Meningitis epidemic hits Burkina Faso and Chad
* Meningococcal meningitis is a bacterial form of meningitis, a serious infection of the thin lining that surrounds the brain and spinal cord.
* The meningitis belt of sub-Saharan Africa, stretching from Senegal in the west to Ethiopia in the east, has the highest rates of the disease.
* In the 2009 epidemic season, 14 African countries implementing enhanced surveillance that reported a total of 78 416 suspected cases, including 4053 deaths, the largest number since the 1996 epidemic.
* Meningococcal polysaccharide vaccines are available to control the disease.
* A new meningococcal conjugate A vaccine developed specifically for Africa should be available by the end of 2010.
Meningococcal meningitis is a bacterial form of meningitis, a serious infection of the meninges that affects the brain membrane. It can cause severe brain damage and is fatal in 50% of cases if untreated.
Several different bacteria can cause meningitis. Neisseria meningitidis is the one with the potential to cause large epidemics. Meningococcal disease was first described in 1805 when an outbreak swept through Geneva, Switzerland. The causative agent, Neisseria meningitidis (the meningococcus) was identified in 1887.
Twelve serogroups of N. meningitidis have been identified, five of which (A, B, C, W135, and X) can cause epidemics. Geographic distribution and epidemic capabilities differ according to the serogroup.
The bacteria are transmitted from person to person through droplets of respiratory or throat secretions. Close and prolonged contact – such as kissing, sneezing or coughing on someone, or living in close quarters (such as a dormitory, sharing eating or drinking utensils) with an infected person – facilitates the spread of the disease. The average incubation period is four days, but can range between two and 10 days.
N. meningitidis only infects humans; there is no animal reservoir. The bacteria can be carried in the throat and sometimes, for reasons not fully understood, can overwhelm the body's defenses allowing infection to spread through the bloodstream to the brain. Although there remains gaps in our knowledge, it is believed that 10% to 20% of the population carries N. meningitidis at any given time. However, the carriage rate may be higher in epidemic situations.
The most common symptoms are a stiff neck, high fever, sensitivity to light, confusion, headaches and vomiting. Even when the disease is diagnosed early and adequate treatment is started, 5% to 10% of patients die, typically within 24 to 48 hours after the onset of symptoms. Bacterial meningitis may result in brain damage, hearing loss or a learning disability in 10% to 20% of survivors. A less common but even more severe (often fatal) form of meningococcal disease is meningococcal septicaemia, which is characterized by a hemorrhagic rash and rapid circulatory collapse.
Initial diagnosis of meningococcal meningitis can be made by clinical examination followed by a lumbar puncture showing a purulent spinal fluid. The bacteria can sometimes be seen in microscopic examinations of the spinal fluid. The diagnosis is supported or confirmed by growing the bacteria from specimens of spinal fluid or blood, by agglutination tests or by polymerase chain reaction (PCR). The identification of the serogroups and susceptibility testing to antibodies are important to define control measures.
Meningococcal disease is potentially fatal and should always be viewed as a medical emergency. Admission to a hospital or health centre is necessary, although isolation of the patient is not necessary. Appropriate antibiotic treatment must be started as soon as possible, ideally after the lumbar puncture has been carried out if such a puncture can be performed immediately. If treatment is started prior to the lumbar puncture it may be difficult to grow the bacteria from the spinal fluid and confirm the diagnosis.
A range of antibiotics can treat the infection, including penicillin, ampicillin, chloramphenicol and ceftriaxone. Under epidemic conditions in Africa in areas with limited health infrastructure and resources, oily chloramphenicol or ceftriaxone are the drugs of choice because a single dose has been shown to be effective on meningococcal meningitis.
There are three types of vaccines available.
* Polysaccharide vaccines have been available to prevent the disease for over 30 years. Meningococcal polysaccharide vaccines are available either bivalent (groups A and C), trivalent (groups A, C and W), or tetravalent (groups A, C, Y and W135) to control the disease.
* For serogroup B, polysaccharide vaccines cannot be developed, due to antigenic mimicry with polysaccharide in human neurologic tissues. Consequently, vaccine against B developed in Norway, in Cuba and Netherlands are outer membrane proteins (OMP).
* Since 1999, meningococcal conjugate vaccines against group C have been available and widely used. A tetravalent A, C, Y and W135 conjugate vaccine has recently been licensed for use in children and adults in the United States and Canada. In 2001, a partnership was created between WHO and PATH to eliminate epidemic meningitis in Africa, through the development of an affordable meningococcal A conjugate vaccine. The Men A vaccine will be manufactured by Serum Institute of India (SIIL) and it is expected to be available by the end of 2010. Unlike polysaccharide vaccines, conjugate vaccines are more immunogenic, particularly for children under two years of age and provide longer immunity.
All of these vaccines have been proven to be safe and effective with infrequent and mild side effects. The vaccines may not provide protection until 10 to 14 days have elapsed following injection.
Meningococcal meningitis occurs in small clusters throughout the world with seasonal variation and accounts for a variable proportion of epidemic bacterial meningitis.
The largest burden of meningococcal disease occurs in an area of sub-Saharan Africa known as the meningitis belt, which stretches from Senegal in the west to Ethiopia in the east. During the dry season between December to June, dust winds, cold nights and upper respiratory tract infections combine to damage the nasopharyngeal mucosa, increasing the risk of meningococcal disease. At the same time, transmission of N. meningitidis may be facilitated by overcrowded housing and by large population displacements at the regional level due to pilgrimages and traditional markets. This combination of factors explains the large epidemics which occur during the dry season in the meningitis belt.
Due to herd immunity (whereby transmission is blocked when a critical percentage of the population has been vaccinated or in contact with the bacteria), and other reasons only poorly understood, these epidemics occur in a pluri-annual cyclic mode.
Global public health response
WHO promotes a two-pronged strategy comprising epidemic preparedness and epidemic response. Preparedness focuses on surveillance, from case detection and investigation and laboratory confirmation. This implies strengthening surveillance and laboratory capacity for early detection of epidemics, establishing national and sub-regional stocks of vaccine and developing or updating national plans for epidemic management (including preparedness, contingency and response). WHO regularly provides technical support at the field level to countries facing epidemics.
Epidemic response consists of prompt and appropriate case management with oily chloramphenicol or ceftriaxone and reactive mass vaccination of epidemic districts. It is estimated that a mass reactive immunization campaign, when promptly implemented, can prevent up to 70% of cases.
Meningitis epidemics in the African meningitis belt constitute an enormous public health burden. WHO is committed to eliminating meningococcal disease as a public health problem and ensuring routine health services are able to control sporadic cases in the shortest possible time. The availability and affordability of conjugate vaccines is essential if this goal is to be reached.