Multiple facial papules on a HIV-positive man - Clinical Advisor

Multiple facial papules on a HIV-positive man

Slideshow

  • May 2015 Dermatology Clinic

    May 2015 Dermatology Clinic

A man, aged 42 years, infected with human immunodeficiency virus (HIV) presented with several small, dome-shaped, flesh-colored papules with central umbilication on his face. The papules were mildly itchy at times, and the patient reported that they have been increasing in number over the last few weeks. The patient was on medication for HIV infection, specifically highly active antiretroviral therapy (HAART), and compliant with the regimen. He had not experienced these skin symptoms before. 



This The Clinical Advisor CME activity consists of 3 articles. To obtain credit, read Blistering patch on 
infant’s forearm and Well-demarcated pink plaques. Then take the post-test here.


This The Clinical Advisor CME activity consists of 3 articles. To obtain credit, read Blistering patch on 
infant's forearm and Well-demarcated pink plaques. Then take the post-test here.Molluscum contagiosum is a cutaneous and mucocutaneous viral infection that is commonly observed...

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This The Clinical Advisor CME activity consists of 3 articles. To obtain credit, read Blistering patch on 
infant’s forearm and Well-demarcated pink plaques. Then take the post-test here.


Molluscum contagiosum is a cutaneous and mucocutaneous viral infection that is commonly observed in school-aged children, sexually active persons, and immunocompromised persons. The infection is caused by themolluscum contagiosumvirus (MCV), a large double-stranded DNA virus from the Poxviridae family. In immunocompetent patients, MCV infection presents as a small cluster (11-20) of skin-colored papules that are 3 mm to 5 mm in diameter.1

MCV papules are clinically differentiated from lesions formed by other cutaneous diseases by the presence of a central umbilication. Generally, the papules are benign and asymptomatic, although erythema and itchiness at the site of infection are reported in a subset of patients. In immunodeficient hosts, the MCV can cause severe and persistent infection with myriad lesions that tend to be recalcitrant to treatment.2

MCV is transmitted through skin-to-skin contact with the infected site, contaminated fomites (e.g., bath towels and clothing), and vertical transmission during labor. The virus can also be spread by autoinoculation, moving from the initial site of infection to other sites on the body. In 30% of patients, acute eczema develops around the papules approximately one month after onset of infection.3 Papules can appear on any cutaneous or mucocutaneous site on the body including the genital, perianal, orbital, and oral regions.

Although data is limited, several studies have estimated the worldwide prevalence of MCV infection to be 5.0% to 7.5%. The prevalence is increased in immunocompromised populations (5.0-18%) and has been reported to be as high as 30% in patients with advanced acquired immune deficiency syndrome (AIDS).4

In healthy individuals, MCV infection is often self-limiting and generally clears completely within several months. On average, 11 to 20 papules appear on the body during the course of infection but spontaneously resolve within 2 months.1 However, as mentioned above, in an immunodeficient host, MCV infection can be severe and persistent, with hundreds of lesions that tend to be recalcitrant to treatment. Extensive infection is indicative of an advanced immunodeficient state.

MCV infection is typically a straightforward clinical diagnosis to make, but difficulties may arise if the presentation involves a solitary lesion or if the lesions are inflamed. In these situations, dermatoscopy or a recently developed real-time polymerase chain reaction (PCR) are useful for sensitive and specific detection of the MCV.5 The classic dermatoscopic pattern of MCV consists of crown vessels at the periphery of the lesion with a radial distribution. These crown arrangements are also seen in nevus sebaceous, sebaceous adenoma, and sebaceous hyperplasia. Both MCV and sebaceous tumors feature whitish structures when viewed through a dermatoscope, but in lesions caused by the MCV, these structures have characteristic shapes that resemble round and four-leaf clovers.6

There is no single best therapy for MCV infection in an immunodeficient patient, and there is no treatment approved by the FDA for MCV infection in any patient population. While MCV lesions will resolve spontaneously over time in an immunocompetent host, infection in a patient with HIV or a similarly compromised state can lead to hundreds of lesions all over the body which may be resistant to conventional treatment methods.2 A cost-effective and potential first-line treatment to consider is a salicylic acid/lactic acid preparation.7 Curettage and cryotherapy with liquid nitrogen are effective in immunodeficient patients with mild infection but should not be employed in treating severely immunocompromised patients due to the risk of additional skin infections, including candidiasis, warts associated with human papillomavirus, and Staphylococcal pyoderma.7 If the MCV infection affects the face, trichloroacetic acid is an efficacious therapy.7 Cantharidin is used by many dermatologists in the United States as an off-label therapy for MCV infection, but the compound is not currently approved by the FDA and therefore is often acquired from Canada.8 Several immunomodulators have been studied and proven successful in the treatment of MCV infection in immunodeficient patients, including 5% imiquimod cream, interferon-alpha injections, and cidofovir.2 A study published in 2000 found 5% imiquimod to be effective in completely eradicating lesions in adults with advanced but stable HIV infection. The immunodeficient subjects in the study experienced a better overall response to the imiquimod therapy than their immunocompetent counterparts.9 Patients should be strongly advised against scratching the lesions in order prevent transmission and autoinoculation.7

The facial lesions on the patient in our case were classic for MCV infection, and a clinical diagnosis was made without the use of dermatoscopy. His lesions were successfully treated with curettage. He has not experienced a recurrence of symptoms. 


Kelly R. Stiegel, BS, is a medical student and Maura Holcomb, MD, is a dermatology resident at Baylor College of Medicine in Houston.



This The Clinical Advisor CME activity consists of 3 articles. To obtain credit, read Blistering patch on 
infant’s forearm and Well-demarcated pink plaques. Then take the post-test here.


References


  1. Brown J, Janniger CK, Schwartz RA, Silverberg NB. Childhood molluscum contagiosum. Int J Dermatol . 2006;45(2):93-99.
  2. Nguyen HP, Franz E, Stiegel KR, et al. Treatment of molluscum contagiosum in adult, pediatric, and immunodeficient populations. J Cutan Med Surg . 2014;18(5):299-306.
  3. Silverberg NB, Sidbury R, Mancini AJ. Childhood molluscum contagiosum : Experience with cantharidin therapy in 300 patients. J Am Acad Dermatol . 2000;43(3):503-507.
  4. Stefanaki C, Stratigos AJ, Stratigos JD. Skin manifestations of HIV-1 infection in children. Clin Dermatol. 2002;20(1):74-86.
  5. Basta-Juzbašic´ A, ˇCeovic´ R. Chancroid, lymphogranuloma venereum, granuloma inguinale, genital herpes simplex infection, and molluscum contagiosum . Clin Dermatol. 2014;32(2):290-298.
  6. Ku SH, Cho EB, Park EJ, et al. Dermoscopic features of molluscum contagiosum based on white structures and their correlation with histopathological findings. Clin Exp Dermatol . 2015;40(2):208-210.
  7. Mankahla A, Mosam A. Common skin conditions in children with HIV/AIDS. Am J Clin Dermatol. 2012;13(3):153-166.
  8. Pompei DT, Rezzadeh KS, Viola KV, et al. Cantharidin therapy: Practice patterns and attitudes of health care providers. J Am Acad Dermatol. 2013;68(6):1045-1046.
  9. Liota E, Smith KJ, Buckley R, et al. Imiquimod therapy for molluscum contagiosum. J Cutan Med Surg . 2000;4(2):76-82.

This The Clinical Advisor CME activity consists of 3 articles. To obtain credit, read Blistering patch on 
infant’s forearm and Well-demarcated pink plaques. Then take the post-test here.


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