[Paris meeting of pediatrics. Group of Biology Applied to Pediatrics. Paris 14 October 1978. Abstracts].
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The emergence of aztreonam-avibactam resistance among NDM-producing Escherichia coli represents a major therapeutic and infection control concern. Four cases of aztreonam-avibactam-resistant (AZAR) NDM-producing E. coli, recovered from three blood cultures and one rectal surveillance culture in a hospital of Paris, prompted an investigation based on whole-genome sequencing. The three isolates responsible for bloodstream infection, which were clonally related, belonged to the ST405 and produced NDM-5, DHA-1, CTX-M-15, and TEM-1 β-lactamases. They also had a penicillin-binding protein 3 (PBP3) modified by the insertion of four amino acids (YRIK). On the other hand, the isolate recovered from the rectal swab belonged to another sequence type (ST2083). It produced NDM-5, CMY-42, and TEM-1 β-lactamases and had an altered PBP3 by the insertion of four other residues (YRIN). Epidemiological investigation identified endoscopic retrograde cholangiopancreatography as a potential risk factor, leading to the detection of three additional patients infected with the ST405 clone after exposure to the same duodenoscope. The outcome of the bloodstream infections was favorable except for one patient. In total, seven patients infected or colonized by AZAR NDM-5-producing E. coli were identified over a 5-month period in 2025, six with duodenoscope exposure.IMPORTANCEThis study underlines the emergence of aztreonam-avibactam resistance among NDM-producing Escherichia coli isolates in France. To our knowledge, this report describes the first clonal outbreak due to aztreonam-avibactam-resistant NDM-producing E. coli.
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Unilateral, intraorganal injection of parental lymph node cells into thyroid lobes of F1 hybrid rats elicited an intense, local graft-versus-host reaction within the injected lobes containing massive numbers of lymphocytes. Surprisingly, significant mononuclear cell infiltration was also seen within the contralateral (noninjected) thyroid lobes, even when the isthmus had been divided. The local graft-versus-host reaction spread from the injected gland to involve the regional lymph nodes and spleen. Migration of 51-cr-labeled donor lymph node cells was documented in these same tissue sites; lesser numbers of labeled cells were found in distant lymph nodes, including the contralateral cervical nodes. However, no significant label was found in the contralateral thyroid lobes. Microscopic evaluation of noninjected glands revealed intense infiltration of mononuclear cells around and within follicles, reminiscent of lesions induced by immunization with thyroid extract in Freund's complete adjuvant. The absence of donor cells in the inflammatory reactions within noninjected thyroid lobes raises the possibility of an autoimmune rather than graft-versus-host pathogenesis.
An enzymatic and immunologic study of 18 patients with trichinosis leads to the following conclusions: The stage of muscular invasion in trichinosis is accompanied by a release of cellular enzymes representative of striated muscle fibres in nearly all the cases. This release can be observed by a study of the LDH iso-enzymes at a time when immunological techniques are not always significantly positive. The specific aspect of this phenomenon can be proposed with reservations since there does not exist any interference with other enzymatic systems such as the gamma-GT and furthermore no other evident cause of muscular lysis is present. The existence of a blood hypereosinophilia completes the biological picture. These early modifications of the enzymatic activities are most probably transient.
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