Meningococcal disease

Neisseria meningitidis colonises a substantial proportion of the general population harmlessly, but in a very small percentage of individuals it can invade the bloodstream, affecting the entire body, most notably limbs and brain, causing serious illness.

DIC can cause ischemic tissue damage when upstream thrombi obstruct blood flow and hemorrhage because clotting factors are exhausted.

In meningococcal meningitis this is caused by the bacteria invading the cerebrospinal fluid and circulating through the central nervous system.

Sub-Saharan Africa, the Americas, Western Europe, the UK, and Ireland still face many challenges combating this disease.

[citation needed] The patient with meningococcal meningitis typically presents with high fever, nuchal rigidity (stiff neck), Kernig's sign, severe headache, vomiting, purpura, photophobia, and sometimes chills, altered mental status, or seizures.

Anyone with symptoms of meningococcal meningitis should receive intravenous antibiotics prior to the results of lumbar puncture being known, as delay in treatment can greatly worsen the prognosis.

Typically, the first symptoms include fever, nausea, myalgia, headache, arthralgia, chills, diarrhea, stiff neck, and malaise.

Later symptoms include septic shock, purpura, hypotension, cyanosis, petechiae, seizures, anxiety, and multiple organ dysfunction syndrome.

Infected fluid from the meninges then passes into the spinal cord, causing symptoms including stiff neck, fever and rashes.

[citation needed] Even with antibiotics, approximately 1 in 10 people who have meningococcal meningitis will die; however, about as many survivors of the disease lose a limb or their hearing, or experience permanent brain damage.

It takes up to several days for the toxin to be neutralized from the body by using continuous liquid treatment and antibiotic therapy.

Twelve serogroups (strains) exist, with six having the potential to cause a major epidemic - A, B, C, X, Y and W135 are responsible for virtually all cases of the disease in humans.

Laboratory personnel and medical staff are at risk of exposure to N. meningitides or to patients with meningococcal disease.

Hospital Infection Control Practices Advisory Committee (HICPAC) recommendations regarding immunization of health-care workers that routine vaccination of health-care personnel is recommended, Any individual 11–55 years of age who wishes to reduce their risk of meningococcal disease may receive meningitis A, C, Y and W-135 vaccines and those older than 55 years of age.

Under certain circumstances if unvaccinated health-care personnel cannot get vaccinated and who have intensive contact with oropharyngeal secretions of infected patients and who do not use proper precautions should receive anti-infective prophylaxis against meningococcal infection (i.e., 2-day regimen of oral rifampicin or a single dose of IM ceftriaxone or a single dose of oral ciprofloxacin).

[citation needed] Travelers to or residents of areas where N. meningitidis is highly endemic or epidemic are at risk of exposure should receive primary immunization against meningococcal disease.

Because the meningococcal organism is transmitted by respiratory droplets and is susceptible to drying, it has been postulated that close contact is necessary for transmission.

Meningitis occurs sporadically throughout the year, and since the organism has no known reservoir outside of man, asymptomatic carriers are usually the source of transmission.

[27] Additionally, basic hygiene measures, such as handwashing and not sharing drinking cups, can reduce the incidence of infection by limiting exposure.

[39][40] An updated 2013 Cochrane review investigated the effectiveness of different antibiotics for prophylaxis against meningococcal disease and eradication of N. meningitidis particularly in people at risk of being carriers.

During follow up no cases of meningococcal disease were reported and thus true antibiotic preventative measures could not be directly assessed.

Early complications include: raised intracranial pressure, disseminated intravascular coagulation, seizures, circulatory collapse and organ failure.

Later complications are: deafness, blindness, lasting neurological deficits, reduced IQ, and gangrene leading to amputations.

It may be that climate change[44] contributes significantly the spread of the disease in Benin, Burkina Faso, Cameroon, the Central African Republic, Chad, Côte d'Ivoire, the Democratic Republic of the Congo, Ethiopia, Ghana, Mali, Niger, Nigeria and Togo.

[45] Further complicating efforts to halt the spread of meningitis in Africa is the fact that extremely dry, dusty weather conditions which characterize Niger and Burkina Faso from December to June favor the development of epidemics.

IRIN Africa news has been providing the number of deaths for each country since 1995,[46][47][48][49] and a mass vaccination campaign following a community outbreak of meningococcal disease in Florida was done by the CDC.

[51] From the Greek meninx (membrane) + kokkos (berry), meningococcal disease was first described by Gaspard Vieusseux during an outbreak in Geneva in 1805.

In 1884, Italian pathologists Ettore Marchiafava and Angelo Celli described intracellular micrococci in cerebrospinal fluid, and in 1887, Anton Wiechselbaum identified the meningococcus (designated as Diplococcus intracellularis meningitidis) in cerebrospinal fluid and established the connection between the organism and epidemic meningitis.

Charlotte Cleverley-Bisman , who had all four limbs partially amputated aged seven months due to meningococcal disease. [ 42 ]
The distribution of meningococcal meningitis in the African meningitis belt