Treatment of Pertussis

Vaccinating yourself and your children will not prevent your new baby from getting it. The vaccine has one of the lowest efficacy rates and you can still spread the germs that cause it even if you are not currently infected. Pertussis isn’t as deadly for infants as you are led to believe it is. When they say the mortality rate for pertussis in infants under 6 months is 0.5%, or 1 out of every 200, that is including all the infants who are formula fed, who live with smokers, who have health problems, etc. There’s a big difference between a baby in those circumstances and a breastfed baby living in a healthy environment.

Vitamin C in the treatment of Pertussis:

 Vitamin C, Infectious Diseases, & Toxins by Thomas E. Levy, MD, JD

pg. 116: Otani (1936) found that pertussis bacteria seemed to be especially susceptible to the effects of vitamin C in the test tube, with high enough dose having a killing, bactericidal effect. It was also demonstrated that a culture of pertussis bacteria in which vitamin C had been added possessed a “strongly reduced” infectivity in test animals.

 

Pg. 118: The bacteria causing pertussis can be killed in culture by vitamin C, and the effects of the pertussis toxin also appear to be lessened by vitamin C…

…adequate regular dosing of vitamin C should prevent pertussis from ever being contracted.

 

 

The primary function of Vitamin C is not to kill the bacteria. It does inhibit them, but the main action in any toxin-mediated disease is to neutralize the toxin, and to support the liver so that when the liver is reducing the amount of endotoxin,  the liver works much more efficiently.   It does not stop the disease. It modifies it, and makes the cough milder.

 

 Vitamin C also puts petrol into the tank of macrophages and phagocytes, and in vitro increases their activity levels. Therefore, in the body, it should increase the effectiveness of the immune system in general, as well as dealing with the specifics of the toxin issue, and inhibiting the bacteria itself.

You can dissolve Vitamin C (sodium ascorbate powder) in breast milk. You can use a dropper or dribble it into the inside of the cheek. Don’t squirt it in their mouths in case they inhale it and that would trigger the vagus nerve.

 

The Bowl tolerance Method:

 

You give your child a small dose (1/4 tsp) of the C in liquid you choose every half hour to an hour until they have a loose stool. The amount of Vitamin C it took them to get there is just past tolerance. You then cut back 1/4 tsp and that’s saturation. Each person has a different level. Everyone will tolerate more when we are sick.

 

 For Breast feeding Mothers:

 

It takes about 8 hours for the vitamin C you take to get through to the breast milk. A Pinch is about 250 mg. If I thought my child was really sick, then I would calculate Vitamin C for her at 375 mg/kg of body weight, and give that over waking hours, and perhaps a larger dose given just before bedtime.

 

 Also, a good vitamin and mineral supplement to help your body deal with emotional stress, Halibut Liver oil, and about 10 grams of vitamin C spread out over your waking hours. You can use powdered sodium ascorbate, and mix it (10 grams = 2 heaped teaspoons) in with 1.25 liters of water in a water bottle. Drink it gradually throughout the day.

 

The Progression:

 

 First they get a cold. Then after a week, they start the odd cough, and after about two weeks, the cough gets stronger. At the end of the cough, which might be a month later, they will bring up globs of fairly thick mucus. This is because it pools down to the bottom of the lungs because the toxin from the bacteria has cut off most of the hairs in the bronchial that sweeps the mucus up and around. The cough sounds dry and that’s because the mucus membranes aren’t being kept as moist as they normally are. Most children, as long as they are getting that mucus up, and do not pool it (where secondary bacterial infections can set it) only have problems when they are coughing. The rest of the time they act normal. Coughing can be provoked by touching the back of the tongue, eating food, or running around. Towards the end of the illness, if they get worked up and tense up, it triggers the cough.

 

 To help a baby during the cough:

 

Turn the baby round, with its back to yours. Split your legs, so the baby is supported around the tummy but the legs are straight down. Your hands make a net around the baby’s ribcage and tummy, and when the baby coughs, lean forward slightly and use the hands as a very gentle net so that the baby has something for the tummy to push against. They haven’t learned to control their abdominal muscles to get an efficient cough yet, so t hands make it much easier for them. If it is whooping cough, then you will get a thick clear mucus glob ejected. If it is whooping cough, then the cough will become more regular.

 

The cough is caused by the bacteria adhering to the bronchial walls, and secreting a toxin, which cuts off the cilia (hairs) in the bronchials. These hairs sweep the mucus up and spread throughout the throat. The bronchial hairs move the mucus around all the time, so that it replaces, and at the same time, gets rid of any pathogens. This mucus is part of the innate immune system. It is linked to the BALT (Bronchial associated lymphatic tissue). You must keep the mucus moving. Whooping cough cuts off the hairs, and tries to stops the mucus from  moving. As long as you keep the mucus moving, your baby should not get a secondary infection.

The other thing the toxin can do is get into the blood-stream, and irritate the body. If the baby’s immune system is not good then this toxin can get to the brain as well. If the mucus is not gotten out, bacteria will grow and cause a secondary bacterial infection, which they will want to treat with antibiotics. Whooping cough in rare cases can cause long-lasting bronchial problems. However, that is if you treat it the way the doctors do, with antibiotics. Antibiotics do not deal with the pooling mucus, or manage it, or deal with the toxin. If you keep the mucus moving there should be nor further problems other than the cough itself.

Whooping cough will last approximately 100 days, but mainly as an irritating annoyance only. After a bout of whooping cough, for the next 6 – 9 months, any cold that the child gets, the child will start to whoop, or cough, the same way as they did with whooping cough. The reason for that is that it takes a long time for the hairs to grow back, and so any infection without proper hairs in the bronchials, will result in mucus pooling.
It is this mucus pooling that has to trigger a cough strong enough, to get the mucus from the bottom of the bronchials up to the top. If they are coughing until they are purple, then your doses of vitamin C are too small. Bump them right up to the level of 375 milligrams per kilo of body weight over the waking hours, as a starting dose. If your dose is right, within 8 hours there should be a two third reduction in the coughing.

 

Testing for Pertussis:

 This one is useless:

Isolation of B. pertussis by culture is 100% specific; however, sensitivity of culture varies because fastidious growth requirements make it difficult to transport and isolate the organism. Although the sensitivity of culture can reach 80%–90% under optimal conditions, in practice, sensitivity typically ranges from 30%–60% (57). The yield of B. pertussis from culture declines in specimens taken after 2 or more weeks of cough illness, after antimicrobial treatment, or after previous pertussis vaccination (58). Within 3 weeks after onset of cough, culture is only 1%–3% sensitive (59). Although B. pertussis can be isolated in culture as early as 72 hours after plating, it takes 1–2 weeks before a culture result can definitively be called negative (60). Culture is essential to isolate B. pertussis for antimicrobial susceptibility testing and for molecular subtyping of strains.  
 
Direct fluorescent antibody (DFA) tests provide rapid results (hours), but are generally less sensitive (sensitivity: 10%–50%) than culture. With use of monoclonal reagents, the specificity of DFA should generally be >90%; however, the interpretation of the test is subjective, and interpretation by an inexperienced microbiologist can result in lower specificity (61). Because of the limitations of DFA testing, CDC does not recommend its use.

 

The only Pertussis diagnostic tests that the CDC endorses are culture and Nasophyngeal PCR. Tests other than the PCR have a high false positive or false negative rating. However, many medical articles still say that there are no reliable correlates of protection (antibody test) for Pertussis.

 

Whooping cough cannot be correctly diagnosed without a nasopharyngeal swab because other pathogens like adenovirus can cause an identical syndrome, as can other bacteria, so the swab must be tested with the PCR (polymerase chain reaction) test.  

 
Doctors will give you Erythromycin, which does not shorten, or do anything to lessen the course of the disease. It can make babies irritable, bother the stomach, and suppress the immune system further. It can simply make the situation worse. There is no reason to use antibiotics, unless the mucus they spit up becomes green in color. Make sure the child drinks enough liquids, to keep the mucus as thin and easy to get up as possible.

 

 

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Pertussis-Epidemiology and Transmission of Disease

Epidemiology and Transmission of Disease

Pertussis infection is unique to humans. There are no animal reservoirs, and the organism cannot survive for a prolonged period in the environment. Localized to the respiratory tract, the organism is transmitted primarily by aerosol droplets from an infected person to a susceptible one. The infection is highly contagious, with attack rates ranging from 50% to 100%. The highest attack rates occur among persons with exposure within 5 feet of a coughing patient.[5]

In the pre-vaccine era, pertussis was predominantly an infection of children aged 1 to 5 years, with maternal immunity providing passive protection during an infant’s first year of life. At that time, an average of 175,000 US cases were reported per year (incidence of approximately 150 cases per 100,000 population).[6] The incidence of disease declined steadily over the two decades after introduction of whole-cell pertussis vaccine, reaching an all-time low of just over 1000 reported cases in 1976.[7,8] Since then, the incidence of infection has continued to rise, with almost 26,000 cases reported to the CDC in 2004 (Figure 1).[9]

 

 Pertussis is the only vaccine-preventable disease on the rise in the US and it is severely underreported. CDC estimates that, at best, one-third of cases are believed to be reported to the CDC;[10] other estimates place the reported cases at 1 in 10 to 1 in 20 of the true incidence.[11] Although pertussis incidence remains highest among young infants, rates are also on the rise in adolescents and adults and there may be significant under-reporting in these age groups, especially those with mild or atypical infection.[7] Compared with surveillance data from 1994 to 1996, the pertussis incidence rate among adolescents and adults increased 62% and 60%, respectively, from 1997 to 2000.[7]

Increased incidence of pertussis in adolescents and adults relates to waning immunity and, likely, to a combination of previous underreporting and recent improvements in reporting processes. The longer the duration since vaccination, the higher the attack rate (Figure 2).[12] Data from a seroprevalence study by Cattaneo et al showed a peak in antibody titers at 4 to 6 years of age, coinciding with DTaP booster dosing, followed by a decline, and a second peak between 13 and 17 years of age.[13] Similar findings were documented by the National Health and Nutrition Examination Survey (NHANES), which reported a protracted decline interrupted by a peak in persons aged 40 to 45 years.[14] Since no pertussis-containing vaccine had been given past the age of 6 years, these spikes in adolescents and older persons clearly represent natural pertussis exposure. These persons not only represent potential cases, but a reservoir of disease that puts those most susceptible to significant morbidity and mortality (ie, those at the extremes of age) at risk of exposure.

Pertussis has been estimated to account for up to 17% of prolonged cough illness in adults.[15,16] Among adults with cough illness, the incidence of confirmed pertussis has been estimated at 170 to 630 cases per 100,000.[17,18] The rates among adolescents were almost 2-fold higher. Data from a prospective acellular pertussis vaccine efficacy trial (APERT) extrapolate the burden of pertussis to be nearly 1 million US cases annually in persons 15 years old.[11]

Given the large disease burden in adolescents and adults estimated by these studies, the limited number of confirmed cases of pertussis (defined in Table 1 ) in older children, adolescents, and adults is striking. A large proportion of these cases may be atypical and undiagnosed. However, according to recent data from Bisgard et al,[19] in cases where the source of pertussis was identifiable, adolescents and adults were the primary source of infection for 20% and 56%, respectively, of infants with pertussis.

Contact with infected adolescents and adults is a common source of B. pertussis infection in infants and unprotected, young children. Widespread silent transmission of pertussis within families has been reported.[20] In a study of risk factors for pertussis-related hospitalizations, siblings were the most common source (53%), followed by parents (20%), other relatives (12%), neighbors (8%), and day-care contacts (3%).[21] In a case-control study, infants of adolescent mothers (aged 15 to 19 years) were 6-fold more likely to contract pertussis, compared with infants of older mothers (aged 20 to 29 years).[22]

Details of the pathogenesis of pertussis infection have been extensively reviewed elsewhere.[23] In brief, the development of pertussis infection begins with entry of B. pertussis into the respiratory tract of a susceptible host. The organism produces adhesion and bacterial surface attachment factors that allow its attachment to cilia in the respiratory mucosa. Tracheal cytotoxin and other toxins are produced and released into the local environment, damaging the cilia and respiratory epithelium. These changes disturb clearance of pulmonary secretions and probably result in development of the coryza and cough observed during the catarrhal phase of the illness. Even as local damage increases, attracting host immune cells, the actions of additional toxins probably inhibit phagocyte functions, thereby protecting the proliferating organisms from clearance. In some cases, the proliferation of B. pertussis continues until organisms reach the alveoli, resulting in pneumonia.

Pertussis symptoms are nonspecific in nature, making the clinical diagnosis challenging. The type and severity of symptoms that develop are highly variable, as is the time frame over which they appear and resolve. Adolescents and adults, as well as those partially protected by pertussis vaccine, frequently have mild clinical disease (or even asymptomatic disease) that goes undiagnosed. Although illness may be milder in adolescents and adults, they are a reservoir of infection and may transmit whooping cough to unimmunized or partially immunized infants. Of great concern, health care providers often do not recognize the varied clinical presentations and do not consider a pertussis diagnosis in patients with chronic cough.[17] Furthermore, management of pertussis is complicated by the fact that infected persons are most contagious early in their illness, before they become symptomatic.

Despite significant interpatient variability, generalizations can be made about the clinical course of illness ( Table 2 ).[5,24] Pertussis infection develops in four sequential stages, beginning with an incubation period during which infected individuals are asymptomatic followed by three stages of symptomatic illness. The incubation period of pertussis infection commonly lasts for 7 to 10 days, but can be as short as 4 days or as long as 21 days. The first stage in which symptoms can be observed is the catarrhal stage. This stage, which typically lasts 1 to 2 weeks, is characterized by the insidious onset of coryza, sneezing, low-grade fever, and a mild, occasional, nonspecific cough that gradually becomes more severe. In young infants, this stage is often characterized by excessive sneezing or “throat clearing.”

During the next stage, the paroxysmal stage, many pertussis patients have bursts, or paroxysms, of numerous, rapid coughs, apparently due to impaired mucociliary clearance. At the end of the paroxysm, a long inspiratory effort is oftentimes associated with a high-pitched whoop. Post-tussive vomiting and cyanosis can also occur. The paroxysmal attacks increase in frequency during the first 1 to 2 weeks, remain at the same level for 2 to 3 weeks, and then gradually decrease.

During the convalescent stage, which lasts for weeks to months, recovery is gradual, with cough becoming less paroxysmal and then disappearing.

The symptomatology of infants during the paroxysmal stage of infection is different from that in adolescents and adults. Although very young infants do experience paroxysms of coughing, they often do not “whoop.” Although the absent whoop in adolescents and adults is usually associated with milder disease, the whoop may be absent in infants because they lack sufficient musculature in the chest wall to take the deep inhalation that creates the whooping sound. The whoop may appear later in the disease as infants gain in size and strength. Infants may also exhibit clinical symptoms such as gagging, gasping, or eye bulging. Occasionally, they may also present with bradycardia or cyanosis. Pertussis is often ignored in the differential diagnosis of cough illness in young infants due to the absence of a “whoop” and the frequency of concomitant respiratory infections.

Life-threatening complications are most common in infants <3 months of age,[19,21] but infection can also be severe in some adult cases. Secondary bacterial pneumonia is diagnosed in up to one quarter of young infants with pertussis[21,25] and is the most common complication and the cause of most pertussis-related deaths across age groups. Data from 1997 to 2000 indicate that pneumonia occurred in up to 5.2% of all reported pertussis cases, and 11.8% of infants <6 months of age.[7] Other complications include seizures (0.8% of all cases, 1.4% of infants <6 months of age) and encephalopathy (0.1% of all cases, 0.2% of infants <6 months of age).

Death due to pertussis is rare (0.2%). The vast majority (90%) occurs in children younger than 6 months of age with no predisposing conditions.[2] Risk factors for death among infants include premature birth, Hispanic ethnicity, and having a young mother.[2,26] Pertussis has also been linked to sudden infant death (3% to 5%).[27,28] Other less severe complications in infants include otitis media, anorexia, and dehydration. Pressure effects of severe paroxysms may lead to pneumothorax, epistaxis, subdural hematomas, hernias, and rectal prolapse. Additional complications identified in adolescents and adults include urinary incontinence, rib fracture, unilateral hearing loss, herniated disk, and precipitation of angina pectoris.[5,24]

Laboratory confirmation of pertussis infection is not as straightforward as that of many other infectious diseases. Most local laboratories are not equipped to make the diagnosis of B. pertussis infection. The preferred approach is polymerase chain reaction (PCR) testing and a culture of the organism from a posterior nasopharyngeal specimen obtained using two separate Dacron swabs.[29] For proper collection, the swab must touch the epithelial cells of the posterior nasopharyngeal wall. Culture is the only method from which antibiotic susceptibilities can be measured and molecular typing determined. Isolation of the organism is compromised by recent antibiotic therapy effective against pertussis (ie, macrolide/azalide or trimethoprim-sulfamethoxazole), by delay in specimen collection beyond the first 2 weeks of illness, and in vaccinated persons.

Serologic testing for B. pertussis is limited by a lack of standardization and should not be obtained for clinical decision making.[30] However, because of its convenience, serology continues to be the most common method used to diagnosis pertussis, especially in the later stages of the infection, making it an important tool in our understanding of disease frequency.[31] Various enzyme-linked immunosorbent assay (ELISA) techniques are available in commercial laboratories, although there is little evidence of sensitivity or specificity relative to clinical infection.[32] None of the commercially available serologic tests for pertussis is FDA-licensed for the routine diagnosis of infection.[14] Direct fluorescent antibody (DFA) is no longer considered useful for diagnosis of pertussis due to low sensitivity and variable specificity.

Pertussis Vaccination of Children

DTaP vaccine, which contains purified, inactivated components of B. pertussis cells (along with tetanus and diphtheria toxoids), has been available in the United States for more than a decade. Since 1997, the CDC recommends DTaP for all doses of the vaccination series for infants and children <7 years of age. The primary immunization series consists of three doses given at 4- to 8-week intervals, beginning at 6 weeks to 2 months of age. A fourth dose is given 6 to 12 months after the third dose. Children who have received all four primary doses before the fourth birthday should receive a fifth (booster) dose before entering school. A fifth dose is not necessary if the fourth dose was administered on or after the fourth birthday.

Point estimates of vaccine efficacy across trials of infants ranged from 80% to 85%.[24] In comparative studies, the acellular pertussis vaccine was significantly more effective than the whole-cell DTP, which is no longer available in the United States. Local and systemic adverse reactions occurred less frequently among infants vaccinated with acellular pertussis vaccine than among those vaccinated with whole-cell pertussis.[34]

Pertussis Vaccination of Adolescents and Adults

The availability of a less reactogenic acellular pertussis vaccine combined with evidence of substantial pertussis infection among adolescents and adults led to reconsideration for the need for acellular pertussis boosters among older subgroups.

Specific formulations of Tdap for adolescents 10 to 18 years, Boostrix® (GlaxoSmithKline), and for adolescents and adults 11 to 64 years, Adacel® (sanofi pasteur), were recently licensed for use in the United States. They contain tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis. In a randomized, controlled, multicenter clinical trial, 10- to 18-year-olds were vaccinated with one dose of Boostrix or a US-licensed Td vaccine.[35] Each subject had completed his or her routine childhood vaccinations against diphtheria, tetanus, and pertussis according to the CDC recommended schedule. Boostrix was comparable to the Td vaccine based on immunogenicity. In both treatment groups, >99.9% of subjects had anti-diphtheria and anti-tetanus concentrations greater than 0.1 IU/mL, indicating seroprotection against these two diseases. In the Boostrix treatment group, anti-pertussis antibodies levels following primary immunization exceeded (by 1.9 to 7.4 times) those observed in infants, in whom efficacy against pertussis disease was previously demonstrated. The overall safety profile was comparable between the Boostrix and Td vaccine groups.

Adacel was evaluated in four principal clinical trials in which 7206 individuals (4185 adolescents and 3021 adults) who had not received tetanus or diphtheria toxoid-containing vaccines within 5 years were enrolled. The trials consisted of one randomized, controlled trial that compared Adacel vaccine to a licensed Td vaccine,[36] one lot consistency trial, and two concomitant administration trials (one with hepatitis B vaccine and one with influenza vaccine). Across trials, a total of 3393 adolescents and 2448 adults received Adacel vaccine and 792 adolescents and 573 adults received Td vaccine. In the largest Adacel trial, the seroprotection rate (of at least 0.1 IU/mL) for tetanus and diphtheria was 99.8% and 100%, respectively.[36] Pertussis antibody geometric mean titers (GMTs) following one dose of Adacel were 2.1- to 5.4-fold higher than those observed among infants following three doses of DTaP. Overall, Adacel vaccine was well tolerated, with local and systemic adverse reactions occurring at similar rates in the Adacel and Td vaccine groups. The ACIP recently revised its recommendations for pertussis vaccination. The immunization schedule now includes a Tdap booster dose for all adolescents at 11 to 12 years of age ( Table 3 ).[37,38] The ACIP also calls for catch-up vaccination of those aged 13 to 18 years who did not receive the Td booster. Finally, because of the importance of controlling pertussis, those in this age range who received the Td booster are encouraged to get the new Tdap vaccine after a suggested 5-year interval. This interval may be shortened to as little as 2 years in the presence of increased risk (eg, during outbreaks or periods of increased pertussis activity in the community).[7]

The ACIP also recommends a single dose of Tdap booster to replace the next scheduled dose of tetanus diphtheria vaccine among persons 19 to 64 years of age. In addition, adults who have or who anticipate having close contact with a vulnerable infant (ie, an infant who has not received two to three doses of DTaP) should receive a single dose of Tdap booster.[39]

In February 2006, the ACIP recommended a single dose of Tdap booster as soon as feasible for health care workers in hospital or ambulatory care settings who have direct patient contact. The Committee stated that priority should be given to vaccination of health care workers with direct contact with infants <12 months of age. Other health care workers should receive a single dose of Tdap booster according to the routine recommendation and interval guidance for use of Tdap among adults.[39]

Widespread administration of Tdap vaccination should have a substantial impact on pertussis. By way of example, adolescent pertussis immunization programs were recently implemented countrywide in Canada, but started earlier in the Northwest Territories and Newfoundland. Following introduction of an adolescent booster dose, pertussis incidence in the Northwest Territories decreased from 7.9 per 100,000 in the late 1990s to 0.2 per 100,000 in 2004.[40] In Newfoundland, no person vaccinated with the Tdap booster has been diagnosed with pertussis to date.[41]

Pertussis is an often serious, potentially deadly community-acquired illness in persons of all ages. Infected adolescents and adults may suffer substantial morbidity and also are a reservoir for disease transmission to infants. Newly available Tdap vaccines are safe and effective in preventing infection. The addition of a pertussis booster to the previously available tetanus and diphtheria booster will not only directly benefit vaccine recipients but may allow for greater control of the pertussis reservoir in adolescents and adults, potentially leading to decreased incidence in infants who are at highest risk for severe complications including death. If widely administered, Tdap vaccination should have a substantial impact on pertussis.

Epidemiology and Transmission of Disease

J Am Board Fam Med.  2006;19(6):603-611.  ©2006 American Board of Family Medicine.

Medscapetoday

 

 

 

Pertussis (Whooping Cough)

     In the pre-vaccine era, 93% of Pertussis cases occurred in children between 1-5 years old. Since the 1980’s, the high incidence rate shifted to children over 5 years of age and older. In 2005, booster vaccines were recommended for adolescents and adults between the ages of 11-64 years old.

 

      From 1985-1987, 25% of reported cases were in children 10 years of age and over. From 1995-1998, that number increased to 42%. The largest majority of cases have been in the vaccinated populations. During the 1980’s, 1990’s and 2000’s, the number of adolescents and adults acquiring Pertussis has increased to spite high vaccination rates. (1) (2) (3) (4) (5)

              “Although pertussis incidence remains highest among young infants, rates are also on the rise in adolescents and adults and there may be significant under-reporting in these age groups, especially those with mild or atypical infection. Compared with surveillance data from 1994 to 1996, the pertussis incidence rate among adolescents and adults increased 62% and 60%, respectively, from 1997 to 2000.”

 

     There has also been an increase in babies under 1 year acquiring Pertussis. The number of cases in babies under 3 months of age from 1990-1997 did not lower. From 1999-2000, 48% of cases were in this age group. In 2001, 62% were under 3 months old. (6)

 

     According to a 2000 CDC MMWR report: “Despite record high vaccination coverage levels with 3 doses of DTaP among U.S. children aged 19–35 months, pertussis continues to cause fatal illness among vulnerable infants. During 1980–1998, the average annual incidence of reported pertussis cases and deaths among U.S. infants increased 50%. The increased morbidity and mortality occurred primarily among infants aged <4 months, who were too young to have received the recommended three DTaP vaccinations at ages 2, 4, and 6 months.” (7)

 

 

     Pertussis has always been endemic despite a vaccine.  It has a natural circulation every 2-5 years. This has not changed since the introduction of the vaccine, and thus indicates that the vaccine may prevent some disease, but has had little impact on transmission amongst the population. The efficacy of the DTaP is roughly 85% effective but waning immunity occurs after 2-5 years. In a case controlled study, it was found that infants of adolescent Mothers, aged 15-19 years, were 6 times more likely to acquire Pertussis compared to infants of older Mothers aged 20-29 years. Death from Pertussis is rare today. The majority of deaths, 90%, are in babies under 6 months of age. DTaP is also a reactive vaccine which means it does not prevent carriage or transmission of the disease. Therefore, vaccinated adolescents, adults and children can serve as reservoirs and transmitters to unprotected infants. (8) (9)

 

 

     Some epidemiologists believe B. Pertussis has mutated by changing its DNA and genetic coding.  Scientists in the Netherlands observed changes in the structure of the circulating wild-type bacteria when compared with those who were vaccinated. The differences were the outer membrane protein pertactin and the pertussis toxin itself. Similar genetic changes have been observed in Poland, Finland and the U.S. Any changes would thus render mutated bacteria immune to vaccination. As far as changing its character, many new cases lack the common ‘whoop’, yet 30% of cases were infected. Some cases were misdiagnosed as atypical asthma.(10) (11)

 

 

     In 2005, Tdap vaccines were recommended for adolescents over age 9 and adults under age 65 due to waning immunity from the DTaP vaccine given in infancy or childhood. There are no pertussis vaccines approved for children 7–9 years of age or for persons older than 64 years. The efficacy is similar and ‘inferred’ to that of DTaP. It is unknown if immunizing adolescents and adults will actually reduce the risk of transmission to infants. Nor is it known how long this vaccine may provide some people with protection. (12)

 

     

In the early 1900’s, it was questioned whether the control of Whooping Cough was even practicable. It has and remains to this day a more severe disease in infancy than in any other age group. A vaccine has not changed that fact. Generations passed have always known that the proper care in treatment of whooping cough would not lead to fatality, and most fatalities were the result of other complications mainly in the immune suppressed. (15)

 

 

Footnotes: 

 

       1.        Medscape Today. Epidemiology and Transmission of Disease. http://www.medscape.com/viewarticle/549508_2

 

2.        CDC MMWR, September 05, 1997 / 46(35);822-826. Pertussis Outbreak Vermont, 1996.  http://www.cdc.gov/mmwr/preview/mmwrhtml/00049244.htm

 

3.        The New England Journal of Medicine. Vol. 331:16-21. July 7, 1994. The 1993 Epidemic of Pertussis in Cincinnati — Resurgence of Disease in a Highly Immunized Population of Children.  http://content.nejm.org/cgi/content/full/331/1/16

 

4.        CDC MMWR, March 27, 1987 / 36(11);168-71. Epidemiologic Notes and Reports Pertussis Surveillance — United States, 1984 and 1985. http://www.cdc.gov/mmwR/preview/mmwrhtml/00000893.htm

 

5.        See #1

 

6.        CDR Weekly 21, June 2001. Enhanced surveillance of laboratory confirmed cases of Bordetella pertussis, England and Wales: 1999 to January-March quarter 2001. www.hpa.org.uk/cdr/archives/2001/cdr2501.pdf

 

7.        CDC, MMWR. July 19, 2002 / 51(28);616-618 Pertussis Deaths — United States, 2000. http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5128a2.htm

 

8.        Medscape Today. Epidemiology and Transmission of Disease. http://www.medscape.com/viewarticle/549508_2

 

9.        Clinical Infectious Diseases.Epidemiological, Clinical, and Laboratory Aspects of Pertussis in Adults. 01 JUNE 1999 Supplement, Volume 28, Number S2.  James D. Cherry. http://www.journals.uchicago.edu/toc/cid/28/s2

 

8.        Medscape Today. Epidemiology and Transmission of Disease. http://www.medscape.com/viewarticle/549508_2

 

9.        Clinical Infectious Diseases.Epidemiological, Clinical, and Laboratory Aspects of Pertussis in Adults. 01 JUNE 1999 Supplement, Volume 28, Number S2.  James D. Cherry. http://www.journals.uchicago.edu/toc/cid/28/s2

 

10.     See #9.

 

11.     Emerging Infectious Diseases. Changes in Predominance and Diversity of Genomic Subtypes of Bordetella pertussis Isolated in the United States, 1935 to 1999.Terri Hawes Hardwick, et al. http://www.cdc.gov/ncidod/EID/vol8no1/01-0021.htm

 

12.     Adacel Tdap Package Insert. www.fda.gov/cber/label/adacelLB.pdf

 

13.     IS THE CONTROL OF MEASLES AND WHOOPING-COUGH PRACTICABLE? Am J Public Health (N Y). 1916 March; 6(3): 265–268. FRANCiS GEORGE CURTIS, M. D., Chairman, Board of Health, Newton, Mass. Read at a General Session of the American Public Health Association, Rochester, N. Y., September 10, 1915.

 

14.   Whooping Cough. Am J Public Health Nations Health. 1936 May; 26(5): 523–524.

 

15.     A STATISTICAL STUDY OF WHOOPING COUGH. FREDERICK S. CRUM, PH. D., Am J Public Health (N Y). 1915 October; 5(10): 994–1017.