Live Flu Vaccines Increase Infectious Bacteria Counts 100-Fold in Mice

Live Flu Vaccines Increase Infectious Bacteria Counts 100-Fold in Mice

If presumably safer "attenuated" flu vaccines are supposed to protect against influenza and its sometimes deadly complications, then why do vaccinated mice have up to 100-fold higher levels of flu-associated pathogenic bacteria than non-vaccinated mice? 

A concerning new study published in mBio, an open access journal of the American Society of Microbiology, titled, "Live Attenuated Influenza Vaccine Enhances Colonization of Streptococcus pneumoniae and Staphylococcus aureus in Mice," reveals that live attenuated influenza vaccines (LAIVs) lead to the rapid and sustained overgrowth of pathogenic bacteria in the upper respiratory tract of mice at colonization densities up to 100-fold higher than non-vaccinated mice.

This is the first study of its kind to demonstrate that vaccination with a live attenuated viral vaccine can dramatically alter the colonization behavior of human bacterial pathogens in a manner very similar to that following infection from 'wild-type', i.e. naturally circulating, flu infections. 

Influenza infection is well known to contribute to serious health complications, but this is the first time that a vaccine strain of flu has been found to induce similar alterations in disease-linked bacteria.

The authors describe the typical adverse effects of influenza infection:

"Infection with influenza viruses increases susceptibility to severe lower and upper respiratory tract (LRT and URT, respectively) bacterial infections resulting in complications, such as pneumonia, bacteremia, sinusitis, and acute otitis media (11). Bacterial infections may be a primary cause of mortality associated with influenza virus infection in the absence of preexisting comorbidity (12, 13). Primary influenza virus infection increases acquisition, colonization, and transmission of bacterial pathogens (14), most notably the pneumococcus Streptococcus pneumoniae and Staphylococcus aureus (11, 15)."

Because secondary bacterial infections following influenza infection are the main cause of harm and even death commonly attributed to influenza itself, these findings may have broad implications for immunization policies that, at present, do not take into account that, while vaccines may reduce the risk of one infectious disease, they may be increasing the risk of other equally, or more, concerning pathogens.

The authors discuss the possible mechanisms through which influenza may influence increased disease susceptibility:

"Although the underlying mechanisms, while well studied, are not entirely defined, they likely include a combination of influenza virus-mediated cytotoxic breakdown of mucosal and epithelial barriers (16–18) and aberrant innate immune responses to bacterial invaders in the immediate postinfluenza state, characterized by uncontrolled pro- and anti-inflammatory cytokine production, excessive leukocyte recruitment, and extensive immunopathology (11, 19–22). When coupled with diminished epithelial and mucosal defenses, such an environment becomes increasingly hospitable for bacterial pathogens to flourish and invade in the days and first few weeks following influenza virus infection."

The researchers emphasized the importance of their finding insofar as, "Influenza infection causes individuals to become transiently susceptible to excess bacterial infections, particularly Streptococcus pneumoniae and Staphylococcus aureus."

Because, "bacterial infections are a leading cause of severe disease during influenza epidemics," the implication is that the immune-altering effects of live flu vaccines may include suppressing innate immune defenses, making the host more susceptible to the very secondary bacteria infections most likely to cause flu-associated harm. 

In addition to finding that live attenuated influenza vaccines prime the upper respiratory tract for increased bacterial growth, they found an increase in the persistence of bacterial carriage, also in a manner nearly identical to that seen following wild-type influenza virus infections.  Even 28 days following LAIV vaccination, far after viral clearance from the nasopharyngeal tract was complete (approximately 7 days after the vaccine), mice saw excess bacterial proliferation relative to PBS controls between 2- to 4-fold higher between days 1 and 3 post-infection.

While the researchers did not find that LAIVs increased morbidity or mortality associated with bacterial disease of the lower respiratory tract of the mice, they cautioned:

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