Meningococcal Disease

and the fraudulent "science" blaming smoking and secondhand smoke

The New England Journal of Medicine, 2001

Meningococcal Disease. NE Rosenstein, BA Perkins, DS Stephens, T Popovic, JM Hughes. N Engl J Med 2001 May 3;344(18):1378-1388. Review. "The acquisition of infection depends on the chance that a person will encounter and acquire a virulent bacterium. In households where a case of meningococcal disease has occurred, the risk of invasive disease in family members is increased by a factor of 400 to 800. In the United States, blacks and persons of low socioeconomic status have consistently been found to be at higher risk for meningococcal disease than whites and persons of higher socioeconomic status. Black race and low socioeconomic status are likely to be markers for differences in factors such as household crowding, urban residence, and exposure to tobacco smoke. Active or passive exposure to tobacco smoke, as well as concurrent viral infection of the upper respiratory tract, increases the risk of meningococcal disease by enhancing the formation and spread of respiratory droplets or diminishing the functional and mechanical integrity of the respiratory mucosa as a barrier to invasion." These are merely ad hoc rationalizations for false claims that are based on using deficient measures of exposure to the bacterium, and the use of multivariate analysis to generate confounded results.

Rosenstein et al. / NEJM 2001 full article

The corrupt and fraudulent report of the Centers for Disease Control (Rosenstein Again), 2005

Prevention and Control of Meningococcal Disease. Recommendations of the Advisory Committee on Immunization Practices (ACIP). Prepared by Oleg O. Bilukha, MD, PhD. Nancy Rosenstein, MD. Division of Bacterial and Mycotic Diseases, National Center for Infectious Diseases. MMWR May 27, 2005 / 54(RR07);1-21. "Persons who have deficiencies in the terminal common complement pathway (C3, C5--9) (15,16) and those with anatomic or functional asplenia (17) are at increased risk for acquiring meningococcal disease. Antecedent viral infection, household crowding, chronic underlying illness, and both active and passive smoking also are associated with increased risk for meningococcal disease (18--25). During outbreaks, bar or nightclub patronage and alcohol use also have been associated with higher risk for meningococcal disease (26--28). In the United States, blacks and persons of low socioeconomic status (SES) have been consistently at higher risk for meningococcal disease (12,13). However, race and low SES are likely risk markers rather than risk factors for this disease. A multistate case-control study in which controls were matched to case-patients by age group indicated that in a multivariable analysis (controlling for sex and education), active and passive smoking, recent respiratory illness, corticosteroid use, new residence, new school, Medicaid insurance, and household crowding all were associated with increased risk for meningococcal disease, whereas income and race were not (18). Additional research is needed to identify groups at risk that might benefit from prevention efforts." See how they make the excuse that race and low SES are only "risk markers," for what, they do not specify; while ignoring the fact that smokers are more likely to be exposed to the bacterium, due to lower SES. Furthermore, multivariable analysis of proxy variables (which are merely inadequate substitutes for true measures of exposure) not only does not prevent confounding, it is a proven recipe for creating confounding, in order to blame false "risk factors," namely smoking and passive smoking.

"Since the early 1990s, outbreaks of meningococcal disease have occurred with increasing frequency in the United States. During July 1994--June 2002, a total of 76 outbreaks were identified (annual median: 10; range: 4--16) (11), including 48 (63%) outbreaks caused by serogroup C, 19 (25%) by serogroup B, and nine (12%) by serogroup Y. These outbreaks occurred in 32 states and involved 247 patients (accounting for <2% of total cases of meningococcal disease in the United States during this period). Of the 76 outbreaks, 26 (34%) were community-based and accounted for 53% of all outbreak-related cases. Of the 50 (65%) outbreaks that were organization-based, 13 (26%) occurred in colleges; 19 (38%) in primary and secondary schools; and nine (18%) in nursing homes." "During 1991--2002, the highest rate of meningococcal disease (9.2/100,000) occurred among infants aged <1 year," for which there is no mention of useful prenatal preventive measures.

MMWR 2005 full article / Centers for Disease Control

The incidence of meningococcal disease does NOT decline when smoking declines.

If the anti-smokers' claims were true, they'd have reductions in the rates of disease to crow about. But the frauds ignore this inconvenient fact in order to continue falsely blaming smoking and passive smoking, and making empty health promises for which they are never held accountable. And their media stooges cover up for them, just as they have covered up about the rising rates of asthma and preterm birth.

Guidelines for control of meningococcal disease. Laboratory Centre for Disease Control Consensus Conference. Canadian Medical Association Journal 1994; 150: 1825-1831. (Based on Canada Communicable Disease Report 1994;20:17-27). "The average annual reported incidence rate of meningococcal disease in Canada increased from 0.83 per 100 000 people between 1980 and 1984 to 1.38 per 100 000 in the period 1985 to 1992. This increase has been accompanied by a change in the relative proportion of isolates that are serogroup B or C. In 1985, 46% of isolates grouped were serogroup B and 24% were serogroup C. In 1992, 24% were serogroup B and 56% were serogroup C. The incidence of meningococcal disease is greatest in childhood. Age-specific incidence rates (per 100 000) during the period 1986 to 1992 were 18.8 for infants less than 1 year old, 5.8 for children 1 to 4 years old, 1.9 for those aged 5 to 19 years and 0.5 for adults 20 years and over. Beginning in 1989 the incidence in the age group 5 to 19 has more than doubled (mean incidence for 1986 to 1988 was 1.09 per 100 000 people and for 1989 to 1992 it was 2.45 per 100 000, p <0.001)."

LCDC - CMAJ 1994 full article

"Surveillance of meningococcal infections by the National Reference Center (NRCM). Meningococcal diseases occur as sporadic cases with an annual incidence below 1 per 100,000 inhabitants in France. The NRCM receives an average of 1,000 strains of Nm per year from approximately 700 collaborating laboratories in France, for confirmation and typing. Approximately half of the strains are from invasive infections, mainly meningococcemia or meningitis. Strains of serogroup B are prominent (more of 50% of the strains) with a relatively stable incidence at 270± 28 cases per year. An increasing incidence of meningococcal diseases, mainly associated with an increasing incidence of serogroup C, was observed since 2001. However, periodic fluctuation in the incidence of serogroup C has yet been observed. A peak of incidence of serogroup C was yet observed in 1992 with 191 cases (40.2%), followed by a continuous decrease until 1995 with 56 cases (15%) and then a continuous increase reaching 235 cases (38.2%) in 2002, but a decrease to 31% is observed in 2003. The incidence of serogroup W135, first detected in 1994, reached 9.8% in 2002, but decreased to 5,9% in 2003. Serogroup Y is stably found in 2-3% of the invasive infections, but mainly in immunocompromised patients and in the elderly. Case fatality rates vary between 8 to 10% per year. They are mostly associated with sepsis and purpura fulminans." (Annual Report of Neisseria meningitidis. The Pasteur Institute, 2003.)

Annual Report of Neisseria meningitidis, 2003 / Pasteur Institute

The Changing Epidemiology of Meningococcal Disease in the U.S. With An Emphasis on College Health Issues. A Publication of the National Foundation for Infectious Diseases, May 1999. Cases of invasive meningococcal disease reported to the CDC's National Notifiable Diseases Surveillance System among 15 to 24 year-olds rose steadily from 1991 to 1996, then declined slightly in 1997 (the last year for which complete data were available) (Fig. 1, p.7.) "From the post-World War II era until recently, rates of meningococcal disease have remained stable, with an annual incidence of 1-2 cases per 100,000 population. Although streptococcus pneumoniae is the leading cause of bacterial meningitis among all age groups combined, N. meningitidis is the major cause of bacterial meningitis among older children and young adults. However, the epidemiology of meningococcal disease has changed in recent years. Among the most pronounced recent changes are: An increase in disease incidence overall between 1992-1996; Disproportionate increases in cases in older children and young adults," as well as changes in the strains which cause the disease (p. 8). Lasker Legislators former US Reps. Paul G. Rogers and John Edward Porter, and anti-smoker Fred Hassan of Schering-Plough are trustees of the NFID; predictably, they attempt to blame smoking anyway (pp. 7 & 12).

The Changing Epidemiology of Meningococcal Disease / National Foundation for Infectious Diseases (pdf, 26 pp)

Correlating Epidemiologic Trends With the Genotypes Causing Meningococcal Disease, Maryland. M. Catherine McEllistrem; John A. Kolano; Margaret A. Pass; Dominique A. Caugant; Aaron B. Mendelsohn; Antonio Guilherme Fonseca Pacheco; Kathleen A. Shutt; Jafar Razeq; Lee H. Harrison. From: Emerg Infect Dis 2004;10(3):451-456. "Two changes occurred in the epidemiology of meningococcal infection in Maryland during the 1990s. First, meningococcal incidence in persons 15-24 years of age substantially increased and then declined; nearly half of infections in this age group were caused by serogroup C Neisseria meningitidis. From 1990 to 1997, the incidence increased from 0.9 to 2.1 cases per 100,000 in this age group (p = 0.01) before declining to baseline in the late 1990s. By the mid-1990s, infection in persons 15-24 years accounted for nearly 30% of all meningococcal infections in Maryland, compared to 16% in 1990 to 1991. This increase was caused mostly by sporadic infections. Only three outbreak clusters were recognized, all caused by serogroup C and representing seven total cases with six cases in persons 15-24 years: two cases in 1995 in children aged 12 and 15 years, who lived on the same street; two cases in 1997, in Maryland college students ages 19 and 21 years, and three cases associated with a party in 1999, in young adults ages 18, 20, and 21 years. Although the case-fatality rate in persons 15 to 24 years is generally low, during the 1990s, 2.5% of infections in this age group were fatal. The increase in meningococcal incidence in this age group that was observed in Maryland was also seen in other regions of the United States."

McEllistrem et al. EID 2004 / Medscape
McEllistrem et al. EID 2004 / Centers for Disease Control

Another Act of Scientific Fraud, from the Harvard School of Public Health, funded by the National Institute of Environmental Health Sciences [sic], and the Bill & Melinda Gates Foundation.

(Association of Secondhand Smoke Exposure with Pediatric Invasive Bacterial Disease and Bacterial Carriage: A Systematic Review and Meta-analysis. C-C Lee, NA. Middaugh, SRC Howie, M Ezzati. PLoS Med 2010;7(12): e1000374.) Once again, it's based on the fraudulent premise that "controlling" for surrogate "risk factors" such as income can make up for failure to identify exposure to the true causal factor, through exposure to an infected person. With high odds ratios from household exposure such as the 400 to 800 noted above, "controlling" doesn't work.

Lee - PLoS Med 2010 full article

A Phage Causes Meningitis Virulence

A chromosomally integrated bacteriophage in invasive meningococci. E Bille, J-R Zahar, A Perrin, S Morelle, P Kriz, KA Jolley, MCJ Maiden, C Dervin, X Nassif, CR Tinsley. J Exp Med 2005 Jun 20;201(12):1905-13. A virus that infects meningococci integrates into the bacterial genome, and the integrated regions are found in the hyperinvasive strains but not the nonpathogenic strains. "No gene satisfied the condition that it be present in all 29 invasive isolates and none of the 20 noninvasive isolates. However, a single group of genes (NMA1792–NMA1799) of 8 kb (Fig. 1 A) was associated significantly with the hypervirulent isolates... This gene cluster was present in 100% (29/29) of these isolates and absent from 90% (18/20) of the noninvasive isolates. Another amplicon corresponding to a frame (NMA0776) that was highly similar (42% DNA base identity, 53% amino acid identity) to one of the genes (NMA1797) in the above cluster showed the same distribution. It was striking that these two groups were the only genes to have this extreme distribution. The genes showing the next highest degree of association with the virulent strains (NMA1283–NMA1285, part of a possible prophage pnm2; reference 6) were present in 9 out of 20 of the noninvasive isolates. These were the only genes to have this extreme distribution; the probability of finding a gene having as significant an association with the invasive isolates as the above group by chance alone was calculated as 0.007. Thus, the 8-kb genetic island is specifically present in isolates belonging to the invasive complexes of N. meningitidis." Over 90% of cases of invasive meningococcal disease in young adults were caused by meningococci which carried this integrated region, while the age distribution of nonpathogenic strains showed the classic profile of age dependence (highest in infancy, then falling rapidly, Fig. 5.) "The carriage of virulence determinants by phages is not an uncommon situation in bacterial pathogens. The cholera toxin is carried by a prophage of the f1/M13 family, whereas the shiga and diphtheria toxins are carried on lysogenic lambdoid phages." It is usually a disadvantage for a pathogen to kill its host quickly; however, such a trait may be associated with some advantage such as the ability to spread rapidly.

Bille et al. / J Exp Med 2005 full article

Other fraudulent studies on which the anti-smokers base their claims.

All of them deliberately exploit confounding resulting from deficient measurement of exposure.

Risk factors for meningococcal disease: a case control study in south west England. JM Stuart, KA Cartwright, JA Dawson, J Richard, ND Noah. Community Med 1988;10:139-146. No abstract available.

Effect of smoking on meningococcal carriage. JM Stuart, KA Cartwright, PM Robinson, ND Noah. Lancet 1989 Sep 23;2(8665):723-725. "Questionnaires were posted to 138 meningococcal carriers and their controls, and to 52 carriers of Neisseria lactamica and their controls. Carriers were matched to controls by age, sex, and area of residence. There were no differences in environmental or medical factors between N lactamica carriers and their controls, nor in household crowding, housing conditions, frequency of physical exercise, or upper respiratory disorders between meningococcal carriers and their controls. Active smoking and the presence of other smokers in the household were independently associated with meningococcal carriage; the risk of carriage increased significantly with heavier smoking." Note that Neisseria lactamica is one of the strains which is not associated with invasive disease, and it is not stated whether the meningococcal strains were carrier or invasive strains.

Stuart et al. - Lancet 1989 abstract / PubMed

A cluster of Neisseria meningitidis serogroup C disease in Phoenix: risk factors for disease. P Zeitz, H Jafari, C Kioski, et al. [Abstract 1388]. In: Programs and abstracts of the 33rd Interscience Conference on Antimicrobial Agents and Chemotherapy, New Orleans, LA, October 17-20, 1993. No abstract available. Note that PS Zeitz was a coauthor with Thomas E. Novotny of: Smoking in Delaware: economic costs and deaths attributable to cigarette smoking in the state, 1985. Del Med J. 1988 Dec;60(12):735-6, 739. No abstract available - but which is based on the anti-smokers' fraudulent SAMMEC computer program.

Smoking, the environment and meningococcal disease: a case control study. RE Stanwell-Smith, JM Stuart, AO Hughes, P Robinson, MB Griffin, K Cartwright. Epidemiol Infect 1994;112:315-328. "This case control study investigated environmental factors in 74 confirmed cases of meningococcal disease (MD). In children aged under 5, passive smoking in the home (30 or more cigarettes daily) was associated with an odds ratio (OR) of 7.5 (95% confidence interval (CI) 1.46-38.66). ORs increased both with the numbers of cigarettes smoked and with the number of smokers in the household, suggesting a dose-response relationship. MD in this age group was also significantly associated with household overcrowding (more than 1.5 persons per room) (OR 6.0, 95% CI 1.10-32.8), with kisses on the mouth with 4 or more contacts in the previous 2 weeks (OR 2.46, 95% CI 1.09-5.56), with exposure to dust from plaster, brick or stone in the previous 2 weeks (OR 2.24, 95% CI 1.07-4.65); and with changes in residence (OR 3.0, 95% CI 1.0-8.99), marital arguments (OR 3.0, 95% CI 1.26-7.17) and legal disputes in the previous 6 months (OR 3.10, 95% CI 1.24-7.78). These associations were independent of social class. Public health measures to lower the prevalence of cigarette smoking by parents of young children may reduce the incidence of MD. The influence of building dust and stressful life events merits further investigation."

Stanwell-Smith et al. - Epidemiol Infect 1994 abstract / PubMed

Outbreak of serogroup C meningococcal disease associated with campus bar patronage. PB Imrey, LA Jackson, PH Ludwinski, AC England 3d, GA Fella, BC Fox, LB Isdale, MW Reeves, JD Wenger. Am J Epidemiol. 1996 Mar 15;143(6):624-630. "Between February 1991 and April 1992, eight undergraduates at a US residential university and one at a nearby 2-year college contracted serogroup C meningococcal disease... Disease was associated with cigarette smoking (p = 0.012), recent patronage of campus-area bars (p = 0.034), estimated amount of time spent in campus-area bars (p = 0.0003), and, especially, recent patronage of one specific bar, bar A (p = 0.0006; odds ratio = 23.1, 95% confidence interval 3.0-571.5). In carriage surveys, 1,528 throat cultures taken from (primarily student) noncases yielded only five (0.3%) strains that were identical by MEE to those from cases. Two of these were found among 22 cultures obtained from bar A employees in spring 1992." Smoking is falsely blamed by residual confounding due to the imprecision of the measure of exposure used, "recent patronage of one specific bar," with an odds ratio of 23.1, which although high is still not as exact as determining exposure to the carrier of the disease - the measure considered necessary in real epidemiology. Had they engaged in real epidemiology, they might have narrowed the relevant exposure down to contact with one infected person.

Imrey et al. - Am J Epidemiol 1996 abstract / PubMed

Tobacco smoke as a risk factor for meningococcal disease. M Fischer, K Hedberg, P Cardosi, BD Plikaytis, FC Hoesly, KR Steingart, TA Bell, DW Fleming, JD Wenger, BA Perkins. Pediatr Infect Dis J 1997;16:979-983. "Since 1992 the US Pacific Northwest has experienced a substantial increase in the incidence of serogroup B meningococcal disease." [Despite their anti-smoking crusade! How amazing! -cast] "We performed a case-control study comparing 129 patients in Oregon and southwest Washington with 274 age- and area-matched controls. We used conditional logistic regression analysis to determine which exposures remained associated with disease after adjusting for other risk factors and confounders and calculated the proportion of disease attributable to modifiable exposures. RESULTS: After adjustment for all other significant exposures identified, having a mother who smokes was the strongest independent risk factor for invasive meningococcal disease in children < 18 years of age [odds ratio (OR), 3.8; 95% confidence interval (CI) 1.6 to 8.9)], with 37% (CI 15 to 65) of all cases in this age group potentially attributable to maternal smoking. Adult patients were more likely than controls to have a chronic underlying illness (OR 10.8, CI 2.7 to 43.3), passive tobacco smoke exposure (OR 2.5, CI 0.9 to 6.9) and to smoke tobacco (OR 2.4, CI 0.9 to 6.6). Dose-response effects were seen for passive smoke exposure and risk of disease in all age groups. CONCLUSION: Tobacco smoke exposure independently increases the risk of developing meningococcal disease." This claim is illegitimate because they did not attempt to determine exposure to infected carrier(s). Their so-called risk factors and confounders are NOT actual risks or confounders in fact, merely proxies; so their "adjustments" do not do what they are purported to do. And, the supposed "independence" of the relationship is biologically meaningless and pertains only to the steadiness of the statistical calculations.

Fischer et al. - Pediatr Infect Dis 1997 abstract / PubMed

Risk factors for sporadic meningococcal disease in North America. M Fischer, L Harrison, M Farley, et al. [Abstract 552 Fr]. In: Abstracts of the 36th Annual Meeting of the Infectious Diseases Society of America, Denver, CO, November 12-15, 1998. No abstract available.

Maternal cigarette smoking and invasive meningococcal disease: A cohort study among young children in metropolitan Atlanta, 1989-1996. HR Yusuf, RW Rochat, WS Baughman, PM Gargiullo, BA Perkins, MD Brantley, DS Stephens. Am J Public Health 1999 May;89(5):712-717. "RESULTS: The crude rate of meningococcal disease was 5 times higher for children whose mothers smoked during pregnancy than for children whose mothers did not smoke (0.05% vs 0.01%). Multivariate analysis revealed that maternal smoking (risk ratio [RR] = 2.9; 95% confidence interval [CI] = 1.5, 5.7) and a mother's having fewer than 12 years of education (RR = 2.1; 95% CI = 1.0, 4.2) were independently associated with invasive meningococcal disease. CONCLUSIONS: Maternal smoking, a likely surrogate for tobacco smoke exposure following delivery, appears to be a modifiable risk factor for sporadic meningococcal disease in young children." This is all that appears in the abstract. However, in the full article, rates were lower in blacks than whites; and, among whites but not blacks, children of mothers who were less than 20 years old had eight times the rate of disease than older mothers; children of Medicaid recipients and mothers with less than 12 years of education had seven times the rate of non-recipients and mothers with more than 12 years of schooling respectively, and children of unmarried mothers had six times the rate of children of married mothers.

Yusuf et al. - AJPH 1999 abstract / PubMed
Yusuf et al. - AJPH 1999 full article / UCSF (pdf, 6 pp)

Changing carriage rate of Neisseria meningitidis among university students during the first week of term: cross sectional study. KR Neal, JS Nguyen-Van-Tam, N Jeffrey, RC Slack, RJ Madeley, K Ait-Tahar, K Job, MC Wale, DA Ala'Aldeen. BMJ 2000 Mar 25;320(7238):846-849. "Carriage rates for meningoccoci increased rapidly in the first week of term from 6.9% on day 1, to 11.2% on day 2, to 19.0% on day 3, and to 23.1% on day 4. The average carriage rate during the first week of term in October among students living in catered halls was 13.9%. By November this had risen to 31.0% and in December it had reached 34.2%. Independent associations for acquisition of meningococci in the autumn term were frequency of visits to a hall bar (5-7 visits: odds ratio 2.7, 95% confidence interval 1.5 to 4.8), active smoking (1.6, 1.0 to 2.6), being male (1.6, 1.2 to 2.2), visits to night clubs (1.3, 1.0 to 1.6), and intimate kissing (1.4, 1.0 to 1.8). Lower rates of acquisition were found in female only halls (0.5, 0.3 to 0.9). The most commonly acquired meningococcal strain was C2a P1.5 (P1.2), which has been implicated in clusters of invasive meningococcal disease at other UK universities."

Neal et al. - BMJ 2000 full article / PubMed Central
Neal et al. / BMJ 2000 full article

Parental smoking, socioeconomic factors, and risk of invasive meningococcal disease in children: a population based case-control study. P Kriza, M Bobakb, B Kriza. Arch Dis Child 2000 Aug;83(2):117-121. "Invasive meningococcal disease was strongly associated with parental smoking; rate ratios adjusted for socioeconomic factors were 3.5 (95% confidence interval 1.4-8.7) for smoking of mother, 3.2 (1.5-6.9) for smoking of father, and 2.7 (1.3-5.4) for every 20 cigarettes smoked at home on an average day. The risk of the disease was strongly inversely related to maternal education and, less strongly, to ownership of a car and of a weekend house, father's education, crowding, and the number of siblings, but these associations were reduced or eliminated in multivariate models. The type of heating and cooking (used as proxies for indoor air pollution) were not associated with the disease. CONCLUSION The risk of invasive meningococcal disease in children is strongly influenced by parental smoking and unfavourable socioeconomic circumstances."

Kriza et al. / Arch Dis Child 2000 full article

Household crowding a major risk factor for epidemic meningococcal disease in Auckland children. M Baker, A McNicholas, N Garrett, N Jones, J Stewart, V Koberstein, D Lennon. Pediatr Infect Dis J. 2000 Oct;19(10):983-990. "With the use of a multivariate model and controlling for age, ethnicity, season and socioeconomic factors, risk of disease was strongly associated with overcrowding as measured by the number of adolescent and adult (10 years or older) household members per room [odds ratio (OR), 10.7; 95% confidence interval (CI), 3.9 to 29.5]. This would result in a doubling of risk with the addition of 2 adolescents or adults to a 6-room house. Risk of disease was also associated with analgesic use by the child, which was thought to be a marker of recent illness (OR 2.4, CI 1.5 to 4.0); number of days at substantial social gatherings (10 or more people for > 4 h; OR 1.8, CI 1.2 to 2.6); number of smokers in the household (OR 1.4, CI 1.0 to 1.8); sharing an item of food, drink or a pacifier (OR 1.6, CI 1.0 to 2.7); and preceding symptoms of a respiratory infection (cough, "cold or flu," runny nose, sneezing) in a household member (OR 1.5, CI 1.0 to 2.5). CONCLUSION: Some of these identified risk factors for meningococcal disease are modifiable. Measures to reduce overcrowding could have a marked effect on reducing the incidence of this disease in Auckland children." This conclusion is appropriate.

Baker et al. - Pediatr Infect Dis J 2000 abstract / PubMed

Carriers of Neisseria meningitidis in household contacts of meningococcal disease cases in Catalonia (Spain). N Cardenosa, A Dominguez, A Orcau, H Panella, P Godoy, S Minguell, N Camps, JA Vazquez; Working Group on Meningococcal Disease. Eur J Epidemiol. 2001;17(9):877-884. "Bivariate analysis identified five statistically significant risk factors for meningococcal carriage: age (5-9 years old), meningococcal A+C vaccination, severe household overcrowding, social class and heavy active smoking (>20 cigarettes a day). Multivariate analysis revealed that of these five variables, only heavy active smoking remained statistically significant when the other factors were controlled." This is merely another demonstration that multivariate analysis is worthless for determining true causes.

Cardenosa et al. - Eur J Epidemiol 2001 abstract / PubMed

Cluster of serogroup C meningococcal disease associated with attendance at a party. R Finn, C Groves, M Coe, M Pass, LH Harrison. South Med J. 2001 Dec;94(12):1192-1194. "An unexplained increase has occurred in the incidence of invasive meningococcal disease in adolescents and young adults... We investigated a cluster of serogroup C meningococcal disease in 3 previously healthy young adults who had attended a party in Maryland... The only common exposure was attendance at the party, where a large number of people reportedly smoked tobacco or marijuana and/or drank alcohol... The PFGE analysis of the 3 case isolates showed identical molecular subtypes... This investigation strongly suggests that transmission of the cluster strain occurred at the party. Transmission may have occurred in part as a result of the recently described risk factors of binge drinking and smoking. Taken together, these findings suggest that some of the recent increase in invasive meningococcal disease may be due to modifiable risk factors." Presumably they think that smoking and drinking caused a pathogenic strain of N. meningitidis to appear by magic, or perhaps that GOD did it to punish them for their "sins."

Finn et al. - South Med J 2001 abstract / PubMed

Risk factors for invasive disease among children in Spain. I Pereiro, J Diez-Domingo, L Segarra, A Ballester, A Albert, A Morant. J Infect 2004 May;48(4):320-329. "The risk factors related to invasive disease by Hib were exposure to tobacco smoke (number of smokers, adjusted OR (aOR) 1.74, 95% confidence interval (CI) 1.02-2.96) and living with more than four people (aOR 3.72, 95% CI 1.3-3.7). For N. meningitidis, there is a dose-response relationship; if more than 60 cigarettes are smoked daily at home, the aOR is 3.61 (95% CI 1.04-12.57). If there are more than four people living in the household, aOR 1.69 (95% CI 1.01-2.85). In children under two years of age, having siblings less than 15 years of age (OR 1.76, 95% CI 0.75-4.17) and attending a day nursery represents a risk for suffering invasive pneumococcal disease (aOR 4.21, 95% CI 1.28-13.83). CONCLUSIONS: Among the variables tested, the modifiable risk factor is smoking; if smoking was reduced at home, the number of cases of invasive disease could be reduced in children, mainly in those under 5 years of age. Identification and vaccination of these risk groups would significantly reduce these diseases." This is weaseling for the sake of propaganda, because vaccination (and also antibiotic treatment as part of prenatal care) would reduce the number of cases, even if no one stopped smoking.

Pereiro et al. - J Infect 2004 abstract / PubMed

Fetal growth, maternal prenatal smoking, and risk of invasive meningococcal disease: a nationwide case-control study. HT Sorensen, R Labouriau, ES Jensen, PB Mortensen, HC Schonheyder. Int J Epidemiol 2004 Aug;33(4):816-820. 462 cases of meningococcal disease hospitalized between 1980 and 1999 and 9240 controls in Denmark. "The adjusted odds ratios (OR) of meningococcal disease associated with low birthweight (<2500 g) varied between 1.6 (95% CI: 1.1, 2.3) in infants <12 months to 1.5 (95% CI: 1.0, 2.3) in children >60 months of age at hospitalization for meningococcal disease. Premature children had an increased risk of meningococcal disease during the first year of life only (adjusted OR = 1.3, 95% CI: 1.1, 1.9). The effect of low birthweight was very similar among mature and premature children. The adjusted OR for maternal smoking was 1.8 (95% CI: 1.4, 2.2). CONCLUSIONS: Low birthweight is associated with an increased risk of meningococcal disease throughout childhood, while an effect of prematurity persists only for 12 months. Maternal prenatal smoking was associated with the risk of meningococcal disease." The leading cause of low birthweight is preterm birth, and the leading cause of preterm birth is chorioamnionitis - which is also also associated with lower socioeconomic class, and which nothing currently being done in the health care system is preventing.

Sorensen et al. - Int J Epidemiol 2004 abstract / PubMed

Risk factors for invasive meningococcal disease in southern Queensland, 2000-2001. BJ McCall, AS Neill, MM Young. Intern Med J 2004 Aug;34(8):464-468. "Univariate analysis found that IMD was associated with sharing bedrooms with two or more people (odds ratio (OR) 4.3; 95% confidence interval (CI) 1.2-17.0, P = 0.01), any exposure to tobacco smoke (smoker or passive exposure; OR 2.3; 95% CI 1.1-4.8, P = 0.02), passive exposure to tobacco smoke (OR 2.4; 95% CI 1.0-5.6, P = 0.03) and recent upper respiratory tract infection (OR 1.9, 95% CI 0.9-4.1, P = 0.06). Children who were breast-fed were less likely to develop IMD (OR 0.3; 95% CI 0.1-1.1, P = 0.04). Attendance at a childcare centre was not associated with an increased risk of IMD. In multivariate analysis, IMD was associated with children under 6 years of age who shared a bedroom with two or more people (OR 7.4; 95% CI 1.5-36.1, P = 0.01) or who had a primary carer who smoked (OR 9.1; 95% CI 2.1-39.9, P = 0.003). DISCUSSION: This is the second Australian study that identifies links between risk of IMD and exposure to cigarette smoke. The risk of IMD in young children could be further reduced if primary caregivers did not smoke. This information may contribute a new perspective to antismoking campaigns." Because the option of antibiotic treatment does not even occur to them, it is clear that manufacturing propaganda for anti-smoking campaigns is in fact the only goal of these worthless quacks.

McCall et al. Intern Med J 2004 abstract / PubMed

Is it exposure to cigarette smoke or to smokers which increases the risk of meningococcal disease in teenagers? PG Coen, J Tully, JM Stuart, D Ashby, RM Viner, R Booy. International Journal of Epidemiology 2006;35(2):330-336. "Passive smoking appears to increase the risk of meningococcal disease (MD) in adolescents. Whether this effect is attributable to exposure to cigarette smoke or contact with smokers is unknown... We conducted a prospective population-based case–control study with age, sex matched-controls in 1:1 matching. Participants were 15–19 year old with MD recruited at hospital admission in six regions (65% of the population of England) from January 1999 through June 2000, and their matched controls. Data on potential risk factors were gathered by confidential interview, including seven passive smoking variables. Factor analysis was performed to assess the dimensionality of the passive smoking exposure variables. The data were analysed with univariate and multivariate conditional logistic regression... 144 case–control pairs were recruited (51% male; median age 17.6). Factor analysis identified two independent factors representing passive smoking (P < 0.01), one associated with ‘exposure to smoke’, the other with ‘smoker contact’. Only smoker contact was a significant risk factor for MD (OR = 1.8; 95% CI 1.0–3.3; P = 0.05). In multivariate analysis this factor was still associated with MD independently of potential confounders such as active smoker status and household crowding. Conclusion Contact with smokers is associated with increased risk of MD in adolescents. This is more likely to be due to higher carriage rates in smokers than to exposure to smoke and emphasizes the importance of public health measures to stop smoking. In epidemiological studies that assess risk from passive smoking, exposure to smoke should be differentiated where possible from contact with smokers." This study actually illustrates how anti-smokers deliberately use deficient measures of exposure in order to falsely blame smoking, but it also fails to observe that the gold standard in real epidemiology is exposure to an infected carrier.

Coen et al. / Int J Epidemiol 2006 abstract

Other Studies

Sporadic meningococcal disease in adults: results of a 5-year population-based study. DS Stephens, RA Hajjeh, WS Baughman, RC Harvey, JD Wenger, MM Farley. Ann Intern Med 1995;123:937-940. Of 44 adult patients (over age 18) in Atlanta, "Twelve of the 15 patients with meningococcal respiratory infection were older than 50 years of age or were immunocompromised (or both), and three fourths of the 15 patients had disease caused by serogroups B, Y, and W-135. Overall, two thirds of adults older than 24 years of age with meningococcal disease had one or more immunocompromising conditions (for example, low complement 50 level [CH50], corticosteroid use, congestive heart failure, multiple myeloma, human immmunodeficiency virus infection)."

Stephens et al. / Ann Intern Med 1995 full article

Neisseria meningitidis: an overview of the carriage state. SP Yazdankhah, DA Caugant. J Med Microbiol 2004 Sep;53(Pt 9):821-932. "While most meningococcal strains recovered from patients belong to a limited number of clonal groups worldwide, strains isolated from carriers comprise numerous genotypes, with only a small proportion of the strains representing invasive clones. During the carriage state, co-colonization with other pathogenic and non-pathogenic bacteria may lead to genetic exchange, which may result in the emergence of new meningococcal clones. The high diversity of meningococcal carrier strains, compared with hypervirulent strains, supports the idea that transmissibility, not invasion, is essential in the life cycle of N. meningitidis... In nonepidemic settings, approximately 10 % of healthy individuals at any time carry N. meningitidis in the upper airway... Rates of transmission and carriage increase in closed and semi-closed populations, such as military recruits, university students and in the household contacts of a case of meningococcal disease... A recent study showed that the carriage rate might be underestimated when using conventional nasopharyngeal swabbing. By using immunohistochemistry for detection of N. meningitidis in patients undergoing tonsillectomy, it was found that meningococci were present in 45 % of the samples, while only 10 % were positive by culture of nasopharyngeal swabs." Patient strains are encapsulated, and capsular proteins are the main targets for mucosal and humoral immunity. However, half of carrier strains are unencapsulated, and capsule production can switch on and off rapidly, enabling them to evade the immune system. "Because of mixed colonization with other bacteria and because of its duration, the carrier state is an ideal condition for horizontal gene transfer between different strains of meningococci, and between meningococci and other commensal bacterial species." A 2003 study in Greece found no strains that were resistant to rifampicin, cefaclor, chloramphenicol, ceftriaxone or ciprofloxacin.

Yazdankhah & Caugant / J Med Microbiol 2004 full article

Factor H-binding protein is important for meningococcal survival in human whole blood and serum, and in the presence of the antimicrobial peptide LL-37. KL Seib, D Serruto, F Oriente, I Delany, J Adu-Bobie, D Veggi, B Aric̣, R Rappuoli, M Pizza. Infect Immun 2009 Jan;77(1):292-299. Binding of factor H (fH), an inhibitor of the complement alternative pathway, to fHBP enables N. meningitidis to evade killing by the innate immune system. Strains with mutant factor H-binding protein survive poorly.

Seib - Infect Immun 2009 abstract / PubMed

Binding of Complement factor H to Neisseria meningitidis is Specific for Human fH and Inhibits Complement Activation by Rat and Rabbit Sera. DM Granoff, JA Welsch, S Ram. Infect Immun 2009 Feb;77(2):764-769. Human fH decreased rat and rabbit C3 deposition on the bacterial surface and decreased group C bactericidal titers, and caused an fH dose-dependent increase in CFU/ml of bacteria in blood of rats.

Granoff / Infect Immun 2009 abstract

Late Repression of NF-κB Activity by Invasive but Not Non-Invasive Meningococcal Isolates Is Required to Display Apoptosis of Epithelial Cells. AE Deghmane, H El Kafsi, D Giorgini, A Abaza, MK Taha. PLoS Pathog 2011 Dec;7(12):e1002403. "Meningococcal invasive isolates of the ST-11 clonal complex are most frequently associated with disease and rarely found in carriers. Unlike carriage isolates, invasive isolates induce apoptosis in epithelial cells through the TNF-α signaling pathway. While invasive and non-invasive isolates are both able to trigger the TLR4/MyD88 pathway in lipooligosaccharide (LOS)-dependant manner, we show that only non-invasive isolates were able to induce sustained NF-κB activity in infected epithelial cells."

Deghmane / PLoS Pathog 2011 full article

Antibiotic Use is Protective

Meningococcal carriage, alcohol consumption, and campus bar patronage in a serogroup C meningococcal disease outbreak. PB Imrey, LA Jackson, PH Ludwinski, AC England 3d, GA Fella, BC Fox, LB Isdale, MW Reeves, JD Wenger. J Clin Microbiol 1995 Dec;33(12):3133-3137. Prevalence of meningococcal carriage of any strain among 85 campus bar workers was 3.8 times that among 867 health center clients; "this prevalence ratio was roughly 2.5 after adjustment for alcohol consumption and bar patronage. Recent antibiotic usage was protective (prevalence odds ratio = 0.3) among health center clients and bar workers." The type of antibiotics used are not specified, and protection would have been higher if they had focused on antibiotics which are effective against N. meningitidis.

Imrey et al. - J Clin Microbiol 1995 full article / PubMed Central
Imrey et al. / J Clin Microbiol 1995 full article (pdf, 6 pp)

Dynamics of meningococcal long-term carriage among university students and their implications for mass vaccination. DAA Ala'Aldeen, KR Neal, K Ait-Tahar, JS Nguyen-Van-Tam, A English, TJ Falla, PM Hawkey, RCB Slack. J Clin Microbiol 2000 Jun;38(6):2311-6. "During freshers week, 2,453 students were screened over 4 consecutive days. The carriage rate rose rapidly in the first week of the term, from 6.9% on day 1, through 11.2% on day 2 and 19% on day 3, to 23.1% on day 4. The average carriage rate in residents of residential halls where shared catering facilities are available during the first week was 13.9%. By November, the carriage rate was 31.0%, and in December it had reached 34.2%. In March, the rate was 28.0%." Several strains switched their serological markers during these months.

Ala'Aldeen et al. - J Clin Microbiol 2000 full article / PubMed Central
Ala'Aldeen et al. / J Clin Microbiol 2000 full article

Study Contradicts Anti-Smoker Dogma

Risk factors for meningococcal disease in university halls of residence. SJ Nelson, A Charlett, HJ Orr, RM Barker, KR Neal, C Taylor, PN Monk, MR Evans, JM Stuart. Epidemiol Infect 2001 Apr;126(2):211-217. "A retrospective ecological study was undertaken to identify social and environmental factors associated with increased incidence of meningococcal disease in university halls of residence. A standardized questionnaire was sent to UK universities and colleges of higher education outside London, for distribution to halls containing at least 50 students. Incidence rate ratios of invasive meningococcal disease were obtained for a range of social and environmental variables. Multi-variable Poisson regression analysis identified 3 factors as having a strong association: a high proportion of first year undergraduate residents (P = 0.0008), decreasing smokiness of the hall bar (P < 0.0001), and opening of hall bar before 1990 (P = 0.0001). The inverse relationship between disease incidence and smokiness of bars was an unexpected finding, and may be due to confounding factors. Universities should continue to promote awareness of meningococcal disease, encourage vaccination of first year students against serogroup C disease, and where appropriate, take measures to reduce overcrowding." Note that they instantly suspect that confounding is to blame for an association between invasive meningococcal disease and "decreasing smokiness of the hall bar," in contrast to their automatic acceptance that smoking is to blame.

Nelson et al. Epidemiol Infect 2001 abstract / PubMed


cast 01-04-12