Clinical symptoms of meningitis were first documented during the Bubonic Plague in the Middle Ages. It wasn’t until an outbreak of the disease in 1805 in Geneva, Switzerland that meningitis was first identified. In 1877, the first causative agent, Neisseria Meningitidis, was isolated1.
During the 20th century, meningitis was prevalent during both World Wars, due in large part to the poor living conditions of soldiers. In 1944, the infection was successfully treated for the first time with intravenous and intrathecal penicillin, and by 1950 clinical trials established high doses of intravenous penicillin as the most effective treatment for meningitis1.
First documented on the West Coast of Africa in 1909, meningitis has been a huge burden on the African continent in the last century in the form of cyclical epidemics. The “Meningitis Belt”, a region of Africa hit hardest by the disease, stretches from Senegal and Gambia in the East to Ethiopia and Western Eritrea in the West. This area is home to a population of over 300 million,
and is suffers massive epidemics about every 8-12 years. Such an epidemic usually follows a local outbreak, and can last up to one or two years, marked by periodic waxing and waning of infection levels until an endemic level is again reached.
It is important to define epidemics in relative terms. For example, in Africa, the incidence of infection is 100-800 infected per 100,000. This figure reaches up to 1,000 per 100,000 in some isolated village. In comparison, an epidemic in Finland and Norway in 1974 resulted in a caseload of 15-25 infected per 100,000, a figure that is comparable to endemic rates of meningitis in Africa between cyclical epidemics. The ratio between epidemic and mean endemic rates of infection are higher in developing countries than in developed countries2.
Herd immunity may be the cause of the cyclical nature of epidemics in Africa. Once infected during an epidemic, a person develops humoral immunity to the disease. As more are infected, more develop this immunity, and the rate of infection is slowed until it is no longer at epidemic proportions. After a number of years, this herd immunity wanes, and large-scale infection becomes predominant again.
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Meningitis infects the nasopharyngeal cavity of humans. From there, it is transmitted from person to person via respiratory droplets that emanate from the nasopharynx. Often, the disease is spread by asymptomatic carriers, and is rarely contracted through contact with an infected patient. The incubation period is from 1 to 10 days, with most around 4 days.
The reason for such a high incidence of transmission and infection in the Meningitis Belt may be climate related. The area is characterized by low levels of rainfall (300 to 1,100 mm of rainfall annually) as well as frequent duststorms. These factors can lead to damage to mucosal barriers to infection, directly inhibiting mucosal immune defenses2. Removing this key barrier to meningitis infection drastically increases the danger of contracting the disease.
In the Meningitis Belt, these climate factors are most pronounced in the dry season, so that the incidence of meningitis is highest during that time. In the United States, meningitis cases occur mostly in the winter, peaking at late winter/early spring. This is a result of the necessity of remaining indoors for many at risk populations due to the weather in much of the country.
At risk populations include: the immunosuppressed, such as the elderly and the very young; college students, refugees, and military recruits, who often live in close quarters, facilitating the spread of disease; and those exposed to active and passive tobacco smoke, due to the compromised nature of their nasopharyngeal mucosal surfaces.
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N Meningitidis
N Meningitidis is the only form of bacterial meningitis responsible for epidemic levels of meningitis infection worldwide.
Serogroup A
Serogroup A has been the historically significant cause of meningitis epidemics worldwide. It is frequently responsible for infection in the Meningitis Belt, and has been documented as the cause of explosive epidemics in areas of the world as diverse as Brazil, North American, Finland, Nepal, and Saudi Arabia.
Serogroup B
Serogroup B is associated with sporadic and isolated outbreaks of disease rather than widespread epidemics. Brief spikes in meningitis incidence in Oregon, Cuba, and Norway have been attributed to this serotype.
Serogroup C
Serogroup C, like Serogroup A, is another significant cause of epidemic meningitis. It has been responsible for epidemics in Brazil and Viet Nam, and is notable for its perpetual presence in the Meningitis Belt along with Serogroup A.
H. Influenza
H Influenza is the most important cause of childhood meningitis worldwide, and is responsible for a the most significant number of endemic instances of meningitis. H Influenza type b, or Hib, is the causative agent of virtually all infections resulting from this particular pathogen. Hib causes over 3 million cases of serious disease each year, marked by meningitis and pneumonia, of which at least 300,000 to 700,000 result in death. Treated early, it has a fatality rate of under 10%, but up to 30% of patients who recover suffer residual neurological effects3. It is rarely seen in patients younger than 3 months and older than 6 years, with most patients aged 4-18 months. The disease manifests itself as meningitis in developed countries, and as pneumonia in developing countries. Since the early 1990s, the disease has been all but eradicated from the United States, Australia, Western Europe, New Zealand, and Canada, due to the availability of a safe and effective vaccine. However, the disease still represents a large burden in the developing world, causing hundreds of thousands of needless deaths every year. In fact, up to 15% of children in non-immunized parts of the world harbor Hib particles in their nasopharynxes4.
S Pneumoniae
Death by pneumonococcal infection represents the leading cause of vaccine-preventable fatalities. Around 40% of all adults and children, healthy or otherwise, exhibit colonization of their nasopharyngal cavities by S Pneumoniae without showing symptoms of adverse effects. While new seroptypes emerge constantly, serotypes 6, 14, 18, 19, and 23 account for 60% to 80% of all infections worldwide5. This disease often infects infants ages 6 months to 4 years, as well as the elderly. In fact, almost every child experiences pneumonococcal otitis media, a clinical manifestation of S Pneumoniae, before the age of 5. The recent development of antibiotic-resistance has proven dangerous in terms of stemming epidemics. While antibiotic resistance occured at a rate of less than .02% in 1987, it has now jumped to 3%, with communities within the US reaching 30% and regions of the world experiencing 80% resistance. This resistance has been evidenced in only 10 strains, all of which remain virulent. Virtually all resistant straints are of the serotypes 6A, 6B, 9V, 14, 19A, and 23F5.
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