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59-Year-Old Man in ER with Generalized Body Rash

Can you diagnose this case?

David L. Kaplan, MD, University of Missouri Kansas City, University of Kansas

Signs and Symptoms

A 59-year-old man presented to the emergency department with a generalized body rash that had developed 3 days before presentation.

His past medical history was notable for HIV infection (viral load, 46 copies/mL; CD4 count, 265 cells/mm3), type 2 diabetes, and hypertension. He noted that he had received a flu shot 2 days before the rash had begun.

He complained of pruritus and described the rash as dry and scaly without drainage. His medications included antiretroviral therapy (tenofovir/emtricitabine and dolutegravir) for his HIV and atenolol for his hypertension. He also had recently been prescribed a statin, a calcium-channel blocker, and an angiotensin-converting enzyme inhibitor. On further questioning, however, he reported that he had not yet started taking these new medications. He denied exposures to new topical cosmetic creams, foods, or pets, and he denied having any other systemic symptoms. He had an allergy to glyburide, and he worked as a cleaner at a public school.

Physical examination revealed a dry, scaly rash with some excoriated pustules and papules that were crusted. The lesions were present over the patient’s neck, chest, abdomen, back, and perioral regions, as well as on the extremities involving the interdigital spaces of the hands and feet. There was fissuring of skin over the flexor and extensor surfaces.

What explains this man’s rash?

Choose one to reveal diagnosis and discussion

Sézary syndrome
Scabies
Atopic dermatitis
Drug reaction

Answer: Crusted Scabies

See the full case at Consultant360

A dermatologist was consulted and evaluated the patient in emergency department. Scrapings of the lesions were taken, and microscopic analysis revealed a high burden of mites consistent with Sarcoptes scabiei.

DISCUSSION

Scabies is a cutaneous infestation by S scabiei, a whitish 8-legged mite. The mite is transmitted by way of direct human contact. Female mites, when fertilized, begin burrowing into the skin and extend the burrowing by 2 mm each day, creating a tunnel. These female mites lay their eggs in the burrows, which hatch in 3 to 4 days; the larvae make way to the surface, feed, molt, mature, are fertilized, and start the cycle again.

The pathogenesis of this disease is not completely understood. The epidermis is infiltrated by a large number of activated T cells, which appear to be capable of inducing keratinocyte proliferation. This is thought to contribute to an ensuing deregulated inflammatory process, with a large production of various cytokines.1

Scabies lesions are small, erythematous, excoriated papules with a hemorrhagic crust. They are intensely pruritic and are the result of a type IV delayed hypersensitivity reaction. Burrows are thin, reddish or brownish linear lesions that are 2 to 15 mm in length. The burrows often can be obscured by excoriations or by the manifestations of secondary infections. The distribution is common in the webs of the fingers, the flexor aspects of the wrists, and the extensor aspects of elbows.

Symptoms begin 3 to 6 weeks after primary infestation and within 3 days for subsequent infestations. The burden of mites decreases after the initial infestation, and this reduction is a function of host cellular immunity. Healthy people with scabies generally have fewer than 100 mites.

Crusted scabies, also known as Norwegian scabies or keratotic scabies, can occur in immunocompromised persons such as those with HIV/AIDS, leprosy, and lymphoma. Crusted scabies begins with poorly defined erythematous patches that quickly progress into a scale; the scale progresses into warts and eventual crusts and fissures. Lesions are most common on the scalp, hands, and feet. The lesions of crusted scabies usually have a foul odor, and the mites number in the hundreds of thousands.

The patient’s history and the distribution of lesions are helpful in making a diagnosis. Crusted scabies should be suspected in immunocompromised individuals with itching that is out of proportion to the severity of lesions. Skin scrapings are viewed microscopically to look for large numbers of mites and eggs, distinguishing crusted scabies from a typical scabies infestation.

Topical permethrin lotion, 5%, or oral ivermectin dosed at 200 µg/kg is sufficient for the usual case of scabies. However, crusted scabies has a high failure rate with topical treatments, and thus 2 doses of oral ivermectin, 200 µg/kg 7 days apart, has been shown to be effective. Antihistamines for itching and systemic antibiotics for secondary infection may be required. In addition, household members and close personal contacts with symptoms should also be treated.

Our patient was given oral ivermectin and was advised to stay at home for 24 hours, since he worked at a school. He followed up with the dermatologist in 10 days, at which time his symptoms and lesions had been improving.

Symptoms begin 3 to 6 weeks after primary infestation and within 3 days for subsequent infestations. The burden of mites decreases after the initial infestation, and this reduction is a function of host cellular immunity. Healthy people with scabies generally have fewer than 100 mites.

DISCUSSION

Sézary syndrome is a cutaneous T-cell lymphoma deriving from skin CD4+ or central memory T cells. It is characterized by circulating malignant (Sézary) cells in peripheral blood. Patients commonly present with erythroderma, generalized lymphadenopathy, and intensely pruritic lesions. However, the lesions of this Sézary syndrome develop over weeks or months, whereas those of crusted scabies develop over a shorter time period. Skin biopsy findings will show predominance of nonspecific infiltrate of inflammatory T cells. In addition, results of a peripheral blood smear will show Sézary cells, with the diagnosis being confirmed via immunophenotyping.

Atopic dermatitis, also known as eczema, is a chronic pruritic inflammatory skin condition associated with elevations in immunoglobulin E (IgE). It is usually diagnosed in childhood, and affected patients have intermittent flares. Patients may also have other IgE-mediated conditions such as asthma or allergic rhinitis. Eczema is characterized by intensely erythematous papules and vesicles that can crust over and scale. Scarring and fissuring can result from chronic lesions secondary to scratching. These lesions look similar to the dry, crusted lesions of scabies. Although the flexor and extensor areas are commonly involved in eczema, the involvement of axillary, gluteal, or groin regions warrants consideration of other diseases.

Topical permethrin lotion, 5%, or oral ivermectin dosed at 200 µg/kg is sufficient for the usual case of scabies. However, crusted scabies has a high failure rate with topical treatments, and thus 2 doses of oral ivermectin, 200 µg/kg 7 days apart, has been shown to be effective. Antihistamines for itching and systemic antibiotics for secondary infection may be required. In addition, household members and close personal contacts with symptoms should also be treated.

Drug reactions are adverse cutaneous reactions that typically manifest in a temporal manner to exposure to a new medication. Their manifestations can range from urticaria to papular eruptions. They can be immediate or delayed reactions. Drug reactions can be morbilliform (maculopapular) in nature and can cause intense pruritus. This can lead to lichenification and fissuring if the reaction continues for days. These lesions can look like scabies lesions; however, a good history is key in making a prompt diagnosis.

The Take-Home Message

Crusted scabies presents as a pruritic, scaly rash with crusts that may mimic other conditions such as eczema or lymphocytic cutaneous infiltrates. It should always be considered in the differential diagnosis of such rashes in an immunocompromised individual, and prompt diagnosis of crusted scabies can reduce transmission and further complications of the infestation, such as secondary bacterial skin infections.

References:

1. Centers for Disease Control and Prevention. Changing the Story of Syphilis. https://www.cdc.gov/std/products/success/changing-the-story-of-syphilis-success-story-508c.pdf, Accessed April 21, 2017/

2. Hicks CB, Clement M. Syphilis: epidemiology, pathophysiology, and clinical manifestations in HIV-uninfected patients. UpToDate. http://www.uptodate.com/contents/syphilis-epidemiology-pathophysiology-and-clinical-manifestations-in-hiv-uninfected-patients, November 21, 2016. Accessed April 21, 2017.

3. French P, Gupta S, Kumar B. Infectious syphilis. In: Gupta S, Kumar B, eds. Sexually Transmitted Infections. 2nd ed. New Delhi, India: Elsevier; 2012:429-457.

4. Bacterial infections. In: Ghom A, Mhaske S. Textbook of Oral Pathology. New Delhi, India: Jaypee Brothers Medical Publishers; 2008:461-483.

5. Brown DL, Frank JE. Diagnosis and management of syphilis. Am Fam Physician. 2003;68(2):283-290.

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