Biofilms and vulvovaginal candidiasis.

Candida species, including C. albicans, are part of the mucosal flora of most healthy women, and inhabit the gastrointestinal and genitourinary tracts. Under favourable conditions, they can colonize the vulvovaginal mucosa, giving rise to symptomatic vulvovaginal candidiasis (VVC). The mechanism by which Candida spp. produces inflammation is unknown. Both, the blastoconidia and the pseudohyphae are capable of destroying the vaginal epithelium by direct invasion. Although the symptoms are not always related to the fungal burden, in general, VVC is associated with a greater number of yeasts and pseudohyphae. Some years ago, C. albicans was the species most frequently involved in the different forms of VVC. However, infections by different species have emerged during the last two decades producing an increase in causative species of VVC such as C. glabrata, C. parapsilosis, C. krusei and C. tropicalis. Candida species are pathogenic organisms that have two forms of development: planktonic and biofilm. A biofilm is defined as a community of microorganisms attached to a surface and encompassed by an extracellular matrix. This form of presentation gives microorganisms greater resistance to antifungal agents. This review, about Candia spp. with a special emphasis on Candida albicans discusses specific areas such as biofilm structure and development, cell morphology and biofilm formation, biofilm-associated gene expression, the cell surface and adherence, the extracellular matrix, biofilm metabolism, and biofilm drug resistance in vulvovaginitis biofilms as an important virulence factor in fungi.

Dermatobia Hominis Infestation Misdiagnosed as Abscesses in a Traveler to Spain.

Dear Editor, A 29-year-old woman presented with abscesses on her buttock and leg attributed to flea bites inflicted 5 days earlier on return to Spain after 2 months in Guinea-Bissau. Ciprofloxacin was ineffective after 7 days, and she was referred for dermatologic evaluation. Examination revealed 4 round, indurated, erythematous-violet furunculoid lesions with a 1.5-2 mm central orifice draining serous material. She reported seeing larvae exiting a lesion, and we extracted several more (Figure 1). Parasitology identified Dermatobia (D.) hominis (Figure 2). Biopsy revealed intense dermal eosinophilic inflammatory infiltrate with a deep cystic appearance, surrounded by acute inflammatory infiltrate and necrotic material. Dermoscopy identified a foramen surrounded by dilated blood vessels and desquamation. A yellowish structure with a luminescent central ring was noted. Ultrasonography identified oval, hypoechoic, and hypovascular structures with inner echoic lines corresponding to cavities with debris and/or larval remains. Larvae were extracted before ultrasonography (Figure 1, b). Recommended treatment included topical antiseptic, occlusion of the infected area with paraffin, and 1% topical ivermectin; treatment resulted in incomplete resolution after 7 days. Furunculoid myiasis is more common in developing countries (1). Cases in Spain are usually imported, since the flies that produce this type of myiasis are not found locally. The species most frequently involved are D. hominis from Central and South America (botfly) and Cordylobia anthropophaga from the sub-Saharan region (tumbu fly) (2). We believe this was the first case in Spain imported from Guinea-Bissau. Several cases have been reported in Spain. Marco de Lucas et al. (3) reported a case in a Colombian male emigrant with multiple subependymal and intraventricular lesions, concentric blooming artifacts, and moderate hydrocephalus due to intracerebral myiasis. Another case was described by Arocha et al. (4). Central European countries continue to report new cases of imported furunculoid myiasis (5). D. hominis is a fly of the Oestridae family, approximately 1.5 cm long, yellowish-white in color, with a plumose edge (6). Larvae induce erythematous papules that sometimes ulcerate and resemble oils or large pustules, with a central orifice of about 1 mm, representing the larval respiratory pore. The lesions are usually painful (especially when larvae are still present) and pruritic, and produce sensations of movement under the skin. Lesions are located predominantly in exposed areas (7) and areas of contact with clothing and footwear, such as feet, buttocks, and external genitalia. Histopathology is not necessary for diagnosis, but usually reveals intense inflammatory infiltrate with abundant eosinophils surrounding larvae. (2) In our patient, ultrasound confirmed absence of living larvae within the cavity. D. hominis larvae show spontaneous movement in positive lesions and can be detected with ultrasound. Lesions in the hypodermis and dermis showed increased echogenicity of surrounding tissue, probably due to edema and inflammation (8). Diagnosis is established by comparing the lesion appearance with images of boils, abscesses, and inclusion of foreign body reaction cysts. Based on failed antibiotic therapy and travel to an endemic zone, myiasis should be considered in the differential diagnosis. Treatment consists of larval extraction through the respiratory orifice using pressure or a fine forceps or punch (9). Topical or oral ivermectin (10) can shorten the time to larval elimination. Physicians should be aware of this condition when travelers from endemic regions present with furuncular lesions, especially if movement is felt within the lesions or if lesions fail to heal. Myiasis is easily diagnosed based on clinical suspicion and epidemiological history, and is simple to treat.