NON-SCALY PLAQUES Group 2

NON-SCALY PLAQUES Group 2
Sy A, Sy J, Sydiongco, Tacata, Tady, Tamondong, Tan E, Tan G, Tan M, Tan S

FIXED DRUG ERUPTION SY, Aaron Keefe S.

FIXED DRUG ERUPTION recur at the same site with each exposure to medications Six or fewer lesions occur, frequently one May be present anywhere on the body, but half occur on the oral and genital mucosa A fixed drug eruption is the term for a drug eruption that occurs in the same skin area every time the person is exposed to the drug.

Clinical Features Begins as a red patch
Evolves to an iris or target lesion identical to erythema multiforme that may eventually blister and erode Lesions of genital and oral mucosa presents as erosions Most lesions are 1 to several cm in diameter. New lesions may be added with continiued /repeated ingestion of the medication. But larger plaques may occur, resembling cellulitis. New lesions may be added, sometimes eventuating in a clinical picture similar to drug-induced erythema multiforme major.

Pathophysiology Exact mechanism is unknown
Recent research suggests a cell-mediated process that initiates both the active and quiescent lesions. Lesion contain intraepidermal CD8+ T-cells with the phenotypic markers of effector memory T-cells. Skin-resident T-cells rapidly produce IFN-γ on exposure to medication. The offending drug is thought to function as a hapten that preferentially binds to basal keratinocytes, leading to an inflammatory response. The newly arriving and residential CD8 cells likely perpetuate tissue damage by their production of the inflammatory cytokines interferon-gamma and tumor necrosis factor-alpha.

Histologic Features An interface dermatitis occuring with intraepidermal and subepidermal vesicle formation, necrosis of keratinocytes and a mixed superficial and deep infiltrate of neutrophils, eosinophils, and mononuclear cells. Stratum corneum is normal in acute stage. Papillary dermal fibrosis and deep perivascular pigment incontinence are commonly present from prior episodes. The contrast between a normal stratum corneum and chronic dermal changes is pathognomonic of fixed drug eruption.

Etiologic Agents Medications usually taken intermittently.
NSAIDS, esp. Pyrazole derivatives, Paracetamol, Naproxen, Oxicams, & Mefenamic Acid – predilection for the lips Sulfonamides, Trimethoprim or the combination – resp. for majority of genital fixed drug eruptions Pyrazole der: Phenylbutazone, phenazone, noramidopyrine. Risk of agranulocytosis.

Possible Etiologic Agents
Include: Barbiturates Dextromethophan Tetracyclines Hydroxyzine Phenolphthalein (in laxative) Lamotrigine Phenylpropanolamine Acetaminophen Erythromycin Ceterizine Chinese & Japanese herbs Celecoxib The risk of developing a fixed drug eruption has been linked to HLA-B22.

Patch Testing needed to determine which drug may be involved
Patch tests with various concentrations of the offending medication can reproduce the lesion on an affected but not unaffected skin. Most useful in pyrazolone derivative- related reactions.

Nonpigmenting Fixed Drug Eruption
large, tender, often symmetrical eythematous plaques Resolve completely within weeks. Pseudoephedrine hydrochloride – most common cause Baboon Syndrome – buttocks, groin, axilla

Treatment Main goal - identify the causative agent and avoid it.
Lesions of fixed drug eruption resolve spontaneously with avoidance of the inciting drug.

Sy, Jamelle D. ERYSIPELAS

ERYSIPELAS St. Anthony’s fire / ignis sacer
an acute beta-hemolytic group A streptococcal infection of the skin involving the superficial dermal lymphatics group B – perineal erysipelas

ERYSIPELAS local redness, heat, swelling, & a highly characteristic raised, indurated border PMN leukocytosis skin lesions: transient hyperemia  vesicles or bullae legs and face are the most frequent sites affected

ERYSIPELAS complications:
septicemia, deep cellulitis, or necrotizing fasciitis complications: operative wounds, fissures, abrasions or scratches, unclean tying of the umbilical cord, venous insufficiency, obesity, lymphedema, and chronic leg ulcers predisposing causes: contact dermatitis from plants, drugs, or dyes, and with angioneurotic edema may be confused with:

TREATMENT Pharmacologic
Vigorous antibiotic therapy for at least 10 days systemic penicillin erythromycin Non-pharmacologic Ice bags and cold compresses

CELLULITIS Sydiongco, Paula

Malaise, chills, fever, and toxicity may occur
Diffuse suppurative inflammation of connective tissue with severe inflammation of dermal and subcutaneous layers of the skin Malaise, chills, fever, and toxicity may occur Lymphangitis, regional lymphadenopathy, or both may be present In severe cases, patients may develop hypotension and area infiltrated and pits on pressure Diffuse suppurative inflammation of connective tissue with severe inflammation of dermal and particularly subcutaneous layers of the skin Involved sites are red, hot, swollen, and tender and localized pain. Erythema rapidly becomes intense and spreads Unlike erysipelas, the borders are not elevated or sharply demarcated. Severe form: area becomes infiltrated and pits on pressure. Central part may become nodular and surrmounted by a vesicle that ruptures & discharges pus & necrotic material.

No racial and sex predilection
No age predilection; individuals older than 45 years Facial cellulitis is more common in children younger than 3 years. Perianal cellulitis is predominantly a disease of children. Site of infection may occur anywhere on the body, but the leg is the most common site of the infection, followed by the arm, and then the head and neck areas. following surgery or trauma wounds, cellulitis can develop in the abdomen or chest areas. morbid obesity, it can also develop in the abdominal area No age predilection is usually described; however, studies found a higher incidence of cellulitis in general among individuals older than 45 years.2,6,9 Moreover, cellulitis at certain anatomic sites may show a predilection for persons in certain age groups Site of infection may occur anywhere on the body, but the leg (particularly in the area of the tibia or shin bone and in the foot) is the most common site of the infection, followed by the arm, and then the head and neck areas. In special circumstances, such as following surgery or trauma wounds, cellulitis can develop in the abdomen or chest areas. In cases of morbid obesity, it can also develop in the abdominal area

Incubation Duration 24 hours or can take days to develop.
less than a week to disappear with antibiotic therapy. months to resolve completely in more serious cases and can result in severe debility or even death if untreated. Not properly treated, it may appear to improve but can resurface months or even years later. Cellulitis can develop in as little as 24 hours or can take days to develop. In many cases, cellulitis takes less than a week to disappear with antibiotic therapy. However, it can take months to resolve completely in more serious cases and can result in severe debility or even death if untreated. If it is not properly treated, it may appear to improve but can resurface months or even years later.

break in the skin such as a fissure, cut, laceration, insect bite, or puncture wound
Risk factors: tinea pedis; elderly and those with immunodeficiency; diabetic people; Immunosuppressive drugs; Chickenpox and shingles; chronic venous insufficiency and varicose veins; pregnancy and obesity Organisms on the skin and its appendages gain entrance to the dermis and multiply to cause cellulitis The vast majority of cases are caused by Streptococcus pyogenes or Staphylococcus aureus Cellulitis usually follows a break in the skin, such as a fissure, cut, laceration, insect bite, or puncture wound. On the leg tinea pedis is the most common portal of entry Patients with toe web intertrigo and/or tinea pedis and those with lymphatic obstruction, venous insufficiency, pressure ulcers, and obesity are particularly vulnerable to recurrent episodes of cellulitis. Organisms on the skin and its appendages gain entrance to the dermis and multiply to cause cellulitis. The vast majority of cases are caused by Streptococcus pyogenes or Staphylococcus aureus. The elderly and those with immunodeficiency (a weakened immune system) are especially vulnerable to contracting cellulitis. Diabetics are more susceptible to cellulitis than the general population because of impairment of the immune system; they are especially prone to cellulitis in the feet because the disease causes impairment of blood circulation in the legs leading to diabetic foot/foot ulcers. Poor control of blood glucose levels allows bacteria to grow more rapidly in the affected tissue and facilitates rapid progression if the infection enters the bloodstream. Neural degeneration in diabetes means these ulcers may not be painful and thus often become infected. Chickenpox and shingles often result in blisters that break open, providing a gap in the skin through which bacteria can enter. Lymphedema, which causes swelling on the arms and/or legs, can also put an individual at risk.

Cellulitis S pyogenes Immunocompetent adults
Perianal cellulitis (children) perianal erythema and pruritus, purulent secretions, painful defecation, and bleeding in the stools S aureus Children Pasteurella multocida dog or cat bite or scratch Pseudomonas aeruginosa after a puncture wound Non–group A streptococci (ie, groups B, C, and G) lymphatic obstruction or venectomy for coronary artery bypass graft Aeromonas hydrophilia, Vibrio vulnificus after exposure to freshwater or seawater In immunocompetent adults, cellulitis is usually due to S pyogenes and, occasionally, S aureus Perianal cellulitis due to group A streptococci is usually observed among children with perianal fissures. It is characterized by perianal erythema and pruritus, purulent secretions, painful defecation, and bleeding in the stools.10 In children, the most common cause of cellulitis is S aureus. Cellulitis from a dog or cat bite or scratch may be caused by the Pasteurella multocida bacteria, which has a very short incubation period of only four to 24 hours. Pseudomonas aeruginosa is another type of bacteria that can cause cellulitis, typically after a puncture wound. Non–group A streptococci (ie, groups B, C, and G) are commonly implicated in cellulitis in patients with lymphatic obstruction or venectomy for coronary artery bypass graft Aeromonas hydrophilia, Vibrio vulnificus, and other bacteria are causes of cellulitis that develops after exposure to freshwater or seawater.

Haemophilus influenzae cellulitis
Haemophilus influenzae type B Children < 6 y.o. Rare in countries where vaccination is available Bacteremia may lead to meningitis, orbital cellulitis, osteomyelitis, or pyarthrosis Culture, needle aspirate Cefotaxime and ceftriaxone; Rifampin Pneumococcal facial cellulitis S pneumoniae Young children Extremity involvement: DM, subs. abuse Head, neck & upper torso involvement: SLE, nephrotic syndrome, hematologic dso. Fever, leukocytosis, and septicemia Penicillin, vancomycin Haemophilus influenzae cellulitis is a cutaneous condition characterized by a distinctive bluish or purplish-red cellulitis of the face prevalent in children under 6 years of age. The condition is Rarely seen in countries where vaccination is available. Bacteremia may lead to meningitis, orbital cellulitis, osteomyelitis, or pyarthrosis. Culture of the blood and needle aspirate of the cellulitis should yeild this organism. Cefotaxime and ceftriaxone are effective; Rifampin should be given to children under 4 y.o. both parents and children unvaccinated to clear the nasal carriage and prevent secondary cases. Pneumococcal facial cellulitis occurs primarily in young children who are at risk for pneumococcal bacteremia.21,22 It may manifest as 2 distinctive clinical syndromes, as follow: Extremity involvement in individuals with diabetes mellitus or substance abuse Head, neck, and upper torso involvement in individuals with systemic lupus erythematosus, nephrotic syndrome, or hematologic disorders. Fever, leukocytosis, and septicemia are universal Penicillin, or resistant cases, vancomycin is excellent S pneumoniae is an uncommon cause of cellulitis in adults. Pneumococcal cellulitis may occur from bacteremia. In a review of pneumococcal skin infection in adults, all such patients had an underlying chronic illness or were immunocompromised by drug or alcohol abuse.

Helicobacter cellulitis
Helicobacter cinaedi Fever, bacteremia, cellulitis and arthritis HIV- infected patients; malignancy, diabetes; and acoholism distinctive red-brown or copper color w/ minimal warmth Ciprofloxacin Tuberculous cellulitis Mycobacterium TB px taking chronic corticosteroids Past history of pulm. TB Four drug treatment Helicobacter cellulitis is a cutaneous condition w/ Fever, bacteremia, cellulitis and arthritis caused by Helicobacter cinaedi. They occur in HIV- infected patients; however malignancy, diabetes; and acoholism are other predisposing condtns. The cellulitis may be multifocal and recurrent, and have distinctive red-brown or copper color w/ minimal warmth. Ciprofloxacin is effective. Tuberculous cellulitis is a skin condition resulting from infection with mycobacterium, and presenting as cellulitis. Unusual manif. Of TB in px who had been on chronic corticosteroids and developed clin. Cellulitis. In biopsy, granulomas and acid-fast bacilli are seen and 4 drug tx resulted in cure. Past history of pulm. TB

Diagnosis Cellulitis is most often a clinical diagnosis Blood cultures usually are positive only if the patient develops generalized sepsis Resemble Cellulitis: deep vein thrombosis: compression leg ultrasound Lyme disease has been misdiagnosed as staph- or strep-induced cellulitis (bullseye rash does not always appear): to rule out Lyme disease is with a blood test, which is recommended during warm months in areas where the disease is endemic.[2] Cellulitis is most often a clinical diagnosis, and local cultures do not always identify the causative organism. Blood cultures usually are positive only if the patient develops generalized sepsis. Conditions that may resemble cellulitis include deep vein thrombosis, which can be diagnosed with a compression leg ultrasound, and stasis dermatitis, which is inflammation of the skin from poor blood flow. There have been many cases where Lyme disease has been misdiagnosed as staph- or strep-induced cellulitis. Because the characteristic bullseye rash does not always appear in patients infected with Lyme disease, the similar set of symptoms may be misdiagnosed as cellulitis. Standard treatments for cellulitis are not sufficient for curing Lyme disease. The only way to rule out Lyme disease is with a blood test, which is recommended during warm months in areas where the disease is endemic.[2]

Children and compromised adults
Complications Gangrene Metastatic abscess Grave sepsis Children and compromised adults

Treatment & Prevention
Rest affected limb & cleaning the wound site and treatment with oral antibiotics Early lesions: Intralesional inj of triamcinolone acetonide 1:10 Mild cellulitis: Flucloxacillin monotherapy (to cover staphylococcal infection) Moderate cases or where streptococcal infection is suspected: combined with oral phenoxymethylpenicillin or intravenous benzylpenicillin, or ampicillin/amoxicillin ; cefazolin or vancomycin Intitial emperic therapy should cover both satph and strep. Intravenous penicillinase-resisitant penicillins or first generation cephalosporin are usually effective If lack of response: MRSA should be considered and treatment strategies chosen depending on whether the infec.. Was hospital or ccommunity acqiured Treatment consists of resting the affected limb or area, cleaning the wound site if present (with debridement of dead tissue if necessary) and treatment with oral antibiotics, except in severe cases, which may require admission and intravenous (IV) therapy.[3] Flucloxacillin monotherapy (to cover staphylococcal infection) is often sufficient in mild cellulitis, but in more moderate cases or where streptococcal infection is suspected then usually combined with oral phenoxymethylpenicillin or intravenous benzylpenicillin, or ampicillin/amoxicillin (e.g. co-amoxiclav in the UK).

Medical advice should be sought:
Severe cases: require admission and intravenous (IV) therapy. Wound: cleaned and dressed appropriately done daily or when they become wet or dirty Medical advice should be sought: wound deep or dirty and retained foreign bodies Pain relief is also often prescribed, but excessive pain should always be considered relevant, as it is a symptom of necrotising fasciitis, which requires emergency surgical attention. As in other maladies characterized by wounds or tissue destruction, hyperbaric oxygen treatment can be a valuable adjunctive therapy, but is not widely available.[4][5] [edit] Prevention Any wound should be cleaned and dressed appropriately. Changing bandages daily or when they become wet or dirty will reduce the risk of contracting cellulitis. Medical advice should be sought for any wounds that are deep or dirty and when there is concern about retained foreign bodies.

TACATA, Patricia TADY, Clarissa Marie
URTICARIA

URTICARIA (HIVES) characterized by wheals surrounded by a red halo or flare severe itching, stinging or pricking annular or polycyclic pattern  clearing of central region and coalescence of lesions

URTICARIA (HIVES) Subcutaneous swellings (angioedema) may accompany the wheals target the gastrointestinal and respiratory tracts resulting in abdominal pain, coryza, asthma and respiratory problems.

ACUTE VS. CHRONIC URTICARIA
days to weeks Produce evanescent wheals that rarely last >12h Resolution within 6 weeks of onset CHRONIC Daily episodes of urticaria and/or angioedema lasting >6w Physical urticaria common

COMMON TRIGGERS Opiates Polymyxin B Tubocurarine
Aspirin and other NSAIDS Tartrazine Benzoate

ETIOLOGIC FACTORS Most frequent cause of acute urticaria
A.DRUGS Most frequent cause of acute urticaria MOST COMMON: Penicillin and related antibiotics Allergic rhinitis or asthma, nasal polyps and food induced anaphylaxis B. FOOD frequent cause of acute urticaria whereas in chronic urticaria food is a less frequent factor MOST COMMON: Chocolate, shellfish, nuts, peanuts, eggs and milk Serum radiallergosorbent tests(RASTs) can be used to detect specific IgE and elimination of diets can be of benefit.

ETIOLOGIC FACTORS C. Food Additives
Natural food additives: yeasts, salicylates, citric acid, egg and fish albumin Synthetic additives: azo dyes, sulfites, penicillin, benzoic acid derivatives With the exception of sulfite and penicillin, most food additives can be avoided by eating only meat produce and dairy products Packaged food are largely prohibited.

ETIOLOGIC FACTORS Streptococcal infections
D. Infections Streptococcal infections Chronic viral infection (Hep B & C) Helminths (ascaris, ankylostoma,filaria) E. Emotional Stress Severe emotional stress no matter what the primary cause Initiating stimulus in CHOLINERGIC URTICARIA F. Neoplasms Associated with carcinomas and Hodgkin’s disease

ETIOLOGIC FACTORS G. Inhalants
Grass pollens, house dust mites, feathers, formaldehyde, etc. H. Alcohol Induced by ingestion of alcohol I. Menthol Rarely causes urticaria

PATHOGENESIS Capillary permeability
Release of histamine from the MAST CELLS (PRIMARY EFFECTOR in urticarial reactions) Serotonin, leukotrienes, prostaglandins, proteases and kinins – other substances that may cause vasodilation and capillary permeability

DIAGNOSIS CLINICAL EVALUATION Clinical grounds
Fixed lesions >24h: Urticarial vasculitis, granuloma annulare, sarcoidosis, cutaneous T – cell lymphoma Skin biopsy: if wheals last >24h CLINICAL EVALUATION Detailed history and physical examination Radiologic sinus evaluation Blood count to detect eosinophilia Review of medications in chronic urticaria Skin biopsy

ANAPHYLAXIS An acute and often life threatening immunologic reaction
Scalp pruritus, diffuse erythema, urticaria and angioedema Most common causes of serious anaphylactic reactions: Penicillins, radiographic contrast agents Hymenoptera stings, shellfish and other food allergens

Treatment Acute Urticaria Antihistamines
Non-sedating Histamines pose a lower risk of psychomotor problem in adults. Avoid the trigger if the cause can be identified Systemic corticosteroids For severe reactions, respiratory and cardiovascular support is essential. Intubation and tracheotomy may be required. Systemic corticosteroids are used if antihistamines are not effective Severe reactions – anaphylaxia Intubation and tracheotomy for progressive cases

Chronic Urticaria Mainstay treatment: Antihistamines
Should be taken on a daily basis and not prescribed to be taken as needed Second generation antihistamine produce less sedation in most patients Second line treatment Phototherapy Calcium channel antagonist Antimalarial medications Methotrexate Corticosteroids produce long term side effects Local treatment Tepid or cold tub baths Topical camphor and menthol 2nd gen antihistamines – Cetirizine, famotidine, loratdine are lipophilic molecules that don’t’ cross the bbb Topical corticosteroids, topical antihistamines and topical anesthetics have no tole in the management of chronic urticaria Topical camphor and menthol for symtomatic relief

Other Urticarial Variants

Angioedema Acute, evanescent, circumscribed edema
Area of predeliction: Eyelids, lips, lobes of ears, external genitalia, or mucous membranes of the mouth, tongue, or larynx Swelling occurs in the lower layers of the skin or in the subcutaneous tissues Frequently begins during night and is found on awakening Two subtypes: Deep form Angioedema associated w/ C1 esterase inhibitor deficiency Usually affects the most distensible tissues Deep form – solitary or multiple sites Angioedema associated w/ C1 esterase inhibitor deficiency- not associated w/ hives, no pruritis

Hereditary Angioedema (HAE)
Quincke edema 2nd – 4th decade, Autosomal dominant inheritance Swelling:  Asymmetrical without urticaria or itching In subcutaneous tissues and abdominal organs mimicking surgical emergencies, and the upper airway (larynx) – life-threatening Little response to antihistamines, epinephrine, or steroids High mortality rate – death often caused by laryngeal edema 3 phenotypic forms: Type I Type II Type III Trigger factors:  minor trauma, surgery, sudden changes in temperature, or sudden emotional stress Type I – Low antigenic and functional plasma levels of a normal C1-EI; replacement therapy with concentrates or FFP Type II – presence of normal or elevated antigenic levels of a dysfunctional protein; Stanozolol (attenuated androgen Type III – normal C1-EI function and normal complement; only in female members of affected families; Danazol

Acquired C1 Esterase Inhibitor Deficiency
 Usually occurs after 4th decade of life  No family history Not associated w/ pruritis or urticaria Two subtypes: A. Acquired angioedema-I Rare disorder associated with lymphoproliferative diseases Treatment: Replacement of C1-EI with concentrates or FFP; antifibrinolytic agents; synthetic Danazol B. Acquired angioedema-II Extremely rare disease Treatment: Immunosuppresive therapy; Synthetic corticosteroids (temporarily effective); Plasmapheresis Acquired angioedema-I – increased catabolism of c1 e1 Acquired angioedema-II - No underlying lymphoproliferative disease

Episodic Angioedema with Eosinophilia
Uncommon disorder w/ no underlying disease Isolated facial edema May occur with fever, weight gain, eosinoophilia and elevated eosinophil major basic protein Treatment: administration of systemic steroidal medications, antihistamines, and IVG

Schnitzler Syndrome Rare disorder
Combination of chronic, non-pruritic urticaria, fever of unknown origin, disabling bone pain, hyperostosis, increased erythrocyte sedimentation rate, and monoclonal IgM gammopathy Age of onset: years old; affects both sex Effective therapy has not been determined Bone pain and urticarial lesion respond to systemic corticosteroids Without gender predilection

Physical Urticarias Occur most frequently in ages 17-40 years old
Most common form dermatographism > cholinergic > cold urticaria Chronic idiopathic urticaria: Dermatographism, delayed pressure, cholinergic, and cold urticaria Other forms: Adrenergic Urticaria Vibratory Angioedema Heat Urticaria Aquagenic Urticaria Solar Urticaria Pressure Urticaria ( Delayed Pressure)

Dermatographism Sharply localized edema or wheal with a surrounding erythematous flare occurring within seconds to minutes after the skin has been stroked Affects 2-5% of the population Arise spontaneously after drug-induced urticaria and persist for months H2 antihistamine may be of benefit Also assoc w/ certain diseases like hypo- and hyperthyroidism, DM

Cholinergic Urticaria
Produced by the action of AcH on the mast cell Characterized by minute, highly pruritic, punctuate wheals or papules 1-3 mm in diameter and surrounded by areas of erythema Area of predilection: trunk and face Persists for min and followed by a refractory period with no lesions of up to 24 hours Palms and soles are spared Trigger factors: exercise, emotional stress, increased environmental temperature, or intradermal injection of nicotine picrate or methacholine Treatment: adequate dosage of antihistamines; Danazol in refractory cases

Cold Urticaria Exposure to cold may develop edema and wheals on the exposed areas; usually on the face and hands Urticaria does not develop during chilling but on rewarming Types: Primary – no underlying systemic disease - Tx: Doxepin, Cyproheptadine; Acrivastine and Cetirizine Secondary - Associated with underlying systemic disease such as cryoglobulinemia Familial Cold Urticaria- produces a Burning sensation with cyanotic centers and surrounding white halos lasting for 24 – 48 hrs - Leukocytosis - Tx: Stanozolol therapy 2nd gen antihistamine - Acrivastine and Cetirizine Familial Cold Urticaria – Leukocytosis is a prominent feature - Stanozolol therapy has been proven effective

Tamondong, Roxanne Tan, Ernie Joe
Erythema Multiforme Tamondong, Roxanne Tan, Ernie Joe

Erythema Multiforme Erythema multiforme minor
Herpes simplex-associated erythema multiforme (HAEM) Strongly associated with preceding herpetic infection

Clinical features Self-limited Recurrent disease Young adults
1-4 weeks Sharply marginated, erythematous macules Raised, edematous papules 24-48 hrs

Classic target or iris lesion
A ring of erythema that forms around the periphery, and centrally the lesions are flatter, more purpuric, and dusky 3 zones: Central dusky purpura Elevated, edematous pale ring Surrounding macular erythema Typical target lesions best seen in palms and soles

Lesions appear symmetrically and acrally
Initial involvement most frequently of the dorsal hands Dorsal feet, extensor limbs, elbows, knees, palms and soles 10% of cases, more widespread lesions occur on the trunk Mucosal involvement in 25% of cases and is limited to the oral mucosa

Atypical HAEM Outbreaks of unilateral or segmental papules and plaques that may be few in number or solitary Lesions may be up to 20cm in diameter Plaques- erythematous and evolve to have a dusky center, which desquamates Subcutaneous nodules may be present

Histology: features of EM and HSV can be seen
Acyclovir – prevents the lesions Prednisone – increase the frequency of attacks

Etiologic factors Preceding orolabial HSV infection
Appear 1-3 weeks (average of 10 days) after the herpes outbreak Not all episodes of EM may follow every episode of herpes

Pathogenesis due to an allergic reaction(medication) or infection(HSV or Mycoplasma) involves damage to the blood vessels of the skin followed by damage to skin tissues. Activated T lymphocytes are present in lesions of Erythema Multiforme. Epidermis – Cytotoxic or Suppressor cells Dermis – Helper T-cells EM minor is linked to HLA type HLA-DQ3

Histopathology Histologic Features are NOT predictive of etiology due to similar feature from EM to TEN(Toxic epidermal necrolysis) Extent of epidermal involvement depends on the duration of the lesion and where in the lesion the biopsy is taken Biopsy- “basket-weave stratum corneum” - suggest acute process where in there was not enough time to produce abnormal keratin

Histopathology Vacuolar interface dermatitis is present with vacuoles and foci of individual cells necrosis out of proportion to the no. of lymphocytes Dermal infiltrate is largely mononuclear and tends to be primarily around the upper dermal vessels and along the dermo- epidermal junction. Eosinophils may be present but rarely prominent and not predictive of etiology

Histopathology of EM must be differentiated from the following:
Fixed Drug Eruption Graft vs Host disease Pityriasis lichenoides Lupus erythematosus -deeper infiltrate w/ eosinophil and neutrophils papillary dermal fibrosis melanophages around post-capillary venules More compact stratum corneum Epithelial disorder resembling Bowens Disease w/ lymphocyte in every vacuole w/ erythrocyte extravasasion neutrophil margination within dermal vessels Compact hyperkertosis a deeper periadnexal infiltrate dermal mucin and basement membrane thickening

Differential Diagnosis when Bullae are prominent:
Pemphigus Bullous pemphigoid Paraneoplastic pemphigus - Prominent mucous membrane involvment Lesions are small erythema prominent at periphery of the bulla May produce atypical target lesions mucosal involvement vacuolar interface dermatitis appear very similar to EM major

Treatment Most cases are self limited and symptomatic treatment may be all that required -Anti-histamine, Moist compress, Topical anesthetics and Acetaminophen Prevention: Sunscreen lotion and sunscreen-containing lip balm – prevent UVB induced outbeaks of HSV Therapy: Oral Anti-viral (acyclovir, valacyclovir or famciclovir) Dapsone – antibacterial that inhibits synthesis of dihydrofolic acid - alternative drug when anti-virals are not effective Systemic Steroids – control inflammation Intravenous Immunoglobulin – to stop disease process

Exfoliative Dermatitis
Genevieve Lynn C. Tan

Dermatitis exfoliativa Pityriasis rubra (Hebra) Erythroderma (Wilson – Brocq)

Extensive erythema and scaling Entire body surface is dull scarlet Small, laminated scales No vesicles and pustules Extensive telogen effluvium

Etiology Result of generalization of preexisting chronic dermatosis (61%) Medications allopurinol, sulfas, gold, phenytoin, phenobarbital, isoniazid, carbamazepine, cisplatin, dapsone, mefloquine, tobramycine, minocycline, nifedipine and iodine Inadequate intake of branched chain amino acids in infants with MSUD Idiopathic

Etiology Sezary syndrome
Generalized exfoliative dermatitis with intense puritus Leonine facies Alopecia Palmoplantar hyperkeratosis Onychodystrophy

Criteria for diagnosis of Sezary syndrome:
Absolute Sezary cell count of at least 1000/mm3 CD4/CD8 ratio >10 Increase Lymphocyte count with evidence of T cell clone Chromosomally abnormal T cell clone

Etiology Hodgkin’s Disease Generalized exfoliative dermatitis Fever
Lymphadenopathy Hepatosplenomegaly ESR

Histopathology Nonspecific Hyperkeratosis Mild acanthosis
Focal parakeratosis

Treatment Drug-induced – stop drug
Application of mild corticosteroid after soaking and occlusion under sauna suit Acitretin, cyclosporin, methotrexate for psoriatic erythroderma Isotretinoin, acetretin, methotrexate for PRP Azathioprine and methotrexate for idiopathic erythroderma unresponsive to therapy

Tan, Marie Dolores Tan, Samantha
Hansen’s disease Tan, Marie Dolores Tan, Samantha

Hansen’s Disease Also known as LEPROSY
Chronic, systemic, infectious disease caused by Mycobacterium leprae Granulomatous or neutrophelic lesions in different parts of the body like: Skin Mucous Membrane Nerves Anterior Segment of the Eye Bones Viscera

Hansen’s Disease Mycobacterium leprae Weakly acid fast Grows 32-35°C
Cultivated in mouse pads and armadillos Favors intracellular location Only bacterium to invade peripheral nerves Phenolic Glycolipid (PGL-1) – unique to leprosy bacillus *T: below the core body T of humans; explains localization of leprosy lesions to cooler areas of the body, and the sparing of the midline and scalp

Epidemiology 10-15 million worldwide
Asia (Indian Subcontinent), Sub-Saharan Africa, South and Central America, Pacific Islands, and the Philippines Most cases in tropical and developing world More common in people who are of low economic status, w/ inadequate housing, unsuitable sanitation, poor nutrition, and lack of education

Epidemiology Men > Female Occurs in all ages
Peak presentations in children aged years old and in adults years old Mode of transmission: controversial (respiratory route: infectious droplets from nasal secretions) Genetic susceptibility

PATHOGENESIS Patient’s immune reaction to the leprosy bacillus: critical element in determining the outcome of infection. TUBERCULOID LEPROMATOUS Granulomas Well-formed, contain helper T-cells Poorly-formed, predominant suppressor T-cells Cytokine profile IFN-γ, IL-2 IL-4, -5, and -10 prominent Cell-mediated immunity Good Downregulated

DIAGNOSIS Identification of M. leprae in the affected tissue
Skin biopsies Skin or nerve lesions Stain: visualize the bacillus with Fite-Faraco stain Slit smears Lesions and cooler areas of the skin Stain: acid-fast stain Multibacillary: organisms found on the skin smears Paucibacillary: negative skin smears (and 5 or fewer lesions) Serologic tests Detects antibodies against M. leprae-unique antigens (PGL-1) PCR detects small numbers of organisms in infected tissue

Diagnostic procedures
Histamine Test Metacholine Sweat Test Skin Sensory Test Lepromin Test (Mitsuda Reaction) Histologic features of Hansen’s disease correlate with the clinical pattern of the disease

Develops clinical disease
Hansen’s Disease Presents with a broad spectrum of clinical diseases Exposure (Spontaneous cure) No clinical disease Develops clinical disease Paucibacillary Multibacillary Most common outcome post-exposure: spontaneous cure If skin disease does appear, initial clinical lesion may be a single hypopigmented patch, perhaps with slight anesthesia, = INDETERMINATE DISEASE

Early indeterminate leprosy
Insidous onset Slight prodromal symptoms “Numbness” – first clinical manifestation First lesion is a solitary, ill-defined hypopigmented macule (sometimes erythematous) Succeeding lesions common: Cheeks, upper arms, thigh, and buttocks Peripheral Nerves not enlarged No plaques No nodules No or very few bacilli on biopsy INDETERMINATE: since the course of the disease cannot be predicted at this stage; the lesion may clear spontaneously or may progress to any other form of leprosy (other forms: next slide)

SPECTRUM OF HOST-PARASITE RESISTANCE in leprosy
High resistance Unstable resistance No resistance Tuberculoid (TT) Borderline Tuberculoid (BT) Borderline (BB) Borderline Lepromatous (BL) Lepromatous (LL) Lesions 1-3 Few Few or many asymmetrical Many Numerous and asymmetrical Smear for bacilli 1+ 2+ 3+ 4+ Lepromin test + Histology Epithelioid cells decreasing → Increasing histiocytes, foam cells, granuloma, xanthoma-like Nerve destruction, sarcoid-like granuloma Spectrum of leprosy has 2 stable poles: Tuberculoid, Lepromatous (these polar forms do not change, the patient remains w/ one or the other form throughout the course of disease) *Ridley and Jopling classifcation or modifications to it have classified cases based on clinical, bacteriologic, immunologic, and histopathologic features

Tuberculoid leprosy Solitary, large, few (<3), asymmetrically distributed lesions Sharply defined and elevated border that slopes down to flattened atrophic centers– “Saucer Right Side Up” appearance Palpable indurations Dry hairless hypo/hyperpigmented lesions Lesions are anesthetic/hyposthenic and anhidrotic Enlarged peripheral nerves (great auricular nerve and ulnar nerve) Muscular weakness and atrophy Common sites of lesion: Face, Limbs or Trunk

Borderline tuberculoid leprosy
Lesions are similar to tuberculoid lesions, but smaller and more numerous (>10-20) Satellite lesions around large macules or plaques Less hair loss Nerves slightly enlarged Common sites of lesion: face and limbs

Borderline leprosy Small, numerous (but countable), cutaneous lesions
Generalized, but asymmetrical lesions Erythematous, irregularly shaped, ill defined borders Erythematous plaques with islands of normal skin – “Swiss Cheese Appearance” Nerves are slightly enlarged, thicker, and tender Anesthesia is only moderate

Borderline Lepromatous Leprosy
Numerous (too many to count), symmetrical lesions: macules, papules, plaques, and nodules Ill-defined outer border and sharply marginated inner border - “Inverted saucer shaped” or “Punched Out” Reverse configuration of tuberculoid type Nerve lesions appear later, enlarged, tender, or both Anesthesia is often absent

Lepromatous Leprosy Numerous, symmetrical macules, papules, plaques, and nodules Lepromas (nodules) on the earlobes, nose, lips, eyebrows Little or no loss of sensation over the lesions No nerve thickening No changes in sweating “Leonine Fascies” Madarosis – lateral thinning of eyebrows Nasal ulceration May begin as such or develop following indeterminate leprosy or from downgrading of borderline leprosy -Leonine fascies: skin thickens over the forehead

Treatment WHO Western Pacific recommendation

Reactional states Characteristic and clinically important aspect of Hansen’s disease Experienced by 50% of patients after institution of multidrug therapy Triggers: intercurrent infections, vaccination, pregnancy, vitamin A, iodides, bromide Severe, abrupt 2 Forms +Management of Reactions Severe: important cause of nerve damage in borderline patients Abrupt: in appearance, vs. Hansen’s disease which changes slowly If the patient feels that the chemotherapy is triggering the reaction, he/she will tend to discontinue the treatment, leading to treatment failure TYPE 1 TYPE 2 Caused/Mediated By: Cell-mediated Immune complexes Occur In: Borderline Leprosy (BT, BB, BL) Lepromatous patients (BL, LL)

Management of reactions
Even though reactions may appear after drug treatment is instituted, it is not advisable to discontinue or reduce anti-leprosy medication. MILD REACTIONS No neurologic complications or severe systemic symptoms Supportive treatment, bed rest, aspirin or NSAIDs TYPE 1 REACTIONS Prednisone Clofazimine TYPE 2 REACTIONS (ENL) Thalidomide: drug of choice; potent teratogen Systemic corticosteroids

prevention BCG vaccination alone provides about 34% prevention against infection BCG + heat-killed M. leprae increases protection to 64% Treat active multibacillary patients and examine exposed persons on an annual basis to detect early evidence of infection Chemoprophylaxis in hyperendemic regions Once yearly multidrug therapy with single dose rifampin+minocycline+clofazamine 80% of patients have close contact with multibacillary patients:

NON-SCALY PLAQUES Group 2

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