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Feature Antibiotics

Speeding new antibiotics to market: a fake fix?

BMJ 2015; 350 doi: (Published 25 March 2015) Cite this as: BMJ 2015;350:h1453

Rapid Response:

Vaccine-driven resistance of bacteria and viruses

Based on the ScienceDaily source: Wellcome Trust Sanger Institute (28 January 2011), “A new study has used DNA sequencing to provide the first detailed genetic picture of an evolutionary war between Streptococcus pneumoniae bacteria and the vaccines and antibiotics use against it over recent decades. Large scale genome sequencing reveals pattern of adaptation and the spread of a drug-resistant lineage of the S. pneumoniae bacteria. The study unmasks the genetic events by which bacteria such as S. pneumoniae respond rapidly to new antibiotics and vaccines.”

“Drug resistant forms of P. pneumoniae first came under the radar in the 1970s…we sequenced 240 samples collected over the course of 24 years from the PMEN1 lineage of S. pneumoniae. By comparing the sequences, we can begin to understand how this bacterium evolves and reinvents itself genetically in response to human interventions.”

“The power of next-generation sequencing exposes S. pneumoniae as a pathogen that evolves and reinvents itself with remarkable speed. The degree of diversity was a real surprise in such seemingly closely related organisms.”

“First the team had to distinguish between a single letter mutations that are passed down ‘vertically’ when cells divide in two, and so called ‘horizontal changes – called recombinations - when chunks of DNA letters are passed across from one bacterium to another and swapped over, changing the structure of their genome.“

“Separating these two kinds of change was the critical first step in unlocking the evolutionary history of the PMEN1 lineage…By looking only at DNA mutations that are passed down through direct ancestry, we constructed an evolutionary tree. When we looked at our tree we could see that the drug-resistant PMEN1 lineage originated around 1970 -- about the time that we saw the introduction of the widespread use of antibiotics to fight pneumococcal disease.”

“We found that genes for antigens -- the molecules that trigger our immune response—were particularly prone to this kind of change, ”says Dr William Hanage, Associate Professor of Epidemiology at Harvard School of Public Health, and visiting Reader at Imperial College London, where he devised the study with scientists at the Welcome Trust Sanger Institute.” ”The remarkable amount of variation at these hotspots hints at ways S. pneumoniae can evade vaccines against these antigens.”

“If the immune system targets these antigens, then the bacteria can simply change them [sic themselves?], like a criminal changes their appearance to evade detection.”

“The authors also identify the difference in the pattern of adaptation in responses to antibiotics and vaccines.”

“With antibiotics, different strains quite often adapt in the same way to become resistant, says Nicholas Croucher, from the Wellcome Trust Sanger Institute, “With vaccines it is different. What we see is a decline in the prevalence of bacteria that are susceptible to the vaccine. This in turn opens the door to bacteria that can evade the vaccine to fill the niche and become the dominant strain.”

“While the latest vaccination measures in the US have almost completely removed the target pneumococcal strains from the population, the pathogen has deep resources to draw on in response. The research suggests that variants that allowed some bacteria to escape the new vaccine were present before the vaccine was introduced. These variants then flourished, expanding to fill a ‘gap in the market’ as the grip of the dominant strain was weakened through vaccination.”

Similar phenomena of adaptation and evasion have been documented with other pathogens such as B. pertussis (Mooi et al. 2009), measles (Super measles warning: Dr Claude Miller, National Health laboratory in Luxembourg 2001), and Haemophilus influenzae strains (Brown et al. 2009), and all other vaccines.

First, vaccination proponents claimed success with all the targeted diseases, while, soon, they reported on outbreaks in fully vaccinated due to waning vaccine immunity (Rouderfer et al. 1994; Witt et al. 2012) and advocated booster doses. Quoting Dr Witt “What was very surprising was the majority of cases were in fully vaccinated children, “GSK never studied the duration of the vaccine protection after the shot given to four- to six-year-olds.”). Ultimately, it became obvious that the causative microorganisms changed themselves to evade the vaccines.

Waaijenborg et al. (2013) also reported, “Children of mothers vaccinated against measles and, possibly, rubella have lower concentration of antibodies and lose protection by maternal antibodies at an earlier age than children of mothers in communities who oppose vaccination. This increases the risk of disease transmission in highly vaccinated populations.”

Octavia et al. (2012) reported, “Australia is experiencing a prolonged epidemic of pertussis that began in 2008…The data suggests increasing selection in favour of strains carrying prn2 and ptxP3 under the pressure of acellular vaccine-induced immunity.”

The upshot? Why not let Nature do its own thing? It does it effectively and intelligently.


Wellcome Trust Sanger Institute.”How bacteria keep ahead of vaccines and antitbiotics.”Science Daily. 28 January 2011.

Croucher et all 2011. Rapid Pneumococcal evolution in response to clinical interventions. Science; 331(6016): 430 DOI:10.1126/science. 1198545.

Weller et al.2004. Vaccination against encapsulated bacteria in humans: paradoxes. Trends in Immunology; 26(2): 85-89.

Rouderfer et al. 1994. Waning immunity and its effects on vaccination schedule. Math Biosci, Nov 1994; 124(1): 59-82.

Witt et al. 2012. Unexpectedly limited durability of immunity following acellular pertussis vaccination in pre-adolescents in a North American outbreak. Clin Infect Dis; advance access March 15: 1-7.

Waaijenborg et al. 2013. Waning of maternal antibodies against measles, mumps, rubella, and Varicella in communities with contrasting vaccination coverage. J Infect Dis; 208(1):10-16.

Octavia et al. 2012. Newly emerging clones of Bordetella pertussis carrying prn2 and ptxP3 alleles implicated in Australian pertussis epidemic in 2008-2010.

Mooi et al. 2009. Bordetella pertussis strains with increased toxin production associated with pertussis resurgence. Emerging Infectious Diseases; 15(8): 1206-1213.

Scheibner. 9 September 2008. Jabbering about jabs. rapid response.

Brown et al. 2009. Invasive Haemophilus influenzae disease caused by non-type b strains in Northwestern Ontario, Canada, 2002-2008. Clin Infect Dis; 49: 1240-1243.

Hiner and Frash. 1988. Spectrum of disease due to Haemophilus influenzae type b occurring in vaccinated children. J Infect Dis; 158(2): 343-346.

Competing interests: No competing interests

27 April 2015
Dr Viera Scheibner (PhD)
scientist/author retired
Blackheath NSW Australia