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BACKGROUND: During a health survey in a remote area in southwest Colombia, it became apparent that a high percentage of the population suffered from chronic pruritus in association with high numbers of ticks and tickbites. OBJECTIVE: To determine the clinical features and severity of tickbite-associated pruritus. METHOD: At twotime points - 8 weeks apart to account for seasonal effects - a cross-sectional study was conducted encompassing physical examination of the population, histological analysis of skin biopsies, and determining serum for antibodies against spotted fever (SFG) rickettsiae and typhus group (TG) rickettsiae. Ticks were identified using morphological criteria, and infection by rickettsiae was determined by PCR. RESULTS: About 94.5% of the population (95% CI 92-97%) showed clinical signs of a pruritic arthropod reaction and of chronic pruritus with lichenoid papules and hyper- and hypopigmented nodules on otherwise noninflamed skin. Pruritus markedly impaired the quality of life in terms of sleeping disturbances. No signs for other diseases were observed. Chronic pruritus appeared to be because of repeated tickbites and scratching, but not because of other dermatological or medical conditions. Antibodies against SFG and TG-rickettsiae were detected at 79.0% (95% CI 73-86) and 3.6% (95% CI 0.7-6), respectively. Ticks were identified as Amblyomma cajennense. CONCLUSION: Remarkably high exposure to tick bites caused an unusually high rate of acute and chronic pruritus and markedly impaired quality of life of the investigated rural community. This underlines the necessity of public health measures and surveillance of rickettsial disease.

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The protozoan parasite Leishmania (Viannia) braziliensis is one of the main causes of cutaneous and mucocutaneous leishmaniasis in South America. Here, we describe three cases of L. (V.) braziliensis infection which were acquired during travelling in Bolivia, Peru or Paraguay and illustrate the phenotypic heterogeneity and therapeutic complexity of the disease. Two patients presented with unusual clinical manifestations, i.e. with prominent regional lymphadenopathy ("bubonic leishmaniasis") and with simultaneously emerged skin and mucosal lesions, respectively. Both patients insufficiently responded to oral treatment with miltefosine; resolution of the lesions was only achieved after a course of intravenous liposomal amphotericin B.

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Macrophages are decisive cells for the course of leprosy as they phagocytose Mycobacterium leprae and have the potential to influence the specific immune response. Expression and release of the myeloid-related protein (MRP) 8 and MRP14 (S100A8 and S100A9) characterize a proinflammatory subtype of macrophage that is prominent in, for example, murine infection with lack of a T helper 1 cell response and in certain highly active chronic inflammations of mice and humans. We investigated cutaneous biopsies of the different forms of leprosy (41 untreated patients) including leprosy reaction type 1 (reversal reaction) and type 2 (erythema nodosum leprosum) (n=18) for expression of MRP8 and MRP14 by subtupes of macrophages. Concomitantly we determined serum levels of MRP8 and MRP14 by sandwich enzyme-linked immunosorbent assay. Expression of MRP8 and MRP14 by CD68-positive macrophages was low in tuberculoid leprosy and rose significantly in borderline tuberculoid leprosy and especially in multibacillary forms, there being expressed by mycobacteria-loaded foam cells. A significant rise of MRP8 and MRP14 expression also occurred in lepra reactions compared to the corresponding non-reactional forms. In type 2 reactions this additional increased was associated with a significant elevation of serum levels. In type 1 it was associated with expression of MRP8 and MRP14 by epitheloid and giant cells, which so far were considered not to express both proteins. In conclusion, we present evidence taht the two prominent proteins MRP8 and MRP14 can be re-expressed in vivo by tissue macrophages in chronic infection, that their increased expression is characteristic for a macrophage subtype associated with high inflammatory but low antimycobacterial activity in the absence of a T helper 1 response, and that their significant rise in serum during erythema nodosum leprosum bears diagnostic and pathophysiological relevance.

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The lepromin test, serum IgM antibodies against Mycobacterium leprae and in situ observations of T cell subsets in biopsies of Mitsuda reaction using monoclonal antibodies were performed on 44 untreated leprosy patients belonging to various classifications of the disease. The Mitsuda reaction was accessed clinically and histologically after 28 days. Clinical reading and histological analysis of Mitsuda reaction showed good agreement. The high positivity in clinical reading correlated with compact granulomas in histology. There is a graduation of Mitsuda reaction that follows the immunological spectrum of the disease. The histological study of Mitsuda reaction is valuable to confirm the immunological condition in doubtful clinical reaction. Anti-PGL-I IgM levels correlated with disease classification, increasing from the tuberculoid towards the lepromatous pole of the disease spectrum. There was an inverse correlation between serum IgM antibody levels and clinical and histological reading of Mitsuda reaction. There were no statistical difference in quantities and distribution of CD4+ and CD8+ T cells in all Mitsuda reactions. The pattern of cellular content of Mitsuda reaction could not be related to the T cells.

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A 39-year-old woman presented with a 6-year history of asymptomatic macules on her back. The patient had no other complaints, and she did not report any case of infectious disease in her family. Examination revealed hyperpigmented macules, presenting irregular edges but with a sharp demarcation, on the midline of the back from the cervical to the lumbar region. Within these hyperpigmented areas, islands of normal appearing skin were observed. There were also some hypopigmented macules on the lateral and posterior aspects of the trunk (Fig. 1). The patient presented thickening of the left ulnar nerve and sensory loss to temperature on the lateral aspect of the left arm. Biopsy specimens were obtained from the hyper- and hypopigmented areas. In the hyperpigmented macule, the biopsy revealed focal areas of hypomelanosis in the epidermis and the presence of melanophages in the superficial dermis, but no acid-fast bacilli were found (Fig. 2a). The Masson-Fontana stain showed an evident pigmentary incontinence (Fig. 2b). The biopsy obtained from the hypopigmented lesion also revealed focal areas of hypomelanosis, but in the superficial dermis an infiltrate of foamy macrophages was observed, as typically found in lepromatous leprosy (Fig. 3a); acid-fast bacilli were found by Fite-Faraco stain. The focal hypomelanosis was confirmed by Masson-Fontana stain (Fig. 3b). Mitsuda's reaction in this patient was negative and slit-skin smears (cutaneous lesion, earlobes, elbows, and knees) were negative for acid-fast bacilli. The patient was treated with multidrug therapy for multibacillary leprosy: rifampin, 600 mg once monthly (supervised), clofazimine, 300 mg once monthly (supervised), dapsone, 100 mg daily, and clofazimine, 50 mg daily, all given for 2 years. After 7 months of treatment, the hypopigmented lesions diminished and the hyperpigmented lesions improved after 2 years of treatment and the sensory loss to temperature was restored.

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