Norwegian scabies - rare case of atypical manifestation*

Human scabies affects all social classes and different races around the world. It is highly contagious, but the exact figures on its prevalence are unknown. A 19-year-old male patient was admitted to the emergency room reporting fever (38°C) and multiple lesions throughout the body, except face, soles, and palms. Lesions were non-pruritic, which hampered the initial diagnostic suspicion. Skin biopsy was performed, and the final diagnosis was crusted scabies (Norwegian). It was concluded that human scabies is a significant epidemic disease, due to its different clinical manifestations, and because it is extremely contagious.


INTRODUCTION
Human scabies is an infestation caused by female mites (Sarcoptes scabiei var. hominis), which lay 40-50 eggs in their 4-6 weeks of life. It is highly contagious and affects all social classes and different races around the world. However, the exact figures on its prevalence is unknown. 1 It is also called Norwegian scabies because it was described in Norway by Danielssen 4). The lesions were non-pruritic, which hampered the initial diagnostic suspicion. No associated comorbidities were found, and the patient was not on any routine medication.
The patient was admitted to the emergency care unit with fever (38°C) without itching, pain, or other clinical manifestations.
Therapy was initiated with intravenous corticosteroids, which worsened the crusted lesions. A week after the admission, a biopsy of the upper right dorsum was done; pathological examination reported crusted scabies as the final diagnosis ( Figure 5). The patient also had an abscess on the gluteal region, which was surgically drained on the eighth day of admission. Sepsis was not observed. Later, as the culture of soft tissues were consistent with Enterococcus faecalis sensitive to vancomycin, teicoplanin, and linezolid, the patient was treated with cefepime (D10) and vancomycin (D5). After 14 days of treatment, the lesions showed signs of regression, and itching and local pain improved significantly ( Figure 6). All persons in contact with the patient, as well as the whole medical and nursing staff, were treated with ivermectin (oral), given the high risk of contagion. The patient was discharged after four weeks of admission, with almost complete regression of lesions.

DISCUSSION
The association between scabies and neurologic deficit is common. However, the patient in this report was free from all kinds of cognitive, sensory, and motor impairment. 2 Serology for HIV and    However, this case is unusual because of the absence of concomitant immunosuppressive diseases. 1,2,4,5 Due to differential diagnoses for hyperkeratotic eczema, psoriasis, and contact dermatitis, the authors opted for a corticoste-important because it destroys the burrows of the mites, which did not occur with the patient in this case report.
Treatment for crusted scabies is difficult in some cases because of the large number of mites, forming hyperkeratotic areas in the skin. Therefore, a prolonged treatment with systemic scabicides is recommended, paying special attention to occacional concomitant infections. 4,5,8 The most common treatment for crusted scabies is a single or recurrent dose of ivermectin (oral), depending on the severity of the case, as with the patient in this case. 2 However, some pesticides and scabicides such as lindane might be applied. 7 Pruridus and focal symptoms can also be treated with deltamethrin and 10% topical precipitated sulfur in petrolatum, for example. 4 Another significant procedure is differential diagnosis with other dermatoses, such as crusted psoriasis -a rare form of the disease manifested by erythematous plaques covered with scabs, 3,8 similar to the patient in this case.q roid therapy, which further aggravated the erythroderma, but with the unusual absence of associated pruritus. 4,6 This symptom affected the diagnosis of scabies. However, the patient later reported that he had overlooked personal hygiene for six months, due to the pain and burning sensation during this procedure. This fact possibly masked the clinical presentation of the disease, raising doubts about its real etiology.

FIgure 6:
Back of the patient after 14 days of treatment