Oral application of vancomycin alters murine lung microbiome and pulmonary immune responses.

Early life exposures to antibiotics negatively impact respiratory health and are associated with an increased risk of childhood asthma. It is explained that the lung is inclined to develop chronic inflammatory phenotypes due to early antibiotic alteration in the gut microbiome. We investigated whether a gut-targeted antibiotic has an impact on the lung microbiome and on pulmonary immunity. Fourteen-day old C57BL/6 mice were administered with vancomycin via oral gavage for 3 days (1 time/day). Control groups were treated with clarithromycin and phosphate-buffered saline (PBS), respectively. Five days after treatment, the cecum and lung microbiome, and pulmonary immune response were analyzed. Vancomycin treatment decreased the relative abundance of the genera Clostridium XIVa and Alistipes and the family Lachnospiraceae in the cecum. Furthermore, the relative abundance of the family Parabacteroidetes and the genus Lactobacillus were increased, whereas the abundance of the phylum Firmicutes was decreased. In the lung, vancomycin treatment reduced bacteria belonging to Clostridium XIVa and the family Lachnospiraceae as compared to those in the clarithromycin treated group. Lung cells from the vancomycin-treated mice released higher levels of interleukin (IL)-4 and IL-13 compared to those from the PBS group, and increased levels of IL-6, IFN-γ, and TNFα compared to lung cells from the clarithromycin and PBS treated mice. Our pilot study suggests that alteration in the gut microbiome could affect bacterial composition and immunity of the lung hence proposes a gut-lung microbiome axis in early life.

Flucloxacillin-induced immune thrombocytopenia.

BACKGROUND: Drug-induced immune thrombocytopenia (DITP) is an adverse drug reaction associated with platelet (PLT) destruction by drug-dependent antibodies. Demonstration of drug-dependent PLT antibodies is often difficult and can only be rendered by extensive laboratory testing. In this report, we present the first serologically confirmed case of DITP caused by the antibiotic flucloxacillin. CASE REPORT: A 68-year-old man developed severe thrombocytopenia that was first suspected to be related to heparin-induced thrombocytopenia. The absence of PLT-activating heparin-dependent antibodies and the abrupt decrease in PLT count to fewer than 20 × 10(9) /L raised the suspicion of DITP. DISCUSSION: Flucloxacillin-dependent antibodies were detected in patient serum using whole PLT enzyme immunoassay and flow cytometry. The glycoprotein (GP) specificity was identified to be against GP IIb/IIIa complexes using the monoclonal antibody immobilization of PLT antigens assay. Interestingly, antibody binding was abolished when EDTA plasma was used and restored after adding calcium. CONCLUSION: In summary, DITP should be considered in cases of acute thrombocytopenia during treatment with flucloxacillin.