Alevizos Alevizos

Christina Antoniou

Dimitris Rigopoulos

George Larios

Heleni Papadogiorgaki

Katerina Lima

Katerina Malouchou

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145Acta Dermatovenerol Croat                     2008;16(3):145-148                        CASE REPORTExtensive Atypical Genital Herpes Simplex Type 2 Infection as an Initial Manifestation of Acquired  Immune Deficiency SyndromeDimitris Rigopoulos1, Katerina Malouchou1, Alevizos Alevizos2, George Larios1, Heleni Papadogiorgaki3, Katerina Lima4, Christina Antoniou11Department of Dermatology and Venereology, Andreas Sygros Hospital, School of Medicine, University of Athens; 2Department of General Practice/Family Medicine, Health Center of Vyronas; 3Department of Microbiology, Andreas Sygros Hospital; 4Department of Pathology, Andreas Sygros Hospital, Athens, GreeceCorresponding author:George Larios MD, MSDepartment of Dermatology and VenereologyAndreas Sygros University Hospital5 Ionos Dragoumi Str.16121 AthensGreecelariosgeo@gmail.comReceived: January 10, 2008Accepted: June 20, 2008¸SUMMARY We present a case of an ulcerative lesion of the genitalia starting one year before in a 33-year-old man. Histopathologic examination revealed herpes virus infection, which suggested the existence of cell-mediated immunodeficiency. Human immunodeficiency virus (HIV) infection was confirmed by ELISA and Western blot test. The patient was treated with intravenous acyclovir, which led to complete remission. We underline the importance of early detecting and diagnosing patients with similar clinical manifestation as a sign of significant underlying immunodeficiency.keY woRdS: herpes simplex virus type 2 (HSV-2), human immunodeficiency virus (HIV), acquired immune deficiency syndrome (AIDS), oral candidiasisIntRodUCtIonGenital herpes is a sexually transmitted viral infection, characterized by primary infection with grouped vesicles at the site of inoculation and a course of recurring outbreaks of vesicles at the same site. It is caused by herpes simplex virus type 2 (HSV-2) and less commonly by herpes simplex virus type 1 (HSV-1). In an immunocom-promised host, HSV-2 may cause extensive lo-cal infection with chronic herpetic ulcers or even widespread systemic infection. Herpetic lesions can sometimes be misleading and an accurate di-agnosis may not be reached at the patient’s first encounter with the physician. HSV-2 infections may often be unrecognized as lesions of viral ori-gin, but may be ignored or mistakenly diagnosed as urinary tract infection, candidal yeast infection, allergy, factitial dermatitis, or other genital condi-tions (1). Improved diagnosis of HSV-2 infection 146could reduce inappropriate use of antibiotics and antifungal medications, as well as enable patients to receive effective treatment and take appropriate precautions to prevent the spread of the disease.CASe RepoRtA 33-year-old male was admitted for painful ulcerative lesions of the genitalia which had de-veloped within the past twelve months and had persisted ever since. His medical history included β-thalassemia trait and schizophrenia (satisfac-torily controlled with drug therapy). He also com-plained of recurrent symptomatic HSV-2 genital infections over the past eight years. The patient reported a weight loss of approximately 10 kg and several recurrent episodes of high fever during the past year. In this period, he visited several phy-sicians and was initially given systemic antibiotic treatment for a diagnosis of perianal fistula, while on the next visits he was administered local antibi-otics and corticosteroids plus systemic antibiotics for suspected recurrent febrile bacterial infections. During the last ten days, the patient reported anti-pyretic-resistant hyperpyrexia. On referral he was febrile with a temperature of 39.8 oC, blood pres-sure of 125/80 mm Hg and heart rate of 116 beats/min. Physical examination only revealed cachexia and paleness. White plaques were observed in the soft palate and uvula (Fig. 1). Cutaneous findings consisted of extended bilateral painful ulcerative lesions of the scrotum, penis, crural folds and thighs, which extended to the gluteal cleft area and buttock (Figs. 2 and 3).The lesions were covered with pus and hem-orrhagic exudate. Satellite papules and vesicles coexisted on healthy skin surrounding the main lesions. No other systemic involvement was rec-ognized. Results of laboratory studies were as follows: hemoglobin 7.4 g/dL, hematocrit 24.2%, white blood cell count 6000/μL (82% neutrophil leukocytes, 11% lymphocytes), erythrocyte sedi-mentation rate 122 mm/1 h, albumins 23 g/L, and Figure 1. White plaques covering the soft palate and uvula of the patient.Figures 2 and 3. Bilateral painful ulcerative lesions extending to the gluteal cleft area and buttock.Rigopoulos et al.      Acta Dermatovenerol CroatGenital herpes simplex as initial manifestation of AIDS    2008;16(3):145-148ACTA DERMATOVENEROLOGICA CROATICA147globulins 42g/L. The remaining serum biochemis-try and urinalysis results were all within the ref-erence range. Culture of the ulcerated areas iso-lated a strain of β-hemolytic Streptococcus group F, while Candida albicans was isolated from the soft palate exudate. Histopathologic examination revealed disseminated intraepidermal vesicles which contained inflammatory cells. Several epi-thelial cells were multinucleated and contained intranuclear inclusions characteristic of HSV-2 in-fection (Fig. 4).HSV-2 antigen was detected on the epithelial cells of the lesion using direct immunofluorescence techniques (BIORAD Laboratories). The Herpe-Select Elisa IgG test (Focus Diagnostics) revealed type specific antibodies to HSV-2, whereas IgM antibodies were negative. An in-house developed PCR was also positive for HSV-2. The patient’s history and clinical presentation in conjunction with the diagnosis of HSV-2 infection and atypi-cal nature of the lesions (widespread, ulcerated and chronic) were highly suggestive of a possible underlying acquired immunodeficiency. Our pa-tient reported that he had never been tested for human immunodeficiency virus (HIV) infection be-fore. The HIV-1 infection was confirmed by both ELISA and Western blot methods, while the CD4 lymphocyte count revealed 114 cells/mm3 (16%) and CD8 436 cells/mm3 (61%). HBsAg and anti-HCV tests were negative. The patient was treated with intravenous acyclovir, 500 mg every 8 hours for three weeks. Immediate fever remission and progressive regression of the cutaneous lesions with marked pain reduction were observed shortly after therapy initiation. For oral candidiasis he was treated with per os fluconazole, 100 mg twice a day for two weeks, which resulted in reduction of the white exudate.dISCUSSIonMEDLINE was searched using the key words HSV-2 and HIV. Articles on HSV-2, its epidemiol-ogy and interaction with HIV were reviewed. The seroprevalence of HSV-2 antibodies varies con-siderably among various populations and ethnic groups, and it has increased over the past few years (2). Most of the infected persons are either asymptomatic or, more commonly, have genital symptoms that remain unrecognized (3,4). HSV infections manifesting with persistent anogenital lesions were among the first opportunistic infec-tions to be described in persons with acquired im-mune deficiency syndrome (AIDS) (5). Moreover, several studies have shown that HIV-induced im-mune impairment results in severe, persistent and recurrent genital herpes, as well as in frequent subclinical reactivations (6,7). HSV-2 shedding is significantly associated with HIV serostatus and CD4 cell count <200/mm3 (8). In recent years, a strong epidemiologic association has emerged between HSV-2 and HIV infection. Numerous studies have proved that HSV-2 seroprevalence rates are higher in HIV-positive than in HIV-nega-tive persons (9-14). Similarly to HIV, serologic di-agnosis of HSV-2 infection has been suggested as a marker of lifestyle and sexual behavior (3). In addition, there is evidence that serologically docu-mented HSV-2 infection is a significant risk fac-tor for HIV acquisition (15). Several epidemiologic studies have demonstrated that prevalent HSV-2 is associated with a 2- to 4- fold risk of HIV-1 acquisition (7,15). Considering the particular and extensive clinical presentation of the herpetic in-fection in our patient, we were surprised to find the lesion history to have extended to a period of ap-proximately 12 months back. It seems that in our case, the majority of physicians involved actually misdiagnosed the herpetic infection as being of bacterial origin, without considering the possibility of an atypical manifestation of a viral infection in an immunocompromised host. This probably oc-curred because of the great extension and severity of the lesions and of their atypical form, combined with systemic manifestations (fever, anemia, ca-chexia). Despite the fact that eventually the patient responded favorably to the treatment, such a de-lay in attaining an accurate diagnosis had affected the patient since he had undergone unnecessary administration of several antibiotics, suffered for a longer period while having a low quality of life, and finally much valuable time was wasted before diagnosing the HIV co-infection, while the patient could have also contaminated other individuals during the period of undiagnosed high viral load.Figure 4. Histopathologic examination character-istic of HSV-2 infection.Rigopoulos et al.      Acta Dermatovenerol CroatGenital herpes simplex as initial manifestation of AIDS    2008;16(3):145-148ACTA DERMATOVENEROLOGICA CROATICA148 ACTA DERMATOVENEROLOGICA CROATICAIn conclusion, we report a case of chronic, ex-tensive and atypical HSV-2 infection in an HIV-1 infected patient, emphasizing the fact that in HIV-positive patients, herpetic infection can differ from the classic form and highlighting the importance of similar cases as an alerting clinical sign of profound cellular immune depression. We would also suggest that physicians should on some oc-casions lower the generally used and widely ac-cepted threshold for offering HIV testing (always in accordance with the clinical picture of every indi-vidual patient), with any particular clinical presen-tation and according to the most recent guidelines, even as part of routine care.References1.   Simonsen M, Nahas SC, da Silva Filho EV, Araújo SE, Kiss DR, Nahas CS. Atypical pe-rianal herpes simplex infection in HIV-positive patients. Clinics 2008;63:143-6.2.   Malkin JE. Epidemiology of genital herpes simplex virus infection in developed countries. Herpes 2004;11(Suppl 1):2A-23A.3.   Cowan FM, Johnson AM, Ashley RL, Corey L, Mindel A. Antibody to HSV-2 as a serological marker of sexual lifestyle in populations. BMJ 1994;309:1325-9.4.   Panasiti V, Devirgiliis V, Borroni RG, Spataro A, Melis L, Petrella MC, Pala S. Atypical cu-taneous manifestation of HSV-2 with Candida albicans co-infection in a patient with HIV-1. J Infect 2007;54:e55-7. Epub 2006 May 22.5.   Siegal FP, Lopez C, Hammer GS, et al. Se-vere acquired immunodeficiency in male ho-mosexuals, manifested by chronic perianal ul-cerative herpes simplex lesions. N Engl J Med 1981;305:1439-44.6.   McGrath BJ, Newman CL. Genital herpes simplex infections in patients with the acquired immunodeficiency syndrome. Pharmacothera-py 1994;14:529-42.7.   Corey L, Wald A, Celum CL, Quinn TC. The effects of herpes simplex virus-2 on HIV-1 acquisition and transmission: a review of two overlapping epidemics. J Acquir Immune Defic Syndr 2004;35:435-45.8.   Schacker T, Zeh J, Hu H, Hill E, Corey L. Fre-quency of symptomatic and asymptomatic her-pes simplex virus type 2 reactivations among human immunodeficiency virus-infected men. J Infect Dis 1998;178:1616-22.9.   Serwadda D, Gray R, Sewankambo N, Wab-wire-Mangen F, Chen M, Quinn T, et al. Hu-man immunodeficiency virus acquisition asso-ciated with genital ulcer disease and herpes simplex virus type 2 infection: a nested case control study in Rakai, Uganda. J Infect Dis 2003;188:1492-7.10. Gwanzura L, McFarland W, Alexander D, Bur-ke RL, Katzenstein D. Association between human immunodeficiency virus and herpes simplex virus type 2 seropositivity among male factory workers in Zimbabwe. J Infect Dis 1998;177:481-4.11. Chen C, Ballard R, Beck-Sague C, Dangor Y, Radebe F, Schmid S, et al. Human immu-nodeficiency virus infection and genital ul-cer disease in South Africa. Sex Transm Dis 2000;27:21-8.12. Suligoi B, Dorrucci M, Volpi A, Andreoni M, Zerboni R, Rezza G, and the Italian Serocon-version Study Group. Prevalence and determi-nants of herpes simplex virus type 2 infection in a cohort of HIV-positive individuals in Italy. Sex Transm Dis 2002;29:665-7. 13. Andreoletti L, Piendoir E, Legoff J, Brodard V, Beguinot I, Strady C, et al. High seropre-valence of herpes simplex virus type 2 infec-tion in French human immunodeficiency virus type 1-infected outpatients. J Clin Microbiol 2005;43:4215-7.14. Ramaswamy M, Sabin C, McDonald C, Smith M, Taylor C, Geretti AM. Herpes simplex virus type 2 (HSV-2) seroprevalence at the time of HIV-1 diagnosis and seroincidence after HIV-1 diagnosis in an ethnically diverse cohort of HIV-1 infected persons. Sex Transm Dis 2006;33:96-101.15. Wald A, Link K. Risk of human immunodefi-ciency virus infection in herpes simplex virus type 2-seropositive persons: a meta-analysis. J Infect Dis 2002;185:45-52.Rigopoulos et al.      Acta Dermatovenerol CroatGenital herpes simplex as initial manifestation of AIDS    2008;16(3):145-148

Extensive Atypical Genital Herpes Simplex Type 2 Infection as an Initial Manifestation of Acquired Immune Deficiency Syndrome

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Extensive Atypical Genital Herpes Simplex Type 2 Infection as an Initial Manifestation of Acquired Immune Deficiency Syndrome

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