Abstract Introduction Crusted (Norwegian) scabies is a severe Sarcoptes scabiei infestation characterized by an extraordinarily high mite burden and extreme contagion, classically in immunocompromised or elderly patients. Secondary bacterial infection can cause sepsis, but progression to septic shock is rare and carries a high mortality risk. This case illustrates the diagnostic challenges and the importance of early recognition and multidisciplinary care in immunocompromised hosts. Case Presentation A 65-year-old woman with systemic lupus erythematosus (SLE) on chronic immunosuppression presented with weeks of worsening painful, pruritic dermatitis. She had a year-long rash with prior biopsies read as psoriasis, leading to immunotherapy initiation. On presentation, she was febrile and hypotensive with a diffuse erythematous, desquamating eruption involving 75% of her body and thick hyperkeratotic plaques. Differential diagnoses included erythroderma (psoriatic), Sézary syndrome, and crusted scabies. Given the characteristic skin findings and immunosuppressed state, empiric treatment for crusted scabies was initiated with oral ivermectin, topical permethrin, and isolation precautions. By hospital day 2, she developed septic shock with multiorgan dysfunction requiring vasopressors and mechanical ventilation. Skin biopsy confirmed crusted scabies. Treatment was continued with ivermectin, permethrin, antibiotics, and corticosteroids, leading to rapid improvement in shock and cutaneous disease within a week. Discussion Crusted scabies may harbor millions of mites, allowing transmission through brief contact or fomites, and is frequently misdiagnosed as psoriasis or erythroderma, delaying therapy. Immunosuppression markedly increases risk. Superinfection with Staphylococcus aureus or Streptococcus pyogenes can cause severe soft-tissue infection, bacteremia, and septic shock. Management requires combination of scabicidal therapy with oral ivermectin plus topical permethrin 5% and antimicrobials for suspected superinfection. Keratolytics and repeated topical applications enhance penetration in hyperkeratosis. Strict infection control is essential: isolate the patient with gowns, gloves, and shoe covers until treatment completion; treat close contacts; and decontaminate linens and clothing (≥50 °C for ≥10 min or seal for 3-7 days). Our patient’s rapid hemodynamic recovery following anti-scabietic therapy underscores the role of parasite reduction alongside antibiotics in reversing shock physiology. This case highlights the diagnostic challenge of distinguishing crusted scabies from other dermatoses and the need for a high index of suspicion when rashes fail standard therapy. Immunocompromised patients are at increased risk, and early recognition, isolation, and combined antiparasitic and antimicrobial therapy are critical. When suspicion is high, empiric therapy should begin promptly without waiting for biopsy confirmation to prevent catastrophic outcomes. This abstract is funded by: None
Burton et al. (Fri,) studied this question.