In Part I , we took a look at news articles and data on the increase of scarlet fever in the UK, whilst adding in articles that showed that the LAIV (Live Attenuated Influenza Vaccine) aka the nasal flu shot, has been steadily increased in the UK, in the same time period.
Is it possible that the nasal flu vaccine could somehow result in scarlet fever? Let’s take a look at research for any connections.
Probably the first fact that needs to be illustrated is - Influenza infections increase host susceptibility to bacterial infections in a variety of ways
With influenza, the one we hear about often is pneumonia. In 1918, that seems to have been the pattern, that bacteria, not flu, killed millions . Back to scarlet fever. When penicillin was discovered, the cases and death numbers fell and kept falling. Scarlet fever develops from the organism, S pyogenes, which is classified as a Group A beta-hemolytic streptococcal (GABHS) infection. "Thus, as in the cases of S. pneumoniae and S. aureus, S. pyogenes acts synergistically with influenza viruses and possibly other respiratory viruses in causing secondary bacterial infections. Enhanced adherence and internalization of S. pyogenes to host cells in the presence of influenza virus infection may explain the synergism. 94,95,96
Any form of S. pyogenes infection may potentially lead to systemic manifestations due to release of toxins or superantigens. Scarlet fever typically follows an episode of upper respiratory tract infection,"
Vintage illustration online here and our thanks.
To examine how viral infections and host antiviral immune responses alter the upper respiratory microbiota...following instillation of live attenuated influenza vaccine ...
We found that live attenuated influenza vaccination led to significant changes in microbial community structure, diversity, and core taxonomic membership....The core membership expanded after LAIV administration to include Streptococcus and Bacillales, among others....LAIV administration was associated with clinically meaningful changes in nasal epithelial gene expression that mirrored those expected of natural influenza infection, including activation of interferon-stimulated pathways, which have recently been implicated in diminished antibacterial activity and enhanced bacterial colonization.......Interestingly, we also observed the emergence of Bacteroides, an obligate anaerobe, after intervention in the LAIV group. While the absolute change was statistically significant in that group, the relative abundances were low, and the clinical relevance of this finding in the respiratory tract is not clear. However, these gram-negative microorganisms are typically noted to be anaerobic and associated with the gut microbiota where they can influence the host immune system and play both commensal and pathologenic ecological roles in part due to their diverse metabolic capabilities, including complex carbohydrate metabolism and biofilm formation . It is possible that they may take on similar roles in the upper respiratory tract; thus, further study may be warranted.
Although influenza vaccination is undoubtedly beneficial to reduce influenza and secondary bacterial infections, we recently reported 28 an unexpected effect of LAIV (but not inactivated influenza vaccine) on increased bacterial carriage for up to 28 days after vaccination. Importantly, however, LAIV had no detrimental effect on bacterial infections of the lower respiratory tract.28 Thus, although LAIV is beneficial to reduce influenza and influenza-mediated secondary disease, it might be important to consider the level of risk of bacterial acquisition during the weeks after vaccination when deciding between LAIV and inactivated vaccines.
...when influenza viruses infect a host, severe infections can develop when bacterial pathogens invade. Secondary bacterial infections (SBIs) contribute to a significant proportion of influenza-related mortality, with Streptococcus pneumoniae, Staphylococcus aureus, Streptococcus pyogenes, and Haemophilus influenzae as major coinfecting pathogens. Vaccines against bacterial pathogens can reduce coinfection incidence and severity, but few vaccines are available and those that are, may have decreased efficacy in influenza virus-infected hosts. While some studies indicate a benefit of vaccine-induced immunity in providing protection against SBIs, a comprehensive understanding is lacking.
Here we show, in mice, that vaccination with LAIV primes the upper respiratory tract for increased bacterial growth and persistence of bacterial carriage, in a manner nearly identical to that seen following wild-type influenza virus infections….LAIV, unlike wild-type virus, did not increase severe bacterial disease of the lower respiratory tract. These findings may have consequences for individual bacterial disease processes within the upper respiratory tract, as well as bacterial transmission dynamics within LAIV-vaccinated populations...we find that LAIV vaccination reverses normal bacterial clearance from the nasopharynx [NP] and significantly increases bacterial carriage densities of the clinically important bacterial pathogens Streptococcus pneumoniae (serotypes 19F and 7F) and Staphylococcus aureus (strains Newman and Wright) within the upper respiratory tract of mice.
In the absence of any safety signals despite widespread use of the vaccine, these findings suggest that bacterial density, and thus transmission rates among children and to people in other age groups, may rise following attenuated influenza infections without associated clinical disease….We show that infections with attenuated viruses can result in increases in carriage density of common bacteria or increases in acquisition...Children carrying more bacteria are probably more infectious than those with fewer, and it makes biological sense that such bacteria should evolve to sense viral rhinitis or the host response to it and exploit it as a transmission opportunity.......Again, there was evidence of an increase in S. pneumoniae density with increasing doses of vaccine. In particular, compared with prevaccine levels, a 2.5-fold increase in density was observed after two vaccine doses
Epidemiology of Streptococcus pyogenes, April 3, 2017.
Acute viral respiratory infections, and influenza in particular (Morens, Taubenberger, & Fauci, 2008), are recognized risk factors for invasive S. pyogenes infection, with secondary infections generally occurring within one week of influenza diagnosis (Zakikhany, et al, 2011). The relative importance of influenza as a risk factor for invasive S. pyogenes infection will therefore be highly dependent on the levels of circulating influenza and the populations affected.
Scarlet fever is an infectious disease caused by invasion of the upper respiratory tract by the Gram-positive bacterium Streptococcus pyogenes.1
- pyogenes is responsible for a wide array of infections, including streptococcal sore throat, strep throat, pharyngitis, scarlet fever, impetigo, erysipelas, puerperal fever, necrotizing fasciitis, toxic shock syndrome, septicemia, acute rheumatic fever, acute post-streptococcal glomerulonephritis, and gas gangrene….The bacterium can survive on a dry surface for 3 days to 6.5 months.
The illustration is available here and our thanks to them.
LAIV may increase bacterial transmigration to the middle ear and could thus increase the risk of clinically relevant acute otitis media. These data warrant further investigations into interactions between live attenuated viruses and naturally colonizing bacterial pathogens.
An ideal vaccine provides complete protection from infection or disease against a pathogen population. To minimize the chance of vaccine escape, the vaccine would instill herd immunity in the host population, or the pathogen population would display no diversity with respect to the vaccine-induced immunity and would be unable to escape it. In practice, pathogens are diverse, and vaccines usually provide imperfect protection that differs from that induced by natural infection.117 By changing the pathogen’s immunological environment, vaccines can thus shape evolution. Models of competing strains predict that vaccination against a subset of strains will increase the abundance of untargeted strains.118,119…natural infection induces nonspecific immune memory but the vaccine does not. ...In the United States, high vaccination rates in young children nearly eradicated the targeted serotypes and increased the abundances of the untargeted serotypes such that overall carriage rates have not declined.122 This phenomenon has been named serotype replacement.119...a successful vaccination campaign against one pathogen may affect competing pathogens in unexpected ways.
Interactions between pathogens and commensal microbes are major contributors to health and disease. Infectious diseases however are most often considered independent, viewed within a one-host one-pathogen paradigm and, by extension, the interventions used to treat and prevent them are measured and evaluated within this same paradigm. Vaccines, especially live vaccines, by stimulating immune responses or directly interacting with other microbes can alter the environment in which they act, with effects that span across pathogen species. Live attenuated influenza vaccines for example, while safe, increase upper respiratory tract bacterial carriage density of important human commensal pathogens like Streptococcus pneumoniae and Staphylococcus aureus. Further, by altering the ecological niche and dynamics of phylogenetically distinct microbes within the host, vaccines may unintentionally affect transmission of non-vaccine targeted pathogens. Thus, vaccine effects may span across species and across scales, from the individual to the population level. In keeping with traditional vaccine herd-effects that indirectly protect even unvaccinated individuals by reducing population prevalence of vaccine-targeted pathogens, we call these cross-species cross-scale effects “generalized herd-effects”. As opposed to traditional herd-effects, “generalized” relaxes the assumption that the effect occurs at the level of the vaccine-target pathogen and “herd effect” implies, as usual, that the effects indirectly impact the population at large, including unvaccinated bystanders. Unlike traditional herd-effects that decrease population prevalence of the vaccine-target, generalized herd-effects may decrease or increase prevalence and disease by the off-target pathogen. LAIV, for example, by increasing pneumococcal density in the upper respiratory tract of vaccine recipients, especially children, may increase pneumococcal transmission and prevalence, leading to excess pneumococcal invasive disease in the population, especially among the elderly and others most susceptible to pneumococcal disease.
Patterns are important in science. One must not be afraid to look even though doing so can shatter age-old beliefs. The pattern here is that LAIV, the nasal flu vaccine, like wild-type influenza, may cause S. Pyogenes to adhere to the upper respiratory tract. The bacteria can then spread from those vaccinated to the bystanders. The ability to transmit and to grow is possible. The ability to spread in the environment (schools) is possible. Nobody has studied this and it seems important. If we look at some of the words from these scientific papers, there seems to be warnings amongst the data, showing a need for further research:
- further study may be warranted.
- it might be important to consider the level of risk.
- a comprehensive understanding is lacking.
- pathogens are diverse, and vaccines usually provide imperfect protection.
- vaccines may unintentionally affect transmission of non-vaccine targeted
- it makes biological sense that such bacteria should evolve to sense viral rhinitis or the host response to it and exploit it as a transmission opportunity.
- vaccination with LAIV primes the upper respiratory tract for increased bacterial growth and persistence of bacterial carriage, in a manner nearly identical to that following wild-type influenza virus infections.
In Part IIII, we will conclude with things to ponder and gratitude for those researchers who do seek the truth.
- -- Aren't you asking us to accept a pretty incredible coincidence? --
- -- I'm just saying a coincidence is possible. --
12 Angry Men -- 1957