Crusted scabies complicated by septic shock: a fatal case report with incidental detection of Sarcoptes scabiei DNA in peripheral blood

Abstract

Crusted scabies is a severe form of scabies characterized by massive mite burden and profound immune dysregulation. Secondary bacterial infection is common and may progress to sepsis with fatal outcomes. We report a fatal case of crusted scabies complicated by septic shock in a 58-year-old man with diabetes mellitus and chronic dermatitis. The patient presented with diffuse erythroderma, extensive hyperkeratotic crusts, and deep skin fissures, and several household members had similar pruritic skin lesions. Laboratory investigations revealed marked eosinophilia, extremely elevated serum immunoglobulin E levels, and multiorgan dysfunction. Peripheral blood metagenomic next-generation sequencing identified multiple bacterial pathogens and incidentally detected Sarcoptes scabiei DNA. Despite broad-spectrum antimicrobial therapy, antiparasitic treatment, and intensive supportive care, the patient deteriorated and died. This case highlights crusted scabies as a potentially lethal condition when complicated by severe bacterial infection and underscores the need for cautious interpretation of parasitic DNA detected in blood, particularly in non-invasive ectoparasitic diseases.

Introduction

Scabies, caused by Sarcoptes scabiei var. hominis, is a common ectoparasitic skin disease worldwide. Crusted scabies represents its most severe variant and is characterized by extensive hyperkeratosis, extremely high mite burden, and impaired host immune responses. Patients with crusted scabies are highly contagious and at increased risk of secondary bacterial infection due to profound skin barrier disruption. Although scabies is classically considered a superficial infestation, accumulating evidence suggests that severe forms may be associated with invasive bacterial infection and sepsis.

Metagenomic next-generation sequencing (mNGS) has emerged as an important diagnostic tool in sepsis. However, detection of microbial DNA in blood does not necessarily indicate viable infection and must be interpreted in the appropriate clinical context. Here, we report a fatal case of crusted scabies complicated by septic shock, with incidental detection of Sarcoptes scabiei DNA in peripheral blood.

Case presentation

A 58-year-old male farmer with poorly controlled type 2 diabetes mellitus, gout, and chronic dermatitis for five months was admitted to the intensive care unit with generalized pain for more than three days. He had no history of immunosuppressive therapy.

On admission, vital signs were: temperature 36.5 °C, heart rate 106 beats/min, respiratory rate 22 breaths/min, blood pressure 123/81 mmHg, and oxygen saturation 100% on nasal oxygen at 3 L/min. Physical examination revealed diffuse erythroderma involving nearly the entire body surface, with extensive yellowish hyperkeratotic crusts, scaling, deep fissures, and areas of skin breakdown affecting the scalp, trunk, abdomen, and extremities.

Laboratory tests showed a white blood cell count of 8.80 × 10⁹/L, with rapidly progressive eosinophilia (absolute eosinophil count rising to 4.07 × 10⁹/L, 35.3%). Inflammatory markers were markedly elevated (C-reactive protein 222.11 mg/L; procalcitonin 21.50 ng/mL). Additional findings included severe hypoalbuminemia (24.6 g/L), acute kidney injury (creatinine 574.80 μmol/L), anemia, electrolyte disturbances, and total serum IgE levels exceeding 4000 IU/mL.

Peripheral blood mNGS detected multiple bacterial pathogens, including Staphylococcus aureus, Acinetobacter baumannii, Klebsiella pneumoniae, and Enterobacter cloacae. Staphylococcus aureus was the dominant organism (197 reads; relative abundance 40.61%). Sarcoptes scabiei-specific sequences were also detected (12 reads).

Broad-spectrum antimicrobial therapy with meropenem and linezolid was initiated, later adjusted to vancomycin due to cytopenia. Following dermatologic consultation, oral ivermectin (12 mg, approximately 200 μg/kg) and topical 10% sulfur ointment were administered. Strict infection control measures were implemented. Hospital infection control measures: Due to the highly contagious nature of scabbed scabies (live mites shed with the scab), the hospital implemented the following measures: Physical isolation: Patients are placed in single isolation rooms, with strict restrictions on accompanying personnel. Personal protection: Healthcare workers wear disposable hats, medical masks, isolation gowns, and double-layered gloves when entering the room. Environmental disinfection: Bed sheets and clothing that have come into contact with the patient are soaked in hot water (>60°C) for 30 min, and the floor of the room is cleaned with a chlorine-based disinfectant three times a day using wet methods.Epidemiologic investigation revealed similar pruritic skin lesions in household members(The patient’s wife and daughter).

Despite aggressive treatment and intensive supportive care, the patient developed refractory septic shock and died on hospital day 11.

Discussion

Scabies and sepsis: clinical evidence and pathophysiologic considerations

Although scabies is traditionally regarded as a superficial ectoparasitic infestation, increasing evidence indicates that severe forms—particularly crusted scabies—may be complicated by invasive bacterial infection and sepsis. Multiple case reports and series have described bacteremia, septic shock, and fatal outcomes in patients with crusted scabies, especially in the presence of delayed diagnosis, extensive skin involvement, or comorbidities such as diabetes mellitus or immunosuppression [1], [2], [3], [4], [5].

Secondary bacterial bloodstream infections, most commonly caused by Staphylococcus aureus, including methicillin-resistant strains, have been repeatedly reported and are associated with multiorgan failure and death [3], [4]. In immunocompromised populations, crusted scabies has also been linked to severe gram-negative sepsis, with extensive skin fissuring serving as likely portals of entry [2]. A case series from Indonesia reported mortality rates approaching 50%, with sepsis identified as the leading cause of death among patients with crusted scabies [5].

The mechanisms linking scabies to sepsis appear multifactorial. Extensive hyperkeratosis, fissuring, and excoriation result in profound skin barrier disruption, facilitating bacterial invasion. Scabies mites secrete immunomodulatory proteins that inhibit complement activation and impair local innate immune responses. In addition, host immune dysregulation, characterized by a Th2-skewed response, marked eosinophilia, and extremely elevated IgE levels, may compromise effective antibacterial defense. Importantly, Sarcoptes scabiei itself remains confined to the epidermis and does not directly cause systemic infection; rather, scabies acts as a facilitator of secondary bacterial invasion, as emphasized in international public health guidance [6], [7].

Molecular testing in scabies and interpretation of mNGS findings

Conventional diagnosis of scabies relies on clinical assessment and microscopic identification of mites or eggs, but sensitivity is limited. PCR-based assays targeting Sarcoptes scabiei-specific genomic sequences have demonstrated improved sensitivity when applied to skin scrapings and are recognized by the International Alliance for the Control of Scabies as supportive diagnostic tools [8], [9], [10].

Metagenomic next-generation sequencing enables unbiased pathogen detection and is increasingly used in sepsis evaluation. However, its role in diagnosing ectoparasitic infestations such as scabies remains undefined. Because Sarcoptes scabiei resides exclusively in the stratum corneum, detection of scabies-derived DNA in peripheral blood most likely represents circulating parasite DNA fragments released from extensively damaged skin rather than viable parasitic infection. At present, there is no evidence to support blood-based mNGS as a diagnostic method for scabies, and such findings should be interpreted cautiously in conjunction with clinical and dermatologic features.

Household clustering of pruritic skin lesions provided a crucial epidemiological clue and underscores the importance of early recognition, prompt dermatologic consultation, and strict infection-control measures.

Conclusion

Crusted scabies is a severe and highly contagious condition that may lead to fatal outcomes when complicated by secondary bacterial infection and septic shock. Incidental detection of Sarcoptes scabiei DNA in peripheral blood by mNGS likely reflects disease severity rather than systemic parasitic dissemination. Early recognition, prompt antiparasitic therapy, and strict infection control measures are essential to prevent catastrophic outcomes.

CRediT authorship contribution statement

Ju Wang: Writing – review & editing. Jun Qiu: Project administration. Chaogui Zhang: Supervision.

Ethics statement

Written informed consent for publication was obtained from the patient’s legal representatives. The study was conducted in accordance with the Declaration of Helsinki.

Funding

The authors received no specific funding for this work.

Declaration of Competing Interest

The authors declare that they have no conflicts of interest.