Step 1: Use the timing and triggers. Lesions appearing within 1-2 days of birth, with an afebrile infant, no mucosal involvement, and a mother with autoimmune blistering disease, point to a passively transferred antibody-mediated process rather than infection or a structural defect.
Step 2: Mechanism of neonatal pemphigus. Maternal IgG anti-desmoglein antibodies cross the placenta and cause transient acantholytic blistering in the newborn (neonatal pemphigus). It is self-limiting as maternal antibodies are cleared over weeks, and systemic toxicity/fever is absent.
Step 3: Exclude infection (SSSS). SSSS is caused by staphylococcal exfoliative toxin, typically presents with fever, irritability, periorificial crusting and tender erythroderma with a positive Nikolsky sign, and would not be tied to a maternal autoimmune history. The afebrile, well neonate with a relevant maternal history argues against SSSS.
Step 4: Exclude BP and EB. Bullous pemphigoid is a disease of the elderly and is exceedingly rare neonatally. Epidermolysis bullosa is an inherited mechanobullous disorder triggered by friction/trauma sites, not by maternal antibody transfer, and is not autoimmune. Neither fits the transplacental, afebrile, mucosa-sparing picture.
Key fact: Afebrile neonatal blistering without mucosal disease plus a mother with pemphigus = neonatal pemphigus from transplacental maternal antibodies.