Spread Of Meningococcal Disease Research Articles

Meningococcal Disease in International Travel: Vaccine Strategies

International travel and migration facilitate the rapid intercontinental spread of meningococcal disease. Serogroup A, and to a lesser extent serogroup C, have been responsible for pandemics in the past (mainly in Africa), but in recent years there was an international outbreak due to W135 related to the Hajj pilgrimage. The high carriage rates, persistence and transmissibility, in combination with the high case fatality rate of the Hajj-associated W135 outbreak clone, certainly raise considerable concern about the public health consequences of widespread dissemination of this organism and the potential for future epidemics. Indeed, the now evolving W135 epidemic in Africa mandates that the bivalent meningococcal vaccine should be replaced by the tetravalent meningococcal vaccine, covering A, C, Y and W135 serogroups. The currently available polysaccharide tetravalent meningococcal vaccine, albeit associated with high seroconversion and efficacy rates, has several shortcomings: it is not immunogenic in young children, duration of protective immunity is short, and it has minimal or no effect on nasopharyngeal carriage and therefore transmission of the organism. Immunogenicity of polysaccharide vaccines can be improved by chemical conjugation to a protein carrier, thereby eliciting a T-cell-dependent antibody response. In contrast to polysaccharide vaccines, conjugate vaccines are immunogenic in young infants, induce long-term protection, and reduce nasopharyngeal carriage. The tetravalent conjugate vaccine will be a leap forward in the control of meningococcal epidemics in affected countries. It will also boost the uptake of meningococcal vaccines in travelers, because the duration of protection is longer and it eliminates the problem of immune hyporesponsiveness of serogroup C with repeated dosing. The small risk of travel-associated disease for the general traveler and the unpredictable nature of epidemics make it difficult to provide evidence-based vaccine recommendations. The current recommendation is to vaccinate all Hajj pilgrims, travelers to areas with current outbreaks, travelers to the sub-Saharan meningitis belt, and high-risk individuals (i.e., those with immunodeficiencies).

Emergency or routine vaccination against meningococcal disease in Africa?

The spread of meningococcal disease in sub-Saharan Africa, which extends from Senegal to Ethiopia, has already affected thousands of people in the region and is urgently in need of an intervention. The meningococcal epidemic in Africa is usually caused by serogroup A and sweeps over the region within several weeks; it then disappears and reappears 5-10 years later. Although vaccination against serogroup A and C meningococci may have its limitations, it is still capable of eliminating the disease. In Ghana, the Ministry of Health launched a vaccination campaign which covered 72% of the population and prevented 23% of cases and 18% of deaths. A simple method of identifying an impending epidemic followed by the development of various vaccination strategies is necessary among less developed countries. WHO recommends that emergency vaccination be implemented, while continuous and improved surveillance systems must be used to confront the epidemic. In conclusion, this paper suggests that the meningococcal disease in sub-Saharan Africa would be better dealt with by well organized campaigns rather than by repeated vaccinations of the entire population.

Outbreak of serogroup C meningococcal disease associated with campus bar patronage.

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. A case-control investigation with 20 controls per case, oropharyngeal carriage surveys, and multilocus enzyme electrophoresis (MEE) of serogroup C isolates were used to identify factors contributing to the outbreak. All eight sterile-site isolates from cases were closely related by MEE and were similar (though not identical) to the strain associated with the 1991-1992 epidemic of meningococcal disease in eastern Canada. 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. Some cases in this outbreak may have followed transmission of the epidemic strain in bar A. Campus bar environments may facilitate the spread of meningococcal disease among teenagers and young adults.

Use of single-dose ofloxacin to eradicate tonsillopharyngeal carriage of Neisseria meningitidis

After an outbreak of three cases of serogroup B meningococcal disease at a Norwegian college, 84 of 392 (21%) subjects were tonsillopharyngeal carriers of Neisseria meningitidis. To eradicate meningococcal carriage, 80 volunteers received a single dose of 400 mg of ofloxacin. Three days after treatment, all 75 evaluable volunteers were culture negative for N. meningitidis, and after 7 days none carried the strain that they carried initially, as judged by DNA fingerprinting. A single dose of ofloxacin was found to be 97.2% effective in eradicating carriage of N. meningitidis for a period of 33 days. The carriage acquisition rate among treated students was four times higher than that among nontreated noncarriers (P = 0.02). After ofloxacin treatment, no case of meningococcal disease occurred for 6 months. Ofloxacin may thus prevent the outbreak and spread of meningococcal disease.

Preventing meningococcal infection

Meningococcal disease continues to kill small children and young adults. The disease is usually sporadic, but in England and Wales about 4 people each year still catch the disease from another documented case or a carrier, usually in the same house. Household contacts are 144 times more likely to suffer the disease than the general population,1 even though most are now given chemoprophylaxis. Contacts are at greatest risk of catching the disease in the first week after diagnosis of the index case but remain at risk for several months.1 How should chemoprophylaxis and vaccination be used to prevent the spread of meningococcal disease?

Multilocus Enzyme Electrophoresis – Application to the Study of Meningococcal Meningitis and Listeriosis

Multilocus Enzyme Electrophoresis – Application to the Study of Meningococcal Meningitis and Listeriosis

Prevention of Infection with Neisseria meningitidis and Haemophilus influenzae Type b

MENINGOCOCCAL DISEASE Background Since the first description by Vieusseux in 1805 of an epidemic of "cerebrospinal fever," physicians have been aware of the potential for spread of meningococcal disease. Numerous studies of military recruits in the United States documented conclusively nasopharyngeal acquisition of Neisseria meningitidis during the course of their basic training. In the military setting, attack rates as high as 46% have been reported for exposed susceptible individuals. In the United States, endemic meningococcal disease occurs in 3,000 to 5,000 persons yearly. Secondary cases occur with a frequency of 0.4% in the first month following disease in the index case. The risk to household contacts is approximately 2.2/1,000/yr; this risk is greatest in the week after the onset of illness in the index case but remains in excess of the endemic disease rate for at least 1 month. The risk of secondary meningococcal disease in household contacts (adults and children) of an index case is 1,000 times greater than that for the population as a whole. Carriage Versus Invasive Disease Household contacts, day care center contacts, and bunk mates (military installations) of an index case frequently are noted to have an increased rate of carriage of N meningitidis in the nasopharynx. It has been noted repeatedly that when the carriage rate of N meningitidis is high, invasive disease is more likely to occur.