Research

Elucidating the physics of pathogen-laden respiratory droplet formation

Human respiratory tract is a complicated network of cavities and airways covered with mucosalivary fluid whose fragmentation during respiratory activities (e.g., coughing, talking, etc.) yields micron size droplets. If emitted from an infected individual, these pathogen-laden respiratory droplets (PRDs) can spread pathogens in the air. But the physics of their formation in respiratory tract remains unclear, hindering answers to several important questions: What is the relative contribution of each respiratory activity to disease transmission? What distinguishes superspreaders from the rest of infected population? What physiological factors contribute to the heterogeneity of superemitters in droplet emission? Do asymptomatic patients emit more droplets than the healthy individuals? What is the pathogen load of the PRDs? To answer these and similar questions, we design experimental devices and perform human experiments that help understand the mechanisms and parameters governing PRD formation in different locations in the respiratory tract including bronchiolar airways, trachea, larynx, and oral cavity. The results of this project aim to resolve the prolonged controversy over the relative contribution of different respiratory activities to disease transmission and provide an explanation for the existence of superemitters and their potential connection to superspreaders.

Single-droplet analysis platform for size-resolved bioaerosol composition measurement

Infection via inhalation of bioaerosols is a known route for disease transmission. Yet, accurately assessing the risk they pose requires knowledge about their pathogen load. In the context of disease transmission via PRDs, the number of pathogens in a single PRD is Np = V Cp, where V is the PRD volume and Cp is pathogen concentration in the respiratory fluid (i.e., PFU per ml of respiratory fluid). The gold standard to calculate Cp is plaque assay of nasal/oral respiratory fluid samples. However, this approach is highly sensitive to sampling location and technique and numbers may differ by orders of magnitude. Moreover, the conventional method assumes a linear correlation between PRD volume and pathogen load, implying that larger PRDs, such as those generated from a sneeze, carry more pathogens. Contrarily, depending on the site of PRD formation and the type of infection, smaller PRDs (e.g., those generated in bronchioles) may carry even more pathogens. In our lab, we combine the principles of aerosol science, droplet microfluidics, complex fluids, and virology to develop a single-droplet analysis platform to measure size-resolved composition of bioaerosols including their pathogen load. This information is critical for accurately assessing infection risk and implementing appropriate control measures.

Pathogen aerosolization from contaminated surfaces (aerosolized fomites)

Using a guinea pig model of influenza, we recently provided the first experimental evidence for a new mode of influenza virus transport via 'aerosolized fomites' (i.e., non-respiratory infectious particles aerosolized from contaminated surfaces). Surprisingly, we found that 99% of the emissions from a guinea pig cage are non-respiratory in origin, challenging previous animal studies suggesting airborne transmission occurs entirely via PRDs. More importantly, we demonstrated that an uninfected, virus-immune guinea pig, whose body is contaminated with influenza virus, can transmit the virus through the air to a susceptible partner in a separate cage, in the absence of PRDs. In our lab, we investigate how this finding translates to airborne infectious disease transmission among humans. The key questions are: what are the sources of aerosolized fomites indoors? how important are they compared to transmission via PRDs? can aerosolized fomites contribute to a higher rate of nosocomial infections or transmission in schools?

Aerosolization of pathogens from plant leaf surfaces is thought to contribute to the onset of airborne plant disease outbreaks, posing an escalating threat to the global food supply. It is believed that most bacteria that invade foliage and fungal spores spread between plants (interplant) or between leaves on the same plant (intra-plant) via wind currents, raindrop splashing, and soil dust. The impact of raindrops on an infected leaf could induce pathogen aerosolization, allowing it to travel significant distances in the atmosphere via wind. Climate-induced changes in temperature and humidity conditions may potentially worsen the development of infections. However, the impact of these factors on pathogen aerosolization from leaf surfaces, its viability in the air, and its transmission to other plants remains poorly understood. In our lab, we are also interested in exploring the dynamics of pathogen aerosolization from infected leaf surfaces and the factors shaping airborne plant disease transmission.