________, _______________, _______________, _______________, _______________

Ø  A  _______________, _______________, _______________, _______________, ________________

Ø  N  _______________, _______________, _______________, _______________, _______________

Ø  S  _______________, _______________, _______________, _______________, _______________

ABCD rule illustration: On the left side from top to bottom: melanomas showing (A) Asymmetry, (B) a border that is uneven, ragged, or notched, (C) coloring of different shades of brown, black, or tan and (D) diameter that had changed in size. The normal moles on the right side do not have abnormal characteristics (no asymmetry, even border, even color, no change in diameter).

By Unknown creator; six images merged by User:Stevenfruitsmaak - National Cancer Institute via Skin Cancer Foundation, Public Domain,


Mount Rushmore, South Dakota, USA