SUMMARY Decreases in the diversity of enteric bacterial populations are observed in patients with Crohn’s disease (CD) and ulcerative colitis (UC). Less is known about the virome in these diseases. We show that the enteric virome is abnormal in CD and UC patients. In-depth analysis of preparations enriched for free virions in the intestine revealed that CD and UC were associated with a significant expansion of Caudovirales bacteriophages. The viromes of CD and UC patients were disease- and cohort-specific. Importantly, it did not appear that expansion and diversification of the enteric virome was secondary to changes in bacterial populations. These data support a model in which changes in the virome may contribute to intestinal inflammation and bacterial dysbiosis. We conclude that the virome is a candidate for contributing to, or being a biomarker for, human inflammatory bowel disease and speculate that the enteric virome may play a role in other diseases.

Summary Autophagy is a lysosomal degradation pathway that is important in cellular homeostasis. Prior work showed a key role for the autophagy related 5 (Atg5) in resistance to Toxoplasma gondii. Here we show that the cassette of autophagy proteins involved in the conjugation of microtubule associated protein 1 light chain 3 (LC3) to phosphatidylethanolamine, including Atg7, Atg3, and the Atg12-Atg5-Atg16L1 complex play crucial roles in the control of T. gondii in vitro and in vivo. In contrast, pharmacologic modulation of the degradative autophagy pathway or genetic deletion of other essential autophagy genes had no substantial effects. Rather the conjugation system was required for targeting of LC3 and interferon-γ effectors onto the vacuolar membrane of T. gondii and its consequent disruption. These data suggest that the ubiquitin-like conjugation systems that reorganize intracellular membranes during canonical autophagy are necessary for proper targeting of immune effectors to the intracellular vacuole membranes utilized by pathogens.

We report two fatal cases of rhino-orbital-cerebral mucormycosis associated with COVID-19 infection. Both patients had pre-existing diabetes mellitus type 2, were treated with corticosteroids, and developed ketoacidosis. Both patients rapidly declined owing to rapid extension of the infection into the intracranial cavity. We postulate that additional risk factors for opportunistic fungal infection exist in COVID-19 patients including mechanical ventilation and Sars-CoV-2 induced immunosuppression. The ophthalmologist's role is particularly important in the early diagnosis of mucormycosis associated with COVID-19.

Butane-oxidizing Arthrobacter (ATCC 27778) bacteria were shown to degrade low concentrations of methyl t-butyl ether (MTBE; range, 100 to 800 g/liter) with an apparent half-saturation concentration (K s ) of 2.14 mg/liter and a maximum substrate utilization rate (k c ) of 0.43 mg/mg of total suspended solids per day. Arthrobacter bacteria demonstrated MTBE degradation activity when grown on butane but not when grown on glucose, butanol, or tryptose phosphate broth. The presence of butane, tert-butyl alcohol, or acetylene had a negative impact on the MTBE degradation rate. Neither Methylosinus trichosporium OB3b nor Streptomyces griseus was able to cometabolize MTBE.The prevalent use of methyl t-butyl ether (MTBE) for gasoline oxygenation has led to its introduction into groundwater from spills and leaky underground storage tanks. MTBE is poorly adsorbed, chemically and biologically stable, and very soluble in water, making it very mobile and persistent in the environment. The U.S. Environmental Protection Agency has recently proposed scaling back the use of MTBE in gasoline in light of the increasing frequency with which MTBE is found as a groundwater contaminant nationwide (16; http://www.epa.gov /swerust1/mtbe/browner.pdf). Concentrations of MTBE in groundwater have been reported to range from 0.5 g/liter to Ͼ10 mg/liter. At least 20 states have established MTBE groundwater cleanup levels ranging from 20 to 400 g/liter for groundwater for potable use (http://www.epa.gov/OUST/mtbe /sumtable.htm). The U.S. Environmental Protection Agency has established a health advisory level of 20 to 40 g/liter for MTBE in drinking water (19).Efforts to develop bioremediation processes to help combat MTBE contamination of groundwater have been hampered by the recalcitrance of MTBE. The highly branched nature of MTBE resists most bacterial enzymatic attacks. Only a few pure and mixed bacterial cultures that are able to biodegrade MTBE have been identified (4,6,7,8,17).One potential MTBE biodegradation pathway involves the demethylation of MTBE to form tert-butyl alcohol (TBA) and formaldehyde (11, 17; K. L. Hurt, J. T. Wilson, and J. S. Cho, 5th Int. In Situ On-Site Bioremediation Symp., 1999), although the formation of tert-butyl formate from MTBE has also been observed (8). tert-Butyl formate is then hydrolyzed into TBA. In general, TBA is the first stable metabolite of MTBE, regardless of the type of bacterial cultures used. Hyman et al. (8) presented evidence that TBA is degraded by the same enzyme that degrades MTBE, although a soil microcosm was identified that was able to biodegrade TBA but not MTBE (M. J. Zenker, R. C. Borden, and M. A. Barlaz, 5th Int. In Situ On-Site Bioremediation Symp., 1999). TBA is biodegraded at a slower rate than MTBE (8, 17); thus, it tends to build up over time. If TBA is indeed degraded by the same enzyme that degrades MTBE, then the accumulation of TBA can have a detrimental effect on the MTBE biodegradation rate as a result of enzyme competition. Consequently, the effects of TBA on MTBE b...