#FEMSmicroBlog: When two pathogens interact in one host


Bacteria have the ability to complicate viral infections. The mechanisms responsible for co-infection by two pathogens in one host, and the increased disease severity, have been extensively described. The commentary “Bacterial-Viral Interactions: A Factor That Facilitates Transmission Heterogeneities” in FEMS Microbes explores the mechanisms behind the pathogens’ abilities to influence each other’s shedding. Emilia Bianchini and Richard A. Stein explain for the #FEMSmicroBlog how a better understanding of these interactions may help us limit the transmission of infectious microbes. #FascinatingMicrobes


What is transmission heterogeneity?

When two pathogens interact with each other in the same host, they can enhance each other’s dispersion. Such interaction can contribute to transmission heterogeneities; meaning that an infected individual contributes to more secondary contacts than other infected individuals.

This phenomenon is becoming increasingly recognized while it is not well understood yet. Examples of such interactions are those between two viruses, a bacterium and a virus, or a bacterium and a helminth (parasitic worm).

When two pathogens interact within one host, they can enhance each other’s dispersion leading to more secondary infections.

In humans, the interactions between a bacterium and a virus were described in the context of upper respiratory and urogenital tract infections. For example, a landmark 1960 study investigated infants that were infected with a respiratory virus and Staphylococci bacteria. Interestingly, some of these infants dispersed more Staphylococci from their upper respiratory tract into the air.

This observation became known as the “cloud baby” phenomenon and is not limited to humans. For instance, a 1941 study reported that ferrets infected with the influenza virus shed large numbers of Streptococci.


Two pathogens, one host, different hypotheses

The cellular and molecular mechanisms that explain the enhanced dispersion as a result of bacterial-viral interactions are not well understood. It is possible that the viral infection may increase the number of bacteria or change the characteristics of the mucous that covers the epithelial surface.

One hypothesis is that the swelling of the nasal epithelium during a viral infection may create turbulent airflow and aerosolize bacteria that colonize the nasal lining. This is supported by the enhanced bacterial dispersal observed in some people with allergic rhinitis.

Another hypothesis is that one pathogen elicits an immune response that impairs or delays the clearing of the other pathogen. Yet another hypothesis is that bacterial components could activate inflammatory signaling pathways and enhance viral replication.


Super-spreading events increase transmission

Transmission heterogeneities were described in many infectious diseases, including SARS, COVID-19, influenza, malaria, Ebola hemorrhagic fever, and measles. While the spread of a pathogen was long believed to be homogeneous in a population, transmission heterogeneities are now increasingly recognized as an important contributor to the population-level dynamics of outbreaks.

In super-spreading events, 20% of infected hosts are responsible for 80% of pathogen transmission.

Extreme cases of transmission heterogeneities are called “super-spreading events”. A quantitative expression of this phenomenon is provided by the 20/80 rule. This statistical pattern states that about 20% of hosts in a population contribute to about 80% of the transmission.

Hence, effective infection-control programs should aim to target those 20% of infected hosts causing super-spreading events. The effectiveness of such outbreak-control measures was confirmed in animal studies.


Different factors leading to super-spreading events

As the commentary “Bacterial-Viral Interactions: A Factor That Facilitates Transmission Heterogeneities” in FEMS Microbes presents, many factors are responsible for transmission heterogeneities and super-spreading events. Most of these depend on the pathogen, the host and/or the external environment. Bacterial-viral interactions represent just one of the many ways in which these heterogeneities may be generated, and are an important component to understanding disease outbreaks.

The commentary in FEMS Microbes explains that we need to better understand the mechanisms involved in transmission heterogeneities.

The commentary explains that we need to better understand the mechanisms involved in transmission heterogeneities. This will help us put together a framework based on outbreaks and in-depth analyses of a multitude of mechanisms. Infectious disease outbreaks can thus be managed better, resulting in improved scientific, medical and public health results.


About the authors of this blog

Emilia Bianchini graduated from NYU Tandon School of Engineering with an BSc undergraduate degree in Biomolecular Science in May 2022. Emilia will return to the Tandon School of Engineering in September 2022 to complete a MSc graduate degree in Biomedical Engineering. She enjoys reading, exploring new places, and spending time with her pets.

Richard A. Stein is an Industry Associate Professor at NYU Tandon School of Engineering. He holds an MD from the “Iuliu Haţieganu” University of Medicine and Pharmacy, Cluj-Napoca, Romania, and a PhD in Biochemistry from the University of Alabama at Birmingham. Richard is interested in understanding the spread of infectious diseases in populations. He likes traveling, volunteering at animal shelters, and climbing volcanoes.

About this blog section

The section #FascinatingMicrobes for the #FEMSmicroBlog explains the science behind a paper and highlights the significance and broader context of a recent finding. One of the main goals is to share the fascinating spectrum of microbes across all fields of microbiology.

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