Sharing a Host Plant (Wheat [Triticum aestivum]) Increases the Fitness of Fusarium graminearum and the Severity of Fusarium Head Blight but Reduces the Fitness of Grain Aphids (Sitobion avenae).

We hypothesized that interactions between fusarium head blight-causing pathogens and herbivores are likely to occur because they share wheat as a host plant. Our aim was to investigate the interactions between the grain aphid, Sitobion avenae, and Fusarium graminearum on wheat ears and the role that host volatile chemicals play in mediating interactions. Wheat ears were treated with aphids and F. graminearum inoculum, together or separately, and disease progress was monitored by visual assessment and by quantification of pathogen DNA and mycotoxins. Plants exposed to both aphids and F. graminearum inoculum showed accelerated disease progression, with a 2-fold increase in disease severity and 5-fold increase in mycotoxin accumulation over those of plants treated only with F. graminearum. Furthermore, the longer the period of aphid colonization of the host prior to inoculation with F. graminearum, the greater the amount of pathogen DNA that accumulated. Headspace samples of plant volatiles were collected for use in aphid olfactometer assays and were analyzed by gas chromatography-mass spectrometry (GC-MS) and GC-coupled electroantennography. Disease-induced plant volatiles were repellent to aphids, and 2-pentadecanone was the key semiochemical underpinning the repellent effect. We measured aphid survival and fecundity on infected wheat ears and found that both were markedly reduced on infected ears. Thus, interactions between F. graminearum and grain aphids on wheat ears benefit the pathogen at the expense of the pest. Our findings have important consequences for disease epidemiology, because we show increased spread and development of host disease, together with greater disease severity and greater accumulation of pathogen DNA and mycotoxin, when aphids are present.

Probability and estimated risk of SARS-CoV-2 transmission in the air travel system.

BACKGROUND: As an emerging virus, SARS-CoV-2 and the risk of transmission during air travel is of high interest. This paper is a retrospective estimate of the probability of an infectious passenger in the air travel system transmitting the SARS-CoV-2 virus to a fellow passenger. METHODS: Literature was reviewed from May-September 2020 to identify COVID-19 cases related to air travel. The studies were limited to publicly available literature for passengers; studies of flight crews were not reviewed. A novel quantitative approach was developed to estimate air travel transmission risk that considers secondary cases, the overall passenger population, and correction factors for asymptomatic transmission and underreporting. RESULTS: There were at least 2866 index infectious passengers documented to have passed through the air travel system in a 1.4 billion passenger population. Using correction factors, the global risk of transmission during air travel is estimated at 1:1.7 million; acknowledging that assumptions exist around case detection rate and mass screenings. Uncertainty in the correction factors and a 95% credible interval indicate risk ranges from 1 case for every 712,000 travelers to 1 case for every 8 million travelers. CONCLUSION: The risk of COVID-19 transmission on an aircraft is low, even with infectious persons onboard.

Computational fluid dynamics modeling of cough transport in an aircraft cabin.

To characterize the transport of respiratory pathogens during commercial air travel, Computational Fluid Dynamics simulations were performed to track particles expelled by coughing by a passenger assigned to different seats on a Boeing 737 aircraft. Simulation data were post-processed to calculate the amounts of particles inhaled by nearby passengers. Different airflow rates were used, as well as different initial conditions to account for random fluctuations of the flow field. Overall, 80% of the particles were removed from the cabin in 1.3-2.6 min, depending on conditions, and 95% of the particles were removed in 2.4-4.6 min. Reducing airflow increased particle dispersion throughout the cabin but did not increase the highest exposure of nearby passengers. The highest exposure was 0.3% of the nonvolatile mass expelled by the cough, and the median exposure for seats within 3 feet of the cough discharge was 0.1%, which was in line with recent experimental testing.

Effect of aircraft-cabin altitude on passenger discomfort.

BACKGROUND: Acute mountain sickness occurs in some unacclimatized persons who travel to terrestrial altitudes at which barometric pressures are the same as those in commercial aircraft during flight. Whether the effects are similar in air travelers is unknown. METHODS: We conducted a prospective, single-blind, controlled hypobaric-chamber study of adult volunteers to determine the effect of barometric pressures equivalent to terrestrial altitudes of 650, 4000, 6000, 7000, and 8000 ft (198, 1219, 1829, 2134, and 2438 m, respectively) above sea level on arterial oxygen saturation and the occurrence of acute mountain sickness and discomfort as measured by responses to the Environmental Symptoms Questionnaire IV during a 20-hour simulated flight. RESULTS: Among the 502 study participants, the mean oxygen saturation decreased with increasing altitude, with a maximum decrease of 4.4 percentage points (95% confidence interval, 3.9 to 4.9) at 8000 ft. Overall, acute mountain sickness occurred in 7.4% of the participants, but its frequency did not vary significantly among the altitudes studied. The frequency of reported discomfort increased with increasing altitude and decreasing oxygen saturation and was greater at 7000 to 8000 ft than at all the lower altitudes combined. Differences became apparent after 3 to 9 hours of exposure. Persons older than 60 years of age were less likely than younger persons and men were less likely than women to report discomfort. Four serious adverse events, 1 of which may have been related to the study exposures, and 15 adverse events, 9 of which were related to study exposures, were reported. CONCLUSIONS: Ascent from ground level to the conditions of 7000 to 8000 ft lowered oxygen saturation by approximately 4 percentage points. This level of hypoxemia was insufficient to affect the occurrence of acute mountain sickness but did contribute to the increased frequency of reports of discomfort in unacclimatized participants after 3 to 9 hours. (ClinicalTrials.gov number, NCT00326703 [ClinicalTrials.gov].).

Sleep at simulated 2438 m: effects on oxygenation, sleep quality, and postsleep performance.

INTRODUCTION: Crewmembers on ultra long-range commercial flights have the opportunity for rest and sleep in onboard areas in which the barometric pressure is 75.3 kPa (565 mmHg) or higher, equivalent to a terrestrial altitude of 2438 m (8000 ft) or lower. Sleep at higher altitudes is known to be disturbed, resulting in postsleep neurobehavioral performance decrements. We investigated the effects of sleep at 2438 m on oxygen saturation, heart rate, sleep quantity, sleep quality, postsleep neurobehavioral performance, and mood. METHODS: Twenty men, 30-56 yr of age, participated in a blinded cross-over investigation conducted in a hypobaric chamber to compare the effects of sleep at altitude (ALT, 2438 m) and ground level (GND, 305 m). RESULTS: SpO2 measured before sleep was significantly lower at ALT than at GND, 90.7 +/- 2.0% (average +/- SD) and 96.2 +/- 2.0%, respectively. During sleep, SpO2 decreased further to 86.1 +/- 2.0% at ALT, and 92.3% +/- 2.0% at GND. The percent of time during which SpO2 was below 90% was 44.4% (3.6-86.9%) at ALT and 0.1% (0.0-22.9%) at GND. Objective and subjective measurements of sleep quantity and quality did not differ significantly with altitude, nor did postsleep neurobehavioral performance or mood. DISCUSSION: The absence of significant changes in sleep and post-sleep neurobehavioral performance associated with pronounced oxygen desaturation during sleep was unexpected. Further study is needed to determine if the same effects occur in women and to characterize the changes in respiratory physiology that occur during sleep at 2438 m in both sexes.

A selective reversible monoamine oxidase B inhibitor in smoking cessation: effects on its own and in association with transdermal nicotine patch.

RATIONALE: Monoamine oxidase B (MAO-B) activity is reduced in smokers. A MAO-B inhibitor alone or co-administered with nicotine may mimic the effects of smoking and be a candidate drug for smoking cessation. OBJECTIVE: This study aims to determine the efficacy and safety of EVT302, a selective reversible MAO-B inhibitor, alone and on top of nicotine patch (NP) in smoking cessation. METHODS: This was a randomised, double blind, placebo-controlled phase II, multicentre trial. Smokers (≥10 cigarettes/day) received either EVT302 (N = 145) or placebo (N = 145), or EVT302 (N = 61) or placebo (N = 61) on top of open label NP 21 mg/day for 8 weeks. The main comparison was between EVT302 and placebo without NP. The primary outcome measure was end-of-treatment 4-week continuous abstinence rate (CAR). SECONDARY OUTCOME MEASURES: point prevalence abstinence rate, saliva cotinine concentrations in the groups without NP, urge to smoke, nicotine withdrawal symptoms and assessment of subjective effects of cigarettes. RESULTS: The 4-week CAR was 15.2 % in the placebo, 17.2 % in the EVT302, 26.8 % in the NP + placebo and 32.8 % in the NP + EVT302 groups, respectively. There was no difference between EVT302 and placebo either alone (adjusted OR: 1.45, 95 % CI: 0.65-3.26) or when co-administered with NP. No statistically significant difference occurred for the secondary outcome measures. CONCLUSIONS: The selective, reversible MAO-B inhibitor EVT302 was not superior to placebo in helping smokers quit, in line with data with selegiline and confirms that MAO-B inhibitors are not effective in smoking cessation. Co-administration of NP does not provide a supplementary benefit.