Why your baby stays sick during the 1st year of life. Decreased immunity after vaccinations and Sero
Vaccines= Increased infections. Vaccinations claim to protect against one single disease at the expense of decreasing immunity to every single other infection. Proven by the science below. Strep/Staph anyone? Ear Infections & Pneumonia Anyone? Is this really worth the risk?
Increased Risk of Noninfluenza Respiratory Virus Infections Associated With Receipt of Inactivated Influenza Vaccine “Receipt of TIV could increase influenza immunity at the expense of reduced immunity to noninfluenza respiratory viruses, by some unknown biological mechanism.....Participants who received TIV would have been protected against influenza in February 2009 but then would not have had heightened nonspecific immunity in the following weeks. They would then face a higher risk of certain other virus infections in March 2009, compared with placebo recipients (Figure 1). The duration of any temporary nonspecific immunity remains uncertain but could be of the order of 2–4 weeks based on these observations.” 2012 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3404712/
Pneumococcal conjugate vaccination and nasopharyngeal acquisition of pneumococcal serotype 19A strains.
The rapid increase in multiresistant serotype 19A as a cause of invasive and respiratory pneumococcal disease has been associated in time with the widespread implementation of 7-valent pneumococcal conjugate vaccination (PCV-7) in several countries. Because spontaneous fluctuations in time and antibiotic selective pressure may have induced this serotype 19A increase, controlled studies are needed to assess the role of PCV-7. Five isolates were penicillin-intermediate susceptible and another 3 were nonsusceptible to erythromycin and azithromycin, all in the vaccine groups. CONCLUSION: A 2 + 1-dose PCV-7 schedule was associated with an increase in serotype 19A nasopharyngeal acquisition compared with unvaccinated controls.
Epidemiology of respiratory viral infections in children enrolled in a study of influenza vaccine effectiveness “Influenza-vaccinated children were 1·6 times more likely than unvaccinated children to have a non-influenza influenza like illness…… Non-influenza Influenza Like Ilnesses were more common among fully vaccinated and partially vaccinated subjects than among unvaccinated subjects …Excluding Influenza Like Ilnesses from which no virus was identified made no significant difference to this finding.” 2014 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4181477/ Pneumococcal conjugate vaccines reduce nasopharyngeal carriage of vaccine-type S pneumoniae. Our finding of an inverse relationship between vaccine-type S pneumoniae and Staphylococcus aureus may imply an upcoming shift, not only toward nonvaccine S pneumoniae serotypes17 but also toward higher Staphylococcus aureus carriage rates in children. This would be particularly disturbing in light of the emergence of community-associated methicillin-resistant Staphylococcus aureus (MRSA).This possibility is supported by a recent report of an increased rate of Staphylococcus aureus culture-positive draining ears in vaccinated children compared with controls. http://www.ncbi.nlm.nih.gov/pubmed/15304469 Full study http://jama.jamanetwork.com/mobile/article.aspx?articleid=199212
“Over the following 9 months, TIV (vaccine) recipients had an increased risk of virologically-confirmed non-influenza infections…. “There was no statistically significant difference in the risk of confirmed seasonal influenza infection between recipients of TIV (vaccine) or placebo, although the point estimate was consistent with protection in TIV recipient... TIV recipients had significantly lower risk of seasonal influenza infection based on serologic evidence…However, participants who received TIV (vaccine) had higher risk of Acute Respiratory Infections associated with confirmed noninfluenza respiratory virus infection. Including 2 additional confirmed infections when participants did not report ARI, TIV (vaccine) recipients had higher risk of confirmed noninfluenza respiratory virus infection. The majority of the noninfluenza respiratory virus detections were rhinoviruses and coxsackie/echoviruses, and the increased risk among TIV recipients was also statistically significant for these viruses….” 2012 http://www.ncbi.nlm.nih.gov/pubmed/22423139
Live Attenuated Influenza Vaccine Enhances Colonization of Streptococcus pneumoniae and Staphylococcus aureus in Mice
Community interactions at mucosal surfaces between viruses, like influenza virus, and respiratory bacterial pathogens are important contributors toward pathogenesis of bacterial disease. What has not been considered is the natural extension of these interactions to live attenuated immunizations, and in particular, live attenuated influenza vaccines (LAIVs). Using a mouse-adapted live attenuated influenza vaccine against influenza A (H3N2) virus carrying the same mutations as the human FluMist vaccine, we find that live attenuated influenza vaccine vaccination reverses normal bacterial clearance from the nasopharynx 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. Vaccination with live attenuated influenza vaccine also resulted in 2- to 5-fold increases in mean durations of bacterial carriage. Furthermore, we show that the increases in carriage density and duration were nearly identical in all aspects to changes in bacterial colonizing dynamics following infection with wild-type (WT) influenza virus. Importantly, live attenuated influenza vaccine, unlike WT influenza viruses, had no effect on severe bacterial disease or mortality within the lower respiratory tract. Our findings are, to the best of our knowledge, the first to demonstrate that vaccination with a live attenuated viral vaccine can directly modulate colonizing dynamics of important and unrelated human bacterial pathogens, and does so in a manner highly analogous to that seen following wild-type virus infection.
We sought to understand whether these effects of LAIV vaccination on bacterial proliferation would continue over a longer duration. Mice were infected with pneumococcus 28 days following live attenuated influenza vaccine vaccination—well after viral clearance from the NP was complete (~7 days postvaccination). Despite the 28-day lag between live attenuated influenza vaccine and pneumococcal infection, LAIV continued to yield immediate excess bacterial proliferation relative to PBS controls...
Live attenuated influenza vaccine enhances Staphylococcus aureus dynamics in the Upper Respiratory Tract.
We next sought to test the effects of live attenuated influenza vaccine on carriage of an entirely distinct but important Gram-positive bacterium, Staphylococcus aureus. Live attenuated influenza vaccine was administered 7 days prior to infection with S. aureus strain Wright (Fig. 4A and B) or Newman (Fig. 4C and D). Similar to the previous experiments using two strains of pneumococcus, the density of these two strains of S. aureus following vaccination was increased at all measured time points for both the Wright and Newman strains (Fig. 4A and C), and duration of colonization was significantly extended 3- to 5-fold over that in the PBS controls (Fig. 4B and D). Although vaccination with LAIV, in the longer term, thwarts secondary bacterial infections by inhibiting primary infections with influenza virus (29, 49), the immediate effects of LAIV on bacterial replication and disease have never before been described. Indeed, although vaccines are among our greatest achievements in the constant battle against microbial pathogens, the effects of vaccination on distinct pathogen species unrelated to vaccine-targeted pathogens have, until now, remained entirely unexplored.
Live attenuated influenza vaccine viruses selectively replicate in the Upper Respiratory Tract, partially denude the epithelium (50), and induce robust innate immune responses that ultimately contribute to long-term protective immunity (28). In so doing, Live attenuated influenza vaccine viruses may, like Wild Type influenza viruses, condition the site of replication for enhanced secondary bacterial colonization.
Here, we demonstrated that vaccination with LAIV, like a Wild Type influenza virus, induces swift increases in bacterial density within the Upper Respiratory Tract, with no discernible differences in effects on bacterial dynamics in the NP between the two virus strains. A lag between viral inoculation and excess bacterial replication of at least 3 to 5 days was consistently measured, no matter the bacterial strain. Of particular interest, the type I interferon, IFN-β, known to play a pivotal role in excess pneumococcal colonization following Wild Type influenza virus infections (36), was maximally upregulated at 3 days post-LAIV vaccination, coincident with commencement of excess bacterial proliferation. After the 3- to 5-day threshold following vaccination was met, the murine NP remained conditioned for excess pneumococcal replication for at least 28 days (our furthest time point out) post-vaccination. However, as the delay between vaccination and bacterial infection was increased, the magnitude of the effects of vaccination on bacterial dynamics became considerably more modest, although statistically significant excess growth was measured even when acquisition followed 28 days post-vaccination.
Nature always wins. Vaccines do not equal health! "A trial with a 7-valent pneumococcal-conjugate vaccine in children with recurrent acute otitis media showed a shift in pneumococcal colonisation towards non-vaccine serotypes and an increase in Staphylococcus aureus-related acute otitis media after vaccination. These findings suggest a natural competition between colonisation with vaccine-type pneumococci and Staphylococcus aureus, which might explain the increase in Staphylococcus aureus-related otitis media after vaccination." http://www.ncbi.nlm.nih.gov/pubmed/15183627
"Thus, we conclude that aP (whooping cough) vaccination interferes with the optimal clearance of B. parapertussis and *enhances the performance of this pathogen. Our data raise the possibility that widespread aP vaccination can create hosts *more susceptible to B. parapertussis infection." http://www.ncbi.nlm.nih.gov/pubmed/20200027
"An acellular whooping cough vaccine actually enhances the colonization of Bordetella parapertussis in mice; pointing towards a rise in B. parapertussis incidence resulting from acellular vaccination, which may have contributed to the observed increase in whooping cough over the last decade”. http://www.cidd.psu.edu/research/synopses/acellular-vaccine-enhancement-b.-parapertussis
______________________________________________________________________________________ Rapid Increase in Pertactin-deficient Bordetella pertussis Isolates, Australia CDC admits whooping cough vaccine causing mutation:
"An additional possible contributing factor is evolution of B. pertussis through vaccine-driven adaptation (5). The most prominent recent changes in circulating B. pertussis strains are polymorphisms within genes encoding 2 of the 3 main virulence factors (ptx and prn) contained in the vaccine. Variations have also been reported in ptxP, the promoter of the ptx operon (6)."
"This pattern is consistent with continuing evolution of B. pertussis in response to vaccine selection pressure."
Bordetella pertussis Strains with Increased Toxin Production Associated with Pertussis Resurgence
"We present evidence that in the Netherlands the dramatic increase in pertussis is temporally associated with the emergence of Bordetella pertussis strains carrying a novel allele for the pertussis toxin promoter, which confers increased pertussis toxin (Ptx) production. Epidemiologic data suggest that these strains are more virulent in humans. We discuss changes in the ecology of B. pertussis that may have driven this adaptation. Our results underline the importance of Ptx in transmission, suggest that vaccination may select for increased virulence, and indicate ways to control pertussis more effectively."
"Evolutionary studies using single nucleotide polymorphisms (SNPs) have separated Bordetella pertussis isolates into six major clusters, with recent isolates forming cluster I. The expansion of cluster I isolates was characterised by changes in genes encoding antigenic components in acellular vaccines, including pertactin (Prn). Here, we determined the initial emergence of the pertussis toxin promoter allele, ptxP3, from an evolutionary perspective. This allele was previously shown in a study from the Netherlands to be associated with increased pertussis toxin production as a result of a single base mutation in the ptxP. The ptxP region of 313 worldwide isolates was sequenced, including 208 isolates from Australia collected over a 40 year period. Eight alleles were identified, of which only two predominated: ptxP1 and ptxP3. One novel allele was also found. ptxP3 was only found in SNP cluster I of B. pertussis and its emergence is concurrent with the change to the non-vaccine prn2 allele. Our results suggest that the globally distributed cluster I of B. pertussis has the ability to evade vaccine induced selection pressure."
Pertussis resurgence: waning immunity and pathogen adaptation - two sides of the same coin.
"Pertussis or whooping cough has persisted and resurged in the face of vaccination and has become one of the most prevalent vaccine-preventable diseases in Western countries....The increase in pertussis is mainly found in age groups in which immunity has waned and this has resulted in the perception that waning immunity is the main or exclusive cause for the resurgence of pertussis. However, significant changes in B. pertussis populations have been observed after the introduction of vaccinations, suggesting a role for pathogen adaptation in the persistence and resurgence of pertussis. These changes include antigenic divergence with vaccine strains and increased production of pertussis toxin. Antigenic divergence will affect both memory recall and the efficacy of antibodies, while higher levels of pertussis toxin may increase suppression of the innate and acquired immune system. We propose these adaptations of B. pertussis have decreased the period in which pertussis vaccines are effective and thus enhanced the waning of immunity. We plead for a more integrated approach to the pertussis problem which includes the characteristics of the vaccines, the B. pertussis populations and the interaction between the two."
"Yet another twist has also emerged with the discovery that pneumococcal serotypes undergo microevolution due to mutations in the wcjE (O-acetyltransferase) gene, whereby colonizing strains exhibit phenotypic switching and become invasive strains . Since the introduction of PCV7 (pneumococcal conjugate vaccine), the marked decrease in invasive disease with vaccine serotypes has been accompanied by an increase in disease with non-pneumococcal conjugate vaccine serotypes [10–12]. Among non-PCV7 (pneumococcal conjugate vaccine) serotypes, serotypes 1, 3, and19A have each emerged as major causes of severe pneumonia and empyema [13–17]. The longstanding association of serotype 3 virulence with its large capsule was reaffirmed in a recent capsule switching study , as was the association between more heavily encapsulated serotypes and mortality in invasive pneumococcal disease ." http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4237063/
Emerging, Non-PCV13 Serotypes 11A and 35B of Streptococcus pneumoniae Show High Potential for Biofilm Formation In Vitro. 2015 Apr Since the use of pneumococcal conjugate vaccines PCV7 and PCV13 in children became widespread, invasive pneumococcal disease (IPD) has dramatically decreased. Nevertheless, there has been a rise in incidence of Streptococcus pneumoniae non-vaccine serotypes (NVT) colonising the human nasopharynx. Nasopharyngeal colonisation, an essential step in the development of S. pneumoniae-induced IPD, is associated with biofilm formation. Streptococcus pneumoniae (pneumococcus) is a leading human pathogen that naturally inhabits the upper respiratory tract. It usually colonises the associated mucosal surfaces in early childhood, and persists as a symptomless commensal (carrier state) in the nasopharynx . The widespread use of conjugate vaccines has been very effective in reducing cases of invasive pneumococcal disease, although increases in disease caused by non-vaccine serotypes (NVT) (“serotype replacement”) have subsequently offset some of these reductions. Although the PCV7 (pneumococcal conjugate vaccine) serotype 6B appears to offer cross-protection against the non-(pneumococcal conjugate vaccine) serotype 6A, this is not the case for 19F and the non-(pneumococcal conjugate vaccine) serotype 19A . Indeed, the incidence of infections caused by 19A multiresistant pneumococcus has increased since PCV7 vaccination became common. Non-vaccine serotypes are also on the rise in the current post-PCV7/PCV13 (pneumococcal conjugate vaccine) era. Surveillance program results suggest that pneumococci of various serogroups/serotypes not included in PCV13 (e.g., 11, 12, 15, 22F, 23A, 23B, 33F, 24, 34, and 35B) are rapidly increasing in prevalence worldwide [5–8]. Serotype 6C pneumococci, which are good biofilm formers  and whose CPS is not included in PCV13, were not investigated further. Concerns about serotype replacement have influenced recent policy discussions . Predicting the amount of future replacement is difficult since the reasons underlying a particular non-vaccine serotype increases after vaccine introduction are not fully understood. In the years immediately preceding PCV13 (pneumococcal conjugate vaccine) introduction, no single non-PCV13 serotype seemed an obvious candidate for replacement, based on current rates of disease, antimicrobial resistance, and carriage data. We recently proposed that quantifying the in vitro biofilm formation capacity of isogenic S. pneumoniae transformants expressing different CPSs might help predict the emergence (and eventual expansion) of non-vaccine serotypes that are prone to colonise the human nasopharynx . In that work we showed that clinical isolates and isogenic pneumococcal transformants of serotypes 19F and 19A (but not those of serotypes 19B and 19C) are capable of forming substantial amounts of biofilm in vitro. Strains of serogroup 6 also showed significant biofilm-forming capacity. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4415931/
"The relationship between herd immunity and antigenic drift has a clear implication for devising vacci-nation strategies: that vaccinating too many people can have negative consequences. Because of influenza’s effect on morbidity and mortality during annual epidemics, it would be imprudent to vaccinate fewer people with the hope of reducing antigenic drift. However, in seasons when high numbers of vaccines are administered, or almost equivalently, during seasons when we suspect natural host immunity to be quite high against the circulating strains, we should expect the emergence of immune-escape variants since the evolutionary pressure favoring them is strong. The case can be made that monitoring efforts should be strengthened during these seasons."