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CASE REPORT Table of Contents   
Year : 2008  |  Volume : 19  |  Issue : 2  |  Page : 155-159
Molluscum contagiosum in human immunodeficiency virus infected patients


Department of Oral and Maxillofacial Pathology, Dr. D.Y. Patil Dental College and Hospital, Pimpri, Pune - 411 018, Maharashtra, India

Click here for correspondence address and email

Date of Submission13-Jul-2007
Date of Decision20-Sep-2007
Date of Acceptance20-Sep-2007
 

   Abstract 

Molluscum contagiosum (MC) is a cutaneous lesion caused by a DNA virus from the poxvirus family. Worldwide in distribution, MC is most frequently encountered as an easily treated disease of childhood and has rarely been a cause of serious morbidity. With the advent of new populations of immunocompromised individuals, especially those infected with the human immunodeficiency virus (HIV), MC has emerged as a difficult clinical challenge and the focus of renewed interest for dental professionals.
This article presents four cases of HIV positive patients afflicted by MC along with a review of the literature on this dermatopathological lesion.

Keywords: Molluscum contagiosum, Human immunodeficiency virus; papules, Henderson-Paterson inclusion bodies

How to cite this article:
Chaudhary M, Kulkarni M. Molluscum contagiosum in human immunodeficiency virus infected patients. Indian J Dent Res 2008;19:155-9

How to cite this URL:
Chaudhary M, Kulkarni M. Molluscum contagiosum in human immunodeficiency virus infected patients. Indian J Dent Res [serial online] 2008 [cited 2019 Nov 17];19:155-9. Available from: http://www.ijdr.in/text.asp?2008/19/2/155/40472
Molluscum contagiosum (MC) is a common, self-limiting viral disease of the skin and mucous membranes. It was first described by Bateman in 1817. [1] It is caused by molluscipoxvirus, which belongs to unclassified genus of poxvirus species. [2] MC has a usual incubation period of 14-50 days. [3] It has been recognized for sometime that MC is a common cutaneous disorder in patients with HIV infection. The association between MC and HIV was first reported in 1983.

We report four cases of MC in HIV infected patients (two males and two females) and also describe the histopathologic findings.


   Case Reports Top


Case 1

A 34-year-old female patient reported with the chief complaint of multiple papular eruptions on both cheeks and also on the right shoulder since 1 month. The lesions had grown slowly to attain the present size. A thorough history revealed that the patient was HIV positive. The patient's family history revealed that her husband was also HIV positive and had died two years back due to AIDS. A general physical examination revealed a moderately built patient, with no signs of pallor, icterus, cyanosis, clubbing, or wasting. Local extraoral examination revealed multiple discrete nodules on both cheeks and on the right shoulder [Figure - 1],[Figure - 2]. These lesions were dome-shaped with a central umbilicated area and measured approximately 0.3 cm in diameter. Intraorally, the patient had scrapable white plaques on the dorsum of the tongue, which was diagnosed as acute pseudomembranous candidiasis [Figure - 3].

Case 2

A 30-year-old male patient reported with the chief complaint of papular eruptions on the right pinna and the left nasolabial fold since 2 months. A thorough history revealed that patient was HIV positive. The patient's family history was noncontributory. A general physical examination revealed a moderately built patient, with no signs of pallor, icterus, cyanosis, clubbing, or wasting. Local extraoral examination revealed discrete nodules on the pinna of the right side and on the nasolabial fold of the left side, with each nodule measuring approximately 0.2 cm in diameter [Figure - 4],[Figure - 5].

Case 3

A 35-year-old male reported with the chief complaint of multiple papular eruptions involving the entire face since 2 months. A thorough history revealed that patient was HIV positive. The patient's family history was noncontributory. A general physical examination revealed a moderately built patient, with no signs of pallor, icterus, cyanosis, clubbing, or wasting. Local extraoral examination revealed multiple discrete nodules on the forehead and bilaterally on the cheeks, each nodule measuring approximately 0.1 cm in diameter [Figure - 6].

Case 4

A 32-year-old female reported with the chief complaint of multiple papular eruptions involving the face, predominantly in the periocular region, since 2 months. A thorough history revealed that patient was HIV positive. The patient's family history was noncontributory. A general physical examination revealed a moderately built patient, with no signs of pallor, icterus, cyanosis, clubbing, or wasting. Local extraoral examination revealed multiple discrete nodules in the periocular region bilaterally and also on the entire face. The periocular lesions on the right side measured approximately 0.5 cm in diameter, whereas the lesions on the entire face measured approximately 0.3 cm in diameter [Figure - 7],[Figure - 8].

Histopathology

Biopsy was performed on two of the four patients (cases 1 and 2) and histopathologic section under low-power microscopy [Figure - 9] revealed inverted lobules of hyperplastic, acanthotic squamous epithelium arranged in a lobulated pattern. The centers of these bulbous structures were filled with enlarged, altered keratinocytes, with eosinophilic viral inclusions referred to as Henderson and Paterson inclusion bodies. The inclusion bodies are the result of a virally induced transformation process. Initially, the small virion particle is formed in the cytoplasm of the epithelial cells above the basal layer. These eosinophilic particles grow in size as they progress towards the granular cell layer, causing compression of the nucleus to the periphery of the infected epithelial cells. Histopathologic section under high-power microscopy revealed the inclusion bodies compressing the nuclei of the infected epithelial cells towards the periphery, giving it a crescent-shaped appearance [Figure - 10].


   Discussion Top


MC is a viral disorder of the skin and mucous membranes, characterized by discrete, single or multiple, flesh-colored papules. It was first described by Bateman in 1817. [1] It is caused by molluscipoxvirus, which belongs to unclassified genus of poxvirus species. The genome, like that of all poxviruses, [4] is a single linear molecule of double-stranded DNA. [2]

In 1841, Henderson and Paterson described the intracytoplasmic inclusion bodies that are now known by their names or as 'molluscum bodies.' [5] In 1905, Juliusberg demonstrated transmissibility by a filterable agent. In 1911, Lipshutz granules within the molluscum bodies were described. [6] By restrictive endonuclease analysis of the genomes of isolates, the following four types have been identified: MCV I, II, III, and IV. In one study of 147 patients, MCV I caused 96.6% of infections and MCV II caused 3.4%; however, no relationship was observed between virus type and lesional morphology or anatomical distribution. MCV III and IV are rare. In patients infected with HIV, MCV II causes the majority (60%) of infections. [7]

MC has a worldwide incidence of between 2-8%. Between 5 and 20% of HIV patients have MC infection. Epidemiologic studies suggest that transmission may be related to factors such as warmth and humidity of the climate and poor hygiene. [8] MC is being increasingly diagnosed in the sexually active population. [9] Transmission of molluscipoxvirus in children is thought to occur by intimate skin-to-skin contact or through fomites. In adults, MC is most often sexually transmitted. [10]

MC has been observed in several diseases associated with an immunocompromised state. Solomon and Telner reported a case of eruptive MC in patients with atopic dermatitis. [11] Slawsky et al . reported a patient with epidermodysplasia verruciformis who not only developed MC, but was also diagnosed with extranodal B-cell lymphoma. [12] Cotton et al . described a patient with mixed lymphocytic and histiocytic lymphoma, atypical T-cell infiltration of bone marrow, and malignant thymoma who also had MC. [13]

The incubation period for MC has been reported to be between 14 and 50 days, [2] although there are reports of newborns having lesions as early as 7 days post-partum. [3] The typical lesion is a smooth-surfaced, firm, spherical papule, with an average diameter of 3-5 mm. [14] Giant lesions of up to 1.5 cm have been described [10] and are seen more often in immunocompromised patients. [15] Lesions may be flesh colored or translucent white or light yellow in color. The number of lesions is usually less than 30, but as many as several hundred may be seen. Up to 100 lesions may coalesce to form a plaque. [10] The most distinctive feature of MC is the central umbilication.

It has been recognized for sometime that MC is a common cutaneous disorder seen in patients with HIV infection. The association was first reported in 1983 when it was noted in an autopsy study that two of ten patients with AIDS had lesions of MC. [16] In contrast to HIV seronegative adults, in whom MC lesions are usually genital, lesions in HIV individuals most often involve the face, neck, and trunk. Because this distribution is similar to that seen in children, in whom the spread is thought to occur through fomites or casual contact, transmission in HIV infected patients does not appear to be solely by sexual contact. Differential diagnosis includes basal cell carcinoma, keratocanthoma, Darier's disease, epithelial nevi, atopic dermatitis, cryptococcosis, and histoplasmosis. [15]

Microscopically, the umbilicated papule is characterized by one or more lobules of epidermis extending down into the dermis and opening onto the surface through the narrow pore. A central crater is formed that is filled with keratin fragments and molluscum bodies. Molluscum bodies are large (up to 35 m in diameter) and contain intracytoplasmic inclusion bodies within keratinocytes. The molluscum bodies are a result of the virally induced transformation process that begins in the lower cells of the stratum malpighii, just above the basal cell layer, where it appears as a small, ovoid, eosinophillic structure within the infected epidermal cells. The molluscum body grows as it progresses upwards towards the granular layer, causing compression of the nucleus to the periphery of infected keratinocyte. At the granular layer, the staining of molluscum body changes from eosinophilic to basophilic. [17] Smith et al . showed that hyperkeratosis was a much more frequent finding in skin biopsies of a variety of cutaneous disorders in patients with advanced, compared to asymptomatic, HIV disease. [18]

Earlier, due to the superficial nature of the infection, it was thought that antibodies to molluscipox virus were produced only in a small proportion of cases, but subsequent studies revealed that most patients with molluscipox virus produce antibodies. [18] Shirodaria et al . studied the presence of anticellular antibodies and virus-specific antibodies by immunofluorescence in patients with molluscipoxvirus compared with healthy individuals. Virus-specific antibodies were detected in 73.3% of patients with molluscipoxvirus, and these antibodies were predominantly of the IgG class. Anticellular IgM antibody and fibrillar anticellular IgM antibody were found in 63 and 60% of infected patients, respectively.

MC is a self-limiting disease which, left untreated, will eventually resolve in immunocompetent hosts, though it may be protracted in atopic and immunocompromised individuals. One of the most common, quick, and efficient methods of treatment is cryotherapy. Liquid nitrogen, dry ice, or Frigiderm are applied to each individual lesion for a few seconds. Repeat treatments at 2-3 week intervals may be required. [19]

An easy method to remove the lesions is by eviscerating the core with an instrument such as a scalpel, sharp tooth pick, the edge of a glass slide, or any other instrument capable of removing the umbilicated core. Because of its simplicity, patients, parents, and caregivers may be taught this method so that new lesions can be treated at home. [20]

Curettage is another method of removal. It can be used with and without light electrodessication. This method is more painful and it is recommended that a topical anesthetic cream be applied to the lesions before the procedure. This method has the advantage of providing a reliable tissue sample to confirm the diagnosis. [21] Another reported treatment involves the use of adhesive tape. The adhesive side of the tape is repeatedly applied to and removed from the lesion for 10-20 cycles. This action effectively removes the superficial epidermis from the top of the lesion. [22]

A 25% suspension of tincture of benzoin or alcohol may be applied once a week. This treatment requires some precautions. It contains two mutagens, quercetin and kaempherol. Some of the listed side effects include severe erosive damage in adjacent normal skin that may cause scarring and systemic effects such as peripheral neuropathy, renal damage, adynamic illeus, leucopenia, and thrombocytopenia, especially if used generously on mucosal surfaces. Podofilox is a safer alternative to podophyllin and may be used by the patient at home. The recommended use usually consists of application of 0.05 ml of 5% podofilox in lactate-buffered ethanol twice a day for 3 days. [22]

Cantharidin (0.9% solution of collodion and acetone) has been used with success in the treatment of MC. This blister-inducing agent is applied carefully and sparingly to the dome of the lesion, with or without occlusion, and left in place for at least 4 h before being washed off. Cantharidin can cause severe blistering. It should be tested on individual lesions before treating large numbers of lesions. It should not be used on the face. When tolerated, this treatment is repeated every week until the lesions clear. Usually 1-3 treatments are necessary. [23]

A 10% iodine solution is placed on the molluscum papules and, when dry, the site is covered with small pieces of 50% salicylic acid plaster and tape. The process is repeated daily after bathing. After the lesions have become erythematous in 3-7 days, only the iodine solution is applied. Resolution has been reported in a mean of 26 days. [24] Tretinion 0.1% cream has been used in the treatment of MC. It is applied twice daily to the lesions. Resolution was reported by day 11. Trace erythema at the site of prior lesions was a notable side effect. [25] Oral cimetidine has been successfully used in extensive infections. The histamine-2 receptor antagonist stimulates delayed-type hypersensitivity. One uncontrolled study showed resolution in 9 of 13 patients. In this study, the dosage was 40 mg/kg/day in two divided doses for 2 months. [26],[27]

Another treatment option is the use of potassium hydroxide. In one study, an aqueous solution of 10% KOH was applied topically twice daily to all lesions with a swab. The treatment was discontinued when an inflammatory response or superficial ulcer became evident. Resolution occurred in a mean of 30 days. [28]

The use of pulsed dye laser for the treatment of MC has also been documented with excellent results. The therapy was well tolerated, without scars or pigment anomalies. The lesions resolved without scarring at 2 weeks. Studies show that 96-99% of the lesions resolved with one treatment. [29],[30] Imiquimod 5% cream has been used topically to treat MC by inducing high levels of IFN-α and other cytokines locally. This potent immunomodulatory agent is well tolerated, although application site irritation is common. It has no known systemic or toxic effects in children. [31]

Cidofovir is a nucleoside analog that has potent antiviral properties. Several small studies and case reports describe the successful use of cidofovir, applied topically or administered by intralesional injection, in several virally induced cutaneous diseases. Cidofovir cream (3%) has been used successfully to treat MC in studies, with clearing seen in 2-6 weeks. [32]

The cases presented by us illustrate the nature of MC, which has been less frequently reported in the past. This lesion was seen in patients infected with HIV. The lesion occurred as multiple papules on the face. Clinical diagnosis is somewhat difficult if the history of the underlying disease is not elicited. The histopathological examination confirmed the diagnosis. The patients were advised to apply canthardin 3-4 times a day. Unfortunately follow-up was not possible because of lack of cooperation on the part of the patients.


   Conclusion Top


MC is a common, generally benign, viral infection of the skin. It is common in children, sexually active adults, and in immunodeficient patients. It is caused by the molluscipox virus, a member of the poxviridae family. This virus differs from other poxviruses in that it causes spontaneously regressing, umbilicated tumors of the skin, rather than pox-like vesicular lesions. In immunocompetent, nonatopic patients, MC is usually a self-limiting disease for which treatment is not mandatory. However, when treatment is deemed appropriate, multiple local therapeutic options are available. For patients with impaired immune functions, with widespread and potentially disfiguring eruptions, the usual local destructive therapies are ineffective; antiviral and immunomodulatory medications have been more successful.

 
   References Top

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2.Parr RP, Burnett JW, Garon CF. Structural characterization of the molluscum contagiosum virus genome. Virology 1977;81:247-56.  Back to cited text no. 2  [PUBMED]  
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5.Brown ST, Nalley JF, Kraus SJ. Molluscum contagiosum. Sex Transm Dis 1981;8:227-34.  Back to cited text no. 5  [PUBMED]  
6.Juliusberg M. Zur Kenntnis des virus Molluscum contagiosum. Dtsch Med Wochenschr 1905;31:1598-9.  Back to cited text no. 6    
7.Porter CD, Archard LC. Characterization and physical mapping of Molluscum contagiosum virus DNA and location of sequence capable of encoding a conserved domain of epidermal growth factor. J Gen Virol 1987;68:673-82.  Back to cited text no. 7  [PUBMED]  [FULLTEXT]
8.Postlethwaite R. Molluscum contagiosum: A review. Arch Environ Health 1970;21:432-52.  Back to cited text no. 8  [PUBMED]  
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11.Telner P, Solomon LM. Eruptive molluscum contagiosum in atopic dermatitis. Can Med Assoc J 1966;95:978-9.  Back to cited text no. 11    
12.Slawsky LD, Gilson RT, Hockley AJ, Libow LF. Epidermodysplasia verruciformis associated with severe immunodeficiency. J Am Acad Dermatol 1992;27:448-56.  Back to cited text no. 12  [PUBMED]  
13.Cotton DW, Cooper C, Barrett DF, Leppard BJ. Severe atypical Molluscum contagiosum infection in an immunocompromised host. Br J Dermatol 1987;116:871-6.  Back to cited text no. 13  [PUBMED]  
14.Felman YM, Nikitas JA. Genital Molluscum contagiosum. Cutis 1980;26:28-32.  Back to cited text no. 14  [PUBMED]  
15.Schwartz JJ, Myskowski PL. Molluscum contagiosum in patients with human immunodeficiency virus infection: A review of 27 patients. J Am Acad Dermatol 1992;27:583-8.  Back to cited text no. 15  [PUBMED]  
16.Reichert CM, O'Leary TJ, Levens DL, Simrell CR, Macher AM. Autopsy pathology in the acquired immune deficiency syndrome. Am J Pathol 1983;112:357-82.  Back to cited text no. 16  [PUBMED]  [FULLTEXT]
17.Lever WF, Schaumberg-Lever G. Diseases caused by viruses: Histopathology of the skin. JB Lippincott: Philadelphia; 1983.  Back to cited text no. 17    
18.Shirodaria PV, Matthews RS, Samuel M. Virus-specific and anticellular antibodies in Molluscum contagiosum. Br J Dermatol 1979;101:133-40.  Back to cited text no. 18  [PUBMED]  
19.Janniger CK, Schwartz RA. Molluscum contagiosum in children. Cutis 1993;52:194-6.  Back to cited text no. 19  [PUBMED]  
20.Epstein WL. Molluscum contagiosum. Semin Dermatol 1992;11:184-9.  Back to cited text no. 20  [PUBMED]  
21.Janniger CK, Schwartz RA. Molluscum contagiosum in children. Cutis 1993;52:194-6.  Back to cited text no. 21  [PUBMED]  
22.Arndt KA. Manual of dermatologic therapeutics, 5 th ed. Little Brown: Boston; 1995. p. 339-40.  Back to cited text no. 22    
23.Silverburg NB, Sidbury R, Mancini AJ. Childhood molluscum contagiosum: Experience with cantharidin therapy in 300 patients. J Am Acad Dermatol 2000;43:503-7.  Back to cited text no. 23    
24.Ohkuma M. Molluscum contagiosum treated with iodine solution and salicylic acid plaster. Int J Dermatol 1990;29:443-5.  Back to cited text no. 24  [PUBMED]  
25.Papa CM, Berger RS. Venereal herpes-like molluscum contagiosum: Treatment with tretinoin. Curis 1976;18:537-40.  Back to cited text no. 25    
26.Avella J, Binder H, Madsen J, Ashkenase P. Effect of histamine H2 receptor antagonists on delayed hypersensitivity. Lancet 1978:1:624-6.  Back to cited text no. 26    
27.Dohil M, Prendiville JS. Treatment of molluscum contagiosum with oral cimetidine: Clinical experience on 13 patients. Pediatr Dermatol;13:310-2.  Back to cited text no. 27    
28.Romiti R, Ribeiro AP, Grinblat BM. Treatment of molluscum contagiosum with potassium hydroxide: A clinical approach in 35 children. Pediatr Dermatol 1999;16:228-31.  Back to cited text no. 28    
29.Hammes S, Greve B, Raulin C. Molluscum contagiosum: Treatment with pulsed dye laser. Hautarzt 2001;52;38-42.  Back to cited text no. 29    
30.Hughes PS. Treatment of molluscum contagiosem with the 585-nm pulsed dye laser. Dermatol Surg 1998;24:229-30.  Back to cited text no. 30  [PUBMED]  
31.Barba Ar, Kapoor S, Berman B. An open label safety study of topical imiquimod 5% cream in the treatment of Molluscum contagiosum in children. Dermatol Online J 2001;7:20.  Back to cited text no. 31    
32.Zabawski EJ Jr. A review of topical and intralesional cidofovir. Dermatology Online J 2000;6:3.  Back to cited text no. 32    

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Correspondence Address:
Mayur Chaudhary
Department of Oral and Maxillofacial Pathology, Dr. D.Y. Patil Dental College and Hospital, Pimpri, Pune - 411 018, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0970-9290.40472

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    Figures

  [Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4], [Figure - 5], [Figure - 6], [Figure - 7], [Figure - 8], [Figure - 9], [Figure - 10]

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