f Recent reports of increasing in vitro sulfonamide resistance in Nocardia prompted us to investigate the findings. Despite the reports, there is a paucity of clinical reports of sulfonamide failure in treatment of nocardia disease. We reviewed 552 recent susceptibilities of clinical isolates of Nocardia from six major laboratories in the United States, and only 2% of the isolates were found to have resistant MICs of trimethoprim-sulfamethoxazole and/or sulfamethoxazole. We hypothesize that the discrepancies in the apparent sulfonamide resistance between our study and the previous findings may be associated with difficulty in the laboratory interpretation of in vitro MICs for trimethoprim-sulfamethoxazole and sulfamethoxazole and the lack of quality controls for Nocardia for these agents.
Mycobacterium massiliense is a rapidly growing mycobacterium that is indistinguishable from Mycobacterium chelonae/M. abscessus by partial 16S rRNA gene sequencing. We sequenced rpoB, sodA, and hsp65 genes from isolates previously identified as being M. chelonae/M. abscessus and identified M. massiliense from isolates from two patients with invasive disease representing the first reported cases in the United States.Rapidly growing mycobacterium infections are increasing in the United States (7) and are difficult to speciate by conventional methods. Partial 16S rRNA gene sequencing is the most widely used method for the identification of nontuberculous mycobacteria (6,8,12), but this gene target is often limited by the lack of sequence divergence among closely related Mycobacterium species (15). Mycobacterium chelonae and M. abscessus are two species that share the same 16S rRNA gene sequence, and since distinguishing these two species is clinically relevant, assays targeting base pair differences within the 16S-23S rRNA internal transcribed spacer (ITS) region have been developed (5
In vitro susceptibilities of 369 to 966 bacterial isolates from periodontal lesions to eight antibiotics were determined by agar dilution technique as a means of determining which antimicrobial agents were inhibitory for bacteria frequently associated with destructive periodontal diseases. Although most bacteria were relatively susceptible to the penicillins, greater activity was generally noted with amoxicillin than with either penicillin or ampicillin with the exception of Selenomonas sputigena and Peptostreptococcus. Antibacterial activities obtained with minocycline were significantly higher than with tetracycline for Actinobacillus actinomycetemcomitans and Streptococcus but comparable for most other taxa. Clindamycin and metronidazole both demonstrated excellent activity against the anaerobic Gram‐negative rods but were less effective against some of the capnophilic and facultative organisms. Eikenella corrodens was exceptionally resistant to both of these drugs; and A. actinomycetemcomitans was generally resistant to Clindamycin but relatively susceptible to metronidazole. Erythromycin was considerably less active than the other antibiotics against the majority of the periodontal bacteria. No single antibiotic, at concentrations equivalent to those achieved in body fluids, was uniformly effective in inhibiting all bacteria currently implicated or suspected as etiologic agents of periodontal diseases.
Recent studies show that CD4+CD25+Foxp3+ regulatory cells (Tregs) produce effector cytokines under inflammatory conditions. However, the direct role of microbial agents that serve as toll-like receptor (TLR) ligands in the induction of effector cytokines in Tregs is less clear. Here we show that CD4+Foxp3+Tregs produce the effector cytokine IL-17A during oropharyngeal candidiasis (OPC) and inflammatory bowel disease in a TLR-2/Myd88 signaling dependent manner. TLR-2 ligands promote proliferation in Tregs in the presence and absence of TCR signals and inflammatory cytokines in vitro. The proliferation is directly dependent on TLR-2 expression in Tregs. Consistent with this, Tlr2−/− mice harbor fewer thymically derived Tregs and peripheral Tregs under homeostatic conditions in vivo. However, under Th17 inducing conditions, IL-6 and TLR-2 signaling both in Tregs as well as antigen presenting cells (APC) are critical for maximal ROR-γt and IL-17A up-regulation in Foxp3+ Tregs. The minimal and transient loss of Foxp3 expression and suppressive properties are due to the presence of IL-6 in the milieu, but not the direct effect of TLR-2 signaling in Tregs. Taken together, our data reveal that TLR-2 signaling promotes not only proliferation, but also IL-17A in Tregs, depending on the cytokine milieu. These IL-17A producing Tregs may be relevant in mucosal infections and inflammation.
We have previously suggested that both the lower esophageal sphincter and diaphragm contribute to the high-pressure zone (HPZ) at the gastroesophageal junction. The purpose of this study in anesthetized cats was to compare changes in diaphragmatic electrical activity with changes in the intraluminal pressure profile in the HPZ following either balloon distension of the esophagus or swallowing evoked by pharyngeal stimulation. Intraluminal pressure was continuously recorded by a perfused manometric assembly anchored to the gastric fundus through an abdominal surgical approach. Integrated EMG was simultaneously measured in the costal and crural parts of the diaphragm. Our results indicate that simultaneous relaxation of the lower esophageal sphincter (LES) and crural diaphragm follows both swallowing and balloon distension of the esophagus; during swallowing both inhibitory reflexes depend on the initiation of esophageal peristalsis; crural relaxation abolishes respiratory-induced pressure oscillations in the HPZ during LES relaxation; ventilation is maintained during relaxation of the HPZ in part by continued contraction of the costal diaphragm; and different neural pathways control LES relaxation and crural relaxation. The data support the view that the crural diaphragm augments the intrinsic smooth muscle sphincter mechanism at the gastroesophageal junction and that crural relaxation may be an important factor in mouth-to-gastric transit.
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