Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085437 (bacterial meningitis)
 4,038 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 43-year-old black man had recurrence of acute bacterial meningitis caused by Neisseria meningitidis. He had had three previous episodes of acute meningitis, starting at age 27 years. The patient's serum was found to have an undetectable level of the sixth component of complement. Congenital absence of one of the terminal proteins in the complement system impairs a patient's ability to eradicate bacteria, and increases susceptibility to recurring infections caused by meningococci and other Neisseria species. Though the serum of complement-deficient patients promotes normal opsonization of bacteria, it is unable to kill meningococci directly. The currently available meningococcal vaccine may augment type-specific antibody, but it does not correct the underlying complement deficiency. The role of self-administered antibiotics in preventing recurrent Neisseria infection remains uncertain.
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PMID:Recurrent meningitis in a black man. 291 51

Seventy-seven children with bacterial meningitis were screened for complement deficiency. Both the classical and the alternate pathways were normal in 75 patients. Transiently reduced total haemolytic activity of the classical pathway was documented in a boy with meningococcal meningitis. Total haemolytic activity of both the classical and the alternate pathways were reduced in another patient with pneumococcal meningitis: individual complement components determination indicated predominant activation of the alternate pathway.
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PMID:Screening for complement deficiency in bacterial meningitis. 934 86

Acute bacterial meningitis is a potentially life-threatening infection of the cranial and spinal leptomeninges. Recurrent episodes of meningitis are rarely seen, but when they occur, an extensive investigation has to be made to find out responsible factors. A single episode of acute meningitis may result from bacteriemia, but when followed by recurrent meningitis in pediatric patients, other possible routes of the bacteria invasion to the cerebrospinal fluid (CSF) should be considered. Patients with head injury have the highest risk of acquiring recurrent bacterial meningitis, followed by patients with a congenital anatomic lesion of the skull or duramater, such as meningomyelocele. The underlying cause is a transdural communication between the meningeal space and paranasal sinuses or skin. The first attack of meningitis may occur several weeks to 12 years after the head injury. In addition, recurrent bacterial meningitis may be due to disorders of the immune system, such as complement deficiency. We report a 14-year-old boy, who suffered from recurrent Streptococcus pneumoniae meningitis due to a well-defined defect at the ethmoid roof after a head trauma.
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PMID:Recurrent Streptococcus pneumoniae meningitis in a child with traumatic anterior cranial base defect. 1853 65

Sixty one Tunisian adult patients with bacterial meningitis were screened for complement deficiency. Functional activity of the classical and the alternative pathways of complement (CH50 and AP50 respectively) were measured according to standard haemolytic procedures. Serum concentrations of C3 and C4 were determined by nephelometry. Late complement component (C5-C9) and properdin concentrations were assessed by double-ligand EISA. Complement deficiency was found in eight patients (13%): Seven had late complement component deficiency (three C7 deficiency, two C5 deficiency, one C6 deficiency and one C8 deficiency) and one had partial properdin deficiency. Patients with late complement component deficiency had a mean age of 24 years (range 17-32 years). All deficient patients had meningococcal meningitis. Recurrent meningitis was reported in half of the patients. Our findings demonstrated a high prevalence of complement deficiency in Tunisia suggesting that screening for hereditary complement deficiency should be performed in case of bacterial meningitides and meningococcal disease patients.
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PMID:[Complement protein hereditary deficits during purulent meningitis: study of 61 adult Tunisian patients]. 1938 94