1. Herpes simplex
2. Varicella-zoster
3. Vesicular tinea pedis
4. Dyshidrosis (pompholyx)
5. Scabies
6. Dermatitis herpetiformis

1. Posion-ivy-type contact dermatitis
2. Bullous impetigo
3. Erythema multiforme bullosum (Steven Johnson syndrome)
4. Pemphigoid
5. Pemphigus

• Pemphigus vulgaris
• Blisters and bullae, rupture→erosions, crusting→post-inflammatory changes
• Nikolsky sign—skin slides off with gentle pressure, separating epidermis from basal layer→blister on skin that was not previously involved
• Usually starts with oral ulcers, progresses to skin blisters. Lesions become bigger, more generalized if left untreated.
• Etiology—autoimmunity to pemphigus vulgaris antigen, member of cadherins (cell adhesion molecules) and normal keratinocyte membranes. Blisters result from loss of integrity of normal intercellular attachments within epidermis and mucosal epithelium.
• Find IgG in intercellular regions of epidermis, rarely IgM, IgA, C3.
• Path—Basal cells lose intercellular bridges but remain attached to dermis, causes “tombstone appearance.” Acantholysis=keratinocytes that lose their attachments to other cells, float freely within the blister cavity.
• Rx—steroids, azathioprine, plasmapharesis
• Bullous pemphigoid
• Subepidermal blisters, also autoimmune
• Tense, pruritic blisters on flexor surfaces (vs. intertriginous areas in PV)
NO positive Nikolsky sign, as skin is tense and not fragile, some post-inflammatory changes but not as marked as in PV.
• 
  
• Starts as “hives,” then blisters appear on urticarial regions
• Does not usually start with oral blisters, but mild and transient if present
• Little epidermal change—because it’s subepidermal. Also eosinophils (remember—eos go with hives and allergies)
• IF—shows IgG, C3 along basement membrane
• Autoab against hemidesmosomes (also cell adhesion molecules)
• Rx—steroids, immunosuppressants

b. Secondary syphilis -- maculopapular rash, condylomata lata (flat topped papules -- located at the anus and in skin folds where heat and moisture exist).

c. Rocky Mountain Spotted Fever -- stage 1: erythema chronicum migrans (a red rash that spreads, leaving a clear center -- bulls-eye rash).

d. Meningococcemia --intravascular multiplication of N. meningitidis in the blood can result in a petechial rash (minute hemorrhagic spots the size of a pin that do not blanch when pressed). The rash can enlarge if the organisms multiply in the blood to the leading to fulminant meningococcemia (Waterhouse-Friderichsen syndrome--bilateral hemorrhage into the adrenals).

e. Herpes Zoster (varicella zoster) Virus -- vesicular rash (chicken-pox) that appear on the back of the head and ears then spread to the face, neck, trunk, and extremities. The distinguishing feature from other rashes (small pox) is that lesions will be at different stages (whereas small pox lesions are concentrated on the extremities and are all in the same stage). The lesions are very pruritic (itchy).

f. Coxsackievirus --Coxsackie A: herpangina -- fever, sore throat, and small red-based vesicles over the back of the throat. Hand-foot-mouth disease -- (coxsackie A-16) eruptions of small pearly, gray vesicles on the fingers, toes, palms, and soles often accompanied by painful vesicles and ulceration of the buccal mucous membranes and the tongue with slight fever; disease lasts 4 to 7 days.