Meningococcal bacteria, same as pneumococcus, are able to change their serogroups.
Serogroup B meningococcal disease outbreak in Québec in 2004. The authors believe that it probably happened due to serogroup replacement due to vaccination with the polysaccharide vaccine against serogroup C.
In 15 months after the introduction of the vaccination in Brazil, G2P(4) rotavirus strain has replaced all other strains, even though it was only seen in 19%-30% of cases prior to the introduction of vaccination. Effectiveness of the vaccine (Rotarix) against this strain was 77% among children of 6-11 months of age, and -24% (negative) among children over 12 months of age. More: [1], [2].
It is reported here, that after the introduction of vaccination in Brazil, regular rotavirus strains got replaced with the new GP12(8) strain. Strain replacement also took place in Paraguay==https://www.ncbi.nlm.nih.gov/pubmed/20213281] and in Argentina.
Since the rotavirus genome consists of separate segments, when two different strains of the virus infect the same cell, they can exchange segments and create a new strain. This is the same reassortment, which happens on its own.
A case of gastroenteritis in a 7-year-old girl is reported here. A rotavirus strain was isolated from her stool sample. The strain was reassortant of two other human-bovine strains from the RotaTeq vaccine. However, the girl has not been vaccinated against rotavirus. Moreover, she has not been in contact with anyone who has been vaccinated. Her two brothers also had similar gastroenteritis symptoms, and they also have not been vaccinated or in contact with anyone who has been.
The isolated reassortant strain of the virus turned out to be stable and very contagious. The authors believe that this new virus is most likely circulating in the population. Reassortant viruses have previously been isolated, but only in those recently vaccinated with RotaTeq: [1], [2], [3].
Cases of detecting new virus strains from reassortment of wild virus with Rotarix vaccine strain are reported here.
It is reported here, that 17% of children secreted the virus after vaccination, and 37% of them secreted a double reassortant virus. Some children secreted the virus for a long time after the vaccination, form 9 to 84 days after the last dose.
The authors analyzed the rotavirus genome of the vaccinated children suffering from gastroenteritis in Nicaragua, and found new strains of the virus, which formed due to reassortment between the wild strain and the RotaTeq vaccine strains.
Among children who had diarrhea within two weeks of vaccination, 21% had been infected with the vaccine strain. 37% of the isolated vaccine strains were reassortant from two RotaTeq strains.
Vaccination decreased the Hib incidence in Ontario (Canada) by 57%, but the incidence of serotype f increased by 2.4 times, and the incidence of noncapsulated strains increased by 3 times. Hib incidence decreased by 7% annually in children under the age of 5 years, and the incidence of noncapsulated strains increased by 7% annually in children of 5-19 years of age. Overall, the incidence of H. influenzae has not changed much, but the incidence of meningitis has decreased and the incidence of sepsis has increased.
The noncapsulated strains colonize the upper respiratory tracts in 65% of children.
One year after introduction of vaccination in Brazil, Hib meningitis incidence decreased by 69% (from 2.62 to 0.81 in 100,000). Hia meningitis (H. influenzae type a) increased 8-fold (from 0.02 to 0.16 in 100,000).
Clinical virulence of Hib and Hia is the same. Hia mortality rate was 23%.
Before the introduction of vaccination, Hib incidence in Alaska was the highest in the world. It decreased sharply due to vaccination, but H. influenzae incidence of other serotypes increased, mostly of serotype A and noncapsulated strains.
After the introduction of vaccination, Hib incidence among adults in England decreased, but the overall incidence of H. influenzae disease increased due to a sharp increase in the incidence of noncapsulated strains, especially among the elderly. Mortality rate was 59%.
Hib incidence among adults in England decreased after the introduction of the vaccine (probably due to herd immunity), reached its low in 1998, but increased back to its pre-vaccine levels by 2003. The level of Hib antibodies in adults decreased after the introduction of vaccination.
The same happened among children. At first, Hib incidence decreased sharply, but then began to increase sharply, despite the high vaccination coverage. The number of cases among children has been doubling each year since 1998, and most of those infected are fully vaccinated.
Vaccination decreased the number of Hib cases in Utah children by 99%, but the incidence of H. influenzae infection among adults increased by 11.5 times between 1998 and 2008. Most cases were of serotype F and noncapsulated strains. Mortality rate was 22%.
Before the introduction of vaccination, 24 Hib cases a year were registered in 1989 in British Columbia (Canada). 45-53 cases in a year were registered between 2008 and 2009. Serotype B incidence decreased, and serotype A incidence increased. Previously, mostly children got infected, but now adults were also getting sick.
The number of Hib cases in Illinois increased by 2.5 times (3.5 times among the elderly) between 1996 and 2004.
The number of cases of infection with noncapsulated Hib strain increased by 657%. In 1996, noncapsulated Hib strain was responsible for 17% of disease cases, whereas in 2004, it was responsible for 71% of the cases already. Mortality rate was 13% (21% among elderly).
Mortality rate for serotype F among the elderly was 11%, and 39% for serotype E.
The incidence of serotype F increased 4-fold between 1989 and 1994, and accounted for 17% of all H. influenzae cases. The mortality rate for this serotype was 30% in adults and 21% in children.
Hib incidence in Netherlands decreased after the introduction of vaccination, and reached a low in 1993, but then started to increase again. Probably because the disappearance of bacteria makes “natural booster” more rare, which leads to weakened immunity, and increased susceptibility to infection.
It could also be because vaccination destroyed the strains with a thin capsule, and left the strains with a thicker capsule. More: [1], [2], [3].
Serotype A (Hia) incidence in Ontario is already 76% higher than Hib incidence was in the pre-vaccination era.
A few more articles on replacement of serotype B strains with others: [1], [2], [3], [4], [5], [6], [7], [8], [9], [10], [11].
Nature abhors a vacuum. By preventing girls from getting the infection from two or four strains of HPV, the vaccine only causes them to be replaced with other strains.
There is a decrease in prevalence of the four strains of HPV in young girls, but there is no change in the prevalence of HPV, taking into account all strains of the virus.
Oncogenic strains of HPV, 16 and 18, have been replaced with other oncogenic strains: 31, 51, 53, 56 and 66.
Three more studies with the same conclusions in Italy, Netherlands and the USA.
In response to antibiotics and vaccination, pneumococcus mutates rapidly. Pneumococcal bacteria can change their serotype.
After the beginning of vaccination, a new serotype 35B appeared, which had been rarely seen before, but now it is responsible for an increasing number of pneumococcal infections. This serotype is 5 times more deadly than other serotypes, and is often insensitive to antibiotics.
The incidence of pneumococcus decreased by 2 times within two years after the introduction of vaccination, and remained at about the same level. More: [1].
After the start of vaccination, the incidence of pneumococcal infection in Barcelona increased by 58%, and among children - by 135%.
The incidence of vaccine serotypes decreased by 40%, and for non-vaccine serotypes it increased by 531%.
The incidence of pneumonia and empyema among children under 5 years of age increased by 320%.
After vaccination began, between 1997 and 2003, the incidence of pneumococcal infection in Salt Lake City (Utah) decreased by 27%. The incidence of vaccine serotypes decreased from 73% to 50%. The number of cases from non-vaccine serotypes increased 3 times. Children with non-vaccine serotypes were hospitalized longer. The proportion of cases of pleural empyema complications increased from 16% to 30%, and the proportion of severe cases increased from 57% to 71%. More: [1].
Native children in Alaska suffer from invasive pneumococcal infection 3 times more often than Americans on average. In the first 3 years after the start of vaccination (2001-2003), the incidence of pneumococcal infection among indigenous children under 2 years old in Alaska decreased by 67%. After that, in 2004-2006, the incidence increased by 82%.
The incidence of vaccine serotypes decreased by 96%, and for non-vaccine serotypes it increased by 140%.
The proportion of cases complicated by pleural empyema increased from 2% to 13%. The proportion of cases with pneumonia and bacteremia increased from 40% to 57%.
In 2004, 41% of the population were carriers of pneumococcus. The proportion of seven vaccine serotypes decreased from 41% to 5%, and for non-vaccine serotypes it increased from 47% to 88%.
The incidence of invasive pneumococcal infection among children under 5 years old decreased by 78% between 2002 and 2010, but it increased among children over 5 years old, adults and the elderly. Vaccine strains were replaced by non-vaccine ones. In general, the incidence has not changed. In 2006-2007, an outbreak of pneumococcus was recorded among beggars and drug addicts. (British Columbia, Canada)
In Philadelphia, the incidence of vaccine serotypes among adults decreased by 29% per year in 2002-2008, and non-vaccine serotypes increased by 13% per year. In general, the incidence of pneumococcal infection increased by 7% per year.
44. A few more articles on the replacement of pneumococcal strains from vaccine to non-vaccine: [1], [2], [3], [4], [5], [6], [7], [8], [9], [10], [11], [12], [13], [14], [15], [16], [17]
... and the replacement of pneumococcus with H. influenzae and other bacteria: [1], [2], [3], [4], [5], [6], [7].
Since invasive infection requires colonization of bacteria in the nasopharynx, the goal of vaccination is also to reduce the colonization of pneumococcus.
The pneumococcal conjugate vaccine was first tested on infants in Gambia in 1993, where it was found that while vaccine serotype colonization decreased by 78%-89%, non-vaccine serotype colonization increased by 4.5 times.
Pneumococcus colonization among vaccinated and unvaccinated people in Italy did not differ. The H. influenzae bacteria were more often found among vaccinated ones.
After the start of vaccination, the colonization of vaccine serotypes decreased significantly, but it increased for non-vaccine ones. H. influenzae bacteria were found in vaccinated people 2-5 times more often than in unvaccinated ones. (Sao Paulo, Brazil)
Between 2001 and 2004, in children under the age of 7 in Massachusetts, colonization with seven vaccine serotypes of pneumococcus in the nasopharynx decreased, and colonization with other serotypes increased. In general, the colonization of pneumococcus has not changed. Penicillin resistance increased from 8% to 25% among non-vaccine serotypes, and from 45% to 56% among vaccine serotypes.
Continuation of the previous study. By 2007, vaccine serotypes had virtually disappeared, and were replaced by non-vaccine and penicillin insensitive serotypes. In general, the level of pneumococcal colonization remained at 30%, but it has grown significantly among children under 6 months of age.
The 13-valent vaccine (PCV13) also did not change the colonization of pneumococcus. Colonization of vaccine serotypes decreased, while colonization of non-vaccine serotypes increased by 12% per year.
The level of colonization among PCV13 vaccinated and unvaccinated children did not differ.
Colonization with PCV13 strains was 70% lower among healthy vaccinated children, but not among children with ARI.
In Japan, after the start of vaccination against Hib and pneumococcus, the colonization of vaccine serotypes of pneumococcus decreased, and colonization of non-vaccine serotypes increased. In general, colonization of pneumococcus has not changed. Colonization with a H. influenzae increased.
In England, colonization of vaccine serotypes decreased, while colonization of non-vaccine serotypes increased. In general, colonization increased by 6% (no statistical significance).
Between 1995 and 2003, the incidence of AOM did not change, but the incidence of protracted AOM decreased from 16% to 12%. Pneumococcus in cases of AOM was replaced by H. influenzae, which after the onset of pneumococcal vaccination became the main causative agent of the disease. (Rochester, New York)
Pneumococcus and H. influenzae are responsible for 80% of cases of AOM. M. catarrhalis is responsible for 3-20% of cases. After the start of vaccination against pneumococcus, most cases of AOM are caused by nonencapsulated serotypes of H. influenzae.
A randomized, double-blind study of the effect of pneumococcal vaccine on AOM in children older than 1 year who are prone to it. Hepatitis B and hepatitis A vaccines were used as a placebo.
The incidence of AOM in vaccinated individuals was increased by 25%, although the statistical significance was borderline (CI 0.99-1.57). In children older than 2 years, the vaccine increased the risk of AOM by 45%. In children not too prone to otitis media, the vaccine increased the risk by 66%. Vaccination did not affect the colonization of pneumococcus, since vaccine serotypes were replaced by non-vaccine ones. In children vaccinated against pneumococcus, more Staphylococcus aureus was detected.
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