Elke-Ingrid Grussendorf-Conen

Routine detection of herpes simplex virus and varicella zoster virus by polymerase chain reaction reveals that initial herpes zoster is frequently misdiagnosed as herpes simplex

The differential diagnosis of herpes simplex and zoster may require virological confirmation, yet virus typing is not regarded as necessary in routine dermatological assessment. In an attempt to evaluate the clinical benefits of the routine detection of herpes simplex virus (HSV) and varicella zoster virus (VZV), we analysed skin swabs from 110 patients who were diagnosed at the first clinical visit as having herpes simplex (n = 45) or zoster (n = 65). Viruses were typed using the polymerase chain reaction (PCR) with the general primer pair GPHV‐RU. PCR analysis showed that at the initial clinical presentation, herpes simplex in these patients was not mistaken for zoster but that zoster was incorrectly diagnosed as herpes simplex in nine cases. Thus these results suggest that initial zoster often mimics herpes simplex, hence routine PCR diagnosis of HSV and VZV or alternative rapid diagnostic approaches may be beneficial in these cases.

Clinical features and age distribution of patients with HPV 2/27/57-induced common warts.

Abstract The morphology of common warts depends on the inducing human papillomavirus (HPV) type. In order to assess the impact of the virus type on wart epidemiology we determined the virus type by PCR and recorded anamnestic data of 238 patients with common warts. Warts induced by the related HPV types 2, 27 and 57 predominated in the study population ( n = 202). These warts mostly occurred as multiple verrucae vulgares, mosaic warts or endophytic warts. Patients aged between 10 and 30 years were most affected and they typically displayed a long disease history (mean duration of warts at the time of first clinical examination, 22 months). A different age distribution was observed in HPV 1-induced warts, most of which occurred in children 6–10 years of age. HPV 2-related warts responded only modestly to treatment, as they persisted in approximately 50% of all patients for more than 6 additional months. No sex preference was detected, but an association with atopic diseases was noted as 39.8% of patients with warts containing HPV 2-related viruses showed a history of atopic eczema, pollinosis or asthma as compared with 20.6% of the control population without a history of warts or with short-duration wart disease. Thus, our results indicate that the epidemiology, as well as morphology, of common warts is closely linked to the virus type.

Topical 5% Imiquimod Long-Term Treatment of Cutaneous Warts Resistant to Standard Therapy Modalities

Background: Long-lasting cutaneous warts may represent an unbearable stigma to patients and therefore pose a singular challenge for the physician. Generally, these warts are induced by human papillomavirus (HPV) 2, HPV-27 or HPV-57. Objectives: The present study was conducted to evaluate the efficacy and safety of long-term treatment with imiquimod 5% cream applied to long-lasting (mean duration 6.3 years) common warts, which had been resistant to previous therapeutic interventions. Patients and Methods: Imiquimod cream was self-applied by the patients twice daily. Assessment of response and occurrence of side-effects was performed every 4 weeks until clinical cure or up to a maximum of 24 weeks. A total of 37 patients were recruited. Results: 31 out of 37 patients completed the treatment. 10 out of 37 patients experienced a total clearance of their warts (27%). The mean duration to clearance was 19.2 weeks. 18 patients (49%) showed a reduction of more than 50% and 5 patients (14%) a reduction of less than 50%. Conclusions: Our data demonstrate that the long-term topical application of imiquimod 5% cream is an effective treatment for otherwise therapy-resistant cutaneous warts without causing any meaningful side-effects.

Rearrangements of the upstream regulatory region of human papillomavirus type 6 can be found in both Buschke-Löwenstein tumours and in condylomata acuminata

Clinically malignant Buschke-Löwenstein tumours and benign condylomata acuminata are caused by human papillomaviruses (HPVs), predominantly HPV-6 and -11. In some cases, the HPV-6 genomes found in Buschke-Löwenstein tumours and in verrucous carcinomas differ from HPV-6b isolated from a benign genital wart, by rearrangements of the upstream regulatory region (URR). To evaluate the frequency and role of mutations of the URR of HPV-6 we analysed 42 condylomata acuminata and four Buschke-Löwenstein tumours by the polymerase chain reaction and restriction enzyme cleavage. Using only four different restriction enzymes we could demonstrate four distinct restriction patterns, indicating that naturally occurring HPV-6 isolates display a high degree of DNA polymorphism within the URR. One Buschke-Löwenstein tumour and two condylomata acuminata yielded rearranged URRs with DNA duplications. All three lesions harboured multiple HPV-6 variants, suggesting that cellular or environmental factors facilitate the development of rearrangements. Therefore, rearrangements of the URR may represent only secondary events in condylomata acuminata and Buschke-Löwenstein tumours which do not necessarily confer a higher malignant potential to the infected cell.

Detection of human papillomavirus‐6 in primary carcinoma of the urethra in men

The authors report a case of primary urethral carcinoma which seems to be linked to human papillomavirus (HPV) infection. Southern blot hybridization of phosphorus 32 (32P)‐labeled DNA extracted from the cancer tissue gave a positive reaction with HPV‐6. Specimens of the tumor material subjected to in situ hybridization with 3H‐labeled HPV‐6 DNA showed numerous tumor cell clusters with clearly labeled nuclei. Using immunoperoxidase staining the authors found papillomavirus structural antigen within cell nuclei of the tumor tissue.

HPV 18-induced pigmented bowenoid papulosis of the neck.

We describe the case of a 53-year-old man in whom pigmented bowenoid papulosis developed on the skin of the neck. By polymerase chain reaction with general primers for genital human papillomaviruses (HPV) and subsequent restriction enzyme cleavage we could demonstrate HPV 18-related DNA in two biopsy specimens of the pigmented papules. To our knowledge, this report represents the first case of HPV 18-induced extragenital bowenoid papulosis of the neck.

Papillomavirus Common Antigen in Bowen’s Disease

We studied 173 biopsies of histologically determined Bowens disease and looked for the presence of papillomavirus antigen using immunoperoxidase staining. Fifty-nine of the lesions were located at the head, 49 at the extremities, 36 at the trunk and 29 originated from the genital region. Papillomavirus capsid antigen could be clearly identified in 39 (22.5%) cases. Eleven (38%) of the 29 lesions located on genital skin were positive for papillomavirus capsid antigen while 28 (19.4%) of the 144 biopsies from other skin regions contained viral antigen. Our findings are suggestive of an etiologic relationship between the virus and this dermatosis which represents a special variant of squamous cell carcinoma. They indicate that human papillomaviruses may play an important role in the development of cutaneous malignancies.

Demonstration of HPV-16 Genomes in the Nuclei of Cervix Carcinoma Cells

Specimens of 4 different cervical cancers, 1 flat condyloma of the cervix, 1 condyloma acuminatum, 1 morbus Bowen of the skin and 1 skin wart were subjected to in situ hybridization using human papilloma virus type 16 (HPV-16) DNA nick translated with 3H-TTP as a probe. Within each cervical cancer biopsy we found a certain number of tumor cell clusters with clearly labelled nuclei, while sections of the other skin lesions did not reveal any accumulation of grains within their nuclei. Southern blot hybridization of the DNA extracted from the 4 cervical carcinomas with 32p-labelled HPV-16 DNA gave a positive reaction in 3 tumors. Non-reactivity in the 4th biopsy might be due to a low concentration of HPV-genomes within the total extracted DNA of this tissue part.

Nachweis von HPV-6 DNA beim primären Urethra-Karzinom — Ein Hinweis auf eine virusinduzierte Genese maligner Genitaltumoren

Das primare Urethra-Karzinom ist ein seltener und bezuglich Histologie, lokalem Wachstum und Metastasierung vielfaltiger Tumor. Seit der Erstbeschreibung durch Thiaudierre im Jahre 1834 [3] sind in der Literatur etwa 400 Urethra-Karzinome beim Mann und 1000 bei der Frau beschrieben [6]. Histologisch uberwiegt das Plattenepithelkarzinom (70%), wahrend Adenokarzinome und Ubergangsepithelkarzinome deutlich seltener sind. Die Atiologie des primaren Urethra-Karzinoms ist nicht bekannt. Anamnestisch lassen sich gehauft venerische Erkrankungen, Urethrastrikturen und -traumen eruieren [4].