Category Archives: vaccination

Chickenpox and Shingles Vaccines SHORT

This is the short version. For the long version with references, click here.

Varicella virus

What are chickenpox and shingles?

Chickenpox is a highly contagious rash caused by varicella zoster virus. Chickenpox infection generally confers lifelong immunity. You may develop an infection without symptoms, and this also generally confers immunity. It is normally a very mild rash illness and only very rarely causes serious complications; children with eczema are not at increased risk of complications. Death is very rare. However, in otherwise healthy adults, the chickenpox complication rate is 15-25 times higher and the death rate is 20 times higher.

After a chickenpox infection, the virus hibernates in a nerve. In times of stress or immune suppression, the virus may reawaken and cause shingles. (You cannot catch shingles. You can catch chickenpox, which might later develop into shingles if your immunity is low.) Shingles is associated with 4-5 times higher complication rate and medical costs than chickenpox.

Chickenpox vaccines are typically given twice in early childhood in North America, Germany, and Australia. The shingles vaccine is given to older adults. Most of the developed world does not use these vaccines.

How can I prevent or treat chickenpox and shingles in my child?

Because chickenpox is mild in childhood but potentially serious in adulthood, many people choose to intentionally expose their child and get it over with in childhood. If you choose to do this, avoid people with immune suppression, pregnant women, and infants during the contagious period. Do not mail infectious material and do not intentionally expose others without their knowledge and consent.

It takes about 10-21 days after exposure for the first spots to appear. Chickenpox is contagious from about 2 days before the spots appear to as much as 7 days later, when the spots are all crusted over. A fever often occurs for one or two days before the first spots appear. To prevent infection, avoid children with chickenpox, fever, or unidentified rash.

The vaccine contains a live virus. There have been several reports of people developing chickenpox with vaccine-strain virus shortly after a close contact was vaccinated. To prevent infection, avoid people who have recently been vaccinated against chickenpox or shingles.

Exposure to chickenpox acts as a natural “booster shot” to protect adults against shingles. If you or your child have had chickenpox or the vaccine, prevent shingles by seeking exposure to chickenpox.

You can treat chickenpox with calamine lotion and daily baths with soap and water. Do not use aspirin, Tylenol, or Benadryl (diphenhydramine), and do not use lotions that have diphenhydramine in them. Use ibuprofen to lower a fever only if the fever is over 106°F (41.1°C). You should generally not take steroids during a chickenpox infection; if your child is on steroids, talk to your doctor about whether to stop the steroids until he recovers. Use anti-infectives such as silver nitrate and essential oils on the spots to prevent bacterial infection. If he develops a secondary fever after the spots have appeared, seek immediate medical attention.

How effective are the vaccines at preventing asymptomatic carriage?

Vaccinated people can have asymptomatic infections with both vaccine-strain and wild-type varicella viruses, and have proven to be contagious during that time. However, whether the vaccine reduces, increases, or has no effect on the degree or duration of asymptomatic carriage is unknown.

How effective are the vaccines?

The chickenpox vaccine is more effective when fewer children receive it because natural exposure to chickenpox boosts immunity, so vaccinated children get a natural “booster shot” from their unvaccinated friends. However, in communities where chickenpox vaccination is widespread, effectiveness drops to very low levels within a few years. A few studies found it to be completely ineffective or even reverse-effective (increased the chickenpox rates). When the vaccine fails, people tend to get chickenpox at an older age, when it is more dangerous.

Since exposure to chickenpox boosts immunity and prevents shingles, researchers predicted that widespread chickenpox vaccination would increase shingles rates. They were proven right by numerous studies in many countries using the vaccine. Because shingles is much more dangerous than chickenpox, the vaccine results in overall increased complication rate and medical costs, so the vaccine is neither effective nor cost-effective. Furthermore, the addition of new booster shots and shingles vaccines to fix this problem is not cost-effective and is associated with a higher complication rate than if children had been permitted to get chickenpox naturally.

The shingles vaccine may be as much as 51% effective and last 1 month to 5 years, necessitating numerous booster shots. It is less effective in people over 70 and completely ineffective in people over 80. Exposure to a child with chickenpox would be much more effective and much safer.

Are there other infectious diseases related to chickenpox/shingles vaccination?

MMR vaccination indirectly resulted in increased severity of chickenpox. This increased severity is part of why the CDC recommends chickenpox vaccination. However, most of Europe still agrees that the risks of chickenpox vaccination far outweigh any possible benefit.

What are the risks of the vaccines?

Adverse reactions to the chickenpox vaccine are at least equal to, and some research shows is greater than, adverse reactions to chickenpox infection. The combination MMR and chickenpox vaccine causes a higher fever and more seizures than MMR and chickenpox vaccines given separately. Chickenpox vaccination increases the risks of shingles, multiple sclerosis, heart disease and heart attacks, and brain tumors.

The shingles vaccine is associated with a very high rate of adverse reactions, especially in the oldest groups. The vaccine also causes severe autoimmune reactions, including a doubled risk of arthritis and tripled risk of alopecia.

So what’s the bottom line?

Chickenpox is very mild in childhood and has some long-term health benefits (e.g., decreased risk of multiple sclerosis, heart disease/heart attack, brain tumors), but poses much greater risk and fewer benefits in adulthood. Vaccination may merely delay chickenpox infection until adulthood, when it has considerably more risk. Natural chickenpox infection and repeated exposure to chickenpox decreases the risk of shingles. Conversely, chickenpox vaccination has very low effectiveness against chickenpox, increases the risk of shingles, and results in more severe shingles occurring at younger ages. Shingles is much more dangerous than chickenpox. The shingles vaccine does not appear to be very effective, but research is very limited; it is not effective in the oldest groups and is not yet approved for people under 50. Both vaccines are associated with some serious adverse effects, especially the shingles vaccine.




Chickenpox and Shingles Vaccines

This is a continuation of a series I’ve been helping to write for an education forum. This is the LONG version. For the short version, click here.

Image result for chickenpox virus

Varicella virus

What is chickenpox? What is shingles?

Chickenpox (varicella) is a highly contagious illness caused by a virus known as varicella zoster virus. Cases tend to peak in winter and spring. You can also have chickenpox and develop immunity without ever developing symptoms. Generally speaking, chickenpox infection confers lifelong immunity. In children, chickenpox is generally very mild and only very rarely causes serious complications. However, in otherwise healthy adults, the complication rate is 15-25 times higher. Childhood chickenpox causes death in roughly 1 per 40,000 infections, so the risk of death from chickenpox in the U.S. is lower than the risk of death by lightning strike. However, the death rate from adulthood chickenpox infection is 20 times higher. In fact, even though children make up over 98% of chickenpox cases, adults make up almost half of chickenpox deaths [1-3]. Children with eczema are not at increased risk of complications [1].

After a chickenpox infection, the virus hibernates in a nerve. In times of stress and immune system dysfunction, the virus may reawaken and cause shingles. Shingles is associated with 4-5 times higher complication rate and medical costs than chickenpox [3].

In the U.S., the chickenpox vaccine is given at 12-15 months and again at 4-6 years [4]. The shingles vaccine is recommended for people over the age of 60 [5].

In Canada, the chickenpox vaccine is given alone or with the MMR at 12 mo, 15 mo, 18 mo, and/or 4-6 years, depending on the province [6]. The shingles vaccine is recommended for adults aged 50 and over [7].


How can I prevent chickenpox and shingles in my child?

A longstanding practice is to intentionally expose children to chickenpox because the infection is almost always harmless in children, but much more serious in adults. This practice is regarded as rarely harmful, but poses some risk of exposing immunocompromised people, with the exception that children with a planned exposure can have planned isolation during the potentially contagious period while children with an accidental exposure cannot. If you plan to intentionally infect your child, you should avoid immunocompromised people, pregnant women, and people with severe lung disease until you know for certain that your child is not contagious [1-2]. Also, if you choose to intentionally infect your child, be aware that mailing infectious material is highly illegal, in part because it is unknown how many people might be unknowingly exposed. Exposure is therefore best done in person.

It takes about 10-21 (usually 14-15) days after exposure to chickenpox before you develop the first spots; fever often occurs before the spots appear. The spots disappear within 7-10 days. Chickenpox is most contagious between 2 days before and 3 days after the start of the rash; but it is generally considered that children with chickenpox are contagious until at least 5 days after the onset of the rash or until all of the spots are dry and crusted. It is mainly contracted by direct contact with the spots, but it can be airborne as well. You can also catch chickenpox from direct contact with shingles lesions, but shingles is far less contagious. (You cannot catch shingles from shingles. But you can catch chickenpox from shingles. This is because the first time the virus causes an outbreak in you, it’s always chickenpox.) [1] To prevent chickenpox, avoid exposure to children with chickenpox, fever, or unidentified rash.

The chickenpox vaccine is a live virus vaccine, meaning the virus in the vaccine is capable of causing a chickenpox infection. There have been reported cases of people contracting the disease from a recently-vaccinated individual. For example, one pregnant woman contracted vaccine-strain chickenpox after her child was vaccinated [8]. In another case, an adult woman received the vaccine and both she and her children shortly afterward developed vaccine-strain chickenpox [9]. In yet another very alarming case, a woman who did not develop any symptoms, such as the characteristic rash, passed the vaccine-strain virus on to her newborn, who developed chickenpox [10]. The shingles vaccine is also a live virus [11] and so can be presumed to shed as well. To prevent chickenpox, you should also avoid individuals who have recently received the chickenpox or shingles vaccines, as they should be considered just as contagious as someone who has an asymptomatic chickenpox infection.

However, ironically, the exact opposite should be done to prevent shingles. Regular exposure to chickenpox acts as a natural “booster shot” to protect adults against shingles [12-15]. In fact, working in childcare reduces your chances of developing shingles by 94% [12]! (That’s FAR more effective than the vaccine, as you’ll see later.) If you have been infected with the chickenpox virus in the past, then to prevent shingles, you should seek exposure to chickenpox.


How can I treat chickenpox and shingles in my child?

Even though exposure to chickenpox boosts immunity, and exposing a child with an active infection to people who are already immune would boost their immunity and benefit them by reducing their risk of shingles, it is considered unethical to intentionally expose someone without their knowledge. Thus, you should isolate your child during the contagious period, except to people who are aware of your child’s contagiousness and willing to expose themselves. You should also keep your child away from people who are at higher risk of complications, such as infants, pregnant women, and immunocompromised people.

Generally speaking, you can give anti-fever medicine if your child develops fever. However, research has shown that Tylenol is not effective for chickenpox [1]. Other research has shown that anti-fever medicine degrades some of the immune response and makes the illness last longer, and so giving anti-fever medicine may be counterproductive [16, 17]. Do not give aspirin, which may cause a serious disorder called Reye’s syndrome in children with chickenpox. If you do give aspirin and your child develops vomiting, go to the emergency room, as this is a sign of Reye’s syndrome [1]. In short, Tylenol doesn’t work, ibuprofen might be counter-productive, and aspirin might be dangerous. In other words, it’s probably best not to use anti-fever medicine unless the fever is over 106°F (41.1°C) [18].

Do not give Benadryl, including any creams that have Benadryl in them, because Benadryl toxicity has often been reported in children with chickenpox [1]. Calamine lotion can give effective symptom relief, but make sure it doesn’t have Benadryl (diphenhydramine) in it. Daily baths with soap and water can also help destroy the virus and prevent bacterial infection [1].

Children with eczema are not at increased risk of complications. However, it’s important to note that a steroid cream should not be used during chickenpox, so if a child’s eczema is being treated with a steroid cream, you should stop using the cream while he has chickenpox [1].

An antiviral drug called acyclovir may shorten the length of the illness and reduce its severity, but does not reduce contagiousness. However, it does not reduce complications and has to be started no later than the first day of the rash because if it is started on or after the second day, it is ineffective [1]. Acyclovir also does not reduce complications in adults [2].

The most common complication, occurring in 1-4% of chickenpox infections, is a bacterial infection of the spots [1]. This should be prevented by keeping the spots clean, not breaking them open, and treating them with an anti-infective such as silver nitrate or certain essential oils. A brief fever before the spots appear is common. But if a second fever occurs several days after the spots appear, your child may have a serious bacterial infection and you should seek immediate medical attention [1].

Chickenpox may rarely cause pneumonia. You can prevent this by boosting your child’s immune system during the outbreak and having him breathe in an anti-infective such as certain essential oils. However, if your child develops difficulty breathing or starts looking sicker after he had started to get better (e.g., tired/lethargic, feverish, etc.), you should seek immediate medical attention [1].


How effective are the vaccines at preventing asymptomatic carriage?

Some studies have found that children who were vaccinated may develop shingles with the wild-type virus [19-20]. In other words, even though they never had symptomatic chickenpox, they apparently had an asymptomatic infection with the wild-type virus. This means vaccinated individuals can have asymptomatic infections with the wild-type virus in spite of having been vaccinated. Furthermore, as mentioned earlier, there has been at least one recorded case of an asymptomatic individual passing on vaccine-strain virus to her newborn child [10].

So, in short, vaccinated people can have asymptomatic infections with both the wild-type and the vaccine-strain virus, and can be contagious during that time. However, whether the vaccine affects the degree or duration of asymptomatic contagiousness has not to my knowledge been studied with the chickenpox vaccine. (Other studies have found that some vaccines increase or decrease, but do not eliminate, the length of asymptomatic carriage, as discussed in my previous posts on pertussis, meningococcal, HiB, and pneumococcal.)

Until proven otherwise, vaccinees should be considered at equal risk of asymptomatic carriage.


How effective are the chickenpox and shingles vaccines?

The chickenpox vaccine has highly disputed effectiveness. Because natural exposure to children with the infection boosts immunity, the vaccine is more effective when fewer children receive it [12-15, 21]. We also know, for example, that vaccinees can get both chickenpox [8-9] and shingles [19-20, 22] from the vaccine virus.

A Japanese study reported that 34.2% of chickenpox-vaccinated children developed symptomatic chickenpox within 7 years after vaccination. The study did not continue after 7 years, but it can presumably affect more children who are further away from the date of their vaccine. The study also did not look for evidence of asymptomatic infection. The authors concluded that the vaccine may reduce the severity of the symptoms but is not strong enough to prevent infection [23]. A South Korean study found that chickenpox cases actually increased after the vaccine was introduced, and that symptoms were not milder in vaccinated children [24].

Since exposure to chickenpox boosts immunity and prevents shingles, researchers had long predicted that a decrease in chickenpox might cause an increase in shingles, estimating that it would result in an overall increased mortality rate (because shingles is more dangerous), with the increased disease and complications from shingles cancelling out any benefit from decreased chickenpox [12, 25-26]. In fact, this was the primary reason why nearly all European countries have chosen to forgo chickenpox vaccination. Some researchers even argued that it is unethical to vaccinate children against chickenpox, knowing that it will result in increased overall morbidity and mortality [27].

The researchers who predicted an increase in shingles were proven right when numerous studies in multiple countries using the chickenpox vaccine (including North America, Southeast Asia, and Australia) found that shingles cases increased and occurred in younger and younger ages, that cases of severe complications from shingles increased and occurred in ever younger ages, that chickenpox also occurred at younger and younger ages, and that chickenpox vaccination overall increased complications and medical costs—in other words, it was neither effective nor cost-effective [14-15, 21, 28-34].

Because the vaccines had very little effectiveness and also increased the incidence of shingles, it was necessary to add a booster shot [21] and later a shingles vaccine. The addition of these new vaccine doses is not cost-effective and is associated with a higher rate of complications than if vaccination had never been started [21].

According to CDC, the shingles vaccine lasts 5 years [5]. However, the research is less than inspiring. The study conducted by the shingles vaccine manufacturer, Merck, found that it was at best 51% effective, but many of the patients were only followed for 31 days [11], so all we know for certain is that it might cut your risk in half for the first month after receiving it. Furthermore, they found it to be less than 40% effective for those aged 70 and older, while in people over 80 years old, the vaccine was only as effective as placebo—in other words, completely ineffective [11, 35]. It is also not effective at preventing postherpetic neuralgia (i.e., shingles pain) [35].


Are there other infectious diseases related to chickenpox and shingles vaccination?

After the MMR (measles-mumps-rubella) vaccine was introduced, cases of encephalitis (serious brain inflammation) due to measles, mumps, and rubella essentially disappeared. However, it was replaced with an even greater number of encephalitis cases by other bacteria and viruses that both had and had not been previously associated with encephalitis, including chickenpox encephalitis. Furthermore, these new cases of encephalitis occurred in younger age groups, which post more serious risks [36]. In other words, MMR vaccination triggered more dangerous chickenpox infections, and one of the CDC’s cited reasons for chickenpox vaccination is the potential for severe complications like encephalitis [37]. In most of Europe, it is still argued that because chickenpox is very mild in childhood and very severe in adulthood, and the increased shingles risk offsets any potential benefit, there is no justification for routine childhood chickenpox vaccination [38].


What are the risks of the vaccines?


Some research suggests that adverse events from varicella vaccination are at least equal to the adverse events of chickenpox infection that the vaccine prevented—in other words, there is no net change in adverse events between nearly 100% natural infection rate and nearly 100% vaccination rate [14].

In one study, systemic adverse reactions occurred in 11.9% of the vaccinated children [24]. The manufacturer reports that the vaccine has caused some of the same serious side effects associated with the wild-type disease, such as pneumonitis [10]. There is a combination MMR and chickenpox vaccine called ProQuad which is associated with higher fever and seizure rates compared to children who get MMR and chickenpox vaccination separately [39].

Shingles. Non-immunocompromised individuals can also develop vaccine-strain shingles as shortly as 2 years after vaccination [19-20, 22].

Indirect risks include the following:

Multiple Sclerosis. There is an increased risk of MS in people who contract measles, mumps, rubella, or chickenpox at a later age [40]. Because the vaccines wear off and therefore put the individual at increased risk of infection at a later age, there is an indirectly increased risk of MS in children who receive the vaccine at a young age.

Heart Disease/Attacks. There is a decreased risk of heart disease such as coronary artery disease (CAD) and heart attacks in people who had chickenpox in childhood. Chickenpox reduces the risk of heart disease and heart attacks by 33% [41]. Thus, indirectly, chickenpox vaccination may increase the risk of heart disease and heart attacks.

Brain Tumors. People who have had chickenpox in childhood have a lower risk of certain aggressive brain tumors called gliomas [42-44]. Thus, indirectly, chickenpox vaccination may increase the risk of brain tumors.



One study by the manufacturer of the shingles vaccine, Merck, reported a relatively high adverse reaction and severe adverse reaction rate following shingles vaccination. The complication rate was especially high in those over 80 years old [11, 35].

The shingles vaccine has been noted to cause severe autoimmune reactions, including a doubled risk of arthritis and a tripled risk of alopecia [45]. The manufacturer study also found that people who received the shingles vaccine at the same time as the pneumonia vaccine had less of an immune response [11].

Another study of a newer shingles vaccine that is not currently available in the U.S. found that adverse reactions occurred in 84% of vaccine recipients within 7 days, and adverse reactions that were severe enough to prevent daily activities occurred in 17% of vaccinees [46].


What vaccines are offered against chickenpox and shingles?

(NOTE: These ingredients lists are not complete; they only list the most alarming ingredients.)

Chickenpox (Varicella)

  • ProQuad (U.S.). MMRV (measles-mumps-rubella-varicella) vaccine. Contains live measles, mumps, rubella, and varicella viruses. Ingredients include chick embryo, aborted human fetus lung cells (WI-38), aborted human fetus cells (MRC-5), cow serum, human albumin, monosodium L-glutamate (MSG), human albumin, and neomycin [39].
  • Varivax (U.S.). Varicella-only vaccine. Contains live varicella virus. Ingredients include human embryonic cells, aborted human fetus lung cells (WI-38), guinea pig cells, DNA and protein from aborted human fetus cells (MRC-5), monosodium L-glutamate (MSG), EDTA, and neomycin [10].
  • Varilrix (AU). Varicella-only vaccine. Contains live varicella virus. Ingredients include aborted human fetus cells (MRC-5), human albumin, lactose, cow products, and neomycin [47].


Shingles (Herpes Zoster)

  • Zostavax (U.S.). Contains live varicella virus. Ingredients include porcine (pig) gelatin, monosodium L-glutamate (MSG), residual DNA and protein from MRC-5 (aborted human fetus) cells, neomycin, and calf serum [11].


So what’s the bottom line?

Chickenpox is very mild in childhood and has some long-term health benefits (e.g., decreased risk of multiple sclerosis, heart disease/heart attack, brain tumors), but poses much greater risk and fewer benefits in adulthood. Vaccination may merely delay chickenpox infection until adulthood, when it has considerably more risk. Natural chickenpox infection and repeated exposure to chickenpox decreases the risk of shingles. Conversely, chickenpox vaccination has very low effectiveness against chickenpox, increases the risk of shingles, and results in more severe shingles occurring at younger ages. Shingles is much more dangerous than chickenpox. The shingles vaccine does not appear to be very effective, but research is very limited; it is not effective in the oldest groups and is not yet approved for people under 50. Both vaccines are associated with some serious adverse effects, especially the shingles vaccine.



















































Pneumococcal Vaccine (Pneumonia, Meningitis)

This is the LONG version. See also the SHORT version here.


S. pneumoniae

What are the “meningitis vaccines”?

There are two basic types of meningitis: viral and bacterial. There are no vaccines targeting viral meningitis. There are three vaccines targeting causes of bacterial meningitis: HiB, pneumococcal, and meningococcal. Meningococcal was Weekly Topic 03, HiB was Weekly Topic 05, and pneumococcal will be discussed here.

There are two types of pneumococcal vaccines: conjugated (PCV) and unconjugated (PPSV). PPSV were the first created and are thus the oldest, but were generally recommended only in adults until very recently. PCV are newer and recommended primarily in children. According to the CDC Vaccination Schedule (2015), pneumococcal vaccination (primarily with PCV, followed by one PPSV dose) occurs at 2, 4, 6, and 12-18 months; if the series begins at 12 months, only two doses are recommended, and if it begins at 24 months, only one dose is recommended [1, 2]. In Canada, depending on province/territory, pneumococcal vaccination occurs typically at 2, 4, and 12 months, with a few recommending an additional 6 month dose and/or moving the 12 month dose to 18 months [3].


What is pneumococcus?

Streptococcus pneumoniae, often referred to as pneumococcus, is a bacterium and “one of the most extensively studied microorganisms” [4, p. 591]. It was first isolated in 1881 by Louis Pasteur himself. Some strains have capsules while others do not, but when simultaneously infected with both a capsular strain and a noncapsular strain, the noncapsular bacteria steal the capsular bacteria’s DNA and thereby create a capsule and convert to the same strain as the capsular bacteria. It’s also possible for capsular bacteria to steal other capsular bacteria’s DNA and begin making a new capsule. Since the capsule is how the serotype (strain) is determined, this is termed “serotype switching” or “capsular switching.” Capsular bacteria are 105 times more virulent than noncapsular strains. Based on unique characteristics of their capsules, the bacteria can be divided into over 90 serotypes. The serotypes vary drastically by geographic area; for example, in the 1980s, researchers found that the same 20 serotypes that are responsible for ~90% of infections in the U.S. and Europe were responsible for less than 70% of infections in Asia. Antibiotic resistance or sensitivity also varies significantly by geographic region, though they are generally sensitive to penicillins. [4, 5]

S. pneumoniae is commonly carried asymptomatically by healthy people, though the rates vary by population. For example, carriers may make up 20-60% of school-aged children, 5-10% of adults without children, and 50-60% of military personnel [5]. A study that tested several hundred children for pneumococci approximately every four weeks for two years found that 54% became carriers at least once by age 6 months and 97% became carriers at least once by age 2 years [6]. Carriage seems to be more common after influenza infection [4] and is more likely when the patient has recently had sinusitis, has one or more older siblings, is enrolled in daycare, or lives in the city [7]. One study of penicillin-resistant pneumococcus found asymptomatic carriage ranged from 3 days to 267 days (median 19 days) [8] and one study in mice found that lower number of bacteria was associated with longer carriage while a higher number of bacteria was quickly cleared [9]. Different serotypes are carried for different lengths of time and one study found that the duration of carriage ranged from 5.9 weeks (serotype 15C) to 19.9 weeks (serotype 6B), and that longer duration of asymptomatic carriage correlated to a lower incidence of disease [6]. Pneumococcal disease mostly occurs after new infection with a new serotype rather than after a long period of asymptomatic carriage [4]. Because carriage is so common, disease is relatively very rare.

The incubation period for pneumococcal infections is only 1-3 days and the symptoms include a sudden onset of fever and chills or rigors, as well as pleuritic chest pain; cough with rusty, mucousy sputum; shortness of breath; rapid breathing; low oxygen levels; rapid heart rate; malaise (general feeling of sickness); and weakness. Less commonly, patients also experience nausea, vomiting, and headaches [5]. It is the most common cause of pneumonia in adults; and is one of the most common causes of bacterial meningitis in children and adults, alongside the HiB and meningococcal bacteria discussed previously [4]. S. pneumoniae is also a common cause of otitis media (middle ear infections) [5].

Vaccines targeting S. pneumoniae were first developed in the early 1900s but were not effective and had many adverse effects. A more effective vaccine was developed in the 1930s, but the interest in antibiotics led to the vaccine being largely ignored, rarely used, and ultimately removed from the market. New pneumococcal vaccines were developed in the 1970s and 1980s. [4]


How can I prevent or treat pneumococcal infection in my child?

Conditions that make an individual more susceptible to pneumococcal disease include recent viral infection, immune suppression, and a generally unhealthy lifestyle [4]. Infection and carriage cannot be prevented (discussed later), so the best prevention of disease is to boost the immune system, avoid people who are sick, and engage in a generally healthy lifestyle.

The destruction of S. pneumoniae releases the toxin pneumolysin, which causes inflammation, and this toxin-mediated inflammation is thought to be responsible for the symptoms of pneumococcal disease. Furthermore, the bacteria also produce hydrogen peroxide, an oxidant which causes further damage and is thus also responsible for some of the symptoms of pneumococcal disease. This peumolysin- and hydrogen peroxide-mediated damage is thought to be responsible for enabling the bacteria to migrate into the lungs or bloodstream, causing pneumonia or invasive disease; the bacteria may migrate to the meninges and cause meningitis either through the bloodstream or directly through the nasopharynx (nose and throat). Furthermore, the pneumolysin damages the cilia in the host’s throat, making it more difficult to move mucus up and out, similarly to pertussis. Also similarly to pertussis, antibiotics attack the bacteria but do not repair the damage and thus may shorten the contagious period or prevent disease if given before symptoms develop but do not improve the progression of the disease or the outcome if given after symptoms have already developed. In fact, by killing the bacteria and thus releasing more of the bacteria’s pneumolysin toxin, antibiotics may actually worsen the disease. [4] Furthermore, unfortunately, the most common strains are also the strains most commonly antibiotic-resistant [7]. Addressing this inflammation and oxidation directly by the use of a safe anti-inflammatory and anti-oxidant that is also effective in the treatment of pertussis—such as vitamin C [10]—may help alleviate some of the symptoms and prevent progression to pneumonia and invasive disease.


How effective are the vaccines at preventing asymptomatic carriage?

“These three factors—increased carriage of vaccine-targeted strains, increased carriage of dangerous strains, and increased carriage of other bacteria—suggest ironically that vaccinated (not unvaccinated) children pose significant risk to the vulnerable members of the population and that vaccination therefore should not be relied upon for herd immunity.”

Pneumococcal carriage occurs among vaccinated individuals in proportions similar to unvaccinated individuals. For example, the CDC states, “Studies comparing patterns of pneumococcal carriage before and after PPSV23 vaccination have not shown clinically significant decreases in carrier rates among vaccinees” [5] and a study on PCV7 found that the overall rate of carriage did not change because the decrease in vaccine-targeted serotype carriage occurred alongside an increase in non-vaccine serotypes [11]. The same study found that there was no change in the distribution of asymptomatically carried PPSV23-targeted serotypes, in agreement with the CDC [11]. The CDC goes on to say that carriage of the vaccine-targeted strains may be reduced in recipients of the PCV [5], though it says nothing of serotype replacement (i.e., whether those serotypes are simply replaced by different serotypes, having no net effect on carriage rates). However, studies have demonstrated that extensive serotype replacement occurs with the PCV, with increased carriage occurring in the vaccinated. One study found carriage of nonvaccine serotypes to be 79% in vaccinated children vs. 42.5% in unvaccinated children; another found 39% in vaccinated vs. 21% in unvaccinated; and similar findings have been recorded in other studies [12]. Another study found the overall carriage rate did not change due to simultaneous increases in non-vaccine serotypes and decreases in vaccine-targeted serotypes [13].

The rate of carriage of vaccine-targeted strains is higher among those more recently vaccinated. For example, one study of asymptomatic carriage in children found that 73.1% of the isolates in children <2 years old, 68.9% of the isolates in children 2-5 years old, and 51.2% of the isolates in children >5 years old were vaccine-targeted strains. [7] This indicates that the vaccine increases the risk of asymptomatic carriage of the vaccine-targeted strains. This same study found that all of the invasive strains found in these asymptomatic carrier children were vaccine-targeted strains [7], indicating that vaccinated children may be more likely to be infected with a dangerous strain (because they are less likely to develop disease from it). Another study that compared carriage rates in the same communities before and after widespread use of the PCV7 found that the rate of carriage increased in those younger than 6 months (those most recently vaccinated) and decreased in those older than 36 months (those least recently vaccinated) [11]. Interestingly, this study also found that carriage of H. influenzae B (HiB) slightly and Moraxella catarrhalis significantly increased in the same timespan [11]. Another study duplicated those results, finding no change in S. pneumoniae carriage and increase in M. catarrhalis carriage. It also found that the vaccinated children were more likely to be carriers of pathogenic (disease-causing) bacteria [14]. Yet another study found that decreased pneumococcal carriage is associated with increased Staphylococcus aureus carriage, suggesting that pneumococcal vaccination may result in increased Staph infections [15].

These three factors—increased carriage of vaccine-targeted strains, increased carriage of dangerous strains, and increased carriage of other bacteria—suggest ironically that vaccinated (not unvaccinated) children pose significant risk to the vulnerable members of the population and that vaccination therefore should not be relied upon for herd immunity.

As discussed previously, pneumococcal asymptomatic carriage is more common after influenza infection. [4] I’m unaware of any studies on the effect of the live virus intranasal FluMist influenza vaccination on pneumococcal carriage in humans, but it’s reasonable to believe that FluMist recipients may be more susceptible to pneumococcal carriage than those who received an injected influenza vaccination or no influenza vaccination. This theory holds up to a study in mice, which found that live influenza vaccination increases carriage of S. pneumoniae and Staphylococcus aureus [16].


How effective is the pneumococcal vaccine?

The pneumococcal vaccines are said to protect against otitis media (ear infections), pneumonia, meningitis, and sepsis. If the infection moves past the ears and/or lungs to infect the normally sterile linings of the lungs (empyema), meninges of the brain (meningitis), or the blood (sepsis), it’s referred to as invasive pneumococcal disease (IPD). To explain the effectiveness of the pneumococcal vaccines, we’ll consider:

  1. Special Populations (in whom the vaccines may have varying efficacy),
  2. Serotype Replacement and Capsular Switching (which helps the bacteria avoid the pressures of the vaccine),
  3. Otitis Media, and
  4. Invasive Pneumococcal Disease, which will encompass
    • Pneumonia,
    • Meningitis, and
    • Sepsis

1. Special Populations

Unfortunately, the vaccine is not very effective at producing an antibody response in the populations that might benefit from it most: immune-suppressed patients (those lacking a spleen, infected with HIV, etc.), patients with frequent respiratory infections, the elderly, and young children [4]. Furthermore, after the introduction of the vaccine, there was an increase in drug-resistant IPD in the most susceptible populations (those aged <5 and 65+), and a decrease in drug-resistant IPD in the least susceptible populations (those aged 5-64) [17]. Another study in Alaska confirmed these findings, with an increase in the IPD rate in children under 2 and adults over 45, particularly in Alaska Natives, following PCV7 vaccination of infants and toddlers [13]. This poses particular danger to “the herd,” since the vaccine is associated with an increased incidence of disease in the populations most vulnerable to disease complications.

2. Serotype Replacement and Capsular Switching

It was thought that vaccination would be very effective because the majority of cases were caused by only a few serotypes [4], but some researchers warned that other serotypes may quickly move in to replace them (called “strain replacement” or “serotype replacement”) and that the new serotypes may be more dangerous [12]—in colloquial terms, it was a discussion of whether to fight “the devil you know or the devil you don’t.” They also warned that the pneumococci’s ability to switch its capsule in order to change serotype (“serotype switching” or “capsular-switching”) would mean that after infecting a host that had been vaccinated, the bacteria would simply change its serotype in order to avoid the host’s vaccine-induced defenses, a phenomenon called “vaccine escape” [12, 18] (as is the case with meningococcal bacteria [19]). Unfortunately, these researchers’ predictions were correct.

The CDC states that no change in serotypes was noted following the use of PPSV23 in adults [5]. However, serotype-replacement has been observed with the PCV, the first of which (PCV7) was licensed in 2000. For example, one 2004 CDC study examined only serotype 19A, a serotype not included in the PCV7, and found that it almost tripled in incidence between 1999 and 2004 (another study using the same data found that it more than quadrupled [17]), and that it had become more genetically diverse and more drug resistant. Furthermore, their results indicated that many clones (genetic bases) targeted by the vaccine took up the genetic code for the capsule of serotype 19A—in other words, the vaccine-targeted strains changed into serotype 19A, a strain not targeted by the vaccine, an example of capsular-switching as vaccine escape [18]; unfortunately, other studies have shown serotype 19A to be more dangerous, so the decrease in vaccine-targeted serotypes has nonetheless occurred alongside an increase in at least one more dangerous non-vaccine serotype [20]. Other studies have provided further evidence to support capsular-switching and oppose antibiotic-directed evolution as the causes of increases in non-vaccine serotypes [20, 21], though some studies have found that while drug-resistant bacterial samples decreased, drug-resistant infections caused by non-vaccine serotypes increased [13]. In most populations, serotype replacement occurs within 3-4 years after introduction of the vaccine [13].

[22] Note that this occurred in Salt Lake City, Utah, and may not be representative of the general population.

[22] Note that this occurred in Salt Lake City, Utah, and may not be representative of the general population.

The pre-licensure vaccine trials showed no changes in serotypes in response to vaccination. However, this was likely due to the fact that relatively few children were vaccinated in the trials, whereas post-licensure, the vast majority of children have received the vaccine. When the vaccine is used on a large scale, it pushes the serotypes to switch. [11, 12, 20] Populations where PCV7 use was widespread (such as Alaska Natives) experienced significant serotype replacement while populations where pneumococcal vaccination was low or moderate (such as Navajo and Australian aboriginal children) did not experience serotype replacement. In fact, the proportion of Alaska children receiving the pneumococcal vaccine was significantly higher than either the national average or any other individual state [13]. Ironically, this means the pneumococcal vaccine would be most effective in recipients if fewer children received it—the opposite of what is usually asserted.

Another potential issue is that some studies had incomplete data and so chose to extrapolate from the data they did have, essentially guessing about the data they didn’t have and using those guesses in their final results. For example, the 2004 CDC study mentioned above did not have the serotype data for all of the samples and so estimated the actual number and proportions of serotypes by extrapolating from the data they did have [17, 18]. It’s unclear how this affected the results.

Finally, and most likely to have the greatest effect on the results, many studies are of low methodological quality. A meta-analysis of studies on the effect of pneumococcal vaccination against pneumonia in older adults found that when only high-quality studies were included, the results were very homogenous: they all agreed that the vaccine is ineffective. However, when studies of all quality were included, the results were very heterogeneous: the effectiveness of the vaccine was uncertain. [23] In this regard, pneumococcal vaccine effectiveness studies mirror influenza vaccine effectiveness studies [24].

3. Otitis Media

“the vaccine slightly reduces the incidence of [ear infections] in some children, but increases the incidence of [ear infection] that is difficult to treat or comes back again and again”

At least 60% of acute otitis media (AOM) is viral, pneumococcus makes up about 25% of all AOM causes, and over 80% of children with AOM recover without antibiotics. The vaccine was not licensed for prevention of otitis media, though it was nevertheless widely advertised for that use since its introduction. It has been suggested that the vaccine was advertised for this purpose because ear infections are very common among vaccinated children while the more serious concerns of pneumonia and meningitis are very rare [25]. Although the drug manufacturer and others found the vaccine to result in a 6-7% reduction in AOM (there was approximately a 34% reduction in S. pneumoniae ear infections, but S. pneumoniae only caused 25% of ear infections pre-vaccine, so the total effect on ear infections was minimal) with simultaneous decreases in vaccine-targeted serotype AOM and increases in non-vaccine serotype AOM [14, 26, 27], it is not effective at reducing the incidence of recurrent ear infections [28]. Another study found that while pneumococcal ear infections decreased from 48% of ear infections to 31% of ear infections in pneumococcal-vaccinated children, other bacterial causes of ear infection doubled, more than replacing the drop in pneumococcal ear infections. Interestingly, one of the bacteria that increased was nontypeable H. influenzae [29] (for more information on HiB, please refer to our previous publication on that topic here). Other studies found increases in carriage of M. catarrhalis (which is more difficult to treat) and HiB, and that vaccinated children were more likely to be infected with pathogenic (disease-causing) bacteria, increasing the risk of antibiotic treatment failure and recurrent AOM [11, 14]. Another study found not only that there was no reduction in AOM among pneumococcal-vaccinated children, but also that pneumococcal-vaccinated children were more likely to have ear infections caused by Staphylococcus aureus, which poses serious concerns about antibiotic resistant ear infections caused by methicillin-resistant Staphylococcus aureus (MRSA) [15, 30]. Another study found no decrease in AOM in children who received pneumococcal vaccines compared to children who received hepatitis A or B vaccines [31], which may be an odd choice for comparison, given that the hepatitis A vaccine may cause AOM [32]; this means they compared the AOM rate after pneumococcal vaccines to the AOM rate after another vaccine which can cause AOM; as there was no difference in AOM rate between the PCV-vaccinated and Hep A-vaccinated children, this seems to indicate that PCV increases AOM rates. At any rate, that last odd study aside, the vaccine slightly reduces the incidence of AOM in some children, but increases the incidence of AOM that is difficult to treat or comes back again and again.

4. Invasive Pneumococcal Disease (IPD)

It’s difficult to say what impact the vaccine has on IPD because studies examining all serotypes have observed both a decrease [22] and an increase [21] in IPD. A study in Spain found the proportion of IPD cases caused by non-vaccine serotypes increased from 38% in the prevaccine period to 72% in the



postvaccine period with an increase in the total number of IPD cases [21]. Although about half of the children in the Spain study had received the PCV7, and this is suggested as a possible reason for the increase, the same phenomenon of sharply increased IPD (specifically due to non-vaccine serotype increases significantly outweighing the vaccine-targeted serotype decreases) was observed in Alaska as well, where the vast majority of the children had received the PCV7 (the proportion who had received at least 3 doses of PCV7 ranged from 88% in 2003 to 96% in 2006). Particularly interesting is that the proportion of IPD cases designated serious and requiring hospitalization also increased (i.e., IPD cases increased in number and became proportionately more dangerous) [13]. However, another 2004 study that looked at all serotypes found a simultaneous decrease in vaccine-targeted serogroups and increase in non-vaccine serogroups such that the total number of IPD cases did not change, though the proportion of cases caused by drug-resistant bacteria and the proportion of cases identified as serious or life-threatening increased. Especially important to note was that the cases caused by non-vaccine serotypes were the most severe [22], suggesting that the vaccine-targeted serotypes were replaced with more dangerous serotypes, which, as discussed above, researchers had previously warned might occur. It is interesting to note that the increase in drug resistance was noted in PCV7-targeted serotypes in one study [22] but in non-vaccine serotypes in another study [11], while another study found a decrease in drug resistance [21]. Another study found a decrease in drug-resistant bacteria overall but a total increase in drug-resistant IPD in young children and the elderly; and an increase in drug-resistant IPD caused by vaccine-targeted serotypes with the greatest increase in drug resistance in serotype 19A (the nonvaccine serotype which increased the most in overall number and proportion of cases) [17]. Other more recent studies have found further increases in both 19A and other non-vaccine serotypes as well as a further increase in drug-resistant pneumococcal infections among the vaccinated but not among the unvaccinated, with the risk highest among those who’d received the most doses of vaccine [20].

Why are the results so variable between studies? It’s probably mostly an issue of which populations are included in the study. For example, the CDC study mentioned above, which found a drop in total IPD cases and apparently no change in the seriousness of IPD cases [17, 18], did not include the population reported by another study, where there was no change in total IPD cases and an increase in serious and life-threatening cases [22]. As discussed previously, the proportions of each serotype vary significantly from population to population, so the vaccine may be very effective in one population and very ineffective in another. If a study of the entire nation, which necessarily must sample various populations rather than including every single case across the country, selectively studies the populations where the vaccine is most effective, as the CDC apparently did (probably unintentionally, since they examined data from the designated CDC surveillance sites), this will skew the results. For this reason, I’m afraid all that can really be said is some studies found the vaccine to be productive and others found the vaccine to be counter-productive, and unfortunately we can’t really know which is true for the general population, nor can we accurately predict which populations will be most benefitted by the vaccine or most harmed by it. (And I know that statement will be unpopular with both pro-vaxxers and anti-vaxxers. Sorry, not sorry.)

A. Pneumonia

“…in children, the vaccine may increase or slightly reduce the incidence of pneumonia but increases the incidence of severe pneumonia that is more dangerous and more difficult to treat. [….] …pneumococcal vaccination does not prevent pneumonia in older adults… but was associated with an increase in severe pneumonia requiring hospitalization.”

In 2004, just four years after the PCV7 was licensed, researchers noted an increase in parapneumonic empyema (a very severe form of pneumonia where the lining of the lungs becomes infected, with mortality as high as 30% in non-immunocompromised patients) caused by pneumococci in spite of decreases in pneumococcal disease and pneumococcal pneumonia, data which confirmed previous studies [22]. A Cochrane Review from 2004 found no effect of PCV7 on clinical pneumonia rate [33] while the Cochrane Review from 2009 found that PCV7 slightly decreases the clinical pneumonia rate [34]. However, a more recent study from 2010 found that PCV7 vaccination was associated with an increase in drug-resistant pneumonia among the PCV7-vaccinated but not among the PCV7-unvaccinated [20]. As discussed above, serotype prevalence differs significantly from population to population and so the vaccine may be very effective in one population and very counter-productive in another. This was exemplified in Britain, where the PCV7 was introduced in 2006, and by 2008, health authorities noted that the incidence of empyema (very severe pneumonia) had risen significantly, due in part to the 10-fold rise in serotype 1 (not included in the vaccine). Though the rise in serotype 1 began before introduction of the vaccine and thus cannot be blamed solely on the vaccine, serotype-replacement surely contributed [35]. Spain also saw an overall increase in IPD in children under 2 after introduction of the PCV7, including a more than fourfold increase in pneumonia [21]. Alaska saw the same pattern, with an overall increase in pneumonia cases and an increase in the proportion of pneumonia cases that involved empyema [13]. In other words, in children, the vaccine may increase or slightly reduce the incidence of pneumonia but increases the incidence of severe pneumonia that is more dangerous and more difficult to treat.

A rigorous meta-analysis published in 2009 found that pneumococcal vaccination does not prevent pneumonia in older adults [23]. As in studies of children discussed above, the use of the PPSV in elderly adults was not associated with a decrease in pneumonia, but was associated with an increase in severe pneumonia requiring hospitalization [36].

B. Meningitis

A study in Spain found that though the rates of sepsis and pneumonia increased after introduction of the PCV7, the rate of meningitis decreased. Nevertheless, the decrease in meningitis cases was not great enough to offset the large increases in pneumonia and sepsis [21].

C. Sepsis

Also called septicemia or bacteremia and “blood poisoning,” this refers to a bacterial infection of the blood. A study in elderly adults found a decrease in pneumococcal sepsis following pneumococcal vaccination, but did not examine other potential causes of sepsis [36]. However, as early as 2004, researchers noted that the number of invasive pneumococcal disease cases did not change due to simultaneous decreases in vaccine-targeted serogroups and increases in non-vaccine serogroups, and there was an increase in cases of severe disease (those classified as “serious” or “life-threatening”) [22]. In 2005, researchers noted that though the overall pneumococcal IPD rate decreased, the proportion of IPD cases caused by non-vaccine serogroups increased (a form of serotype replacement), and the proportion of cases caused by drug-resistant bacteria increased [18]. Studies in other countries, such as Spain, confirmed some of these results. Oddly, the Spain study found that sepsis rates overall increased (from a per 100,000 population rate of 14.5 to 21.4 in children <2 and 1.5 to 5.8 in children 2-4) and the specific causes of sepsis that increased in incidence were S. pneumoniae, the species targeted by the vaccine, and E. coli [21]. A study in Alaska also found an increase in bacteremia [13].


So if it’s not effective, why did it get licensed and put on the CDC vaccine schedule?

Of the 12 committee members at the FDA responsible for determining whether to approve Prevnar for licensing, four had financial ties to the drug company making Prevnar. Of those four, three were granted waivers so that they could still vote. [37] For this reason, some believe the committee’s approval of the pneumococcal vaccine was largely a matter of bias. For a long time, Prevnar was the most expensive vaccine on the market. At one time, Prevnar alone accounted for 40% of the cost of vaccination according to the CDC schedule. Financially speaking, Prevnar performed exceptionally well compared to other vaccines.


Are there other infectious diseases related to pneumococcal vaccination?

The use of other bacterial vaccines, particularly pertussis, seems to have contributed to the sudden increase in HiB infections in the 1970s and 1980s. [38] This led to the creation of the HiB vaccine. However, the introduction of the HiB vaccine also seems to have caused the sudden increase in pneumococcal infections, which are more dangerous and less treatable than HiB. This led to the introduction of the pneumococcal vaccine. However, the introduction of the pneumococcal vaccine seems to have caused the sudden increase in meningococcal infections, which are more dangerous and less treatable than pneumococcal infections. This led to the introduction of the meningococcal vaccine. There is concern that meningococcal vaccination will also be followed by the sudden increase of another more dangerous and less treatable bacterial disease. [39, 40]


What are the risks of the vaccine?

Prevnar has a troubled history. As mentioned above, there were significant financial conflicts of interest in the licensing process. Furthermore, a whistleblower came forward in 2004 with allegations that the company was violating certain FDA rules regarding quality control [41]. Many in developing nations such as Argentina were apparently coerced into participating in the Prevnar vaccine trials under threat of having their children taken from them if they refused [42]. It was also halted or outright banned in many countries shortly after introduction due to severe adverse reactions, particularly death, including, but not limited to, the Netherlands [43], Portugal [44, 45], Japan [46], and India [47].

The drug company making Prevnar performed short-term safety studies in which Prevnar was compared to an experimental vaccine. Prevnar was found to cause more seizures and rashes, and higher fevers than the experimental vaccine. Prevnar was not compared to a placebo. [25, 37]

Please note that having had the vaccine once without any serious reactions does not mean serious reactions will not happen with future vaccination. For example, this article reported a case where a patient with previous pneumococcal vaccination nevertheless had a serious local reaction (severe pain and swelling that extended beyond the area of the injection) upon repeat vaccination [48] and, in fact, reactions are more common in those who have had the vaccine before than in those receiving the vaccine for the first time [49].

Seizures. One study conducted by the vaccine manufacturer found seizures to occur four times as often in children receiving the pneumococcal vaccine than in children receiving another experimental vaccine (it was not compared to a saline placebo) [25].

Asthma. One study found the incidence of asthma in pneumococcal-vaccinated children (2.96/1000) was nearly double the incidence in pneumococcal-unvaccinated children (1.66/1000). The authors postulated that this was related to “the hygiene hypothesis of decreased childhood infections” [50]. The hygiene hypothesis notes that children who have fewer childhood infections (including measles and hepatitis A) have a higher incidence of allergies and asthma, and hypothesizes that induction of a Th1 response early in life prevents or even reverses the imbalanced Th1/Th2 ratio in people who are prone to asthma [51].

Thrombocytopenia. The vaccine has been noted to cause relapses of immune thrombocytopenia [52].

Autoimmune Diseases. Pneumococcal vaccination has been shown to cause onset or rebound of the following autoimmune conditions: idiopathic thrombycytopenic purpura, peripheral and central demyelinating disease, Henoch-Schönlein Purpura (a form of leukocytoclastic vasculitis), Guillain-Barre Syndrome, minimal-change nephritic syndrome, neuromyelitis optica (a.k.a., optic neuritis), Sweet’s syndrome, autoimmune hemolytic anemia, systemic lupus erythematosus, migrating arthralgia, angioimmunoblastic lymphadenopathy with dysproteinemia (a type of lymphoma), and chronic fatigue syndrome. It has been involved in at least two cases of bullous phemigoid, myositis, but other vaccines were given simultaneously, so causation with pneumococcal vaccination cannot be demonstrated. These conditions have largely occurred following PPV rather than PCV, as the PCV is too new for most autoimmune conditions to have presented themselves and is given primarily in children, in whom many autoimmune reactions are missed due to age-related difficulty expressing or recognizing symptoms [53]

Local Reactions. Local reactions, such as severe pain and swelling that extends far beyond the area of the injection, have been reported to occur even in those who have previously received pneumococcal vaccination or had extensive laboratory contact with pneumococci with no previous reaction [48]. These local reactions may mimic cellulitis and have high white blood cell counts, leading to unnecessary hospitalization and antibiotic treatment if the treating physician is unaware that this is a typical, noninfectious reaction to the vaccine. A local reaction occurs in as many as 50% of vaccine recipients, with the highest rate in those who have previously had pneumococcal vaccination [49].

Apnea in Preemies. Apnea (temporary suspension of breathing) has been observed in premature infants who receive Prevnar. [54]

Bronchiolitis, Gastroenteritis, Pneumonia. Ironically, one of the most common serious adverse events following this pneumonia vaccine is pneumonia. [54]

Hypotonic-Hyporesponsive Episodes. This is similar to fainting; the child may be awake but have altered consciousness. This is one of the most common serious adverse reactions reported. [54]


What vaccines are offered against pneumococcal?

In the U.S., there are two pneumococcal vaccines, the PCV13 (the replacement for PCV7), which targets 13 strains and is recommended for children under 5 and adults over 64 (and those aged 6+ who are at high risk), and the PPSV23, which targets 23 strains and is recommended for adults over 64 (and those aged 2-64 who are at high risk). (NOTE: These ingredients lists are not complete; they only list the most alarming ingredients.)

  • Prevnar 13: diphtheria-pneumococcal (diphtheria CRM197 protein, pneumococcal 13 serotypes, soy, yeast, ammonium sulfate, polysorbate 80, aluminum) [54]
  • Pneumovax 23: pneumococcal (pneumococcal 23 serotypes, phenol) [55]


So what’s the bottom line?

The bottom line is that S. pneumoniae is so common that almost 100% of the population carries it at some point and develops some degree of immunity by age 2. There are over 90 serotypes, and the bacteria easily change their serotype (serotype switching) to avoid the host’s vaccine-induced defenses. The vaccine does not prevent asymptomatic carriage—in fact, it may increase asymptomatic carriage not only of S. pneumoniae but also of other bacteria—and so cannot contribute to herd immunity and may, in fact, pose greater risk to the herd. The vaccine is said to protect against ear infections, pneumonia, meningitis, and sepsis, but may actually be ineffective for all of these purposes due partly to serotype switching and serotype replacement, and partly to increases in other bacteria. The serotypes not covered by the vaccines are more dangerous, and so the proportion of serious infections is higher in vaccinated children than in unvaccinated children. Because it is mostly ineffective, the risks, no matter how mild, outweigh the benefit.





















[19] See the previous Meningococcal Weekly Topic located here:





[24] Per Cochrane Collaboration: “An earlier review of 274 influenza vaccine studies in all age groups (including most of the studies in this review) showed an inverse relationship between risk of bias and the direction of study conclusions. Conclusions favourable to the use of influenza vaccines were associated with a higher risk of bias. In these studies, the authors made claims and drew conclusions that were unsupported by the data they presented. In addition, industry-funded studies are more likely to have favourable conclusions, to be published in significantly higher-impact factor journals and to have higher citation rates than non-industry-funded studies. This difference is not explained by either their size or methodological quality (Jefferson 2009a). Any interpretation of the body of evidence in this review should be made with these findings in mind.”









[33] NOTE: The link provided goes to the abstract; however, the information about clinical pneumonia is in the full text of the article, not in the abstract.






[39] “Several factors indicate that mass immunisation with pertussis and other non-Hib vaccines may have been responsible for the unprecedented epidemics of invasive bacterial infections such as Hib, during the 1970’s and 1980’s.” (p. 315) Miller, N.Z. (2008). Vaccine Safety Manual.














[53] Shoenfeld, Y., Agmon-Levin, N., & Tomljenovic, L. (2015). Vaccines and Autoimmunity (pp. 193-195, 227, 323, 340, 346, 354). Hoboke, NJ: Wiley Blackwell.



Pertussis (Whooping Cough)

In another forum, I shared some very basic information on whooping cough. Recently, I was asked to post it in a place where it can be widely shared. So here it is!

Weekly Topic 02: Pertussis (Whooping Cough)

Thanks to the recent viral video of a baby with whooping cough, we’re doing pertussis this week.

In the United States, pertussis is currently the least well-controlled vaccine-preventable disease despite excellent vaccination coverage and 6 vaccine doses recommended between 2 months of age and adolescence. [E2]

What is whooping cough?

Whooping cough or “pertussis” is a coughing illness that usually lasts many weeks (“the 100-day cough”); when the child has the typical whooping cough symptoms, it’s called “classic pertussis.” Many pertussis infections are asymptomatic or present as the flu. For example, this study [1] found that among unvaccinated 10 year olds who had not had classic whooping cough, 64% had antibodies against pertussis toxin and 100% had antibodies against other pertussis antigens, indicating that 100% of unvaccinated children without history of whooping cough nevertheless had an infection but fought it off without symptoms. In this same study, they found that 61% of unvaccinated 10 year olds had had whooping cough, indicating that in a given population, about 60% will have classic pertussis and 40% will develop immunity by an asymptomatic or mild flu-like infection. Natural infection confers about 30 years of immunity [2], whereas the vaccine lasts at least one year for only 73% of recipients, and at least 2-4 years for only 34% [3]. When symptoms do appear (i.e., when the child actually gets classic pertussis), it is most severe in newborns.

Whooping cough or pertussis is caused by one of several bacteria:

  • Bordetella pertussis
  • Bordetella parapertussis
  • Bordetella holmesii

What is B. pertussis?

B. pertussis is the first bacteria we discovered that causes whooping cough. It was discovered in 1900 and is the only bacteria used for the whooping cough vaccine. Thanks to the vaccine, the bacteria has evolved and there are now two important strains to know about:

  • Pertactin-deficient or “Non-PRN” B. pertussis is a new strain that makes up 85% of B. pertussis in the U.S. today [4]. (EDIT: A later American study found 91.7% of tested B. pertussis isolates to be Non-PRN [E1]. However, this apparently varies by country and even by region within a country.) According to the CDC, those who are vaccinated are at higher risk of contracting this strain and the risk increases with more vaccine doses given [4]. EDIT: This was later confirmed by other research in humans [E2] and experiments in mice [E3].
  • PtxP3 B. pertussis is a new strain that produces more pertussis toxin and is therefore believed to be more dangerous. It was responsible for recent Australian outbreaks [5]. It is believed that the vaccinated are at higher risk of contracting this strain [6]. EDIT: This is supported by other recent research [E4]. Like Non-PRN B. pertussis, PtxP3 B. pertussis evolved in response to the vaccine. Since this strain first appeared right when whooping cough rates began increasing, it is thought to be the primary reason for the increased incidence of whooping cough [E5].
  • EDIT: The prevailing theory seems to be that the increase in pertussis rates in spite of higher-than-ever pertussis vaccination rates is due to a combination of the vaccine wearing off and vaccine resistance due to Non-PRN and PtxP3 strains [E5].

What is B. parapertussis?

B. parapertussis is another species that causes whooping cough. It was discovered in the 1930s. The vaccine may increase the risk of infection with this species 40-fold [7].

What is B. holmesii?

B. holmesii is a new species that causes whooping cough. It was discovered in 1985. The pertussis vaccine may increase the risk of B. holmesii (DTP) or have no effect on the risk of B. holmesii (DTaP) [8].

What is the popularity of these species and strains?

Knowing how common the different species and strains are can help us predict vaccine-induced risk. A study in Ohio in 2010 [9] found the proportions to be:

  • 42.3% B. pertussis (or mix)
    • estimated 36.0% Non-PRN
    • estimated 6.3% PRN+
  • 42.5% B. parapertussis
  • 15.3% B. holmesii

The only species and strain against which the vaccine protects is PRN+ B. pertussis, which makes up approximately 6.3% of all whooping cough bacteria in circulation (if we take the CDC’s report that 15% of B. pertussis is PRN+). However, the vaccine has no effect on 15.3% of all whooping cough bacteria (B. holmesii) and increases your risk of 78.5% of all whooping cough bacteria (non-PRN B. pertussis and B. parapertussis).

Look up any recent news articles about whooping cough outbreaks. Although they frequently blame the unvaccinated, if they admit how many were vaccinated, it usually disproportionately affects the vaccinated.

EDIT: In fact, the CDC itself says that the unvaccinated are not responsible for the increase in whooping cough cases over the past few decades [E9].

What about herd immunity?

Because the vaccine is so ridiculously ineffective at preventing whooping cough—in fact, it increases your risk of whooping cough, as described above—there’s no such thing as herd immunity for whooping cough. However, even if the vaccine actually prevented whooping cough, it would not contribute to herd immunity because it does not prevent a person from becoming contagious.

A 2013 FDA study [10] found that after being exposed to an animal with classic whooping cough, vaccinated baboons got infected but did not have symptoms and were contagious. In other words, vaccinated people may be protected from developing classic whooping cough caused by PRN+ B. pertussis (which was the strain used in the study and the only strain against which the vaccine protects), but they are not protected against becoming infected and contagious. In this respect, the vaccinated may pose a greater risk to vulnerable people like infants and immunocompromised individuals because they are more likely to get whooping cough caused by newer species/strains and more likely to develop a contagious asymptomatic infection caused by the vaccine-targeted strain. If they have no symptoms, they do not know they are contagious.

ETA: The lead author of the FDA baboon study also gave the New York Times an interview in which he explained that the vaccinated still develop infection when they are exposed and grow the bacteria in the backs of their throats, and thereby are contagious. He described this as “good for you, but not for the population” [E8].

What about getting the vaccine during pregnancy?

Women who get the vaccine during pregnancy develop some antibodies and pass them on to their babies–about 68.8 U/mL [E6]. However, the level of antibodies required to prevent pertussis is 246 U/mL [E7]. Not surprisingly, it has not yet been demonstrated that infants who received the Tdap vaccine during pregnancy have reduced risk of pertussis.

What’s the bottom line?

Many pertussis infections are so mild that they are not recognized as pertussis. Furthermore, the pertussis vaccine offers no real protection. It increases your risk of almost 80% of whooping cough bacteria and protects against only 6%. It also makes you susceptible to becoming a contagious asymptomatic carrier. There is no evidence that getting it during pregnancy protects your baby.





[4] see page 6:


[6] see slide 18:



UPDATE 9/16/16: Looks like the above link no longer works. Here’s an archived version of the link:















Please note that the exact proportions of species and strains differs from country to country, so the vaccine-targeted strain may make up less or more of the total in your region. The U.S. studies mentioned above should be used only as a rough estimate.

A Brief History of Pertussis Vaccines

Previously, I wrote about the dangers of attempting to protect an infant by cocooning (vaccinating all of his adult contacts against whooping cough), demonstrating how doing so actually increases the risk to the infant rather than decreasing it. I discussed how I’ve never been a fan of influenza or HPV vaccination, but how, due to research published primarily in the last couple years, I’ve come to feel similarly about pertussis vaccination.

Whooping cough deaths and cases dropped dramatically prior to introduction of the vaccine. They continued to drop after the introduction of the vaccine, decreasing by about 99% between the mid-1940s and 1970. Vaccination rates fell in concert with rising concerns about the safety of the DTP vaccine in the 1970s-1990s. However, vaccination rates have steadily risen since then and are now at an all-time high. Nevertheless, since the 1980s, the incidence has steadily increased in spite of simultaneously increasing rates of pertussis vaccination.

As I was reading studies and articles about the many possible explanations for this paradoxical increase, I came across what was to me a fascinating and detailed (and apparently award-winning) article authored by Dr. Geier, a former researcher at the National Institutes of Health (NIH) and advisor to the Centers for Disease Control and Prevention (CDC), about the history of pertussis vaccines. After reading it, I’m amazed at how much disinformation abounds on the internet about this topic! You may not be as fascinated by the topic as am I—in which case, you can skip this one and wait for my next blog post—but I found it so interesting that I summarized the article and filled in the few blanks from a few other sources. So without further ado, I present to you a brief history of pertussis vaccination.


And So It Starts

In 1906, researchers Bordet and Gengou developed a technique to grow B. pertussis in a laboratory, which paved the way for the creation of a pertussis vaccine. The first whole cell pertussis (wP) vaccine was produced by Bordet and Gengou in 1912 and by 1914, there were six U.S. manufacturers of pertussis vaccines. Pertussis vaccines sans formal testing were used sporadically between 1914 and 1925. The first clinical trials of wP vaccines were published in 1925 and 1933, with the 1933 study reporting serious adverse effects for the first time in its listing of two deaths that occurred within 48 hours of vaccination. The first modern wP vaccine, which was combined with diphtheria and tetanus toxoids, was created in 1942 by Dr. Pearl Kendrick. Because the wP vaccine does not inactivate endotoxin or pertussis toxin, it may be associated with some or all the side effects of pertussis infection from fever to seizures, shock, and death. Evidence of the dangerous side effects of the wP vaccine as compared to the aP vaccine were reported as early as the 1930s and considered conclusive by the 1950s, with the first deaths reported in 1933 and the first published reports of irreversible brain damage appearing in 1947 and 1948. By 1948, there were a dozen manufacturers of DPT. The “mouse toxicity test,” which essentially determined the toxicity of the vaccine by seeing how many mice died from it, was introduced to ensure licensure of safer vaccines; however, researchers concluded in 1963 that there was no correlation between mouse safety and human safety. From the late 1940s to the early 1960s, physicians continued to use wP vaccines because they had no other choice on the market and because manufacturers hid the presence of endotoxin in the vaccine and its associated risk. Vaccine manufacturers began a successful lobbying campaign of pediatric societies and state legislators in the 1940s, ultimately resulting in legislation requiring DTP vaccination prior to school entry in most states by the mid-1960s. However, with such widespread vaccination came the first published reports of irreversible brain damage and deaths resulting from the vaccine, with these reports being published almost every year from the early 1950s through the early 2000s, with additional published reports coming out of other countries. This causal relationship was deemed definite by a report from the National Institutes of Health (NIH) in 1963. Criticism of the wP vaccine due to its high rate of adverse effects, cited at 93% in a 1984 study, increased through the 1970s and peaked in the 1980s.


A Better Option?

The first aP vaccine was created in the 1920s and it was obvious from at least the 1930s that it was associated with fewer adverse events than the wP vaccine. Lederle Laboratories patented a new aP vaccine in 1937, which was shown clinically to be 94% protective against disease, making it significantly more effective than the wP vaccine, and was used widely in the 1940s. However, new federal laws were passed which would require expensive and labor-intensive efficacy testing of aP vaccines, and so Lederle ceased production of its more expensive but more effective and less reactogenic aP vaccine in 1948 and began producing a wP vaccine instead. Another aP vaccine was produced in 1954 but never licensed or marketed in the U.S. due to the higher cost of production and increased clinical trial requirements. Eli Lilly Company created an aP vaccine and named it Tri-Solgen. Tri-Solgen was associated with significantly fewer adverse reactions compared to wP vaccines and was sold widely from 1962-1977, at one point capturing up to 65% of the U.S. market for pertussis vaccines. Merck Sharp & Dohme produced another aP vaccine in 1960 which was found to be both safer and more effective than the wP vaccines, but ceased production by 1963 due to the cost. The following year, 1964, Merck also removed all wP vaccines from the market citing a fear of lawsuits due to damages caused by its wP vaccine because they had a safer and more effective aP product that didn’t sell. Many other aP vaccines were produced but never marketed due to their cost and to similar concerns about legal liability due to having a safer and more effective product (the aP vaccine) but continuing to sell the more dangerous and less effective product (the wP vaccine). Due to these concerns, the market severely contracted and only four manufacturers were still producing DTP vaccines by the 1970s. Lilly ceased production of all biologic products in 1975 and sold the rights to its high quality aP vaccine Tri-Solgen to Wyeth. However, the yield was low and when Wyeth reformulated it to increase its yield, the government required new safety and efficacy trials. Wyeth determined the cost, both financial and legally, wasn’t worth it and ceased production of Tri-Solgen; specifically, Wyeth’s concerns were the same as Merck’s had been—that the studies would show the aP Tri-Solgen to be safer and more effective than Wyeth’s wP vaccine, making them legally liable for continuing to market an inferior product. Hence, the only aP vaccine on the market became unavailable after 1977. By 1984, Wyeth also completely stopped production of pertussis vaccines, again due to concerns of legal liability from its failure to produce its safer product. The end result was that only two pertussis vaccine manufacturers remained in the U.S., and both produced only the wP vaccine.


Trouble in Paradise

In 1975, two babies in Japan died from DPT vaccination, and these were two of 37 SIDS deaths linked to vaccination; in response, the Japanese government initially banned the DTP vaccine, but later in the year resumed vaccination in children over age 2. The following year, 1976, the government sent Dr. Sato to the NIH to study aP vaccine production. His aP vaccine was tested between 1978 and 1981 and found to be nearly 100% effective and significantly less reactogenic, and so the Japanese government mandated switching to aP vaccination in 1981. During this period, infant deaths plummeted, bringing Japan from a high 17th place in world comparison of infant mortality rates to 1st place with the lowest infant mortality rate in the world. (Coincidentally, when they reintroduced vaccinations in children as young as 3 months of age in 1988, their SIDS rate quadrupled.)

Also in the 1970s, rising awareness of vaccine adverse effects led to a reduction in the pertussis vaccine compliance rate. Pertussis is an epidemic disease–i.e., there are periodic outbreaks every 3.3 years with low disease rates in the interepidemic periods–but the interepidemic period that correlated to the lowest pertussis vaccine compliance rates was an unusually long interepidemic period with the lowest whooping cough incidence on record. In the 1970s, the U.K. determined that the benefits of continued use of wP vaccination outweighed its risks, while Sweden determined the opposite, pointing out that no one had died from pertussis since 1970 and that the causal relationship between wP vaccines and encephalopathies was too great to ignore, and banned the wP vaccine. Most studies of efficacy look only at the ability of the vaccine to produce an antibody response—termed by some “research efficacy.” However, because the presence of antibodies does not necessarily correlate to immunity, a study of actual disease rates may be used to determine the ability of the vaccine to prevent disease—termed by some “clinical efficacy.” The wP vaccines were determined to be 45-48% clinically effective while the Japanese aP vaccines when tested in Sweden were found to be 55-69% clinically effective. Even when the Swedish scientists compared a two-dose regimen of aP vaccines to a five-dose regimen of wP vaccines, the aP vaccines were found to be more effective.

In the 1970s and 1980s in the U.S., several factors contributed to consideration of abandoning wP vaccination, including: the relative absence of whooping cough in the population; improvements in medical treatment of whooping cough; the serious adverse effects of the wP vaccine, which led to health clinics requiring parents to sign an informed consent prior to receiving a wP vaccine; several SIDS deaths in 1979 which the CDC deemed to be caused by a particular lot of the wP vaccine, causing the FDA to order a recall of the defective lot, followed by a reversal of the recall and efforts by manufacturers to prevent future recalls (e.g., Wyeth began spreading lots out across the country rather than sending an entire lot to one area so that adverse effects of any one lot would not be noticed as quickly in the future); and numerous lawsuits beginning in 1981 which were ironically successful because it was argued that the manufacturers had known how to produce a safer aP product but chose not to. (Unsuccessful lawsuits had been filed previously.) In 1982, a television program about the adverse effects of DPT vaccination raised parental awareness so much that attorneys trying the cases were flooded with hundreds of requests for representation. The vaccine manufacturers attempted to stop the cases by harassing the expert witnesses, leading at least one to file a suit against them. Nevertheless, by 1985, 219 such lawsuits had been filed. Pressure from parents and especially from a group formed in 1982 called Dissatisfied Parents Together led the American Academy of Pediatrics (AAP) to conduct over 8 months of hearings to develop recommendations for the creation of a federal compensation program for vaccine-injured children. Due to the AAP’s recommendations and to the large-scale civil litigation against vaccine manufacturers, Congress introduced the National Compensation Act in 1983, which sought to limit liability for vaccine injuries. One manufacturer agreed to settle out of court for $26 million and then cite its case as an example of why the act was needed. In 1986, the U.S. Congress passed the National Vaccine Injury Act, which established, among other things, the National Vaccine Injury Compensation Program (NVICP) and essentially ended litigation against vaccine manufacturers. However, with the threat of litigation gone, manufacturers were no longer under pressure to produce a safer aP vaccine. Foreseeing that this would happen, the Congress also stipulated in the Act that the IOM hold hearings and make recommendations for improving vaccines in general and the pertussis vaccine specifically.


Safety Wins

As previously stated, the causal link between DPT and neurological sequelae was deemed definite by the NIH in 1963. However, after receiving several generous donations from vaccine manufacturers and being staffed and/or headed by former and current employees of vaccine manufacturers, the AAP and the Pediatric Neurology Society “mysteriously” reported in 1992 that there was no such link. This was followed by several heavily manufacturer-funded researchers publishing articles that also attempted to deny the link. Backing up a few years, we’ll examine what the government saw. In 1985, the Institute of Medicine (IOM) published a report stating, among other things, that in spite of its initially higher costs, the aP vaccine saves on overall medical costs as compared to the wP vaccine, and the United States would save millions of dollars if the wP vaccine was replaced by the aP vaccine due to the high rate of adverse reactions; it advised that the highest priority should be given to making the switch. However, this recommendation was put on the back shelf and when another IOM committee convened in 1990, only five years later, they were surprised to learn that data presented in the meeting came from their own archives. Nevertheless, the evidence against the wP vaccine was so overwhelming that, regardless of the opinions of those bought by the manufacturers, the IOM determined that the causal link between wP vaccination and encephalitis was definite. The IOM convened a third time in 1993 to again discuss the DTP vaccine and determined that it definitely causes permanent brain damage. Even the AAP failed to argue the point, instead merely notifying its members of the IOM’s position. In 1992, the FDA approved the use of aP for the boosters given at 18 months and 6 years of age. In 1996, the FDA approved the use of aP for the entire schedule. Finally, by the beginning of 2001, the wP vaccine had been removed from the U.S. market, though American manufacturers continue to produce the cheaper (in every sense of the word) wP vaccines for sale in the third world.


“The development and acceptance of acellular pertussis vaccine in the United States demonstrates that scientific evidence alone is not always enough to change harmful medical practices. Given the powerful resistance to change demonstrated by the pharmaceutical industry, it took years of litigation, consumer advocacy, international scientific development, and congressional action to create a new norm for childhood immunization. It would seem that open discussion of vaccine problems in the scientific and medical communities, along with policies that preclude those with a conflict of interest from determining vaccine policy, might help to prevent similar difficulties in the future in the rapidly expanding vaccination field.” (Geier & Geier, 2002, p. 284]




Centers for Disease Control and Prevention (1997). “Vaccination: Use of acellular pertussis vaccines among infants and young children recommendations of the Advisory Committee on Immunization Practices (ACIP).” Morbidity and Mortality Weekly Report, 46(RR-7):1-25. Retrieved from < >.

Fine, P.E.M., & Clarkson, J.A. (1982). “The recurrence of whooping cough: Possible implications for assessment of vaccine efficacy.” The Lancet, 319(8273):666-669. doi: 10.1016/S0140-6736(82)92214-0.

Geier, D., & Geier, M. (2002). “The true story of pertussis vaccination: A sordid legacy?” Journal of the History of Medicine, 57:249-284. Retrieved from < >.

Hieb, L. (2015). “How vaccine hysteria could spark totalitarian nightmare.” WND. Retrieved from < >.

Howson, C.P., Howe, C.J., Fineberg, H.V., eds. (1991). “B pertussis and rubella vaccines: A brief chronology.” In Adverse Effects of Pertussis and Rubella Vaccines: A Report of the Committee to Review the Adverse Consequences of Pertussis and Rubella Vaccines. Institute of Medicine Committee to Review the Adverse Consequences of Pertussis and Rubella Vaccines. Retrieved from < >.


Jabs for Love

DISCLAIMER: This blog post is not about pertussis vaccination overall. This blog post is about pertussis cocooning. Any rabbit trail I make is really meant to point back to the overall purpose of this blog post, which is pertussis cocooning. Did I mention this blog post is about pertussis cocooning? I now return you to your regularly scheduled program.


Jabs for Love

Some of my readers may be aware that I am pregnant and due to deliver in late May. I’ve recently been asked whether I want adults who plan to visit my newborn to get the whooping cough (pertussis) vaccine. This question probably arose from the CDC’s recent recommendation that adult contacts of a newborn get vaccinated so as to decrease the baby’s risk of contracting it from them [1], and from simple love—I love your unborn child and want to do everything in my power to protect him/her if I can—“jabs for love,” if you will. I generally answered privately because these days, if you express the slightest reservations over or even the strongest scientific evidence against any vaccine in any form for anybody or for any reason, you are labeled “anti-vaxx,” but I’ve been asked to share it more publicly.

Well, I would like to state that I’m not “anti-vaxx,” but I’m not sure what that label even means (nor “pro-vaxx” for that matter). And honestly, the medical profession (some of you may also be aware that I’m an ER nurse) has an equally vague term—“vaccine hesitant”—which is applied to anyone who hesitates over or questions the safety, efficacy, or necessity of any vaccine for all or for any unique individual. (For example, one of my coworkers in the ER was allergic to the flu vaccine. Because of her refusal to get one every year due to her allergy, she is technically “vaccine hesitant.”) In that case, I stand with the majority of nurses (Footnote 1) as “vaccine hesitant” due to my “hesitancy” over the influenza vaccine, which has basically been deemed worthless by a dozen Cochrane Reviews (Footnote 2). Over time, I’ve come to feel the same about the HPV vaccine, and I’ve rather recently discovered some things about the pertussis vaccine that makes me reconsider the wisdom of cocooning. And now, I’m going to put myself in mortal danger of being brutally murdered by “Big Pharma” or whoever it is “anti-vaxxers” are afraid of, by giving my answer to pertussis publicly rather than privately. Sharpen your pitchforks. 😉


Problems with Cocooning

I’ve seen some people suggest that the pertussis component of the adult TdaP (and pediatric DTaP) vaccine sheds, due to a misunderstanding of a certain FDA baboon study. This is not true. (The FDA news release [2] is vague and can easily be misunderstood to mean that, but if you read the study itself [3], it’s very clear, as I’ll discuss in my first point below.) If you stop to think about it, the TdaP (and DTaP) contains acellular pertussis (the aP portion), which includes only some of the components of the bacterium, not the entire bacterium. So how can you develop the growth of (be “colonized” or “infected” with) the bacteria when you’re only getting bits and pieces of it? (If someone gives you—but don’t ask me why they would—a cat’s tail and whiskers, can the cat come to life and claw you? Yes. …If you’re on LSD.) And if you can’t get an entire bacterium from the vaccine, how can you give an entire bacterium to someone else?

So I’m not afraid of the TdaP shedding and therefore won’t ask adult contacts of my newborn to avoid it for that reason. Because it just doesn’t make scientific sense.

However, although the TdaP doesn’t shed like live virus vaccines do, it:

1) Increases the risk that the recipient will become an asymptomatic carrier of B. pertussis following exposure and thereby infect others, as demonstrated in baboons in the aforementioned FDA study [2, 3] and in immunized children in an Israeli study reported by the CDC [4]. The FDA study demonstrated that following exposure to an infected baboon, baboons who had been vaccinated with acellular pertussis (as in the TdaP and DTaP vaccines) became asymptomatic carriers for 6 weeks after colonization and baboons who had been vaccinated with whole cell pertussis (as in the DTP or DTwP vaccine) became asymptomatic carriers for 3 weeks after colonization. These asymptomatic carriers then infected other baboons, demonstrating that pertussis bacteria may leap from one asymptomatic carrier to someone who is susceptible to infection by the bacteria because they were low-responders to vaccination, non-responders to vaccination, no longer immune due to waning immunity from the vaccine, or unvaccinated (Footnote 3). It’s unknown whether the bacteria can leap from one asymptomatic carrier to another asymptomatic carrier until it infects a susceptible individual.

2) May make those who do get sick with B. pertussis have milder symptoms such as no “whoop” to their cough. According to the CDC, “Adolescents and adults and children partially protected by the vaccine may become infected with B. pertussis… Pertussis infection in these persons may be asymptomatic, or present as illness ranging from a mild cough illness to classic pertussis with persistent cough (i.e., lasting more than 7 days). Inspiratory whoop is not common.” [5, p. 216] Unfortunately, this makes it harder to diagnose and more likely they’ll infect others, as in a case affecting six infants in Texas [6, para. 1] and another case affecting four newborns in Australia [7], both of which involved immunized nurses who infected newborn babies with pertussis due to a failure of physicians to diagnose their atypical symptoms.

3) Increases the risk of pertussis infection (whooping cough) caused by non-PRN strains of pertussis (pertussis bacteria lacking pertactin, a key antigen in the vaccine), as reported by the CDC. Non-PRN strains now make up over 50% of all B. pertussis isolates and a study of 752 pertussis cases in 2012 found 85% were caused by non-PRN strains. Interestingly, the vaccinated who are up-to-date on their pertussis vaccinations are more likely to become infected by these strains than the unvaccinated, reflecting a tendency for these strains to selectively attack the vaccinated. [8, pg. 6]

4) And potentially increases the risk of contracting B. parapertussis, another cause of whooping cough, 40-fold [9, 10]. I say “potentially” because this study was done in mice.

Pertussis cases have increased in spite of increasing pertussis vaccination. The FDA states, “the rates of [pertussis] infection in the U.S. have been rising over the last 30 years, despite vaccination of over 95% of children nationwide. The U.S. is now experiencing levels of pertussis comparable to those seen in the 1950s, with 48,000 cases reported in 2012.” [11, para. 3] The above four points have all been suggested as reasons for this paradoxical increase.

The FDA also states that the effects of cocooning (vaccinating all of a newborn’s adult or other contacts, which is being implemented this year in the U.S.) are unclear [11]. However, Australia, which had implemented cocooning efforts as early as 2009, abandoned it in 2012 because it was found to be ineffective at preventing pertussis infection in newborns [12].

So in summary, pertussis vaccination of adult contacts increases the risk of asymptomatic infection (increasing the risk of the infant contracting the disease); increases the risk of atypical symptomatic disease (again increasing the risk of the infant contracting the disease); increases the risk of infection and disease caused by the majority of pertussis strains (increasing the risk of the adult contact contracting the disease, therefore potentially increasing the risk of the infant contracting the disease); and potentially increases susceptibility to B. parapertussis (also increasing the risk of the adult contact contracting the disease, therefore potentially increasing the risk of the infant contracting the disease). Furthermore, cocooning has epidemiologically been found ineffective at preventing whooping cough in newborns.

So no, I won’t ask my family and friends to get vaccinated against pertussis. It just doesn’t make scientific sense.

I’m not going to tell you what to do for yourself. Getting any vaccine due to the perceived benefits to yourself, even very falsely perceived benefits as in the case of the influenza vaccine, is your choice.

However, if you want to get the vaccine solely in order to protect my child—don’t. According to the best scientific evidence from the FDA and CDC, and epidemiological evidence from Australia, you may actually be increasing my child’s risk of infection. Now, I’m not going to shriek, “Don’t visit my child if you have/haven’t gotten X vaccine, you horribleterribleawfulcrazyinsane person!!!” because I’m not ruled by fear, as are so many in these vaccine discussions. All I’m saying is that I will never ask you to protect my child by doing something that is more likely to harm him than to help him.


A Slight Rabbit Trail…

I think the pertussis vaccine is similar to the HiB vaccine. Once upon a time, B was the most common strain of Haemophilus influenzae (a bacterium, not a virus), accounting for over 80% of invasive H. influenzae disease in children, but now it’s significantly less common, having decreased by 99% in children (probably thanks to vaccination of children, which has also correlated to a decreased incidence of HiB in adults). Nowadays, the A and C-F strains are the most common, and the HiB vaccine offers no protection against those strains. Unfortunately, invasive H. influenzae disease, which carries a 22% fatality rate in adults, is increasing in overall incidence, probably as a result of the vaccine inadvertently shifting strain dominance from B, against which the vaccine offers protection, to strains A and C-F, against which it offers no protection [13]. In other words, the overall effect of the vaccine has been to increase all-type H. influenzae infections in spite of a 99% decrease in type B infections, including a sharp increase in the incidence of dangerous invasive H. influenzae disease. So while HiB vaccination made sense when the vaccine was first introduced, and was associated with a sharp reduction in HiB infections (a good thing!), it now has the effect of increasing overall H. influenzae infection and invasive disease rates. It would make more sense today to vaccinate against HiF (the new most common typeable strain) or against all-type H. influenzae [13], if possible, than to continue use of a vaccine that increases the overall risk rather than decreasing it.

Similarly, the introduction of the pertussis vaccine in the U.S. in the 1930s correlated to a sharp reduction in whooping cough rates (Footnote 4). However, by a process of natural selection, the vaccine has resulted in different strains not included in the vaccine gaining dominance, and, for probably manifold and complex reasons we don’t yet fully comprehend, recently increasing the overall incidence of whooping cough infections.



Like the HiB vaccine, it may be time to either update or retire the pertussis vaccine. Should the pharmaceutical companies produce an HiF or all-type Hi vaccine and update the pertussis vaccine (and I had reason to believe in their safety and efficacy, unlike the HPV and influenza vaccines), I would be far more comfortable receiving for myself or my child or recommending to potential adult contacts of my newborn those vaccines than receiving the current HiB and pertussis vaccines, which seem to rather increase the risk and incidence of infection and disease than to decrease it.

I think I can already feel the pitchforks poking. 😉




Footnote 1: As recently as 2010, the influenza vaccination rate among healthcare providers was so low (30-50%) that the goal was only to get the rate as high as 60% by 2010 [14]. In fact, “as a group, health workers are among the most poorly covered” as regards influenza vaccination [14] and the second most common reason given by healthcare providers for getting the flu shot is “My employer requires me to be vaccinated for flu” with less than half reporting that they think it will prevent them from getting influenza [15]. Today, in an environment where influenza vaccination is often required as a condition of employment with few or no exceptions, the majority of nurses do receive the influenza vaccine at 90.5% in the 2013-2014 season [15], an increase from about 80% in the 2011-2012 season and from about 75% in the 2010-2011 season. This increase is largely attributed to employer mandates (in fact, a 2012 CDC report showed that mandatory vaccination in healthcare institutions raised compliance rates to almost 100%) rather than to a change in attitude regarding flu vaccination [16].

Footnote 2: For those who don’t know, the Cochrane Collaboration is a global, independent, nongovernmental organization that gathers, reviews, and summarizes the latest scientific knowledge from the highest quality research. Because they limit themselves to the highest quality research, and most published research today is very poor and/or biased [17], there are limits to the topics they can discuss. For example, the highest quality type of study is a double-blind, randomized, placebo-controlled trial (RCT), which means the participants are randomly assigned into one of two or more groups, at least one group gets a placebo (an ineffective treatment, such as a sugar pill or an injection of saline or water), and neither the participant nor the person administering the treatment knows whether they’re getting “the real thing” or the placebo. These randomization and double-blind placebo techniques eliminate as much as possible the chance of mind-over-matter—that is, the participant’s expectations interfering with the results—and reduces the chance of one group being lower risk than the other, which might skew the results. However, there are cases where such a study is impossible. For example, if you want to compare the safety of hospital birth to home birth, how do you randomly assign participants to hospital vs. home? Even worse, how do you make both the participant and the healthcare provider delivering the baby unaware of which “treatment” (hospital or home) is being used? Obviously, the mother is going to know whether she’s in her own house! So there are limits to what double-blind, placebo-controlled RCT’s or other high-quality research can study; therefore, by extension, there’s a limit to what the Cochrane Collaboration can review.

However, whether the influenza vaccine actually reduces the incidence of influenza infection is not impossible to study, though it may be difficult to wade through the thousands of studies on the topic to weed out the poor quality, biased ones. With that in mind, what has the Cochrane Collaboration found regarding influenza vaccination? The most recent (2014) Cochrane Review on influenza vaccination in adults reported, “The results of this review provide no evidence for the utilisation of vaccination against influenza in healthy adults as a routine public health measure.” [18]

Why is this? There are many reasons, one of which is the relatively low incidence of influenza. The CDC explains, “ILI [influenza-like illness] is a nonspecific respiratory illness characterized by fever, fatigue, cough, and other symptoms. The majority of ILI cases is not caused by influenza but by other viruses (e.g., rhinoviruses and respiratory syncytial virus [RSV], adenoviruses, and parainfluenza viruses)… [or] bacteria such as Legionella spp., Chlamydia pneumoniae, Mycoplasma pneumoniae, and Streptococcus pneumoniae.” [19, para. 2] In the same document, the CDC concludes, “many persons vaccinated against influenza will still get ILI.” [19, para. 9] In fact, about 200 viruses can cause influenza and ILI [18]. A Cochrane collaborator expounded on the CDC’s statement, explaining that during flu season, only 7% of the population suffers ILI (influenza-like illness), and of those only 11% are caused by influenza and concludes: “…evidence presented here points to influenza being a relatively rare cause of ILI and a relatively rare disease. It follows that vaccines may not be appropriate preventive interventions for either influenza or ILI.” [20, p. 3]

Another reason discussed is the high number of vaccinations that would be necessary to prevent a single case of influenza. The researchers considered the proportion of the vaccinated population that does not respond to the vaccine and subsequently gets influenza or gets a non-influenza ILI or has a vaccine reaction (which may include flu-like symptoms), any of which results in taking sick days from work, versus the proportion of the unvaccinated population that gets ILI (caused by influenza or not), which results in taking sick days from work, but obviously does not have a vaccine reaction because they were unvaccinated. Their conclusion was that so many vaccines would be required to prevent a single case of influenza and that there would be so many side effects and non-influenza ILI cases that the end result is no economic advantage (regarding the number of days lost from work versus the cost of the vaccine as regards financial cost and work days lost to illness due to or in spite of the vaccine) to vaccination. The summarized statement reads, “The preventive effect of parenteral inactivated influenza vaccine on healthy adults is small: at least 40 people would need vaccination to avoid one ILI case… and 71 people would need vaccination to prevent one case of influenza… Vaccination shows no appreciable effect on working days lost or hospitalisation…. The effectiveness of live aerosol vaccines on healthy adults is similar to inactivated vaccines: 46 people… would need immunisation to avoid one ILI case” [18].

Furthermore, statistics regarding influenza complications are likely incorrect. For example, “flu” is often billed as a major cause of pneumonia [e.g., 19; 21; 22] and the CDC lumps flu and pneumonia together in morbidity and mortality statistics [e.g., 23]. However, as reported in the British Medical Journal regarding CDC flu and pneumonia statistics, the vast majority of “flu and pneumonia” deaths involve only pneumonia (for example, 61,777 out of 62,034 or 99.59% in 2001) and of the remaining deaths attributed to flu (257 out of 62,034 or 0.41%), only 7.00% (18 out of 257 “flu” cases or 0.029% of all “flu and pneumonia” cases) were positively identified as influenza [24]. Therefore, given the relative rarity of influenza-related deaths, it should not be surprising that the 2010 Cochrane Review found “no credible evidence that there is an effect [of influenza vaccination] against complications such as pneumonia or death” [25, p. 12].

Significantly, there are also serious issues regarding bias interfering with study results. For example, a Cochrane review of influenza vaccination in children found “Extensive evidence of reporting bias of safety outcomes from trials of live attenuated influenza vaccines [which] impeded meaningful analysis” [26]. This also calls into question the validity of any claims of efficacy made by the companies producing influenza vaccines, or in studies of influenza vaccines, the majority of which are funded by the companies producing them. Furthermore, a meta-analysis or review, such as the Cochrane reviews, are only as good as the studies included in them and may be no more than a summary of the prevailing bias [17]. This makes it even more surprising that the Cochrane Review of influenza vaccination in healthy adults found no overall advantage to vaccination considering that, by their own account, about 70% of the studies included in their review had pharmaceutical industry funding and a high risk of bias, 20% had an unknown risk of bias, and only 10% had a low risk of bias [18].

The results for children are a little more complex than for healthy adults, but it appears that vaccination against influenza is completely ineffective in children under 2 years; is effective for those over age 2, with the live influenza vaccine more effective than the inactivated influenza vaccine; and is of unknown safety in any age group [26]. Interestingly, the Cochrane Review for influenza vaccination in children stated, “This review includes trials funded by industry. An earlier systematic review of 274 influenza vaccine studies published up to 2007 found industry-funded studies were published in more prestigious journals and cited more than other studies independently from methodological quality and size. Studies funded from public sources were significantly less likely to report conclusions favourable to the vaccines. The review showed that reliable evidence on influenza vaccines is thin but there is evidence of widespread manipulation of conclusions and spurious notoriety of the studies. The content and conclusions of this review should be interpreted in the light of this finding.” [26] In other words, even though their review found influenza vaccination to be effective in children over age 2, they caution that the results could be largely due to bias secondary to pharmaceutical industry funding, as discussed above.

The most recent (2010) Cochrane review on influenza vaccination in older adults found that there is no evidence to recommend vaccination against influenza in older adults, either [27].

Footnote 3: “Low” or “poor” responders to vaccination, which seems to be a genetic trait and therefore not correctable by repeated vaccination, are those who develop poor or low-level antibody responses to initial vaccination and weak responses to revaccination, and lose detectable antibody levels long before the antibody response is expected to wane. For example, one study demonstrated loss of detectable antibodies against measles within 2-5 years of vaccination [28]. Low responders are estimated to make up almost 5% of the population in the case of measles vaccination [29]. I am unaware of the proportion of the population thought to be low responders specifically to pertussis vaccination. The sources I’ve found typically examine response to pertussis vaccination in newborns (not practiced in the U.S.), response to only one pertussis vaccination without boosters (not recommended in the U.S.), or response to the whole cell pertussis vaccine (not used in the U.S.).

Non-responders to vaccination refers to people who do not develop any detectable antibody response in spite of receiving the vaccine and all recommended boosters to the vaccine. Although the proportion of non-responders to each vaccine probably varies significantly, non-response occurs in 5-15% of those receiving the hepatitis B vaccine [30] and one study of pertussis vaccination in 137 infants showed similar results, with up to 91% demonstrating an immune response to full vaccination, implying a non-response rate as high as 9% following complete vaccination [31], so pertussis non-response is probably similar to hepatitis B non-response at 5-15%.

As discussed earlier, those who responded normally to vaccination but have had their immunity naturally wane over time and those who have not been vaccinated at all are also susceptible to pertussis. I don’t think it’s possible to even guess at the number of people in the population whose immunity has waned, though guesses have certainly been made. The rate of the completely unvaccinated also seems to be difficult to determine. According to the CDC, about 94.1% of children aged 19-35 months in the U.S. had received at least 3 doses of the DTaP vaccine, but this figure includes children who received only the DT without the pertussis (aP) portion, and I could not find a figure for children who have received absolutely no DTaP vaccines [32]. Therefore, knowing that most of the children reported as having received at least 3 doses of DTaP probably got at least one DTaP (i.e., a vaccine that included the pertussis portion), and that many children may have gotten one or two DTaP vaccines prior to stopping vaccination and therefore were not counted in the statistics in spite of having had some level of pertussis vaccination, 5% (and probably actually much lower) is the best guess I can come up with (understanding it is almost certainly inaccurately high) for how many children aged 19-35 months are completely unvaccinated against pertussis. It’s also definitely inaccurate to consider all completely unvaccinated children or adults to be susceptible to pertussis infection given that having had a naturally-occurring pertussis infection in the past may confer 30 or more years of natural immunity [33], meaning that the unvaccinated may not actually be in the “susceptibles” group. Then again, the same is probably true for the vaccinated who nonetheless developed natural infection. Furthermore, many people develop an appropriate antibody response to vaccination but still develop disease. So again, these are all just best guesses.

In summary, with potentially 5% of the population being non-responders to vaccination, 5-15% of the population being low-responders to vaccination, and 5% being completely unvaccinated, that adds up to about 15-25% of the population being susceptible to pertussis infection, not including those whose (vaccine-induced or naturally-induced) immunity has naturally waned or those for whom an appropriate antibody response is insufficient to confer protection. Then again, as mentioned once or twice in the DISCLAIMER at the beginning of this blog post, this post is really about the newborn’s susceptibility to pertussis related to cocooning, not the susceptibility of non-newborns.

Footnote 4: I mentioned that the introduction of the pertussis vaccine was followed by a sharp reduction in pertussis rates. While true, just so that I don’t come across as uninformed, I want to acknowledge what many anti-vaxxers point out: that the rate of pertussis was already in sharp decline long before the vaccine was introduced, and that the rate of decline did not change after the introduction of the vaccine [34]. Just so you know, yes, I am aware of that, but stating that fact in the body of the post itself would detract from my overall point. Additionally, I have no interest in discussing that topic in this post because, as discussed in the DISCLAIMER at the beginning of the post, this is about pertussis cocooning specifically, not about pertussis vaccination in general. I’ll leave you to do your own research on pertussis vaccination in general and decide whether the TdaP is superior to the Td—or, I suppose, to no vaccination—for your purposes.



  1. Centers for Disease Control and Prevention [CDC] (N.d.). “Surround babies with protection.” National Center for Immunization and Respiratory Diseases, Division of Bacterial Diseases. Last updated 27 Jan 2015. Retrieved from < >.
  2. U.S. Food and Drug Administration [FDA] (2013). “FDA study helps provide an understanding of rising rates of whooping cough and response to vaccination.” Last updated 27 Nov 2013. Retrieved from < >.
  3. Warfel, J.M., Zimmerman, L.I., & Merkel, T.J. (2013). “Acellular pertussis vaccines protect against disease but fail to prevent infection and transmission in a nonhuman primate model.” Proceedings of the National Academy of Sciences, 111(2):787-792. Retrieved from < >.
  4. Srugo, A., Benilevi, D., Madeb, R., Shapiro, S., Shohat, T., Somekh, E., …Lahat, N. (2000). “Pertussis infection in fully vaccinated children in day-care centers, Israel.” Emerging Infectious Diseases, 6(5):526-529. Retrieved from < >.
  5. Atkinson, W., Wolfe, S., Hamborsky, J. (Eds.). (2012). “Chapter 15: Pertussis.” In Epidemiology and Prevention of Vaccine-Preventable Diseases (12th ed.). Washington DC: Public Health Foundation. Retrieved from < >.
  6. Zastrow, R.L. (2011). “Emerging infections: Pertussis on the rise.” American Journal of Nursing, 111(6):51-56. Retrieved from < >.
  7. Woodhead, M. (2011). “Pertussis spread to neonates by immunised staff.” 6minutes. Retrieved from < >.
  8. CDC (2013). “Meeting of the Board of Scientific Counselors, Office of Infectious Diseases: Centers for Disease Control and Prevention: Tom Harkins Global Communication Center: Atlanta, Georgia: December 11-12, 2013.” Retrieved from < >.
  9. Karanikas, A. (N.d.). “Acellular pertussis vaccination enhances B. parapertussis colonization.” The Pennsylvania State University: Center for Infectious Disease Dynamics. Retrieved from < >.
  10. Long, G.H., Karanikas, A.T., Harvill, E.T., Read, A.F., & Hudson, P.J. (2010). “Acellular pertussis vaccination facilitates Bordetella parapertussis infection in a rodent model of bordetellosis.” Proceedings of the Royal Society of Biological Sciences, 282(1807). doi: 10.1098/rspb.2010.0010. < >.
  11. FDA (N.d.). “Maternal and neonatal vaccination protects newborn baboons from pertussis infection.” Last updated 16 Mar 2015. Retrieved from < >.
  12. AAP (2012). “States ending free parent whooping vaccine.” Retrieved from < >.
  13. Rubach, M.P., Bender, J.M., Mottice, S., Hanson, K., Weng, H.Y., Daly, J.A., & Pavia, A.T. (2011). “Increasing incidence of invasive Haemophilus influenzae disease in adults, Utah, USA.” Emerging Infectious Diseases, 17(9):1645-1650. PMID: 21888789. PMCID: PMC3322072. doi: 10.3201/eid1709.101991. Retrieved from < >.
  14. “Annual Influenza Vaccination Requirements for Health Workers.” (2010). American Public Health Association. Retrieved from < >.
  15. CDC (2014). “Influenza vaccination coverage among health care personnel – United States, 2013-14 influenza season.” Morbidity and Mortality Weekly Report, 63(37):805-811. Last updated 19 Sep 2014. Retrieved from < >.
  16. Domrose, C. (2013). “Face flu facts: New mandates raise the stakes in flu vaccination for nurses.” < >.
  17. Ioannidis, J.P.A. (2005). “Why most published research findings are false.” PLoS Med, 2(8):e124. doi: 10.1371/journal.pmed.0020124. Retrieved from < >.
  18. Demicheli, V., Jefferson, T., Al-Ansary, L.A., Ferroni, E., Rivetti, A., & Pietrantonj, C.D. (2014). “Vaccines for preventing influenza in healthy adults (Version 5).” Cochrane Database of Systematic Reviews. doi: 10.1002/14651858.CD001269.pub5. Retrieved from < >.
  19. CDC (2001). “Notice to readers: Considerations for distinguishing influenza-like illness from inhalation anthrax.” Morbidity and Mortality Weekly Report, 50(44):984-986. Retrieved from < >.
  20. Jefferson, T. (2009). “Mistaken identity: Seasonal influenza versus influenza-like illness.” British Medical Journal Clinical Evidence. Retrieved from < >.
  21. American Lung Association (2010). “Influenza and pneumonia.” State of Lung Disease in Diverse Communities. Retrieved from < >.
  22. CDC (N.d.). “Pneumonia can be prevented—Vaccines can help.” National Center for Immunization and Respiratory Diseases, Division of Bacterial Diseases. Last updated 12 Nov 2014. Retrieved from < >.
  23. CDC (2010). “Estimates of deaths associated with seasonal influenza—United States, 1976-2007.” Morbidity and Mortality Weekly Report, 59(33):1057-1062. Retrieved from < >.
  24. Doshi, P. (2005). “Are US flu death figures more PR than science?” British Medical Journal, 331:1412. doi:
  25. Jefferson, T. (2010). “Influenzae.” Retrieved from < >.
  26. Jefferson, T., Rivetti, A., Pietrantonj, C.D., Demicheli, V., & Ferroni, E. (2012). “Vaccines for preventing influenza in healthy children (Version 4).” Cochrane Database of Systematic Reviews. doi: 10.1002/14651858.CD004879.pub4. Retrieved from < >.
  27. Jefferson, T., Pietrantonj, C.D., Al-Ansary, L.A., Ferroni, E., THorning, S., & Thomas, R.E. (2010). “Vaccines for preventing influenza in the elderly (Version 3).” Cochrane Database of Systematic Reviews. doi: 10.1002/14651858.CD004876.pub3. Retrieved from < >.
  28. Poland, G.A. (1998). “Variability in immune response to pathogens: using measles vaccine to probe immunogenetic determinants of response.” American Journal of Human Genetics, 62(2):215-220. PMID: 9463343. PMCID: PMC1376909. doi: 10.1086/301736. Retrieved from < >.
  29. LeBaron, C.W., Beeler, J., Sullivan, B.J., Forghani, B., Bi, D., Beck, C., …Gargiullo, P. (2007). “Persistence of measles antibodies after 2 doses of measles vaccine in a postelimination environment [Abstract].” Archives of Pediatrics and Adolescent Medicine, 161(3):294-301. PMID: 17339511. Retrieved from < >.
  30. Hepatitis B Foundation (N.d.). “Vaccine Non-Responders.” Last updated 21 Oct 2009. Retrieved from < >.
  31. Hanlon, M., Nambiar, R., Kakakios, A., McIntyre, P., Land, M., & Devine, P. (2000). “Pertussis antibody levels in infants immunized with an acellular pertussis component vaccine, measured using whole-cell pertussis ELISA.” Immunology and Cell Biology, 78:254-258. doi: 10.1046/j.1440-1711.2000.00910.x. Retrieved from < >.
  32. CDC (2014). “National, State, and Selected Local Area Vaccination Coverage Among Children Aged 19-35 Months – United States, 2013.” Morbidity and Mortality Weekly Report, 63(34):741-748. Retrieved from < >.
  33. Wearing, H.J., & Rohani, P. (2009). “Estimating the duration of pertussis immunity using epidemiological signatures.” PLoS Pathog, 5(10):e1000647. doi: 10.1371/journal.ppat.1000647. Retrieved from: < >.
  34. Bystrianyk, R., & Humphries, S. (2013). “Vaccines: A peek beneath the hood.” International Medical Council on Vaccination. Retrieved from < >.



16 July 2015: Noticed that all the links in the references were broken. Fixed all the links. Noticed that one link was missing (reference #32). Added link.