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There is a risk of meningitis after neurotrauma and different actions have been taken to reduce this risk. Prophylactic antibiotics are often administered, although at present there is little evidence to support such a regimen. Increasing problems with antibiotic resistance heightens the need for pertinent use of antibiotics.
Even if most of these infections occur early in the course, the risk appears to persist for many years and almost half of the posttraumatic meningitis cases occur after one month. Streptococcus pneumoniae is the most common causative agent and pneumococcal vaccination after neurotrauma is now recommended in several national guidelines. There are, however, no recommendations of when to administer the vaccine. In clinical practice, vaccination is most often performed several weeks after the trauma. Because the risk of meningitis is at the highest shortly after the trauma, vaccination within days would be preferable. Until recently, pneumococcal polysaccharide vaccine (PPSV) was the most common recommendation. During recent years pneumococcal conjugate vaccines (PCV) have been introduced, offering long-term protection and is now recommended in the USA.
Trauma, as well as surgery, activate the innate immune system resulting in, among other things, decreased T-cell function. Patients with injuries of the central nervous system (CNS) may show signs of a specific CNS-injury-induced immune deficiency syndrome (CIDS), which is also characterized by impaired T-cell activity. Accordingly, it can be speculated that ongoing anti-inflammatory response after trauma, here referred to as trauma-induced immune deficiency syndrome (TIDS), and CIDS by impaired T-cell function could negatively affect the response to vaccines, especially to T-cell dependent conjugate vaccines. In the present thesis, focus will be the impact of TIDS and CIDS on the response to T-cell dependent and T-cell independent vaccines.
Vaccination A conjugate vaccine against Haemophilus influenzae type b (Hib) was chosen as the T-cell-dependent antigen. All patients received a single subcutaneous injection of 0.5 ml Act-HIB® (Sanofi Pasteur MSD, Lyon, France) in the upper right arm. A 0.5 ml dose of this vaccine contains 10 μg of Hib polysaccharide conjugated to 24 micrograms of tetanus protein.
All patients also received, at the same time, a single subcutaneous injection of 0.5 ml Pneumovax® (Sanofi Pasteur MSD AB, Lyon, France) (PPSV23) containing 25 μg of purified capsular polysaccharide from each of the 23 serotypes (1, 2, 3, 4, 5, 6B, 7F, 8, 9N, 9V, 10A, 11A, 12F, 14, 15B, 17F, 18C, 19A, 19F, 20, 22F, 23F and 33F) in the upper left arm.
Patients in the NT and NS groups were vaccinated within 10 days after trauma or surgery. Control patients were vaccinated, according to the local routine for pneumococcal vaccination, at least three weeks after trauma or surgery.
Adverse reactions to the vaccine were recorded in the case report form.
Sera collection and analysis Pre-vaccination sera were collected just before vaccination and post-vaccination sera were obtained three and six weeks after vaccination. Samples were stored at -70oC pending analysis. The laboratory was blinded with respect to group assignment of the patients.
IgG antibody concentrations to Hib polysaccharide were determined by enzyme immunoassay which is an established and accredited methodology.
An anti-Hib polysaccharide antibody concentration of 0.15 -1.0 μg/ml has been associated with long-term protection against invasive Hib infection after vaccination of children with Hib polysaccharide vaccine. Based on previous experience in children, a post-vaccination concentration of 10 μg/ml, 10 times the upper supposed protective concentration, was chosen as the target level for a good response to the vaccination in this study.
Serotype-specific anti-polysaccharide binding IgG antibody levels to serotypes 4, 6B, 9V, 14, 18C, 19F and 23F were determined by enzyme immunoassay which is an established and accredited methodology.
A serotype-specific IgG >0.35 μg/ml has been defined as the correlate of protection for invasive disease in infant recipients of (PCV). The true correlate of protection for adults after vaccination with PPSV23 is not known. The value of 1.0 μg/ml was chosen as the target level for a good response to the vaccination in this study.
Allocation: Non-Randomized, Endpoint Classification: Efficacy Study, Intervention Model: Parallel Assignment, Masking: Open Label, Primary Purpose: Prevention
Published on BioPortfolio: 2016-06-20T18:53:21-0400
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A species of gram-negative, aerobic BACTERIA. It is a commensal and pathogen only of humans, and can be carried asymptomatically in the NASOPHARYNX. When found in cerebrospinal fluid it is the causative agent of cerebrospinal meningitis (MENINGITIS, MENINGOCOCCAL). It is also found in venereal discharges and blood. There are at least 13 serogroups based on antigenic differences in the capsular polysaccharides; the ones causing most meningitis infections being A, B, C, Y, and W-135. Each serogroup can be further classified by serotype, serosubtype, and immunotype.
Inflammation of the coverings of the brain and/or spinal cord, which consist of the PIA MATER; ARACHNOID; and DURA MATER. Infections (viral, bacterial, and fungal) are the most common causes of this condition, but subarachnoid hemorrhage (HEMORRHAGES, SUBARACHNOID), chemical irritation (chemical MENINGITIS), granulomatous conditions, neoplastic conditions (CARCINOMATOUS MENINGITIS), and other inflammatory conditions may produce this syndrome. (From Joynt, Clinical Neurology, 1994, Ch24, p6)
Meningitis caused by fungal agents which may occur as OPPORTUNISTIC INFECTIONS or arise in immunocompetent hosts.
A species of ENTEROVIRUS associated with outbreaks of aseptic meningitis (MENINGITIS, ASEPTIC).
A fulminant infection of the meninges and subarachnoid fluid by the bacterium NEISSERIA MENINGITIDIS, producing diffuse inflammation and peri-meningeal venous thromboses. Clinical manifestations include FEVER, nuchal rigidity, SEIZURES, severe HEADACHE, petechial rash, stupor, focal neurologic deficits, HYDROCEPHALUS, and COMA. The organism is usually transmitted via nasopharyngeal secretions and is a leading cause of meningitis in children and young adults. Organisms from Neisseria meningitidis serogroups A, B, C, Y, and W-135 have been reported to cause meningitis. (From Adams et al., Principles of Neurology, 6th ed, pp689-701; Curr Opin Pediatr 1998 Feb;10(1):13-8)
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