Ploidy of Cell-Sorted Trophic and Cystic Forms of Pneumocystis carinii

Once regarded as an AIDS-defining illness, Pneumocystis pneumonia (PcP) is nowadays prevailing in immunocompromised HIV-negative individuals such as patients receiving immunosuppressive therapies or affected by primary immunodeficiency. Moreover, Pneumocystis clinical spectrum is broadening to non-severely-immunocompromised subjects who could be colonized by the fungus while remaining asymptomatic for PcP, thus being able to transmit the infection by airborne route to susceptible hosts. Although the taxonomical position of the Pneumocystis genus has been clarified, several aspects of its life cycle remain elusive such as its mode of proliferation within the alveolus or its ploidy level. As no long-term culture model exists to grow Pneumocystis organisms in vitro, an option was to use a model of immunosuppressed rat infected with Pneumocystis carinii and sort life cycle stage fractions using a high-through-put cytometer. Subsequently, ploidy levels of the P. carinii trophic and cystic form fractions were measured by flow cytometry. In the cystic form, eight contents of DNA were measured thus strengthening the fact that each mature cyst contains eight haploid spores. Following release, each spore evolves into a trophic form. The majority of the trophic form fraction was haploid in our study. Some less abundant trophic forms displayed two contents of DNA indicating that they could undergo (i) mating/fusion leading to a diploid status or (ii) asexual mitotic division or (iii) both. Even less abundant trophic forms with four contents of DNA were suggestive of mitotic divisions occurring following mating in diploid trophic forms. Of interest, was the presence of trophic forms with three contents of DNA, an unusual finding that could be related to asymmetrical mitotic divisions occurring in other fungal species to create genetic diversity at lower energetic expenses than mating. Overall, ploidy data of P. carinii life cycle stages shed new light on the complexity of its modes of proliferation

Le loxoscelisme cutané, à propos d’une observation exceptionnelle de 9 cas consécutifs

International audienceINTRODUCTION:Loxosceles spiders are ubiquitous and responsible for many cases of envenomation in the world. The kind rufescens is present in the Provence and Occitan regions in France. During the summer 2015, we faced many Loxosceles rufescens cases of bites having led to extensive integumental necrosis whose features and singular evolution seems important to report.MATERIAL AND METHODS:We report the cases of nine patients who experienced a spider bite in the summer of 2015 in the Languedoc Roussillon.RESULTS:Of nine patients, eight patients had skin necrosis and five required surgical care. Five patients had a fever and had five other general signs such as important asthenia, joint pain, nausea and dizziness. CRP was very low normal in all patients. Finally, five of the nine patients reported a residual pain.DISCUSSION:L. rufescens is a small spider (7 to 15mm in diameter) having a cytotoxic venom. Loxoscelism diagnosis is usually made by removing a front necrotic skin lesion. Of systemic loxoscelism that have been described, some American species had fatal outcomes. The treatment remains controversial with various options: surgery, antibiotics, antihistaminics, antivenom.CONCLUSION:The diagnosis must be made in endemic areas when confronted to a necrosic integumentary infectious rapidly progressive, unresponsive to antibiotic treatment associated with atypical general signs

Anti-Saccharomyces cerevisiae antibodies in twins with inflammatory bowel disease

Background and aims: An increased occurrence of anti-Saccharomyces cerevisiae antibodies (ASCA) is reported in unaffected members of families with Crohn’s disease. Whether ASCA is a familial trait due to genetic factors or is caused by exposure to environmental factors is unknown. To assess the genetic influence of ASCA we studied its occurrence in a twin population. Patients and methods: ASCA were analysed in 98 twin pairs with inflammatory bowel disease and were related to clinical phenotype and CARD15/NOD2 genotype. Results: ASCA were more common in Crohn’s disease than in ulcerative colitis (40/70 (57%) twins v 5/43 (12%) twins). Associations with ileal Crohn’s disease, stricturing/penetrating behaviour, and young age, but not CARD15/NOD2 were confirmed. ASCA were found in 1/20 (5%) healthy siblings in discordant monozygotic pairs with Crohn’s disease compared with 7/27 (26%) in discordant dizygotic pairs. Using the intraclass correlation coefficient (ICC), no agreement in ASCA titres was observed in discordant twin pairs with Crohn’s disease, in monozygotic (ICC = −0.02) or dizygotic (ICC = −0.26) pairs. In contrast, strong agreement was seen within concordant monozygotic twin pairs with Crohn’s disease (ICC = 0.76). Conclusions: These findings question the concept of ASCA as a marker of genetic susceptibility for Crohn’s disease. The agreement in ASCA titres within concordant monozygotic twin pairs with Crohn’s disease, suggests that the level of increase is genetically determined. We propose that ASCA are a marker of a response to an environmental antigen and that a specific gene(s) other than CARD15/NOD2 determines the level of response and perhaps also specific phenotypic characteristics