Objective: Rare disease Background: Chryseobacterium gleum (C. gleum) is a rare but concerning device-associated infection that can cause urinary tract infections and pneumonia. It produces a biofilm and has intrinsic resistance to a wide array of broadspectrum agents. Risk factors include neonate or immunocompromised states, intensive care unit admission for more than 21 days, broad-spectrum antibiotic exposure, indwelling devices, and mechanical ventilation. Case Report: A 61-year-old cachectic man presented in the United States with community-acquired pneumonia and immediately decompensated, requiring ventilator support. Despite starting broad-spectrum antibiotics, the patient developed fever, leukocytosis, and additional desaturation episodes. The patient's respiratory culture grew numerous C. gleum and few Stenotrophomonas (Xanthomonas) maltophilia. He also had a positive urine streptococcal pneumonia antigen. Broad-spectrum agents were discontinued after prolonged treatment due to a continued worsening clinical picture, and the patient was started on trimethoprim-sulfamethoxazole to cover C. gleum. The patient showed rapid clinical improvement on trimethoprim-sulfamethoxazole, with resolution of symptoms on post-discharge follow-up. Conclusions: To the best of our knowledge, this is the first case report of a documented case of a patient with C. gleum respiratory infection successfully treated solely with trimethoprim-sulfamethoxazole. The expedient identification of C. gleum is essential for proper treatment. The literature has consistently shown isolated respiratory C. gleum strains to be largely susceptible to fluoroquinolones, piperacillin-tazobactam, or trimethoprim-sulfamethoxazole.

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IntroductionResults from recent studies have suggested a role for protease inhibitors in altering mechanisms involved in the initiation and proliferation of cancer cells. One such inhibitor, indinavir, may act as an anti-cancer agent by modulating the alpha-7-nicotinic acetylcholine receptor, which is a pro-carcinogenic protein that has been researched in conjunction with nicotine in lung cancer development. In our study, we compare indinavir's binding affinity towards α7-nAchR and MMP-2, another promoter of malignancy, to determine what extracellular effects the drug has before being internalized to inhibit HIV-1 protease.MethodsA computer program, PyRx, was used to compare indinavir's binding affinity with digital models for α7-nAchR, MMP-2 and HIV-1 protease, which were then compared to the results of in vitro binding assays for these targets.ResultsPyRx testing predicted the highest binding affinity values for indinavir to MMP-2 (mean = 8.77 kcal/mol, S.D. = 0.29), followed by the α7-nAchR (mean = 8.53 kcal/mol, S.D. = 0.15) and HIV-1 protease (mean = 7.5 kcal/mol, S.D. = 0.44). In vitro, indinavir's mean percent inhibition of control values were 103.2 for HIV-1 protease, 5.3 for MMP-2, and 7.7 for the α7-nAchR.ConclusionsBinding affinity values for indinavir to MMP-2 and α7-nAchR were not significantly different. Using PyRx to predict affinity compared with in vitro testing did not yield comparable results. However, indinavir was shown to slightly inhibit both α7-nAchR and MMP-2, which may have ramifications in the drug's delivery to the intracellularly located HIV-1 protease.

Figure 1. Forest plot of symptoms (A) and autoimmune conditions (B) in gender based-celiac disease patients. All P-values are , 0.0001 unless stated otherwise. Univariate analysis used to

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