SummaryTungiasis is caused by penetration of the female sand flea Tunga penetrans into the epidermis of its host. It is endemic in many countries in Latin America, the Caribbean and sub-Saharan Africa. Although superinfection is a common clinical observation, the frequency and the pattern of bacterial pathogens associated with tungiasis have never been investigated systematically. We conducted a prospective clinico-bacteriological study with patients living in a shantytown in Fortaleza, capital of Ceará State (Northeast Brazil), where tungiasis is hyperendemic. Swabs were taken from 78 patients with multiple lesions after surgical extraction of the parasite, and the specimens were cultured for aerobic and anaerobic microorganisms. Ninety-nine specimens were investigated for aerobic bacteria, from which 146 pathogens were identified. The most common species were Staphyloccous aureus (35.5%) and various enterobacteriaceae (29.5%). Bacillus sp., Enteroccous faecalis, Streptococcus pyogenes and Pseudomonas sp. were also isolated. Eighty-four anaerobic cultures yielded 20 pathogens: in eight cases we detected Peptostreptococcus sp., in seven cases Clostridium sp., and in five cases non-identifiable gram-negative bacilli. These results show that secondary infection is very common in tungiasis, and caused by a variety of highly pathogenic microorganisms. It is proposed that T. penetrans acts as a foreign body facilitating biofilm formation within the epidermis. To prevent spreading of pathogens to the surrounding tissue and/or the systemic circulation, sand fleas should be surgically extracted immediately after penetration.keywords tungiasis, clinico-bacteriological study, superinfection, aerobic pathogens, anaerobic pathogens, biofilm formation correspondence Prof.

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Sodium alendronate preserves alveolar bone resorption and has anti-inflammatory and antibacterial activities in experimental periodontitis.

Intestinal mucositis is a common side effect of irinotecan-based anticancer regimens. Mucositis causes cell damage, bacterial/endotoxin translocation and production of cytokines including IL–1 and IL–18. These molecules and toll-like receptors (TLRs) activate a common signaling pathway that involves the Myeloid Differentiation adaptor protein, MyD88, whose role in intestinal mucositis is unknown. Then, we evaluated the involvement of TLRs and MyD88 in the pathogenesis of irinotecan-induced intestinal mucositis. MyD88-, TLR2- or TLR9-knockout mice and C57BL/6 (WT) mice were given either saline or irinotecan (75 mg/kg, i.p. for 4 days). On day 7, animal survival, diarrhea and bacteremia were assessed, and following euthanasia, samples of the ileum were obtained for morphometric analysis, myeloperoxidase (MPO) assay and measurement of pro-inflammatory markers. Irinotecan reduced the animal survival (50%) and induced a pronounced diarrhea, increased bacteremia, neutrophil accumulation in the intestinal tissue, intestinal damage and more than twofold increased expression of MyD88 (200%), TLR9 (400%), TRAF6 (236%), IL–1β (405%), IL–18 (365%), COX–2 (2,777%) and NF-κB (245%) in the WT animals when compared with saline-injected group (P<0.05). Genetic deletion of MyD88, TLR2 or TLR9 effectively controlled the signs of intestinal injury when compared with irinotecan-administered WT controls (P<0.05). In contrast to the MyD88-/- and TLR2-/- mice, the irinotecan-injected TLR9-/- mice showed a reduced survival, a marked diarrhea and an enhanced expression of IL–18 versus irinotecan-injected WT controls. Additionally, the expression of MyD88 was reduced in the TLR2-/- or TLR9-/- mice. This study shows a critical role of the MyD88-mediated TLR2 and TLR9 signaling in the pathogenesis of irinotecan-induced intestinal mucositis.

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