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Meningococcal Disease: Causes, Phases, Prevention Research Paper

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Updated: Apr 22nd, 2022

Introduction

Meningococcal disease is a communicable bacterial disease which is attributable to the meningococcus strain (Neisseria meningitidis) and can cause death if not treated immediately. Meningococcal bacteria exist in several serogroups which include W-135, A, B, C, and Y. The disease is spread through person-to-person contact especially if a person inhales the respiratory droplets of an infected person. It is a major cause of illness, death as well as disability in developed and developing countries across the world. The disabilities may include mental retardation, speech disorders, paralysis, deafness, as well as, loss of limbs. It exists in three clinical forms which include pneumonia, meningeal syndrome, and septic form.

Most susceptible population group

Young children especially those aged five years and below are the most vulnerable to the disease. However, it is also common in older children as well as young adults. Young children are the ones who are most at risk due to their waning immunity. It largely affects the individual who lives in high endemic areas or those whose immunity has been waned by other diseases such as HIV/AIDS.

Cause of Meningococcal disease

The bacteria Neisseria meningitidis resides in the mucosal membrane of the throat as well as the nose, although it does not cause any harm at this point. The World Health Organization (2011) believes that about 5-10% of the world’s population is likely to be asymptomatic carriers. However, in some people, the bacteria may cause the disease by spreading through the bloodstream and therefore causing blood poisoning. The bacteria may also move to the brain, and as a result, cause meningitis. The reasons that cause the bacteria to spread to these parts of the body and cause the disease have not been established. It is these carriers who are significant in the spread of the disease since most infections occur through exposure to asymptomatic carriers. The bacteria spread from person to person through throat secretions as well as respiratory droplets. This happens when an infected person coughs, sneezes, or shares a drinking vessel with a non-infected individual. Climatic factors such as dry seasons as well as dust storms increase its epidemics. One social factor which facilitates its spread is overcrowding which could result from living in an overcrowded house. Meningococcal disease infection is normally introduced into a household through an asymptomatic carrier who is a member of the household. The carriage then spreads to other household members who had not been infected especially children whose immunity to strain the bacteria is still low. The personal characteristic of an individual may also increase the likelihood of infection or severity to an individual. These include concomitant respiratory infections as well as mucosal lesions on the individual. Smoking may also increase the risk of infection or the development of the disease.

The phases of meningococcal disease process

Meningococcal disease occurs as a result of malfunctioning human host defenses. A person’s genetic variation to susceptibility increases the chances of the progression of the disease or the risk of being infected. Thus, abnormalities during gene variation may increase the likelihood of being infected as well as progression to disease.

In the subclinical stages of the disease, haemorrhagic rash, which is normally a feature of meningococcal septicaemia may not be present (Apicella, 2000). In the initial stages, the rash is likely to blanch with pressure. The rash resembles a viral exanthem.

In the clinical stages of the disease, the rash may appear on any part of the body; the palms, as well as soles, are not left out in this case. Initially, purpuric or petechial rash of about 1-2mm in diameter lesions appears (Apicella, 2000). This progresses outwards to produce larger ecchymotic lesions which normally appear in clusters. In children, clinical features could include high temperature, haemorrhagic rash, altered mental state, meningeal irritation, and the unwillingness to make eye contact or to interact.

Antibiotic therapy should begin immediately for those suspected or identified to be infected by the disease. Benzylpenicillin or ceftriaxone is administered to those suspected to be infected as an immediate treatment before being transferred to the hospital or within 30 minutes of their arrival at the hospital (Commonwealth of Australia, 2001). This is done before cerebrospinal fluid as well as blood specimens are taken so as to lower the amount of positive cerebrospinal fluid cultures or blood.

After the initial assessment and administration of antibiotic, a triage nurse has to assess the patient to determine the possibility of meningococcal disease. The presence of petechial or maculopapular rash is used to in early diagnosis of the disease (Commonwealth of Australia, 2001). Diagnostic tests should include blood and throat swab tests as well as serological studies. Others include acid-base balance, electrolyte, and chest x-rays (Commonwealth of Australia, 2001).

The therapy for the disease after Neisseria meningitidis has been identified involves continued administration of benzylpenicillin or the available recommended antibiotic as a sole antibiotic until the therapy is completed (Commonwealth of Australia, 2001). This should be continued for a minimum of three days. When the individual is being discharged from the hospital, a summary discharge which contains details of the prognosis as well as the follow-up needed is sent to the patient’s general practitioner. If found that the patient’s recovery process has no complications, then, he or she is released under the care of the general practitioner. The clinical recovery process is considered successful if no seizures are experienced by the patient (Commonwealth of Australia, 2001).

Some patients may survive death but acquire brain injury, experience seizures, suffer deafness or be amputated. In such cases, the recovery process involves planned, together with, specialised follow-up arrangements during discharge from hospital. However, in case the person infected by the disease does not receive early treatment or an effective antibiotic therapy, then the person may die.

Primary prevention

Primary prevention measures to curb the spread of the disease include practicing basic hygiene measures like avoiding sharing of drinking cups or vessels as well as hand washing to limit exposure to Neisseria meningitidis, and as a result, reduce its infection. Other measures include covering mouth or nose when coughing or sneezing to reduce the likelihood of spreading the bacteria (New Zealand Ministry of Health, 2011).

Whenever it is confirmed that an individual is already infected with the disease, all those who are normally in close contact with the person should be given antibiotics or chemoprophylaxis to reduce the likelihood of the disease spread to other people (Greenwood & Wali, 1980).

Secondary prevention

Prevention of meningococcal disease can be best achieved through vaccination against Neisseria meningitidis. W-135, A, B, C and Y serogroups are nearly responsible for all infection cases of the disease although vaccine against the B serogroup is still being developed. There are several vaccines which can be used to protect individuals against the rest of the strains of meningococcal disease. The lowest age for which an individual is supposed to receive the initial dose of meningococcal vaccine as well as the interval for vaccine doses varies depending on the type of vaccine used.

Children below two years of age can be vaccinated using conjugate meningococcal C vaccines. Children below 12 months have to be given three doses of the vaccine while those above 12 months should only receive one dose of the vaccine (New Zealand Ministry of Health, 2011). According to the American Academy of Pediatrics Committee on Infectious Diseases (2005) children aged 2-10 years are at high risk of being infected by the meningococcal disease and may develop certain chronic conditions of the disease when they travel to or live in hyperendemic areas or countries, and therefore, need to receive primary vaccination.

Prevention programs should also be extended to children above 10 years and younger adults who may be at risk of being infected by the disease. Meningitis W-135, A, C, and Y vaccines should be provided to all children aged 11-12 years as well as adolescents who have not received the vaccination by age 15. Conjugate meningococcal vaccines as well as polysaccharide vaccines can be used to vaccinate adolescents in this age bracket. These vaccines can also be used to immunize adults who live in endemic areas or those planning to move to such areas. Secondary school students and college students who live in dormitories have to receive primary immunization using Meningitis W-135, A, C and Y vaccines since they are at high risk for meningococcal disease. Military recruits who are normally housed together in single units should also receive routine immunization to protect them from being infected by the disease. This also applies to tourists who are planning to travel to countries where Neisseria meningitidis is highly endemic. The American Academy of Pediatrics Committee on Infectious Diseases (2005) reports that both conjugate meningococcal vaccines and polysaccharide vaccines can be used to immunize adults below age 55 years. However, polysaccharide vaccines are not appropriate for adults above age 55 years.

Persons infected with HIV are at high risk for meningococcal disease. It is therefore important to provide primary immunization for such individuals against meningococcal disease (Centers for Disease Control and Prevention, 1997). Meningitis W-135, A, C, and Y vaccines should be provided to HIV-infected individuals aged 11-55 years by immunizing them using the conjugate meningococcal vaccine to reduce their risk to infection.

Conclusion

Meningococcal disease is communicable and can easily spread from person to person through sneezes, coughs or sharing of drinking vessels. This means that basic hygiene measures should be adopted to control its spread. However, immunization using conjugate meningococcal and polysaccharide vaccines remains the most appropriate ways for preventing the spread of the disease.

Reference List

American Academy of Pediatrics Committee on Infectious Diseases. (2005). Policy statement on the prevention and control of meningococcal disease: recommendations for use of meningococcal vaccines in pediatric patients. Pediatrics, 116: 496-505

Apicella, M. A. (2000). Neisseria Meningitidis. In Bennett, J. E., Dolin, R. D, & Mandell, G. L. eds. Principles and Practice of Infectious Diseases, 5th Edition. Churchill Livingstone, 2: 2228-2241.

Centers for Disease Control and Prevention. (1997). Immunization of health-care workers: recommendations of the Advisory Committee on Immunization Practices (ACIP) and the Hospital Infection Control Practices Advisory Committee (HICPAC). MMWR Morb Mortality Weekly Report, 46(18):1-42

Commonwealth of Australia. (2001). Guidelines for the early clinical and public health management of meningococcal disease in Australia. Canberra: Commonwealth Department of Health and Aged Care.

Greenwood, B. M., & Wali, S. S. (1980). Control of meningococcal infection in the African meningitis belt by selective vaccination. Lancet, 1: 729-732.

New Zealand Ministry of Health. (2011). Immunisation: Diseases and vaccines. Web.

World Health Organization. (2011). Global alert and response (GAR): Meningococcal disease. Web.

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