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.
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 ControlIf 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)."
"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.)
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."
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.
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.
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."
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.
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.
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.
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."
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."
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.
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.
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."
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.
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.
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.
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.
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)."
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.
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.
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.
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 / PubMedcast 04-16-06