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Objective: To determine the frequency and clinical forms of oral manifestations associated to Paracoccidioidomycosis (PCM) and Histoplasmosis. Material and Methods: 481 medical records of outpatients referred to the Medical Mycology Department were reviewed since 2009 to 2016. Data were analyzed using descriptive statistical methods. Results: 47 (9.77%) cases had oral manifestations, 29 (61.70%) were associated to PCM and 18 (38.29%) to histoplasmosis. For PCM, male-female ratio was 8:1 and 1:1 for histoplasmosis. The average age for PCM was 48 years old and 53 for histoplasmosis. All the PCM patients had more than 1 oral structure affected: 44.82% were gingival lesions and 27.58% palate. In patients with histoplasmosis, 6 (33.33%) were lesions affecting palate and 6 (33.33%) involving tongue. For both entities, painful ulcers and granulomatous-like lesions were the most prevalent clinical forms; however, we observed a wide range of other oral manifestations. Regarding PCM patient's comorbidities, 3 (10.34%) cases had HIV/AIDS, 8 (27.58%) histoplasmosis and 2 (6.89%) carcinomas. Whereas the comorbidities of patients with histoplasmosis, 2 (11.11%) had HIV/AIDS and 1 (5.55%) had carcinoma. Conclusion: In endemic countries for both mycoses, dentists must be aware of patients with mouth lesions, take advantage of epidemiologic clues that suggest risk factors and be acquainted with all the current diagnostic tests in order to make a quick diagnosis and treatment in highly suspicious cases.

Background Amoebiasis is a parasitic disease caused by Entamoeba histolytica, which affects people living in low- and middle-income countries and has intestinal and extraintestinal manifestations. To date, knowledge on coronavirus disease 2019 (COVID-19) coinfection with enteric parasites is limited, and E. histolytica coinfection has not been previously described. Here we present the case of a patient with COVID-19 who, during hospitalisation, presented a clinical picture consistent with an amoebic liver abscess (ALA). Case presentation A 54-year-old man, admitted as a suspected case of COVID-19, presented to our hospital with dyspnoea, malaise, fever and hypoxaemia. A nasopharyngeal swab was positive for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) by reverse-transcription polymerase chain reaction. After 7 days, he developed diarrhoea, choluria and dysentery. An abdominal ultrasound showed a lesion compatible with a liver abscess; stool examination revealed E. histolytica trophozoites, and additional serology for E. histolytica was positive. After 12 days of treatment with metronidazole, ceftazidime and nitazoxanide, the patient reported acute abdominal pain, and an ultrasound examination revealed free liquid in the abdominal cavity. An emergency exploratory laparotomy was performed, finding 3000 mL of a thick fluid described as “anchovy paste”. Computed tomography scan revealed a second abscess. He ended up receiving 21 days of antibiotic treatment and was discharged with satisfactory improvement. Conclusion Here we present, to the best of our knowledge, the first report of ALA and COVID-19 co-presenting. Based on their pathophysiological similarities, coinfection with SARS-CoV-2 and E. histolytica could change the patient’s clinical course; however, larger studies are needed to fully understand the interaction between these pathogens.

Introduction: Pyogenic granuloma (PG) is a reactive inflammatory vascular lesion of the skin and mucous membranes, characterised by the presence of enlarged venules and seamed and seamless capillaries with plump endothelial cells (EC), and numerous macrophages. EC activation upregulates the synthesis of galectins and induces their translocation to the EC surface promoting angiogenesis and lymphangiogenesis, particularly galectin-1 (Gal-1), Gal-3 and Gal-8. However, the presence and distribution of Gal-1, -3 and -8, as well as their implications in the pathogenesis of PG, has not been considered. Materials and methods: Eight biopsies from patients diagnosed with PG were selected. The presence of PECAM-1/CD31, IL-1β, VEGF-C, VEGFR-2, VEGFR-3, integrin β1, CD44, fibronectin and Gal-1, -3 and -8 was assessed by immunofluorescence staining using confocal laser scanning microscopy. Results and Discussion: Immunostaining revealed that these molecules were present in the enlarged venules with plump ECs, in some macrophages and other immune cells. We propose that macrophages release VEGF-A and VEGF-C inducing VEGFR-2/VEGFR-3 expression and activation, leading macrophages to transdifferentiate into plump ECs that might integrate into pre-existing venules, contributing to the formation of enlarged venules with transluminal bridges and capillaries. EC activation, induced by certain cytokines, has been shown to stimulate galectin expression and changes in the cellular localisation through association and activation of specific EC surface glycoproteins. Therefore, it is plausible that Gal-1, -3 and -8, acting in a concerted manner, could be mediating the transdifferentiation of macrophages into plump ECs and facilitating their migration and incorporation into the new vessels. Lay Summary In this study, immunostaining of pyogenic granuloma (PG) tissue sections showed immunoreactivity for PECAM-1/CD31, IL-1β, VEGF-C, VEGFR-2 and VEGFR-3, and galectin-1, -3 and -8 in enlarged venules with plump endothelial cells (EC), as well as in some macrophages and other immune cells. Interestingly, enlarged and thin-walled transient vessels lined by PECAM-1/CD31 and VEGFR-2 immunopositive ECs that form from pre-existing normal venules in response to VEGF-A (called ‘mother’ vessels [MV]) and that undergo intraluminal bridging evolving into various types of capillaries (called ‘daughter’ vessels [DV]) have been observed in benign and malignant tumours, in physiological and pathological angiogenesis as well as in vascular malformations, suggesting an important role for VEGF-A and VEGFR-2 in such a process. However, it is not only the mechanisms by which the MVs evolve in different types of DVs that remains to be elucidated, but also whether the cells that form intraluminal bridges proceed from locally activated ECs or whether they are derived from bone marrow precursors or from resident macrophages. Given that the formation of homodimers by Gal-1 and Gal-8 and pentamers by Gal-3 to generate gal–glycan lattices at the cell surface and in the extracellular space has been shown, it is possible that in PG tissue Gal-1, -3 and -8, through their binding partners, form a supramolecular structure at the surface of ECs and plump ECs, macrophages and in the extracellular space that might be mediating the transdifferentiation of macrophages into plump ECs and facilitating the migration and incorporation of these cells into the pre-existing venules, thus contributing to the formation of MVs and DVs.

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