Molecular detection and genetic identification of Borrelia garinii and Borrelia afzelii from patients presenting with a rare skin manifestation of prurigo pigmentosa in Taiwan.

OBJECTIVES: To determine the genetic identity of Borrelia spirochetes isolated from patients with an unusual skin lesion of prurigo pigmentosa (PP) in Taiwan. The causative agents responsible for human borreliosis were clarified. METHODS: Serum samples and skin specimens were collected from 14 patients with suspected PP and five controls. Serological testing by Western immunoblot analysis and isolation of Borrelia spirochetes from skin specimens were used to verify the Borrelia infection. Genetic identities of isolated spirochetes were determined by analyzing the gene sequences amplified by PCR assay based on the 5S (rrf)-23S (rrl) intergenic spacer amplicon gene of Borrelia burgdorferi sensu lato. RESULTS: Borrelia spirochetes were isolated from skin biopsies of three patients. Serological evidence of Borrelia infection in these patients was also confirmed by elevated IgG and IgM antibodies against the major protein antigens of B. burgdorferi. Phylogenetic analysis revealed that these detected spirochetes are genetically affiliated to the genospecies of Borrelia garinii and Borrelia afzelii with high sequence homology within the genospecies of B. garinii (91.0-98.7%) and B. afzelii (97%). CONCLUSIONS: This study provides the first evidence of B. garinii and B. afzelii isolated and identified in patients with PP. Whether this unusual skin lesion is a new manifestation of Lyme disease needs to be studied further.

Identification of Helicobacter pylori in skin biopsy of prurigo pigmentosa.

A 23-year-old Chinese man presented with a 3-year history of a pruritic eruption. On examination, pink urticarial papules associated with hyperpigmented reticulated patches were noted on his neck, back, and upper chest. Histopathology revealed vacuolar interface dermatitis and numerous gram-negative rods within a dilated hair follicle. The organisms were reactive with anti-Helicobacter pylori immunohistochemisty. The histologic findings and clinical presentation support the diagnosis of prurigo pigmentosa. Additional testing demonstrated a positive urease breath test and serum H. pylori IgG antibodies. The patient was referred to gastroenterology and treated with appropriate antibiotics. After treatment, esophagogastroduodenoscopy revealed chronic gastritis without evidence of H. pylori infection and his skin showed reticulated hyperpigmented patches without evidence of active inflammatory papules. Although previous reports have associated prurigo pigmentosa to H. Pylori gastritis, this is the first report of H. pylori organisms identified in a skin biopsy of prurigo pigmentosa.

Prurigo nodularis due to Mycobacterium tuberculosis.

Prurigo nodularis (PN) is a rare chronic skin disorder of unknown origin. Here we describe what is believed to be the first case of PN associated with tuberculosis. For the first time, culture and PCR analysis of skin biopsy confirmed the presence of Mycobacterium tuberculosis complex in PN skin lesions. The pruritus and skin lesions resolved following antitubercular therapy. Our case provides further evidence in favour of a link between PN and mycobacterial infection.

[The role of Helicobacter pyroli in the development of skin diseases]. / Rola Helicobacter pylori w powstawaniu chorób skóry.

The paper presents the current state-of-the-art concerning the effect of Helicobacter pyroli infection on the progress of some skin diseases (Raynaud's disease, purpura hyperergica, rosacea, prurigo nodularis, atopic dermatitis, chronic urticaria). The attention was turned to the lack of unanimity among authors respective to the effect of Helicobacter pylori on the progress of some skin diseases, especially those of allergic etiology. The methods of bacteria identification were discussed. The methods are as follows: invasive tests involving endoscopy of the upper segment of the alimentary tract--a traumatic test, histologic examination and bacteria culture as well as noninvasive tests: respiratory test and serological tests able to detect the humoral response to infection or examination of the bacteria genetic material by means of PCR. The therapeutic methods used to eradicate effectively the infection, recommended by the Working Group of the Polish Association of Gastroenterology (a three-component treatment for seven days--a drug able to diminish gastric secretion and two antibiotics) are also discussed.

Helicobacter pylori and prurigo nodularis.

BACKGROUND/AIMS: Numerous data have suggested that there may be a relationship between Helicobacter pylori (H. pylori) infection and extragastric diseases, including dermatological pathologies. We studied some cases of Hide's Prurigo Nodularis (NP), a very itchy skin disease of unknown origin, in order to asses whether there is a pathogenic correlation between PN and H. pylori infection. METHODOLOGY: Prurigo Nodularis had been diagnosed clinically and histologically in 42 outpatients (27 females and 15 males with mean age of 62 +/- 5 years). All patients were screened for H. pylori infection by esophagogastroduodenoscopy, histologic examination and specific immuno-enzymatic determination. Specific pharmacological treatment was administered to all patients with H. pylori infection. RESULTS: H. pylori colonization was observed in 40/42 patients examined and 32/40 patients presented some immunologic alterations. After the pharmacological treatment, endoscopy and rapid urease test confirmed eradication of H. pylori in 39/40 cases; itching was greatly reduced in the latter and microscopic examination of repeated skin biopsies revealed an improved histologic picture in patients affected by PN associated with H. pylori infection. CONCLUSIONS: The concomitant presence of skin disease, H. pylori infection and immune disorders infers that there may be a pathogenic connection between bacterial infection and the inflammatory alteration of PN. We believe that the pharmacologic treatment induced remission of the skin lesions by direct control of H. pylori chronic infection; in fact, H. pylori may have triggered or enhanced the vasculitis which, in turn, may have enhanced the clinical signs and inflammatory histologic component of PN.

Histopathological and bacteriological findings in prurigo nodularis.

Prurigo nodularis is a chronic disease with unknown aetiology. Biopsy specimens of 43 patients with prurigo nodularis were taken for histopathological and mycobacteriological analyses. By conventional histopathology, 25 (58%) samples, and by immunostaining for S100 protein, 31 (72%) samples had changes relevant to prurigo nodularis. Twelve (28%) of the samples were positive for acid fast bacilli in tissue staining by Ziehl-Neelsen technique, including 4 of the 6 samples also positive for mycobacteria in cultivation. The results verified the usefulness of S100 staining in detection of neural hyperplasia in dermal nerves, a feature regarded as diagnostic for prurigo nodularis. They also indicated that atypical mycobacteria may be a contributing factor in prurigo nodularis.

Mycobacteria in prurigo nodularis: the cause or a consequence?

BACKGROUND: Prurigo nodularis (PN) is a chronic skin disorder; its cause remains unknown. OBJECTIVE: We evaluated mycobacteria as a possible cause of PN. METHODS: Forty-three patients with PN were examined. Skin biopsy specimens were obtained for microbiologic and histopathologic studies. The patients were tested for intracutaneous reactivity to 12 mycobacterial antigens with the Mantoux technique. RESULTS: Six specimens (14%) grew mycobacteria in culture: M. avium-intracellulare (3), M. malmoense (1), and Mycobacterium sp. (2). Histopathologically, 12 samples (28%) were positive for acid-fast bacilli, and granulomatous changes were present in one sample. Patients whose cultures were positive for mycobacteria had significantly larger skin reactions to mycobacterial antigens. Two patients underwent 2 years of antituberculous chemotherapy; one had an excellent response and the other a partial response. CONCLUSION: Detection of mycobacteria by culture or staining, combined with elevated skin reactivity to mycobacteria in a high proportion of patients with PN, suggests a mycobacterial cause.