Epidemiology

Clinical meningococcal disease was described as early as 1805 during an outbreak in Switzerland, however, Neisseria meningitidis was not identified as the causative agent of bacterial meningitis until 1887.[2] The disease probably appeared in northern Africa in the 1880s, however cerebrospinal meningitis has been present in Sudan for much longer. The African continent has been vulnerable to epidemic outbreaks since at least 1909. [2]

Major outbreaks were also observed during World War I and II.[2] Group A Neisseria meningitidis seldom caused epidemics in the temperate regions of the developed world after the Second World War, however, it has continued to wreak havoc in Sub-Saharan Africa. [2] This region experienced approximately 340,000 cases and 53,000 deaths between 1951-1960 alone.[2]

In describing epidemics throughout the world, it is useful to keep in mind the degree of impact a particular incidence may have for a given country.[2] European epidemics have rarely experienced epidemics as large as those in Africa. [2] Therefore, epidemic conditions should be defined as that incidence rate which requires emergency control measures in a given country.[2]

The sub-Saharan region of Africa has been particularly vulnerable to meningococcal epidemics.[2] The "African meningitis belt" extends from Ethiopia in the East, to Senegal in the West.[2] Sporadic infections occur in annual seasonal cycles, however epidemics have been further interspersed and less predictable.[2] Outbreaks have occurred in the meningitis belt every 8-12years (as herd immunity develops) during the past 50 years.[4] These cycles become more brief and irregular since the 1980s, especially in regions with greater person-to-person contact and population reshuffling.[4] No periodicity has been observed in other nations, although the three Norwegian outbreaks occurred in 30-40 year intervals. [4]

In the 1960s, meningitis was still considered a permanent public health problem in tropical zones but was no longer thought to be a threat in Europe and North America.[4] However, epidemics have continued to occurr throughout the world since the 1970s.[4] Several countries in North and South America, Asia, and Europe experienced recurrent epidemics and persistent, sporadic infection. Epidemics again spread throughout India, Nepal, and Africa in the 1980s[4]. The wave in the African continent extended beyond the meningitis belt to West Africa.[4] The movement of the disease outside its traditional boundaries could reflect any number of changes in climate, increasingly mobile populations (either voluntary movement or refugee displacement), or the introduction of new strains into susceptible populations.[4]The Eastern Mediterranean region of Africa experienced a meningococcal epidemic in 1988 after the return of pilgrims in 1987[4] Outbreaks have reduced since the early 1990s, after some countries began vaccinating high-risk groups[4]

Over 80% of bacterial meningitis can be traced to three disease causing agents: Neisseria meningitidis, Streptococcus pneumoniae and Hemophilus influenzae type b (Hyperlink).[4] Before the 1990s, H. influenzae was the predominant disease causing agent in the United States, accounting for 45% of cases, with an incidence of 2.9 cases per 100,000 population.[6] In the past few years, however, with the development of the new conjugate vaccine to H. influenzae, the incidence of disease has dropped from 421 cases per 100,000 population to less that 0.7 per 100,000 population.[6] Today in the US, the most common cause of meningitis is S. pneumoniae, accounting for 30-50% of the disease, with an incidence of 0.6-1.2 per 100,000 population.[6] N. meningitidis follows next, accounting for 15-40% of the cases, with an incidence of 0.5-1 per 100,000 population.[6] Neisseria Meningitidis has three serogoups: A, B and C. Serogroup A is the major cause of epidemic meningococcal disease all over the world. Serogroup B and serogroup C cause systemic disease. Disease due to the infectious agents is age specific. Table 1. gives an overview of the age dependence on cause of bacterial meningitis.

Bacteria	No. of cases
*Neisseria meningitidis*	10-30% in adults 30-40% in children up to age of 15 very rare in infants
*Streptococcus pneumoniae*	30-50% in adults 10-20% in children up to 5% in infants
*Hemophilus Influenzae*	1-3% in adults 35-45% in children rare in infants

Meningococcal disease can be categorized into two forms of disease: endemic disease and epidemic disease.[4]The major cause of endemic disease is the menigococcus, Neisseria meningitidis, a Gram- negative bacteria. The endemic disease manifests itself in small clusters or sporadically. The incidence of endemic meningococcal disease range from 1 to 5 per 100000 population in Europe and North America.[4] In developing countries the incidence rates varies from <10 to >20 per 100,000 population.[4] Cerebrospinal meningitis or meningococcal meningitis caused by Neisseria meningitidis is the only disease that occurs in epidemic form. In developing countries, most often epidemic disease is indistinguishable from endemic disease because of the lack of adequate laboratory resources to clearly diagnose the disease. Thus meningococcal meningitis is grouped with the other endemic forms of bacterial meningitis. In addition to the epidemic cases, at least 1.2 million other cases of bacterial meningitis are reported, 135,000 of them being fatal.[4] Under non-epidemic conditions children are more prone to bacterial meningitis, and 50-60% of cases occur in children between 3 months to 5 years of age. [4] In countries within the meningitis belt, children between the ages of 5-10 are most susceptible to the disease.[4]

Meningococcal meningitis requires person-to-person contact. It is spread efficiently when the respiratory droplets of the infected person are spread to other individuals. Common routes of transmission are:

Humans presenting with meningococcal meningitis are the predominant carriers of the organisms. [2] Asymptomatic individuals who carry the organism in the nasopharynx are the second most common reservoir.[2] The infection begins when the bacteria colonize the nasopharynx. The organisms have pilli on their surface to assist in adhering to nasopharyngeal mucosal receptors. [6] Upon colonization; the organism infects neighboring tissues, and ultimately makes its way into the blood stream. [6] After entering the bloodstream, the organism successfully penetrates the blood-brain barrier and invades the subarachnoid space.[6] The host is unable to clear the infection because of the relatively low levels of complement activity and antibodies in the cerebrospinal fluid.[6] Most people present symptoms by three to four days.[7]

Patients may experience a severe, sudden headache, fever, a stiff neck or back, nausea and vomiting, and possibly a rash.[8]

50-60% of adult and adolescent patients will present with signs of swelling such as hypertension and bradycadia.[8]

Patients may develop neurological symptoms such as lethargy, delirium, coma, or convulsions.[8]

About 75% of patients experience petechial or purpuric (hyperlink) rashes that range from tiny, reddish-purple spots to bruise-like marks.⁸ Usually these rashes are found on the armpits, groin, and ankles.[8]

Infants may present with a bulging fontanelle (soft spot), fever, irritability, vomiting, or lethargy.[2]

Elderly patients may or may not demonstrate signs of inflammation such as fever, but may experience an altered level of consciousness and experience confusion or notice that senses have become less acute.[8]

10-20% of those individuals infected with N. meningitidis will develop septicemia.[9]

Septicemic patients progress rapidly, approximately 30% die because of they responded poorly to antibiotics.[9]

balanced diet, adequate rest and sleep, exercise, low stress (all help to maintain a strong immune system) [8]

avoidance of upper respiratory tract illnesses and cigarette smoke inhalation [8]

establishment of emergency preparation and response committee to monitor and respond to rising levels of infection [2]

public education about early symptoms/dispelling misconceptions regarding transmission [2]

policy guidelines for use of vaccine- preparation to ensure timely protection [4]

simplified treatment protocols due to potential shortages, logistical difficulties, and high incidence [2]