Dermatology
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| What is dermatitis? | AKA Eczema, cutaneous inflammation that presents w/erythema, vesiculations, pruritis in acute phase. Chronic phase is characterized by dryness, scaling, lichenification, fissuring, and pruritis. There are multiple types (atopic, seborrhic, nummular, contact) |
| What is contact dermatitis? | Inflammatory eczematous disease, caused by chemicals or metals exert toxic effects w/out inducing a T cell response (contact irritant) or by small reactive chemicals that modify proteins and induce innate and adaptive immune response. |
| What are types of contact dermatitis? | Irritant contact dermatitis (non-specific response of the skin to a direct chemical damage, usually due to detergent not individual, chemical releases mediators of inflammation from epidermal cells) Allergic Contact Dermatitis (delayed type IV hypersensetivity rxn due to exogenous contact antigens, affects 20% of children, response due to interaction of cytokines and T cells, some are applied after photo contact (Confined to UV radiation) |
| When does ACD occur? | When contact w/ a particular substance elicits a delayed hypersensitivity reaction, sensitization requires 10-14 days, and when re-exposure occurs dermatitis appear w/in 12-48 hours. Most common cause is Rhus Dermatitis (poison Ivy/Oak/Sumac) Other causes topic Abx, benzocaine, Vitamin E, Rubber, Nickel, Formaline, Preservatives (some skin care products), Fragrances. |
| How is epidemiology of contact dermatitis? | Females, infants and elderly and individuals w/atopic tendencies have high risk to get irritant contact dermatitis (80% of occupational dermatitis is ICD) ACD all individuals are at risk, risk factors include age, occupation, and hx of atopic dermatitis. Contact dermatitis most common in red hair and fair skin people, women more likely to develop contact due to use of jewelry and fragrances. |
| What are the clinical findings in contact dermatitis? | Main symptom of ACD is pruritis. Presents as eczematous, scaly edematous plaques w/vesiculations distributed in areas of exposure. It is bilateral if exposure is bilateral (usually unilateral) Can't differentiate between ICD and ACD both w/three morphological patterns (acute: erythema, edema, oozing, crusting, tenderness, vesicles, pustules. Subacute: crusts, scales, hyperpigmentation. Chronic: Lichenification) CD is 4-7% of dermato consults, mostly chronic due to nickel and chromate. Occuptational disease burden (after mental illness and musculoskeletal burndens) |
| What is irritant contact dermatitis? | Likelyhood of getting it depends on duration, intensity, concentration of substance. Chemical/physical agents and microtrauma could induce it, friction/ abrasions/ occlusions/ detergents produce ICD Severity depends on quantity and concentration of irritant, duration and frequency of exposure. All types of skin possible, environmental factors like high or low temperature and humidity determine severity. |
| What are factors causing ICD? | Exogenous (inherent toxicity of chemical for human skin, site differences make face/neck/scrotum/dorsal hands more susceptible) Atopic dermatitis major risk for ICD of hand due to impaired barrier function and lower threshold for skin irritation |
| What are clinical findings of ICD? | Mild irritants (erythema, chapped skin, dryness, fissuring (repeated exposures over time) Pruritis from mild to extreme, pain most common symptom when erosions and fissures are present. Severe cases edema, exudate and tenderness Potent irritants produce painful blisters w/in hours post-exposure. It is most common type of CD, affects hands common, for children diaper and dry skin dermatitis most common, due to repititive exposure to water, glazed, parched scalded appearance. In ICD inflammatory cells play a role, but not lymphocytes so no prior sensitization is needed, affects everyone after sufficient exposure. |
| How is pathogenesis of ICD? | Resident epidermal cells, endothelial cells, leukocytes interact under control of cytokines and lipid mediators. Keratinocytes initiate skin inflammatory reactions through cytokine release, environmental factor stimulates release of inflammatory cytokines (IL1, TNF-a), chemotactic cytokines (IL8/10), Growth-promoting cytokines (IL6,7,15,TGF-a), humoral vs cellular immunity cytokines (IL10/12/18), ICAM-1 infiltration of leukocytes. |
| What is ACD? | Common etiological allergens are nickel, balsam of Peru, chromium, neomycin, formaldehyde, fragrance, poison Ivy. Sensitization lasts 10-15 days in man, first step has no clinical consequence but may induce primary ACD (hapten-specific skin inflammation 5-15 days after contact). It results from inflammation caused by type IV HS cellular immune response. Acute lesions (papules/vesicles/weeping/crusting/erythema/edema/ pruritis) Prior sensitization is essential here, and needs re-exposure to occur after 6-12 hours. Chronic lesions fissuring, skin thickening, lichenification, acneiform eruption, hypo/er pigmentation. For children occurs by age 6 months |
| How is pathogenesis of ACD? | Two phases, Sensitization phase (Ag-specific T cells induced draining lymph nodes by Ag captured DC from skin) Elicitation phase (T cells activated after Ag caught by DC produce chemical mediators create inflammation) |
| What is photosensitization? | Photoallergic rxn, sun-exposed areas (face/ V of anterior neck/ dorsal hands/ forearms), spares eyelids/ upper lip. May develop when UV reacts w/chemical agents inducing photosensitization. |
| What is systemic CD? | Generalized dermatitis/ exanthema in flexural areas (Baboon syndrome) Can also develop in previous CD/ positive patch test sites w/systemic exposure to allergen (ingestion/infusion..) Pathophysio similar to ACD, initiated by T cells. Most common causes are metals (mercury/nickel/gold), medications (Abx, steroids, aminophyllin, estradiol topical), plants and herbal products (Balsam of Peru...) |
| What is subjective irritancy? | W/in minutes of contact on face in absence of visible changes, after applying cosmetics/ sunscreens. Uncommon for endogenous, irritant and allergic etiologies to co-exist in development of eczemas (hand and foot) |
| How is CD in children? | Reports are increasing (Ni, topical Abx, preservatives, fragrances and rubber are most common) Eczematous eruption children should be patch tested, particular those w/hand and eyelid eczema. |
| What is atopic dermatitis? | Chronic, relapsing pruritic inflammation of the skin, affects more children than adults (adults have specific morphology and distribution), associated w/increased IgE and hx of allergies. One of the most common skin disorders (20% of children, 1-3% of adults) Primary symptom (pruritis), periods of remission and exacerbation. |
| What are associated findings w/atopic dermatitis? | Asthma, allergic rhinitis, xerosis, (itching and dry skin), chronic relapsing course, morpholgy and age-specific patterns. |
| How is clinical presentation of atopic dermatitis? | Variation of eczema between individuals, most people get acute flares w/inflamed weepy patches. Between flares skin may be normal or chronic eczema w/dry thickened itchy skin. We see Lichenification and Xerosis cutis |
| How is rash distribution in atopic dermatitis? | Infants (Face, behind ears, extensors of limbs, widely distributed eczema, dry scaly red skin w/small scratch marks due to baby nail , 1st place is cheek) Children (2-3 yrs) (trunk, flexors of limbs, may affect genitals, eyelids, earlobes, neck and scalp, can get recurrent itchy blisters on palm fingers or feet (Pompholyx/vesicular hand)) Adults (ankles, flexors of knees and elbows, neck and gluteal fold, diffuse, more dry and lichen than children, recurrent staph infection may occur, may cause ICD in hands (blistered)) |
| How is perioral dermatitis? | Inflammatory rash involving skin around the mouth, may spread to nose, eyes -->periorificial dermatitis. Causes (topical steroids, bacterial/fungal infections, drooling, fluorinated toothpaste, OCP, sunscreen, rosacea. |
| How do we assess severity of atopic dermatitis? | Thickness of lesion, body surface area involved, pruritis, and QoL impact. QoL (child [impair sleep, embaressment, limited lifestyle], Parents [impair sleep, tiredness, angry on drs, auxilliary caregiver for siblings]) |
| What are some comorbidities associated w/atopic dermatitis? | In children and teens (Increased risk of ADHD, autism, anxiety, depression, poor attention span (pruritis)) |
| How is clinical manifestation of atopic dermatitis? | Lesions benign erythematous papules, form erythematous plaques that may display weeping, crusting or scale. Various distribution w/age, xerosis at all stages Pt w/inadequately controlled atopic dermatitis we see 90% dry skin for 5-7 days a week, 50% bleeding/ cracking/ flaking 3-7 days a week, can be associated w/ skin infections Dx gold std (Hanfin and Rajka (3 out of 4: pruritis, typical morphology and distribution according to age, chronic dermatitis, personal/family hx of atopic disease (50-80% of children will have asthma or allergic rhinitis)) |
| How is pathogenesis of atopic dermatitis? | Multifactorial (genetics, skin barrier dysfunction, impaired immune response and environment) may be filaggrin deficiency, T helper produces cytokines (IL4/ IL13 by Th2) that initiate positive feedback loop, reduce KC differentiation and increase epidermal hyperplasia by reducing expression of epidermal structural proteins and may cause itchy lesions Hyperplasia causes lichenification, decreased structural proteins cause pruritis and allergen entry. |
| How is SA superinfection in Atopic dermatitis? | 73-100% of pt w/AD have Staph colonization, helps cause skin exacerbation and increase atopic eczema severity |
| How is family predisposition of atopic dermatitis? | 1 parent has it ->60% risk child has it, 2 parents have it ->80% |
| What are complications of AD? | Secondary infections (Staph, HSV1, Tinea) Psychosocial (sleep disorder, decreased QoL) Extension/generalization, impetigo, Kaposi-Juluisberg, Contact eczema, psycho-emotional impact Viral infection usually appears unilateral (HSV) May be hand blistering, HS to insect bites, |
| What is tx of atopic dermaitis? | Goal is to prevent exacerbation, education, stop itching, prevent scratch damage and space recurrence. Recommendation non-pharmaco (hydration, identify aggrevating allergens, symptomatic tx) Short-term and long-term tx manage it (manage flare and control symptoms between flares) Gentle skin care (tepid bathes w/out scrubbing, specific cleansers instead of soap, pat dry, emollients moisturizers, avoid triggers/irritants, breast feeding during infancy. |
| What are the pharmacologic tx of atopic dermatitis? | Moisturizers (ointments best since less preservatives, no sting or burn) Topical corticosteroids (in acute flares, ointments preferred, face low potency, body and extremities medium potency, side effects include acne, atrophy, striae, telangiectasis) Cleaning (warm water, no perfume, bath oil, cut nails, emolient after bath, no lotions, cotton gloves at night) Immunomodulators (tacrolimus/ pimecrolimus, supress T lymphocytes interest in long term, children 2-17, reduces relapses) Antibacterial (tx co-existing infections systemic Abx (oral not topical) Antihistamines (never topical always oral, for itching and sleep, short term) |
| What is duplimab and crisaborole? | Duplimab indicated for 6 years and older, human monoclonal Ab, tx of moderate to severe AD not controlled by topical therapies or contraindicated tx FDA approved. Crisaborole Phosphodiesterase inhibitor ointment tx mild-moderate AD children > 3 months of age. |
| What are specific questionnares used to diagnose contact dermatitis? | Age, occupation, address, history of contact dermatitis, atopy, stasis, dermatitis, otitis, lichen, psoriasis. onset of symptoms, pruritis, starting (cosmetics, occupation, hobbies, medications) Physical exams (hands, perianal, otitis externa, eyelids, ophthalmo, hair, stasis, dermatitis. Environment (animals, garden, carpet), work, home, cosmetics contact, previous treatment and efficacy. |
| What is patch testing? | Used to determine allergens for allergic contact dermatitis, series of allergens applied to the upper back, removed after 2 days, on day 4-5 patient returns for results, positive reactions show erythema, papules or vesicles. Identification of specific allergen helps find products free of these allergens, it is the gold std for dx of ACD, indicated for any pt w/acute/chronic pruritic/eczematous or lichenified dermatitis sus of secondary ACD. If dermatitis is extensive it should be controlled before PT, can't perform it on a lesion already found, stop immunosupressive tx, or lower dose, refrain from sun tanning 2-4 weeks prior to PT, not done for pregnant/breast feeding pt. |
| How is patch test graded? | According to international guidlines (doubtful, weak positive, strong positive, extreme positive, irritant reaction, negative reaction according to lesion) There are panels that hold different allergens (seen in truetest.com) |
| How is allergen testing? | Not all pt need PT, only if unclear allergen or chronic dermatitis it is needed, positive test is considered only if the rash is gone after removal of allergen. Allergens causing ACD (nickel (most common), chromates (leather, cement), rubber accelerators, fragrances, preservatives, hair dye, cocoamidopropyl betaine, meds (topical) Read positive test at 96 hours, to improve rash avoidance of allergens is required 1-3% of population are allergic to cosmetics ingredients |
| What is immediate contact dermatitis? | After exposure to offending topical agent we see contact utricaria with a wheal and flare reaction, most cases are mild but anaphylactic reactions can sometimes occur, some types of contact urticaria include exposure to cold, dermatographism, pressure, exercise, solar, heat, and choline. Latex allergy may be immediate HS, see burning, stinging, itching w/ or w/out urticaria, may include allergic rhinitis, anaphylaxis (so important to notice it to not wear gloves). Test is prick test to latex, pt withdraw antihistamine w/out dermographism (anaphylaxis, RAST, skin prick). |
| How is the difference in relevancy of tests? | Tests are considered relevant or not in case of the recent frequent exposure to the allergen or not (example of pt who works in a bakery but used to work w/cement, his cement allergy isn't relevant any more) |
| What is the differential diagnosis of CD? | Atopic dermatitis (early age chronic in nature, family hx) Seborrheic dermatitis (on scalp, periauricular, face, sharpe demarcated lesions) Dyshidrotic eczema (hands, symmetrical) Mycoses fungoides and Cutaneous T cell lymphoma May see fingertip dermatitis w/ fissures (florist) |
| How is evaluation of contact dermatitis? | Identify possible irritant and avoid, if not improving reffer to dermatologist, patch test performed in occupational cases w/sus chronic irritant dermatitis exclude ACD. Avoidance (of allergen is key to successful tx, some allergens are cross reactors, we can use special tests to detect presence of metals (Ni, Cr) in products to avoid them |
| How is first line treatment of CD? | Topical corticosteroids, soap substitutes and emollients tx of established contact dermatitis, if infected combined topical corticosteroid + Abx. Long term intermittent use of mometasone furoate in chronic hand eczema, topical tacrolimus effective in nickel ACD |
| How is second line treatment of CD? | PUVA, azathioprine, methotrexate and ciclosporin are used for steroid-resistant chronic hand dermatitis. Several prospective clinical trials to support these treatments. Grenz rays (X-rays produced at low kev, low penetration power) for chronic hand dermatitis showed a significantly better response with this therapy compared with use of topical corticosteroids. Alitretinoin is an endogenous acts as pan-agonist at retinoid receptors, binding with high affinity to both retinoic acid receptors and retinoid X receptor Nickel elimination diets |
| How is ICD prevention done? | Education about irritant avoidance, use personal protective equipment (gloves), use less irritating substances than soap like emollients and soap substitutes, care for months after dermatitis has healed (since skin is vulnerable to flares of dermatitis) |
| What is impetigo? | Common superficial bacterial skin infection, common in children 2-5 yrs, older can get affected, contagious, spread easily, most cases are due to S.aureus/GAS Non-bullous impetigo (most common form, AKA impetigo contagiosum, papules lesions surrounded by redness, progress to form pustules and breakdown to form honey-crust appearance) Bullous/Blistering impetigo (seen in young children, flaccid bullae w/clear yellow fluid later becomes purulent, if ruptures leaves a thick brown crust, common locations in face, extremities and diaper Skin diseases secondarily infected (most common in adults, bacteria penetrates through skin scratch/injury, look for pruritic dermatitis, scabies, eczema, herpes, VZV) |
| How is dx of impetigo? | Clinical dx (easily seen), bacterio exam (if complicated/resistant), Basic lesions (fragile vesicle/bubble pustule break-up may lead to polycyclic circumferential contours) classic locations in children around the mouth, skin, general condition preserved and no fever |
| What is ecthyma? | Ulcerative lesion extending to dermis (deep impetigo), punched out ulcer covered w/yellow crust surrounded by raised margins, heals slowly and scars (unlike impetigo), S.aureus/GAS/Pseudomonas (If IC) AKA ecthyma gangrenosum. It is necrotic covered with thick crust and surrounded by dark halo usually in lower limbs, could be induced by poor hygiene, IC, DM, alcoholism + Strep usually. heals slowly and leaves a scar |
| How is tx of impetigo? and what are its complications? | Disinfection (topical fucidin/mupirocin if localized lesions) If widespread (oral Abx - especially clindamycin) Complications (rare, post-strep glomerulonephritis, RF, control of proteinuria 3 weeks after infectious episode) |
| What is folliculitis? | Superficial bacterial infection of hair follicles (never seen in places where no hair), small raised red occasionally pruritic pustules <5mm diameter, may be STD, usually due to S.aureus, pseudomonas (swimming pools), candidiasis (marked erythema), herpetic... Pustule is fluid filled lesion w/purulent fluid centered by a hair w/perifollicular erythema, variable in number lesions on hairy regions Clinical forms (stye [eyelash], sycosis [beard- shaving induces chronicity and extension]) |
| How is tx of folliculitis? | Cleaning w/antibacterial soap, superficial ones rupture and drain spontaneously, maybe oral/topical anti-staph Abx (mupirocin/retapamulin/clindamycin topical), deep lesions are abscesses and should be drained |
| What is furuncle/Boil? | Acute, round, tender, circumscribed perifollicular abscess generally ends in central suppuration, deep necrotic folliculitis, S.aureus [maybe recurrent if resistant, painful papule/nodule centered by pustule and central necrosis] differential (fungal [candida, dermatophytes], pseudofolliculitis [no pathogen, body rxn, Crohn's disease/eosinophilic folliculitis], Hidradenitis suppurativa (Verneuil's disease): chronicinflammation of the pilosebaceous follicles and sweat glands in areas rich in apocrine glands (axillary, sub- mammary and anoperineal folds), Epidermal inflammatory cyst or superinfected cyst: Preexisting cyst (face) |
| What are complications of furuncle? | Anthrax (conglomerate several boils), furunculosis (chronic boils triggering factors DM/IC), primary abscess, lymphangitis, systemic complications (very rare bacteremia, sepsis), malignant staph of face (emergency, rare, pt manipulates his furuncle of the face usually near labia/nose, causes general staph infection, fever, edema, palpable venuos cord, lead to septic thrombophlebitis, and more severe thrombophlebitis of cavernous sinus [deadly] |
| What is carbuncle? | Coalescence of several inflamed follicules into a single inflammatory mass w/purulent drainage from multiple follicules Subtype of abscess, usually by staph, pt tx by Abx oral, if solitary small furuncle can compress it to promote drainage, larger ones manage as an abscess |
| How is tx of folliculitis and boils? | General hygiene antiseptic use, for boils give systemic oral Abx active on S.aureus, if comorbidities give penicillin M, macrolides in case of allergy/contraindications, duration for 10 days Furunculosis we should perform disinfection of portages armpits ,perineum, nasal vestibule...antiseptic toilet and usage of topical antibiotics (fucidin) |
| What is Whitlow (Panaris)? | • Infection of the ungual fold • Elemental lesion: periungual erythematous and edematous fold, painful • Treatment: local antiseptics; oral antistaphylococcal antibiotic in case of resistance and/or collection and / or complication; incision and drainage in case of purulent collection |
| What is an abscess? | Collection of pus w/in dermis and deeper skin tissues, painful tender fluctuant and erythematous nodules, surmounted by a pustule and a rim of erythematous edema, absent fever, lymphangitis, satellite adenopathies, good general conditions, spontaneous drainage may occur (like a fistula outside) |
| How is abscess tx? | Abscess incision and drainage recommended to clear pus and debris and probe the entire cavity following incision and drainage. Abx recommended for abscesses w/severe or extensive diseases (multiple sites, rapid progress to cellulitis, S&S of systemic illness, ass comorbidities and IS, extremes of age, abscess difficult to drain, associated septic phlebitis, and lack of response to I&D alone |
| What is lymphangitis? | Due to S.aureus/GAS, linear inflammatory erythema between site of inflammation and first regional lymph node, palpable lymph node, maybe febrile. Tx systemic Abx |
| What is superficial septic thrombophlebitis? | • Superficial septic venous thrombosis • Linked to thrombogenic activity of S. aureus, risk of deep spread and septic emboli • Clinical presentation: Common form: Venous Inflammatory cord at the point of infusion, indurated on palpation, fever • Treatment: Removal of catheter / gateway to an infection. Antiseptics; systemic antibiotic therapy if resistance / complication; rare form: malignant staphylococcal disease of the face |
| What is cellulitis? | • Cellulitis is a very common infection occurring in up to 3% of people per year • Most do not require hospitalization • Results from an infection of the dermis that often begins with a portal of entry that is usually a wound, maceration between toes (strepto component), or fungal infection (e.g., tinea pedis) • Presents as a spreading erythematous, non-fluctuant tender plaque • More commonly found on the lower leg • Streaks of lymphangitis may spread from the area to lymph nodes |
| What are risk factors for cellulitis? | Local trauma (bug bites, laceration, abrasion, puncture wound) – Spread of a preceding or concurrent skin lesion (furuncle, ulcer) Secondary cellulitis from blood-borne infection or from direct spread of subjacent infections (e.g. osteomyelitis) is rare • Following a preexisting skin infection due to compromise of skin barrier (intrerdigital strep, tinea pedis) • Inflammation (local dermatitis, radiation therapy) • Edema and impaired lymphatics in the affected area |
| What are etiologies of cellulitis? | • 80% of cases are caused by gram positive organisms • Group A streptococcus is most common; other strep less so • Staphylococcus aureus is less common but occurs with open wound or penetrating trauma as with needle injection with drug abuse • Think of other organisms if there have been unusual exposures or conditions: Pasteurella multocida (animal bites) • Eikenella corrodens (human bites) • MRSA (with concurrent MRSA elsewhere/illicit drug use/purulent drainage) |
| What is tx of cellulitis? | • It is important to recognize and treat cellulitis early as untreated cellulitismay lead to sepsis and death • The following guidelines are for empiric antibiotic therapy: For outpatientswith nonpurulent cellulitis: empirically treat for β-hemolytic streptococci (group A streptococcus) as cephalexin, amoxicillin, amoxicillin-clavulanate, dicloxacillin, or clindamycin • For outpatients with purulent cellulitis (purulent drainage or exudate in the absence of a drainable abscess)/injection drug use/other penetrating trauma/MRSA presence elsewhere: empirically choose treatment to cover community-associated MRSA as well as strep, as clindamycin; work with dermatology and infectious disease specialists • For unusual exposures: cover for additional bacterial species based on such exposure; work with dermatology and infectious disease specialists |
| How is post tx of cellulitis? | • Monitor patients closely and revise therapy if there is a poor response to initial treatment; usually a 5 day course of antibiotics is sufficient • Treat underlying derm disorder/condition, as venous eczema • Elevation of the involved area • Treat tinea pedis, toe maceration (strep) if present • Consideration of concurrent oral steroid treatment to decrease post- inflammatory lymphatic damage; more studies needed • For hospitalized patients: empiric therapy for MRSA should be considered • Cultures from abscesses and other purulent skin and soft tissue infections (SSTIs) are recommended in patients to be treated with antibiotic therapy but if case has a typical presentation, they need not be performed |
| What are MRSA risk factors? | • Healthcare-associated MRSA (HA-MRSA) and community-associated MRSA (CA- MRSA) risk factors include: . Antibiotic use •Prolonged hospitalization •Surgical site infection •Intensive care •Hemodialysis •MRSA colonization • Proximity to others with MRSA colonization or infection • Skin trauma • Cosmetic body shaving • Group facilities • Sharing equipment that is not cleaned or laundered between users/body contact as in sports |
| What is erysipelas? | • Erysipelas is a superficial cellulitis with marked dermal lymphatic involvement (causing the skin to be edematous or raised) Main pathogen is group A streptococcus • Also caused by Staph aureus, Haemophilus, and others • Usually affects the lower extremities and face • Presents with pain, bright erythema, and plaque-like edema with a sharply defined margin to normal tissue • Plaques may develop overlying blisters (bullae) • May be associated with a high white count (>20,000/mcL) • May be preceded by chills, fever, headache, vomiting, and joint pain |
| What is tx of erysipelas? | • Immediate empiric antibiotic therapy should be started (cover most common pathogen - Streptococcus) Such as penicillin V, amoxicillin, clindamycin, macrolide, and others • Monitor patients closely and watch the therapy if there is a poor response to initial treatment • Elevation of the involved area • Treat tinea pedis, erythrasma, or intertrigo |
| What are some generalities related to HSV infection? | Primary infection is first contact w/HSV1 or HSV2 could be symptomatic or asymptomatic Initial non-primary infection is second or more exposure Recurrence is clinical expression in a pt previously infected by same viral type (if got before HSV1 and now gets HSV2 not recurrence) Shedding: finding HSV1 in an asymptomatic pt Reactivation clinical recurrence or asymptomatic viral secretion. |
| How is epidemiology of HSV? | HSV is a DNA virus two types 1 and 2, very homologous, HSV1 affects upper body and HSV2 usually genitals, although HSV1 could be found in genitals, HSV2 is increasing in teens (typical genital lesions for a teen pt) Genital herpes is 1st cause of genital ulcer disease in developed countries. |
| What are risk factors for getting HSV2 infection? | Female, early first intercourse, number of sexual partners, hx of STI, HIV +, low socioeconomic level |
| How is primary oral infection (Acute Herpetic Stomatitis)? | Usually HSV1 in small children from 6 months, when no maternal Abs, IP 3-6 days, preceded by pain, dysphagia and sialorrhea, in context of general malaise w/fever>39C Gums swollen and bleeding, gray erosions on oral mucosa, set w/ a red border and becomes an ulcer covered with white coat. |
| How is primary genital infection? | HSV2 mainly, maybe HSV1. Young women get acute vulvovaginitis, extreme painful and brutal febrile malaise. Man get less intense, and confused with recurrent herpes presentation, burn urination, dysuria, anitis, anorectitis or erosions may be seen man or woman especially homos. |
| Describe the women vuvlvaginitis caused by acute genital herpes? | -Efflorescence-vesicles on the mucous membrane is swollen vulva are mostly ephemeral -Erosions rounded contours polycyclic ulcers sometimes, also extending toward the anus -Herpetic lesions often coexist on the vaginal walls and cervix, but the pain make gynecological examination impossible -They often beyond the skin side, the root of the thighs, buttocks and pubic area, lymphadenopathy -Sensitive groin are constant, frequent urine retention, exacerbation of pain by urination very painful The spontaneous healing, request 2-3 weeks |
| What are other symptoms of primary herpetic infection? | Skin (get finger eczema that we should be careful of to not get the infection) Opthalmo (keratoconjuctivitis, blisters on swollen eyelids cervical lymphadenopathy) ENT (herpetic angina, acute rhinitis, nasal obstruction, perinasal vesicles, and cervical lymphadenopathy) |
| What are severe presentations of primary herpetic infection? | IC (almost always HSV1, extensive lesions necrotic and persistent, may be generalized/systemic) Atopic (gingivatomastitis severe, kaposi's sarcoma which is generalized crusting of children skin by hemorrhagic vesicles rapid spread) Pregnant women (increased risk of hepatitis or fulminant encephalitis) Newborn (rare but severe in utero transmission, growth retardation, uterine, ocular, cardiac issues) Neonatal herpes (mucucutaneous, neurological [15% MR] or systemic [60% MR]) |
| How is recurrent herpes? | Clinical presentation (80% HSV infections go latent and recur after febrile infection, UV, rules, stress, trauma, regional surgery, morphine, sex) Seen anywhere on body, IMPORTANT decrease recurrence with age |
| Describe the clinical features of recurrent herpetic infection depending on location | Herpes labialis [sore on vermilion and skin] herpes nasal [folliculitis] herpetic stomatitis [painful erosions] herpetic keratitis [corneal ulcerations cause vision loss w/uveitis] genital herpes [HSV2 but difficult dx erosion, fissure...], signs on the location of primary sx, healing needs 7-15 days for vesicles and erosion crusts. |
| Describe clinical features of recurrent herpetic infection depending on severity and skin reaction. | IC (frequent recurrence, prolonged atypical presentations, ulcers, blisters, pustules) Systemic involvement (meningoencephalitis, esophagitis [HSV1], hepatitis [rare, pregnant and IC], pulmonary [elderly/IC] Skin reaction (may be followed by erythema multiforme, maculopapular lesion in target blistering associated with mucosal involvement, most HSV is most common cause of recurrent erythema multiforme) |
| How is dx of HSV? | Collect fluid from vesicle then either culture virus (2-3 days), Ag search (IF, ELISA, 1-5 hrs poor sensitivity), PCR (best), Tzanck test (effects of groups, MCNs), serology (Igs 10 days after 1st test) |
| How is tx of HSV? | Topical not effective (only used before recurrence when there is a tingling sensation) Acyclovir (PO/PRL, imp used effective and cheap), Valacyclovir (better but more costly), Foscarnet (if resistant HSV) Normal dose: 200mg 5time/day for 10 days adults/ 5mg/kg/8h for children or valcyclovir 500 one tablet BID/10 days If recurrence same tx but for 5 days, may get preventive tx if >6 recurrences/year 400mg 2 tablets BID/day for several months Followup (support and QoL evaluation) |
| How is tx of neonatal HSV and pregnant women HSV? | Neuro/systemic neonatal (acyclovir IV 60mg/kg/day for 21 days) for mucocutaneous same for 14 days Pregnant (<1 months predelivery same as normal but continue till delivery, if before last month give it normally for 10 days) Cesarian section done if there are lesions during labor or if no lesions but primary infection since <1 month and untreated. Vaginal delivery in case of no lesions w/primary infection since >1 month/ recurrence since more than 7 days |
| What is Herpes zoster? | • Herpes zoster or shingles: localized rash due to varicella zoster virus (VZV) • Resurgence of virus remaining latent after primary infection or chickenpox • Unilateral dermatomal distribution is characteristic of the disease |
| How is the typical presentation of herpes zoster? | I) Pre-eruptive stage: Unilateral pain superficial half-belt, burning or itching sometimes with a fever of 38 ° C, dysesthesia and satellite lymphadenopathy ii) Eruptive phase: • rash erythematous vesicular unilateral vesicles lining macules, are grouped in bunches, first translucent and then troubles erosions and crusts • Successive outbreaks occur leaving depigmented scars • The duration varies from 15 to 20 days up to 3-4 weeks • Unilateral radicular topography (intercostal) guide the diagnosis |
| What are other locations of herpes zoster? | • Zona ophthalmic: this is the most common cranial nerve herpes zoster. The eruption registered in one or more of the three branches of the trigeminal nerve, especially in its ophthalmic branch (V1). Ocular complications may occur (keratitis, iridocyclitis, optic nerve, paralysis of the oculomotor nerve) • Zona geniculate (Ramsey-Hunt syndrome): to seek before any peripheral facial paralysis. The eruption set in the area of Ramsey- Hunt, causing pain in the ear and mouth • Zona of the limbs: band sometimes making rash limb length in an area corresponding to one or more roots • Zona of the oral mucosa: stomatitis, pharyngitis or laryngitis with unilateral erosions |
| How is biological workup of herpes zoster? | Rarely useful in the diagnosis: - Serology: elevated IgM from the 3rd day - Viral culture (from vesicles or erosions) - PCR |
| How is evolution and prognosis of herpes zoster? | - In the typical form, the evolution is good in 3-4 weeks. Residual pain may persist for several weeks - In the immune compromised patients (AIDS), the rash is often necrotic with superficial ulceration, which can spread throughout the body. The pains are intense. Internal involvement as meningitis or hepatitis may occur |
| How is tx of Herpes zoster? | • i) For typical presentation: rest. Disinfection of the lesions. Use analgesics or sedatives. Aciclovir or valaciclovir orally may shorten the duration of the eruption. Postherpetic neuralgia is difficult to treat and sometimes we use antidepressants • ii) Severe forms: immune compromised, ophthalmic zoster, elderly. Hospitalization and start IV of aciclovir at effective dose (15-20 mg / kg 3 times daily) leading to a healing of the lesions. Monitoring of renal function is necessary in the treatment with aciclovir if repeated infusions |
| What is impetigo? | Common superficial bacterial skin infection, most commonly seen in children 2-5 yrs, older and adults can be affected, contagious, easily spread w/close contact, mostly due to S.aureus, S.pyogenes, combination. Two types: non-bullous (AKA impetigo contagiousum, most common form, papules surrounded by erythema, progress form pustule enlarge and break down to form thick honey crusts) Bullous (seen in young children, flaccid bullae w/clear yellow fluid later becomes purulent, leave thick brown crust, common locations are face, extremities and diaper area) |
| What is secondarily infected skin disease? | Most common form in adults, bacteria penetrate skin barrier via scratch/injury, search systematically for pruritic dermatitis, scabies, pediculosis, eczema, herpes and chickenpox |
| How is dx of impetigo? | Clinical, bacterio exam (complicated cases, resistant, abnormal) Basic lesion/clinical aspect (bubble fragile pustule breakup honey crust, may result in polycyclic circumferential contours) Classic location (children around mouth and all areas may be affected, general condition preserved, no fever and possible satellite lymph node) |
| What is ecthyma? | Ulcerative lesion extends to epidermis, punched out ulcers covered w/yellow crust surrounded by raised margins. Heals slowly and may scar, S.aureus /Strep may be the cause. Deep impetigo (ulcer of dermis GAS, precariousness, ecthyma gangrenosum, immunocompromised can be caused by pseudomonas) Covered with thick crust and surrounded by dark inflammatory halo located on lower limbs, for adults induced by poor hygiene, immune suppression, diabetes, chronic alcoholism, caused by strep, heal slowly and leave a scar |
| How is tx of impetigo? | Topical mupirocin ointment or fucidic acid (as effective as oral Abx if localized lesion and healthy pt w/no outbreak, otherwise use Abx) Disinfection (70% alcohol bactericidal) Oral Abx (when extensive or affecting several people (close contact, most important is clindamycin) |
| What are complications of impetigo? | Rare (post-strep glomerulonephritis, RF) Control of proteinuria 3 weeks post infectious episode. |
| What is folliculitis? | Superficial bacteria infection of hair follicules, small raised erythematous and occasionally pruritic pustules <5mm diameter. Genital folliculitis may be STD, commonly S.aureus, if there has been an exposure to hot tub/swimming pool consider pseudomonas as a possible cause. Pustules associated w/erythema in groin may be candidiasis Variable in number (thighs, perineum, arms, thorax, back) Clinical forms include stye (eyelash) and sycosis (beard -induced by shaving chronicity), may be pseudomonas |
| What is tx of folliculitis? | Antibacterial soap, superficial pustules drain and rupture spontaneously. Oral/topical anti staph mupirocin/retapamulin, clindamycin, deep lesions of folliculitis small follicular abscess should be drained |
| What is a furuncle/boil? | A furuncle (boil) is an acute, round, tender, circumscribed, perifollicular abscess that generally ends in central suppuration. Deep and necrotic infection of the pilosebaceous follicle S. aureus +++. If recurrent abscess evolution undergoing small family epidemics: toxinogenic research infection (Panton-Valentiner leucocidinresponsible for necrosis) and chronic carriage Clinical feature: inflammatory papule or nodule, painful, centered by a pustule on a hairy area (the hair has disappeared due to necrosis); evolution towards a central necrotic zone in a few days |
| What is furuncle differential? | • Other infectious folliculitis: ->fungal: dermatophytes (kerion of the scalp: inflammatory dermatophyte, folliculitis to pityrosporum), Candida albicans, ->gram-negative bacillae • Pseudofolliculitis (non infectious): Crohn's disease, eosinophilic folliculitis • Hidradenitis suppurativa (Verneuil's disease): chronic inflammation of the pilosebaceous follicles and sweat glands in areas rich in apocrine glands (axillary, sub- mammary and anoperineal folds) • Epidermal inflammatory cyst or superinfected cyst: Preexisting cyst (face) |
| What are furuncle complications? | • Anthrax: conglomerate of several boils • Furunculosis: boils of chronic evolution, disrupted role of triggering factors such as diabetes or immunosuppression • Primary abscess • Lymphangitis • Systemic complications (very rare): bacteremia, septic secondary localizations • Malignant Staphylococcal disease of the face: emergency case, rare |
| What is malignant staph disease of the face? | • Secondary to the inadvertent manipulation of a furuncle of the face localized in an area delimited by the internal canthus, the labial commissure and the wing of the nose • Decreasing of the general state, fever, with edema of the face, possible indurated venous cord palpable • Mechanism: superficial septic thrombophlebitis; severe complication: thrombophlebitis of the cavernous sinus (vital risk involved) |
| What is a carbuncle? | A carbuncle is a coalescence of several inflamed follicles into a single inflammatory mass with purulent drainage from multiple follicles • Furuncles and carbuncles are a subtype of abscesses, which preferentially occur in skin areas containing hair follicles exposed to friction and perspiration Common areas include the back of the neck, face, axillae, and buttocks • Usually caused by Staphylococcus aureus • Patients are commonly treated with oral antibiotics • For a solitary small furuncle: warm compresses to promote drainage may be sufficient • For larger furuncles and carbuncles: manage as you would an abscess |
| How is tx of folliculitis and boils? | • General hygiene measures: Frequent hand washes with chlorhexidine or polyvidone iodine antiseptics; avoid the handling of boil • Local antiseptic care in a topical form (solution, creams, ointments): chlorhexidine, polyvidone iodine. . For boils: systemic oral antibiotic therapy active on the S. aureus, if comorbidities and / or risk of complications: penicillin group M (oxacillin or cloxacillin). Macrolides or pristinamycin in case of allergy and / or contra-indication • duration of treatment: 10 days |
| What is tx of folliculitis and boils? | General hygiene measures (wash, don't handle boil) • Local antiseptic care in a topical form (solution, creams, ointments): chlorhexidine, polyvidone iodine. . For boils: systemic oral antibiotic therapy active on the S. aureus, if comorbidities and / or risk of complications: penicillin group M (oxacillin or cloxacillin). Macrolides or pristinamycin in case of allergy and / or contra-indication • duration of treatment: 10 days • In case of furunculosis: In addition to the previous measures: • Disinfection of the portages, armpits, perineum, nasal vestibules and external auditory canal, • Antiseptic toilet and application (repeated, sequential) of topical antibiotic (fucidic acid, mupirocine except on the mucous membranes ...) |