Abstract
The host-to-host transmission of respiratory infectious diseases is fundamentally enabled by the interaction of pathogens with a variety of fluids (gas or liquid) that shape pathogen encapsulation and emission, transport and persistence in the environment, and new host invasion and infection. Deciphering the mechanisms and fluid properties that govern and promote these steps of pathogen transmission will enable better risk assessment and infection control strategies, and may reveal previously underappreciated ways in which the pathogens might actually adapt to or manipulate the physical and chemical characteristics of these carrier fluids to benefit their own transmission. In this article, I review our current understanding of the mechanisms shaping the fluid dynamics of respiratory infectious diseases.
Highlights
Mucosalivary fluid (MS) is composed mostly of water (99.5%) and a mixture of proteins (0.3%) and inorganic and trace substances (0.2%)
While the extensive work by the Flügge school established a nuanced understanding of respiratory infectious disease transmission in TB, it was soon erroneously reduced to the notion that only ballistic droplet emissions that remain in the liquid state are the major route of respiratory infectious disease transmission
In the context of respiratory diseases, the generation of mucosalivary droplets and their emission as part of a multiphase turbulent gas cloud, coupled to their evolution in the environment through multiphase droplet and phase-change physics of evaporation and condensation, determine the nature, composition, and size of the droplets or the droplet nuclei/residue inhaled by a potential host
Summary
The notion that diseases could be contracted through inhalation of so-called bad air dates back millennia and was the foundation of the long-held miasma theory, which posited that epidemics spread through the inhalation of noxious vapors originating from decomposing matter. Here, and contrary to today’s nomenclature of droplets versus aerosols, Flügge termed all respiratory emissions “droplets,” irrespective of their size and final state (liquid droplet or droplet residue/aerosol), as long as they were not yet deposited In these experiments, collection was done hours after emission, allowing ample settling to occur and not differentiating between liquid and dried droplets. While the extensive work by the Flügge school established a nuanced understanding of respiratory infectious disease transmission in TB, it was soon erroneously reduced to the notion that only ballistic (large) droplet emissions that remain in the liquid state are the major route of respiratory infectious disease transmission This dramatic reduction changed the view of respiratory infectious disease transmission from the airborne dry resuspended dust route to that of ballistic liquid droplet infection [32, 33]. The problem with this dichotomy, as we know, is that it is false
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