Complications des otites moyennes chroniques

Objectif de l’étude : Rapporter la fréquence des complications des otites moyennes chroniques et présenter notre expérience dans leur prise en charge.Matériel et méthodes : Etude rétrospective concernant la période allant du 1er janvier 2000 au 31 décembre 2009. Les complications ont été réparties en 2 grands groupes : extracrâniennes et intracrâ-niennes.Résultats : 57 patients sur 350 reçus pour OMC ont présenté une complication, soit une fréquence de 18,38 %. Le cholestéatome était le plus grand pourvoyeur de ces complications (84,2%). Dix-neuf patients présentaient plus d’une complication, soit au total 76 cas. Les complications extracrâniennes ont été les plus fréquentes, 63 cas (83%), dominées par la mastoïdite extériorisée profuse (68,3%). Les complications intracrâniennes au nombre de 13 (17%) étaient dominées par la méningite purulente otogène (46,2%). La mastoïdectomie associée à une antibiothérapie à large spectre, occupait une place im-portante dans la prise en charge de ces complications. Elle a été réalisée chez 45 patients (79%). La mortalité a été estimée à 3,5% (2 cas de décès). Un drainage neurochirurgical a été effectué dans 4 cas (8,6 %).Conclusion : Cette étude se caractérise par un taux de complications d’OMC plus élevé que ceux rappor-tés dans la littérature, ainsi que par la prédominance des formes étendues et des associa-tions de complications chez un même patient.Mots clés : Otite moyenne chronique, Complications, Cholestéatome.The objective of this study : was to report the frequency and our experience of management of complications of chronic otitsmedia.Methods : We conducted a retrospective study covering 10 years period (from 1st January 2000 to 31 December 2009). Complications were divided into 2 groups: extracranial and intracranial.Results : Among 350 patients received for chronic otitis media, 57 presented complications, such as a rate of 18.38%. Cholesteatoma was the largest provider of these complications in order of 84.2%. Nineteen (19) patients had more than one complication. So, a total of 76 cases of complications were listed. Subperiostal mastoiditis was the most common findings, 68.3% of the extracranial complications. The intracranial complications, (17%), were domi-nated by otogenic purulent meningitis (46.2%). Radical mastoïdectomy with broad spectrum antibiotics occupied an important place in the management of these complications, performed in 45 patients (79%). Neurosurgical drainage was performed in 4 cases (8.6%). Mortality was estimated at 3.5% (2 deaths).Conclusion : COCM are characterized, in this study, by an elevated rate compared to that reported in the literature, the prevalence of extended forms and associations of complications in the same patient.Keys words : Chronic otitis media, Complications, Cholesteatoma

Atg5-Independent Sequestration of Ubiquitinated Mycobacteria

Like several other intracellular pathogens, Mycobacterium marinum (Mm) escapes from phagosomes into the host cytosol where it can polymerize actin, leading to motility that promotes spread to neighboring cells. However, only ∼25% of internalized Mm form actin tails, and the fate of the remaining bacteria has been unknown. Here we show that cytosolic access results in a new and intricate host pathogen interaction: host macrophages ubiquitinate Mm, while Mm shed their ubiquitinated cell walls. Phagosomal escape and ubiquitination of Mm occured rapidly, prior to 3.5 hours post infection; at the same time, ubiquitinated Mm cell wall material mixed with host-derived dense membrane networks appeared in close proximity to cytosolic bacteria, suggesting cell wall shedding and association with remnants of the lysed phagosome. At 24 hours post-infection, Mm that polymerized actin were not ubiquitinated, whereas ubiquitinated Mm were found within LAMP-1–positive vacuoles resembling lysosomes. Though double membranes were observed which sequestered Mm away from the cytosol, targeting of Mm to the LAMP-1–positive vacuoles was independent of classical autophagy, as demonstrated by absence of LC3 association and by Atg5-independence of their formation. Further, ubiquitination and LAMP-1 association did not occur with mutant avirulent Mm lacking ESX-1 (type VII) secretion, which fail to escape the primary phagosome; apart from its function in phagosome escape, ESX-1 was not directly required for Mm ubiquitination in macrophages or in vitro. These data suggest that virulent Mm follow two distinct paths in the cytosol of infected host cells: bacterial ubiquitination is followed by sequestration into lysosome-like organelles via an autophagy-independent pathway, while cell wall shedding may allow escape from this fate to permit continued residence in the cytosol and formation of actin tails

LprG-mediated surface expression of lipoarabinomannan is essential for virulence of Mycobacterium tuberculosis

Mycobacterium tuberculosis employs various virulence strategies to subvert host immune responses in order to persist and cause disease. Interaction of M. tuberculosis with mannose receptor on macrophages via surface-exposed lipoarabinomannan ( LAM) is believed to be critical for cell entry, inhibition of phagosome-lysosome fusion, and intracellular survival, but in vivo evidence is lacking. LprG, a cell envelope lipoprotein that is essential for virulence of M. tuberculosis, has been shown to bind to the acyl groups of lipoglycans but the role of LprG in LAM biosynthesis and localization remains unknown. Using an M. tuberculosis lprG mutant, we show that LprG is essential for normal surface expression of LAM and virulence of M. tuberculosis attributed to LAM. The lprG mutant had a normal quantity of LAM in the cell envelope, but its surface was altered and showed reduced expression of surface-exposed LAM. Functionally, the lprG mutant was defective for macrophage entry and inhibition of phagosome-lysosome fusion, was attenuated in macrophages, and was killed in the mouse lung with the onset of adaptive immunity. This study identifies the role of LprG in surface-exposed LAM expression and provides in vivo evidence for the essential role surface LAM plays in M. tuberculosis virulence. Findings have translational implications for therapy and vaccine development