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1.
J Fungi (Basel) ; 6(4)2020 Sep 29.
Article in English | MEDLINE | ID: mdl-33003309

ABSTRACT

BACKGROUND: In this last decade, a huge increase in African anthropophilic strains causing tinea capitis has been observed in Europe. The Belgian National Reference Center for Mycosis (NRC) conducted a surveillance study on tinea capitis in 2018 to learn the profile of circulating dermatophytes. METHODS: Belgian laboratories were invited to send all dermatophyte strains isolated from the scalp with epidemiological information. Strain identification was confirmed by ITS (Internal Transcribed Spacer) sequencing. Mutation in the squalene epoxidase (SQLE) gene was screened by PCR. RESULTS: The main population affected by tinea capitis was children from 5-9 years. Males were more affected than females. The majority of the strains were collected in the Brussels area followed by the Liege area. Among known ethnic origins, African people were more affected by tinea capitis than European people. The major aetiological agent was Microsporum audouinii, followed by Trichophyton soudanense. One strain of Trichophyton mentagrophytes has been characterized to have a mutation on the squalene epoxidase gene and to be resistant to terbinafine. CONCLUSIONS: African anthropophilic dermatophytes are mainly responsible for tinea capitis in Belgium. People of African origin are most affected by tinea capitis. The monitoring of terbinafine resistance among dermatophytes seems necessary as we have demonstrated the emergence of resistance in T. mentagrophytes.

2.
Acta Clin Belg ; 73(5): 356-363, 2018 Oct.
Article in English | MEDLINE | ID: mdl-28954600

ABSTRACT

Case report We report the case of a young Cameroonian woman who presented with cough, hyperthermia, weight loss, pancytopenia, and hepatosplenomegaly. A positive HIV serology was discovered and a chest radiography revealed a 'miliary pattern'. Bone marrow aspiration pointed out yeast inclusions within macrophages. Given the morphological aspect, the clinical presentation and immunosuppression, histoplasmosis was retained as a working hypothesis. Antiretroviral and amphotericin B treatments were promptly initiated. Review Given the immigration wave that Europe is currently experiencing, we think it is important to share experience and knowledge, especially in non-endemic areas such as Europe, where clinicians are not used to face this disease. Histoplasmosis is due to Histoplasma capsulatum var. capsulatum, a dimorphic fungus. Infection occurs by inhaling spores contained in soils contaminated by bat or bird droppings. The clinical presentation depends on the immune status of the host and the importance of inoculum, varying from asymptomatic to disseminated forms. AIDS patients are particularly susceptible to develop a severe disease. Antigen detection, molecular biology techniques, and microscopic examination are used to make a rapid diagnosis. However, antigen detection is not available in Europe and diagnosis needs a strong clinical suspicion in non-endemic areas. Because of suggestive imagery, clinicians might focus on tuberculosis. Our case illustrates the need for clinicians to take histoplasmosis in the differential diagnosis, depending on the context and the patient's past history.


Subject(s)
AIDS-Related Opportunistic Infections , Histoplasmosis , Adult , Amphotericin B/administration & dosage , Amphotericin B/therapeutic use , Anti-Retroviral Agents/administration & dosage , Anti-Retroviral Agents/therapeutic use , Antifungal Agents/administration & dosage , Antifungal Agents/therapeutic use , Bone Marrow Cells/microbiology , Bone Marrow Cells/pathology , Female , HIV Infections/diagnosis , HIV Infections/drug therapy , Histoplasma , Humans , Pancytopenia
3.
Clin Chim Acta ; 438: 401-14, 2015 Jan 01.
Article in English | MEDLINE | ID: mdl-25236333

ABSTRACT

The link between vascular calcification (VC) and increased mortality is now well established. Over time, as clinical importance of this phenomenon has begun to be fully considered, scientists have highlighted more and more physiopathological mechanisms and signaling pathways that underlie VC. Several conditions such as diabetes, dyslipidemia and renal diseases are undoubtedly identified as predisposing factors. But even if the process is better understood, many questions still remain unanswered. This review briefly develops the various theories that attempt to explain mineralization genesis. Nonetheless, the main purpose of the article is to provide a profile of the various existing biomarkers of VC. Indeed, in the past years, a lot of inhibitors and promoters, which form a dense and interconnected network, were identified. Given importance to assess and control mineralization process, a focusing on accumulated knowledge of each marker seemed to be necessary. Therefore, we tried to define their respective role in the physiopathology and how they can contribute to calcification risk assessment. Among these, Klotho/fibroblast growth factor-23, fetuin-A, Matrix Gla protein, Bone morphogenetic protein-2, osteoprotegerin, osteopontin, osteonectin, osteocalcin, pyrophosphate and sclerostin are specifically discussed.


Subject(s)
Diabetes Mellitus/metabolism , Dyslipidemias/metabolism , Renal Insufficiency, Chronic/metabolism , Vascular Calcification/metabolism , Biomarkers/metabolism , Bone Morphogenetic Protein 2/genetics , Bone Morphogenetic Protein 2/metabolism , Calcium-Binding Proteins/genetics , Calcium-Binding Proteins/metabolism , Diabetes Complications , Diabetes Mellitus/genetics , Diabetes Mellitus/physiopathology , Dyslipidemias/complications , Dyslipidemias/genetics , Dyslipidemias/physiopathology , Extracellular Matrix Proteins/genetics , Extracellular Matrix Proteins/metabolism , Fibroblast Growth Factor-23 , Fibroblast Growth Factors/genetics , Fibroblast Growth Factors/metabolism , Gene Expression Regulation , Humans , Osteoprotegerin/genetics , Osteoprotegerin/metabolism , Renal Insufficiency, Chronic/complications , Renal Insufficiency, Chronic/genetics , Renal Insufficiency, Chronic/physiopathology , Risk Assessment , Signal Transduction , Vascular Calcification/etiology , Vascular Calcification/genetics , Vascular Calcification/physiopathology , alpha-2-HS-Glycoprotein/genetics , alpha-2-HS-Glycoprotein/metabolism , Matrix Gla Protein
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